FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Gach, J
Venzon, D
Monica, V
Brandon, K
Franchini, G
Forthal, D
AF Gach, Johannes
Venzon, David
Monica, Vaccari
Brandon, Keele
Franchini, Genoveffa
Forthal, Donald
TI Vaccine-induced Antibody that Captures but Does Not Neutralize SIVmac251
Increases the Rate of Infection after Low-dose, Repeated Rectal
Challenge
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Gach, Johannes; Forthal, Donald] Univ Calif Irvine, Irvine, CA USA.
[Venzon, David; Monica, Vaccari; Franchini, Genoveffa] NCI, Bethesda, MD 20892 USA.
[Brandon, Keele] Leidos Biomed Res Inc, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA OA14.02
BP 75
EP 75
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600129
ER
PT J
AU Huang, Y
Tomaras, G
Andersen-Nissen, E
Dintwe, O
Morris, L
Grunenberg, N
Issacs, A
DiazGranados, C
Sinangil, F
Laher, F
Swann, E
DeRosa, S
Ferrari, G
Montefiori, D
Gilbert, P
McElrath, J
Corey, L
Gray, G
AF Huang, Ying
Tomaras, Georgia
Andersen-Nissen, Erica
Dintwe, One
Morris, Lynn
Grunenberg, Nicole
Issacs, Abby
DiazGranados, Carlos
Sinangil, Faruk
Laher, Fatima
Swann, Edith
DeRosa, Stephen
Ferrari, Guido
Montefiori, David
Gilbert, Peter
McElrath, Julie
Corey, Lawrence
Gray, Glenda
CA HVTN097
TI The Relationship between Immune Responses to Tetanus Vaccine, Hepatitis
B Vaccine and a Pox-protein HIV Vaccine Regimen
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Huang, Ying; Andersen-Nissen, Erica; Grunenberg, Nicole; Issacs, Abby; DeRosa, Stephen; Gilbert, Peter; McElrath, Julie; Corey, Lawrence] Fred Hutchinson Canc Res Ctr, 1124 Columbia St, Seattle, WA 98104 USA.
[Tomaras, Georgia; Ferrari, Guido; Montefiori, David] Duke Univ, Med Ctr, Durham, NC 27706 USA.
[Andersen-Nissen, Erica] Hutchinson Ctr Res Inst South Africa, Cape Town, South Africa.
[Dintwe, One] Univ Cape Town, Rondebosch, South Africa.
[Morris, Lynn] Univ KwaZulu Natal, Durban, South Africa.
[Morris, Lynn; Laher, Fatima; Gray, Glenda] Univ Witwatersrand, ZA-2050 Johannesburg, South Africa.
[DiazGranados, Carlos] Sanofi Pasteur, Swiftwater, PA USA.
[Sinangil, Faruk] Global Solut Infect Dis, Princeton, NJ USA.
[Swann, Edith] NIAID, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Gray, Glenda] South African Med Res Council, Tygerberg, South Africa.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA OA14.04
BP 76
EP 76
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600131
ER
PT J
AU Janes, H
Cohen, K
Sobieszczyk, M
Frahm, N
Karuna, S
Sanchez, B
Magaret, C
Adams, E
Hammer, S
Gilbert, P
McElrath, J
AF Janes, Holly
Cohen, Kristen
Sobieszczyk, Magda
Frahm, Nicole
Karuna, Shelly
Sanchez, Brittany
Magaret, Craig
Adams, Elizabeth
Hammer, Scott
Gilbert, Peter
McElrath, Juliana
TI Vaccine-induced CD8+T Cell Immunity Strongly Predicts Lower HIV
Infection Risk in HVTN 505
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Janes, Holly; Cohen, Kristen; Frahm, Nicole; Karuna, Shelly; Sanchez, Brittany; Magaret, Craig; Gilbert, Peter; McElrath, Juliana] Fred Hutchinson Canc Res Ctr, 1124 Columbia St, Seattle, WA 98104 USA.
[Sobieszczyk, Magda; Hammer, Scott] Columbia Univ, Med Ctr, New York, NY 10027 USA.
[Adams, Elizabeth] NIAID, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA OA17.03
BP 85
EP 85
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600148
ER
PT J
AU Parsons, M
Lloyd, S
Center, R
Swiderek, K
LaBranche, C
Montefiori, D
Keele, B
Lifson, J
Venturi, V
Davenport, M
Amarasena, T
Kent, S
AF Parsons, Matthew
Lloyd, Sarah
Center, Robert
Swiderek, Katherine
LaBranche, Celia
Montefiori, David
Keele, Brandon
Lifson, Jeffrey
Venturi, Vanessa
Davenport, Miles
Amarasena, Thakshila
Kent, Stephen
TI Partial Efficacy of a Broadly Neutralizing Antibody against
Cell-associated SHIV Infection
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Parsons, Matthew; Lloyd, Sarah; Amarasena, Thakshila; Kent, Stephen] Univ Melbourne, Melbourne, Vic 3010, Australia.
[Center, Robert] Burnet Inst, Melbourne, Vic, Australia.
[Swiderek, Katherine] Theraclone, Seattle, WA USA.
[LaBranche, Celia; Montefiori, David] Duke Univ, Durham, NC 27706 USA.
[Keele, Brandon; Lifson, Jeffrey] NCI, Bethesda, MD 20892 USA.
[Venturi, Vanessa; Davenport, Miles] UNSW, Sydney, NSW, Australia.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA OA19.02
BP 90
EP 90
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600159
ER
PT J
AU Steinhardt, J
Guenaga, J
Mckee, K
Louder, M
O'Dell, S
Chiang, CI
Lei, L
Doria-Rose, N
Mascola, J
Li, YX
AF Steinhardt, James
Guenaga, Javier
McKee, Krisha
Louder, Mark
O'Dell, Sijy
Chiang, Chi-I
Lei, Lin
Doria-Rose, Nicole
Mascola, John
Li, Yuxing
TI Rational Design of Bispecific Antibodies Targeting HIV-1 Env to Achieve
Enhanced Anti-viral Potency and Breadth
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Steinhardt, James; Chiang, Chi-I; Lei, Lin; Li, Yuxing] Inst Biosci & Biotechnol Res, Rockville, MD USA.
[Guenaga, Javier] Scripps Res Inst, IAVI Neutralizing Antibody Ctr, San Diego, CA USA.
[McKee, Krisha; Louder, Mark; O'Dell, Sijy; Doria-Rose, Nicole; Mascola, John] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA OA19.01
BP 90
EP 90
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600158
ER
PT J
AU Hessell, AJ
Jaworski, JP
Pandey, S
Kahl, C
Reed, J
Sutton, WF
Stanton, JJ
Pegu, A
Chen, XJ
Axthelm, MK
Lewis, A
Graham, BS
Mascola, JR
Sacha, JB
Haigwood, NL
AF Hessell, Ann J.
Jaworski, J. Pablo
Pandey, Shilpi
Kahl, Christoph
Reed, Jason
Sutton, William F.
Stanton, Jeffrey J.
Pegu, Amarendra
Chen, Xuejun
Axthelm, Michael K.
Lewis, Anne
Graham, Barney S.
Mascola, John R.
Sacha, Jonah B.
Haigwood, Nancy L.
CA Passive Immunotherapy
TI Durable Marked Attenuation and Clearance of SHIV Infection in Infant
Macaques with Human Neutralizing mAbs as Post-exposure Treatment Within
48 Hours
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Hessell, Ann J.; Jaworski, J. Pablo; Pandey, Shilpi; Kahl, Christoph; Sutton, William F.; Stanton, Jeffrey J.; Axthelm, Michael K.; Lewis, Anne; Sacha, Jonah B.; Haigwood, Nancy L.] Oregon Hlth & Sci Univ, Oregon Natl Primate Res Ctr, Portland, OR 97201 USA.
[Hessell, Ann J.; Reed, Jason; Axthelm, Michael K.; Sacha, Jonah B.; Haigwood, Nancy L.] Oregon Hlth & Sci Univ, Vaccine & Gene Therapy Inst, Portland, OR 97201 USA.
[Pegu, Amarendra; Chen, Xuejun; Graham, Barney S.; Mascola, John R.] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA OA19.03
BP 91
EP 91
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600160
ER
PT J
AU Lynch, R
Madden, P
Boritz, E
Coates, E
Dezure, A
Koup, R
Graham, B
Douek, D
Ledgerwood, J
Mascola, J
AF Lynch, Rebecca
Madden, Patrick
Boritz, Eli
Coates, Emily
Dezure, Adam
Koup, Richard
Graham, Barney
Douek, Daniel
Ledgerwood, Julie
Mascola, John
CA VRC 601 Study Team
TI Virus Fitness after Infusion with Broadly Neutralizing Antibody VRC01
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Lynch, Rebecca] George Washington Univ, Washington, DC 20052 USA.
[Lynch, Rebecca; Madden, Patrick; Boritz, Eli; Coates, Emily; Dezure, Adam; Koup, Richard; Graham, Barney; Douek, Daniel; Ledgerwood, Julie; Mascola, John] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA OA19.04
BP 91
EP 91
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600161
ER
PT J
AU Astronomo, RD
Lemos, MP
Narpala, S
Czartoski, J
Westerberg, K
Fleming, L
Gross, M
Hural, J
Tieu, HV
Baden, L
Rodriguez, B
Hammer, S
Frank, I
Ochsenbauer, C
Grunenberg, N
Ledgerwood, JE
McDermott, A
Mayer, K
McElrath, MJ
AF Astronomo, Rena D.
Lemos, Maria P.
Narpala, Sandeep
Czartoski, Julie
Westerberg, Katharine
Fleming, Lamar
Gross, Mary
Hural, John
Hong Van Tieu
Baden, Lindsey
Rodriguez, Benigno
Hammer, Scott
Frank, Ian
Ochsenbauer, Christina
Grunenberg, Nicole
Ledgerwood, Julie E.
McDermott, Adrian
Mayer, Kenneth
McElrath, M. Juliana
TI Rectal and Vaginal Biopsies from Men and Women Infused Intravenously
with VRC01 Show Protection in Ex Vivo HIV-1 Challenge
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Astronomo, Rena D.; Lemos, Maria P.; Czartoski, Julie; Westerberg, Katharine; Fleming, Lamar; Gross, Mary; Hural, John; Grunenberg, Nicole; McElrath, M. Juliana] Fred Hutchinson Canc Res Ctr, 1124 Columbia St, Seattle, WA 98104 USA.
[Narpala, Sandeep; Ledgerwood, Julie E.; McDermott, Adrian] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Hong Van Tieu] New York Blood Ctr, New York, NY 10021 USA.
[Baden, Lindsey] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Rodriguez, Benigno] Case Western Reserve Univ, Cleveland, OH 44106 USA.
[Hammer, Scott] Columbia Univ, Med Ctr, New York, NY 10027 USA.
[Frank, Ian] Univ Penn, Philadelphia, PA 19104 USA.
[Ochsenbauer, Christina] Univ Alabama Birmingham, Birmingham, AL USA.
[Mayer, Kenneth] Fenway Hlth, Boston, MA USA.
[Mayer, Kenneth] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Mayer, Kenneth] Harvard Med Sch, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA OA19.05
BP 92
EP 92
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600162
ER
PT J
AU Carballo-Dieguez, A
Balan, IC
Giguere, R
Dolezal, C
Leu, CS
Brown, W
Ho, T
Tuswa-Haynes, C
Lama, J
Piper, J
Richardson, B
McGowan, I
Cranston, RD
AF Carballo-Dieguez, Alex
Balan, Ivan C.
Giguere, Rebecca
Dolezal, Curtis
Leu, Cheng-Shiun
Brown, William, III
Ho, Titcha
Tuswa-Haynes, Camagu
Lama, Javier
Piper, Jeanna
Richardson, Barbra
McGowan, Ian
Cranston, Ross D.
CA MTN-017 Protocol Team
TI High Levels of Adherence to a Rectal Microbicide Gel and to Oral PrEP
Achieved in MTN-017
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Carballo-Dieguez, Alex; Balan, Ivan C.; Giguere, Rebecca; Dolezal, Curtis; Leu, Cheng-Shiun; Brown, William, III; Ho, Titcha; Tuswa-Haynes, Camagu] New York State Psychiat Inst & Hosp, HIV Ctr Clin & Behav Studies, New York, NY 10032 USA.
[Carballo-Dieguez, Alex; Balan, Ivan C.; Giguere, Rebecca; Dolezal, Curtis; Leu, Cheng-Shiun; Brown, William, III; Ho, Titcha; Tuswa-Haynes, Camagu] Columbia Univ, New York, NY 10027 USA.
[Lama, Javier] Asociac Civil Impacta Salud & Educ, Lima, Peru.
[Piper, Jeanna] NIAID, Div AIDS, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Richardson, Barbra] Univ Washington, Sch Publ Hlth & Community Med, Seattle, WA 98195 USA.
[McGowan, Ian; Cranston, Ross D.] Univ Pittsburgh, Pittsburgh, PA 15260 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA OA20.01
BP 93
EP 93
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600164
ER
PT J
AU Palanee-Phillips, T
Roberts, S
Montgomery, E
Reddy, K
Govender, V
Naidoo, L
Siva, S
Gaffoor, Z
Pather, A
Kiweewa, FM
Hlahla, K
Makinini, B
Bunge, K
Schwartz, K
Torjesen, K
Brown, E
Soto-Torres, L
Baeten, J
AF Palanee-Phillips, Thesla
Roberts, Sarah
Montgomery, Elizabeth
Reddy, Krishnaveni
Govender, Vaneshree
Naidoo, Logashvari
Siva, Samantha
Gaffoor, Zakir
Pather, Arendevi
Kiweewa, Flavia Matovo
Hlahla, Kudzai
Makinini, Bonus
Bunge, Katie
Schwartz, Katie
Torjesen, Kristine
Brown, Elizabeth
Soto-Torres, Lydia
Baeten, Jared
CA ASPIRE Study Team
TI Frequency of Partner-related Social Harms and their Impact on Adherence
to the Dapivirine Vaginal Ring during the MTN020/ASPIRE HIV Prevention
Trial
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Palanee-Phillips, Thesla; Reddy, Krishnaveni] Wits Reprod Hlth & HIV Inst, Johannesburg, South Africa.
[Roberts, Sarah; Baeten, Jared] Univ Washington, Seattle, WA 98195 USA.
[Montgomery, Elizabeth] RTI Int, Womens Global Hlth Imperat, Res Triangle Pk, NC USA.
[Govender, Vaneshree; Naidoo, Logashvari; Siva, Samantha; Gaffoor, Zakir; Pather, Arendevi] MRC, Tygerberg, South Africa.
[Kiweewa, Flavia Matovo] MU JHU Res Collaborat, Kampala, Uganda.
[Hlahla, Kudzai] UC UCSF Collaborat Res Programme, Harare, Zimbabwe.
[Makinini, Bonus] John Hopkins Univ Res Project, Coll Med, Blantyre, Malawi.
[Bunge, Katie] Univ Pittsburgh, Pittsburgh, PA 15260 USA.
[Schwartz, Katie; Torjesen, Kristine] FHI 360, Durham, NC USA.
[Brown, Elizabeth] FHCRC SCHARP, Seattle, WA USA.
[Soto-Torres, Lydia] NIAID, Div AIDS, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA OA20.03
BP 94
EP 94
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600166
ER
PT J
AU Husnik, MJ
Brown, ER
Marzinke, M
Livant, E
Palanee-Phillips, T
Hendrix, C
Kiweewa, FM
Nair, G
Soto-Torres, LE
Schwartz, K
Hillier, SL
Baeten, JM
AF Husnik, Marla J.
Brown, Elizabeth R.
Marzinke, Mark
Livant, Edward
Palanee-Phillips, Thesla
Hendrix, Craig
Kiweewa, Flavia Matovu
Nair, Gonasagrie
Soto-Torres, Lydia E.
Schwartz, Katie
Hillier, Sharon L.
Baeten, Jared M.
TI Novel Implementation of a Real-time Adherence Monitoring Strategy within
a Phase III, Blinded, Placebo-Controlled, HIV-1 Prevention Clinical
Trial
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Husnik, Marla J.; Brown, Elizabeth R.] Fred Hutchinson Canc Res Ctr, 1124 Columbia St, Seattle, WA 98104 USA.
[Marzinke, Mark; Hendrix, Craig] Johns Hopkins Univ, Baltimore, MD 21218 USA.
[Livant, Edward] Magee Womens Res Inst & Fdn, Pittsburgh, PA USA.
[Palanee-Phillips, Thesla] Univ Witwatersrand, ZA-2050 Johannesburg, South Africa.
[Kiweewa, Flavia Matovu] MUJHU Res Collaborat, Kampala, Uganda.
[Nair, Gonasagrie] Ctr AIDS Programme Res South Africa, Durban, South Africa.
[Soto-Torres, Lydia E.] NIH, Bldg 10, Bethesda, MD 20892 USA.
[Schwartz, Katie] FHI 360, Durham, NC USA.
[Hillier, Sharon L.] Univ Pittsburgh, Pittsburgh, PA 15260 USA.
[Baeten, Jared M.] Univ Washington, Seattle, WA 98195 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA OA20.05
BP 95
EP 95
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600168
ER
PT J
AU Kwong, PD
Stewart-Jones, GBE
Xu, K
Zhou, TQ
AF Kwong, Peter D.
Stewart-Jones, Guillaume B. E.
Xu, Kai
Zhou, Tongqing
TI Targeted Deglycosylation as a Means of Vaccine Focusing
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Kwong, Peter D.; Stewart-Jones, Guillaume B. E.; Xu, Kai; Zhou, Tongqing] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA OA21.02
BP 96
EP 96
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600171
ER
PT J
AU Chen, XJ
Duan, HY
Cheng, C
Boyington, J
Tian, M
Cheng, KL
Wang, LS
Zhang, Y
Frederick, A
Mascola, J
AF Chen, Xuejun
Duan, Hongying
Cheng, Cheng
Boyington, Jeffery
Tian, Ming
Cheng, Kwei-Ling
Wang, Lingshu
Zhang, Yi
Frederick, Alt
Mascola, John
TI Glycan-masking Improves the CD4bs-specificity of Antibodies Elicited by
eOD-GT8 60mer
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Chen, Xuejun; Duan, Hongying; Cheng, Cheng; Boyington, Jeffery; Wang, Lingshu; Zhang, Yi; Mascola, John] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD USA.
[Tian, Ming; Cheng, Kwei-Ling; Frederick, Alt] Harvard Med Sch, Boston, MA USA.
[Tian, Ming; Cheng, Kwei-Ling; Frederick, Alt] Childrens Hosp, 300 Longwood Ave, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA OA21.06LB
BP 98
EP 98
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600175
ER
PT J
AU Xu, K
Zhou, TQ
Mascola, JR
Kwong, PD
AF Xu, Kai
Zhou, Tongqing
Mascola, John R.
Kwong, Peter D.
TI Development of a Soluble HIV-1 Env Trimer Immunogen Stabilized in the
Pre-fusion Closed State from Strain CH505
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Xu, Kai; Zhou, Tongqing; Mascola, John R.; Kwong, Peter D.] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA OA21.05
BP 98
EP 98
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600174
ER
PT J
AU Huang, J
Kang, B
Ishida, E
Griesman, T
Wheatley, AK
Khurana, S
Narpala, SR
McDermott, AB
Poole, A
Bailer, RT
Koup, RA
Alexander, J
Smith, J
Migueles, SA
Golding, H
Wohlbold, TJ
Chromikova, V
Krammer, F
Gurwith, M
Connors, M
AF Huang, Jinghe
Kang, Byong
Ishida, Elise
Griesman, Trevor
Wheatley, Adam K.
Khurana, Surender
Narpala, Sandeep R.
McDermott, Adrian B.
Poole, April
Bailer, Robert T.
Koup, Richard A.
Alexander, Jeffrey
Smith, Jonathan
Migueles, Stephen A.
Golding, Hana
Wohlbold, Teddy John
Chromikova, Veronika
Krammer, Florian
Gurwith, Marc
Connors, Mark
TI Upper Respiratory Tract (URT) Administration of a Replication Competent
Ad4-H5-Vtn Vaccine Induces Durable Neutralizing Antibody Responses in
Humans
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Huang, Jinghe; Kang, Byong; Ishida, Elise; Griesman, Trevor; Poole, April; Migueles, Stephen A.; Connors, Mark] NIAID, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Wheatley, Adam K.; Narpala, Sandeep R.; McDermott, Adrian B.; Bailer, Robert T.; Koup, Richard A.] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Khurana, Surender; Golding, Hana] US FDA, Rockville, MD 20857 USA.
[Alexander, Jeffrey; Smith, Jonathan; Gurwith, Marc] PaxVax Inc, San Diego, CA USA.
[Wohlbold, Teddy John; Chromikova, Veronika; Krammer, Florian] Icahn Sch Med Mt Sinai, New York, NY 10029 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA OA22.05
BP 101
EP 101
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600180
ER
PT J
AU Hural, J
Metch, B
Grunenberg, N
Allen, M
Coombs, R
Dragavon, J
Puren, A
Singh, B
Maenza, J
AF Hural, John
Metch, Barbara
Grunenberg, Nicole
Allen, Mary
Coombs, Robert
Dragavon, Joan
Puren, Adrian
Singh, Beverly
Maenza, Janine
TI HIV Vaccine Trials Network (HVTN) 910: Long-term Follow-up of HIV
Vaccine-induced Seropositivity (VISP) among HIV Vaccinees
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Hural, John; Metch, Barbara; Grunenberg, Nicole] Fred Hutchinson Canc Res Ctr, HIV Vaccine Trials Network, Vaccine & Infect Dis Div, 1124 Columbia St, Seattle, WA 98104 USA.
[Allen, Mary] NIAID, Div Aids, NIH, Bethesda, MD 20892 USA.
[Coombs, Robert; Dragavon, Joan; Maenza, Janine] Univ Washington, Seattle, WA 98195 USA.
[Puren, Adrian; Singh, Beverly] NICD, NHLS, Johannesburg, South Africa.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA OA22.06
BP 101
EP 101
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600181
ER
PT J
AU Richardson, SI
Lambson, BL
Scheepers, C
Bhiman, JN
Garrett, N
Abdool-Karim, S
Carrington, M
Moore, PL
Mkhize, NN
Morris, L
AF Richardson, Simone Irene
Lambson, Bronwen L.
Scheepers, Cathrine
Bhiman, Jinal N.
Garrett, Nigel
Abdool-Karim, Salim
Carrington, Mary
Moore, Penny L.
Mkhize, Nonhlanhla N.
Morris, Lynn
TI Enhanced Effector Functionality of a V2 Broadly Neutralizing Antibody
with a Novel IgG3 Fc Allotype
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Richardson, Simone Irene; Lambson, Bronwen L.; Scheepers, Cathrine; Bhiman, Jinal N.; Moore, Penny L.; Mkhize, Nonhlanhla N.; Morris, Lynn] Natl Inst Communicable Dis, Ctr HIV & STIs, Johannesburg, South Africa.
[Richardson, Simone Irene; Lambson, Bronwen L.; Scheepers, Cathrine; Bhiman, Jinal N.; Moore, Penny L.; Mkhize, Nonhlanhla N.; Morris, Lynn] Univ Witwatersrand, Fac Hlth Sci, Johannesburg, South Africa.
[Garrett, Nigel; Abdool-Karim, Salim; Moore, Penny L.] Univ KwaZulu Natal, CAPRISA, Durban, South Africa.
[Carrington, Mary] Ragon Inst MGH MIT & Harvard, Cambridge, MA USA.
[Carrington, Mary] Frederick Natl Lab Canc Res, Leidos Biomed Res Inc, Canc & Inflammat Program, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA PD02.05LB
BP 113
EP 113
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600203
ER
PT J
AU Chakrabarti, BK
Boliar, S
Shukla, B
Ghobeh, A
Chen, WZ
Patil, S
Guenaga, J
Dimitrov, D
Wyatt, R
AF Chakrabarti, Bimal K.
Boliar, Saikat
Shukla, Brihaspati
Ghobeh, Ali
Chen Weizao
Patil, Shilpa
Guenaga, Javier
Dimitrov, Dimiter
Wyatt, Richard
TI Direct Access to the Co-receptor Binding Site in Virus Is Dependent on
Mass of the Inhibitory Molecule and the Length of Variable Loops, V1/V2
of Env
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Chakrabarti, Bimal K.; Boliar, Saikat; Shukla, Brihaspati; Patil, Shilpa] THSTI, Faridabad, Haryana, India.
[Ghobeh, Ali; Guenaga, Javier; Wyatt, Richard] IAVI, New York, NY USA.
[Chen Weizao; Dimitrov, Dimiter] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA PD05.02
BP 120
EP 120
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600214
ER
PT J
AU DeKosky, BJ
Normandin, E
Cheng, C
Duan, HY
Chen, XJ
Kong, R
Ransier, A
Darko, S
Tian, M
Cheng, HL
Menis, S
Kwong, PD
Douek, DC
Schief, WR
Alt, FW
Mascola, JR
AF DeKosky, Brandon J.
Normandin, Erica
Cheng, Cheng
Duan, Hongying
Chen, Xuejun
Kong, Rui
Ransier, Amy
Darko, Sam
Tian, Ming
Cheng, Hwei-Ling
Menis, Sergey
Kwong, Peter D.
Douek, Daniel C.
Schief, William R.
Alt, Frederick W.
Mascola, John R.
TI High-throughput Paired Heavy: Light Antibody Sequencing Enables Genetic
Analyses of Broadly Neutralizing Antibody Lineage Development
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [DeKosky, Brandon J.; Normandin, Erica; Cheng, Cheng; Duan, Hongying; Chen, Xuejun; Kong, Rui; Ransier, Amy; Darko, Sam; Kwong, Peter D.; Douek, Daniel C.; Mascola, John R.] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Tian, Ming; Cheng, Hwei-Ling; Alt, Frederick W.] Boston Children s Hosp, HHMI, Boston, MA USA.
[Menis, Sergey; Schief, William R.] Scripps Res Inst, IAVI, La Jolla, CA 92037 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA PD05.03
BP 121
EP 121
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600215
ER
PT J
AU Shen, CH
Soto, C
Stewart-Jones, GB
Lemmin, T
Kwong, PD
AF Shen, Chen-Hsiang
Soto, Cinque
Stewart-Jones, Guillaume B.
Lemmin, Thomas
Kwong, Peter D.
TI N-linked Glycan Taxonomy and the HIV-1 Glycan Shield
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Shen, Chen-Hsiang; Soto, Cinque; Kwong, Peter D.] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Stewart-Jones, Guillaume B.] Univ Oxford, Oxford, England.
[Lemmin, Thomas] Univ Calif San Francisco, San Francisco, CA 94143 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA PD05.04
BP 121
EP 121
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600216
ER
PT J
AU Asokan, M
Pegu, A
Gorman, J
Doria-Rose, N
Ko, SY
Schmidt, S
Narpala, S
Del Prete, G
Chen, XJ
Choe, M
Li, H
Todd, JP
Hatziiannou, T
McDermott, A
Koup, R
Keele, B
Shaw, G
Lifson, J
Kwong, P
Mascola, J
AF Asokan, Mangaiarkarasi
Pegu, Amarendra
Gorman, Jason
Doria-Rose, Nicole
Ko, Sung-Youl
Schmidt, Stephen
Narpala, Sandeep
Del Prete, Gregory
Chen, Xuejun
Choe, Misook
Li, Hui
Todd, John-Paul
Hatziiannou, Theodora
McDermott, Adrian
Koup, Richard
Keele, Brandon
Shaw, George
Lifson, Jeffrey
Kwong, Peter
Mascola, John
TI Construction and Characterization of Chimeric SHIVs Displaying V1V2
Epitopes that Bind Germline Precursors of Broadly Neutralizing Human
Antibodies
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Asokan, Mangaiarkarasi; Pegu, Amarendra; Gorman, Jason; Doria-Rose, Nicole; Ko, Sung-Youl; Schmidt, Stephen; Narpala, Sandeep; Chen, Xuejun; Choe, Misook; Todd, John-Paul; McDermott, Adrian; Koup, Richard; Kwong, Peter; Mascola, John] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Del Prete, Gregory; Keele, Brandon; Lifson, Jeffrey] NCI, ACVP, Leidos Biomed Inc, NIH, Bethesda, MD 20892 USA.
[Li, Hui; Shaw, George] Perelman Sch Med, Philadelphia, PA USA.
[Hatziiannou, Theodora] Aaron Diamond AIDS Res Ctr, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA PD06.01LB
BP 123
EP 123
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600217
ER
PT J
AU Yacoob, C
Pancera, M
Vigdorovich, V
Oliver, BG
Sather, DN
Glenn, J
Feng, JL
McGuire, AT
Stamatatos, L
AF Yacoob, Christina
Pancera, Marie
Vigdorovich, Vladimir
Oliver, Brian G.
Sather, D. Noah
Glenn, Jolene
Feng, Junli
McGuire, Andrew T.
Stamatatos, Leonidas
TI Interactions of Germline VRC01-Class Antibodies with HIV-1 Env: The Role
of CDRH3
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Yacoob, Christina; Pancera, Marie; Glenn, Jolene; Feng, Junli; McGuire, Andrew T.; Stamatatos, Leonidas] Fred Hutchinson Canc Res Ctr, 1124 Columbia St, Seattle, WA 98104 USA.
NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Vigdorovich, Vladimir; Oliver, Brian G.; Sather, D. Noah] Ctr Infect Dis Res, Bethesda, MD USA.
Univ Washington, Seattle, WA 98195 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA PD06.02LB
BP 123
EP 123
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600218
ER
PT J
AU Duan, HY
Tian, M
Cheng, C
Chen, XJ
Cheng, HL
Dekosky, BJ
Joyce, MG
Dao, M
Kimble, M
Lin, S
Du, Z
Chen, YW
Chen, YM
Cantor, E
Huang, PY
Jain, S
Schief, WR
Haynes, BF
Alt, FW
Mascola, JR
AF Duan, Hongying
Tian, Ming
Cheng, Cheng
Chen, Xuejun
Cheng, Hwei-Ling
Dekosky, Brandon J.
Joyce, M. Gordon
Dao, Mai
Kimble, Michael
Lin, Sherry
Du, Zhou
Chen, Yiwei
Chen, Yimin
Cantor, Elizabeth
Huang, Pei-Yi
Jain, Suvi
Schief, William R.
Haynes, Barton F.
Alt, Frederick W.
Mascola, John R.
TI Selective Activation of VRC01-class Germline Antibodies in Knock-in Mice
with Diverse Precursor Repertoires
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Duan, Hongying; Cheng, Cheng; Chen, Xuejun; Dekosky, Brandon J.; Joyce, M. Gordon; Mascola, John R.] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Tian, Ming; Cheng, Hwei-Ling; Dao, Mai; Kimble, Michael; Lin, Sherry; Du, Zhou; Chen, Yiwei; Chen, Yimin; Cantor, Elizabeth; Huang, Pei-Yi; Jain, Suvi; Alt, Frederick W.] Harvard Med Sch, Boston Childrens Hosp, Boston, MA USA.
[Schief, William R.] Scripps Res Inst, La Jolla, CA 92037 USA.
[Haynes, Barton F.] Duke Human Vaccine Inst, Durham, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA PD06.03LB
BP 124
EP 124
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600219
ER
PT J
AU Soumana, D
Pancera, M
Chen, GY
Soto, C
Kwong, PD
AF Soumana, Djade
Pancera, Marie
Chen, Gwo-Yu
Soto, Cinque
Kwong, Peter D.
TI Structural Characterization of HIV-1 Entry Inhibitors
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Soumana, Djade; Pancera, Marie; Chen, Gwo-Yu; Soto, Cinque; Kwong, Peter D.] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA PD08.02
BP 128
EP 128
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600227
ER
PT J
AU Francis, JN
Nishimura, Y
Smith, A
Welch, B
Martin, M
Kay, M
AF Francis, J. Nicholas
Nishimura, Yoshiaki
Smith, Amanda
Welch, Brett
Martin, Malcolm
Kay, Michael
TI Preclinical Characterization of a Potent D-peptide Inhibitor of HIV
Entry: Cholesterol-conjugated PIE12-trimer
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Francis, J. Nicholas; Welch, Brett; Kay, Michael] Navigen, Salt Lake City, UT USA.
[Francis, J. Nicholas; Smith, Amanda; Welch, Brett; Kay, Michael] Univ Utah, Salt Lake City, UT 84112 USA.
[Nishimura, Yoshiaki; Martin, Malcolm] NIAID, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA PD08.04LB
BP 129
EP 129
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600229
ER
PT J
AU Mason, R
Biris, K
Doria-Rose, N
Welles, H
Nguyen, R
O'Dell, S
Bailer, R
Mascola, J
Roederer, M
AF Mason, Rosemarie
Biris, Kristin
Doria-Rose, Nicole
Welles, Hugh
Nguyen, Richard
O'Dell, Sijy
Bailer, Robert
Mascola, John
Roederer, Mario
TI Next Generation SIV Broadly Neutralizing Antibodies Mediate Complete
Neutralization of SIVmac239
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Mason, Rosemarie; Biris, Kristin; Doria-Rose, Nicole; Welles, Hugh; Nguyen, Richard; O'Dell, Sijy; Bailer, Robert; Mascola, John; Roederer, Mario] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA PD08.05LB
BP 130
EP 130
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600230
ER
PT J
AU Lee, A
Donofrio, G
Dussupt, V
Kong, R
Georgiev, I
Doria-Rose, N
Slike, B
Grande, R
Bryson, M
Mascola, J
Robb, M
Polonis, V
Michael, N
Krebs, S
AF Lee, Anna
Donofrio, Gina
Dussupt, Vincent
Kong, Rui
Georgiev, Ivelin
Doria-Rose, Nicole
Slike, Bonnie
Grande, Rebecca
Bryson, Mary
Mascola, John
Robb, Merlin
Polonis, Victoria
Michael, Nelson
Krebs, Shelly
TI Isolation of HIV Specific Monoclonal Antibodies Using a Combined
Antigen-specific and B Cell Culture Supernatant Method
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Lee, Anna; Donofrio, Gina; Dussupt, Vincent; Slike, Bonnie; Grande, Rebecca; Bryson, Mary; Robb, Merlin; Polonis, Victoria; Michael, Nelson; Krebs, Shelly] Walter Reed Army Inst Res, US Mil HIV Res Program, Washington, DC USA.
[Lee, Anna; Donofrio, Gina; Dussupt, Vincent; Slike, Bonnie; Grande, Rebecca; Bryson, Mary; Robb, Merlin; Krebs, Shelly] Henry M Jackson Fdn Adv Mil Med, Bethesda, MD USA.
[Kong, Rui; Doria-Rose, Nicole; Mascola, John] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Georgiev, Ivelin] Vanderbilt Univ, 221 Kirkland Hall, Nashville, TN 37235 USA.
NR 0
TC 0
Z9 0
U1 3
U2 3
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P01.01
BP 132
EP 132
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600231
ER
PT J
AU Cale, E
Gorman, J
Radakovich, N
Crooks, E
Osawa, K
Ozorowski, G
Asokan, M
Doria-Rose, N
Ward, A
Kwong, P
Mascola, J
Binley, J
AF Cale, Evan
Gorman, Jason
Radakovich, Nathan
Crooks, Ema
Osawa, Keiko
Ozorowski, Gabriel
Asokan, Mangai
Doria-Rose, Nicole
Ward, Andrew
Kwong, Peter
Mascola, John
Binley, James
TI A Broadly Neutralizing HIV-1 Antibody with a Non-projecting CDRH3 Loop
Engages the V1V2 Apex of Native Envelope Glycoprotein Trimers
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Cale, Evan; Gorman, Jason; Radakovich, Nathan; Asokan, Mangai; Doria-Rose, Nicole; Kwong, Peter; Mascola, John] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Crooks, Ema; Osawa, Keiko; Binley, James] San Diego Biomed Res Inst, San Diego, CA USA.
[Ozorowski, Gabriel; Ward, Andrew] Scripps Res Inst, La Jolla, CA 92037 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P01.07
BP 135
EP 135
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600237
ER
PT J
AU Gorman, J
Geng, H
Joyce, MG
Zhou, TQ
Kwong, PD
AF Gorman, Jason
Geng, Hui
Joyce, M. Gordon
Zhou, Tongqing
Kwong, Peter D.
TI Combining Env Trimer Engagement with Germline V1V2-and CD4bs-directed
Antibodies
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Gorman, Jason; Geng, Hui; Joyce, M. Gordon; Zhou, Tongqing; Kwong, Peter D.] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P01.09
BP 136
EP 136
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600239
ER
PT J
AU Duerr, R
Soni, S
Banin, A
Tuen, M
Courtney, C
Nanfack, A
Mayr, L
Redd, A
Ding, SL
Finzi, A
Meli, J
Ngai, J
Kong, XP
Gorny, MK
Nyambi, P
AF Duerr, Ralf
Soni, Sonal
Banin, Andrew
Tuen, Michael
Courtney, Colleen
Nanfack, Aubin
Mayr, Luzia
Redd, Andrew
Ding, Shilei
Finzi, Andres
Meli, Josephine
Ngai, Johnson
Kong, Xiangpeng
Gorny, Miroslaw K.
Nyambi, Phillipe
TI Three Related HIV-1 Cross-superinfected Individuals Exchange Similar
Viral Strains, but Evolve Different Immunological Responses
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Duerr, Ralf; Soni, Sonal; Banin, Andrew; Tuen, Michael; Courtney, Colleen; Nanfack, Aubin; Mayr, Luzia; Kong, Xiangpeng; Gorny, Miroslaw K.; Nyambi, Phillipe] NYU, Sch Med, New York, NY 10003 USA.
[Redd, Andrew] NIAID, NIH, Bethesda, MD USA.
[Ding, Shilei; Finzi, Andres] Univ Montreal, Montreal, PQ, Canada.
[Meli, Josephine; Ngai, Johnson] Med Diagnost Ctr, Yaounde, Cameroon.
[Nyambi, Phillipe] Manhattan Vet Affairs Harbor Healthcare Syst, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P01.20
BP 141
EP 141
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600249
ER
PT J
AU Wang, YM
Dell, SO
Guenaga, J
Chiang, CI
Lei, L
Wilson, R
Doria-Rose, N
Mascola, J
Wyatt, R
Hedestam, GK
Li, YX
AF Wang, Yimeng
Dell, Sijy O.
Guenaga, Javier
Chiang, Chi-I
Lei, Lin
Wilson, Richard
Doria-Rose, Nicole
Mascola, John
Wyatt, Richard
Hedestam, Gunilla Karlsson
Li, Yuxing
TI HIV-1 Env Immunogen-elicited Cross-reactive Tier 2 Virus Neutralizing
Antibody Response in Non-human Primates
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Wang, Yimeng; Wyatt, Richard; Li, Yuxing] Scripps Res Inst, La Jolla, CA 92037 USA.
[Wang, Yimeng; Chiang, Chi-I; Lei, Lin; Li, Yuxing] Univ Maryland, College Pk, MD 20742 USA.
[Dell, Sijy O.; Doria-Rose, Nicole; Mascola, John] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Guenaga, Javier; Wilson, Richard; Wyatt, Richard; Li, Yuxing] Scripps Res Inst, IAVI Neutralizing Antibody Ctr, La Jolla, CA USA.
[Hedestam, Gunilla Karlsson] Karolinska Inst, Stockholm, Sweden.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P01.24
BP 143
EP 143
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600253
ER
PT J
AU Gift, SK
Wieczorek, L
Krebs, SJ
Molnar, S
Donofrio, G
Chenine, AL
Sanders-Buell, E
Kijak, G
Chang, D
Doria-Rose, N
Rolland, M
Tovanabutra, S
Sriplienchan, S
Nitayapan, S
Connell, RJO
Eller, LA
Mascola, J
Michael, NL
Robb, ML
Polonis, VR
AF Gift, Syna K.
Wieczorek, Lindsay
Krebs, Shelly J.
Molnar, Sebastian
Donofrio, Gina
Chenine, Agnes-Laurence
Sanders-Buell, Eric
Kijak, Gustavo
Chang, David
Doria-Rose, Nicole
Rolland, Morgane
Tovanabutra, Sodsai
Sriplienchan, Somchai
Nitayapan, Sorachai
Connell, Robert J. O.
Eller, Leigh-Anne
Mascola, John
Michael, Nelson L.
Robb, Merlin L.
Polonis, Victoria R.
TI Development of Autologous Neutralizing Antibodies in HIV-1
CRF01_AE-infected Patients Spanning the First Three Years of Infection
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Gift, Syna K.; Wieczorek, Lindsay; Krebs, Shelly J.; Molnar, Sebastian; Donofrio, Gina; Chenine, Agnes-Laurence; Sanders-Buell, Eric; Kijak, Gustavo; Chang, David; Rolland, Morgane; Tovanabutra, Sodsai; Eller, Leigh-Anne; Michael, Nelson L.; Robb, Merlin L.; Polonis, Victoria R.] US Mil HIV Res Program, Bethesda, MD USA.
[Gift, Syna K.; Wieczorek, Lindsay; Krebs, Shelly J.; Molnar, Sebastian; Donofrio, Gina; Chenine, Agnes-Laurence; Sanders-Buell, Eric; Kijak, Gustavo; Chang, David; Tovanabutra, Sodsai; Eller, Leigh-Anne; Robb, Merlin L.] Henry M Jackson Fdn Advancement Mil Med, Bethesda, MD USA.
[Doria-Rose, Nicole; Mascola, John] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Sriplienchan, Somchai; Nitayapan, Sorachai; Connell, Robert J. O.] Armed Forces Res Inst Med Sci, Bangkok, Thailand.
[Michael, Nelson L.; Polonis, Victoria R.] Walter Reed Army Inst Res, Silver Spring, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P01.30
BP 146
EP 146
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600259
ER
PT J
AU Lei, L
Tran, K
Chiang, CI
Wang, YM
Arendt, HE
DeStefano, J
Xiao, YL
Wyatt, RT
Li, YX
AF Lei, Lin
Tran, Karen
Chiang, Chi-I
Wang, Yimeng
Arendt, Heather E.
DeStefano, Joanne
Xiao, Yongli
Wyatt, Richard T.
Li, Yuxing
TI Antibody Responses Elicited by Cleaved Soluble HIV-1 Envelope Trimers in
Guinea Pigs Revealed by Single B Cell Sorting and Cloning
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Lei, Lin; Chiang, Chi-I; Wang, Yimeng; Li, Yuxing] Univ Maryland, Inst Biosci & Biotechnol Res, College Pk, MD 20742 USA.
[Tran, Karen; Wyatt, Richard T.] Scripps Res Inst, IAVI Neutralizing Antibody Ctr, La Jolla, CA 92037 USA.
[Arendt, Heather E.; DeStefano, Joanne] Int AIDS Vaccine Initiat, New York, NY USA.
[Xiao, Yongli] NIAID, Lab Infect Dis, NIH, Rockville, MD USA.
Scripps Res Inst, Dept Immunol & Microbial Sci, La Jolla, CA 92037 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P01.34LB
BP 148
EP 148
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600263
ER
PT J
AU Montefiori, D
Seaman, M
Korber, B
Wagh, K
Morris, L
Zolla-Pazner, S
Lu, S
Corey, L
Scarlatti, G
D'Souza, P
AF Montefiori, David
Seaman, Michael
Korber, Bette
Wagh, Kshitij
Morris, Lynn
Zolla-Pazner, Susan
Lu, Shan
Corey, Larry
Scarlatti, Gabriella
D'Souza, Patricia
TI Tier 1 Strains of HIV-1: Time to Break an Old Habit?
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Montefiori, David] Duke Univ, Med Ctr, Durham, NC 27706 USA.
[Seaman, Michael] Harvard, Beth Isreal Deaconess Med Ctr, Cambridge, MA USA.
[Korber, Bette; Wagh, Kshitij] Los Alamos Natl Lab, Los Alamos, NM USA.
[Korber, Bette; Wagh, Kshitij] New Mexico Consortium, Los Alamos, NM USA.
[Morris, Lynn] Natl Inst Communicable Dis, Johannesburg, South Africa.
[Zolla-Pazner, Susan] Icahn Sch Med Mt Sinai, New York, NY 10029 USA.
[Lu, Shan] Univ Massachusetts, Sch Med, Amherst, MA 01003 USA.
[Corey, Larry] Fred Hutchinson Canc Res Ctr, 1124 Columbia St, Seattle, WA 98104 USA.
[Scarlatti, Gabriella] Global HIV Vaccine Enterprise, New York, NY USA.
[D'Souza, Patricia] NIAID, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P01.33LB
BP 148
EP 148
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600262
ER
PT J
AU Levendosky, K
Barnable, P
Mizenina, O
Zydowsky, TM
O'Keefe, BR
Derby, N
Teleshova, N
Fernandez-Romero, JA
AF Levendosky, Keith
Barnable, Patrick
Mizenina, Olga
Zydowsky, Thomas M.
O'Keefe, Barry R.
Derby, Nina
Teleshova, Natalia
Fernandez-Romero, Jose A.
TI Comparative Assessment of the Potency and Breadth of Activity of
Griffithsin and Broad Neutralizing Antibodies Against HIV
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Levendosky, Keith; Barnable, Patrick; Mizenina, Olga; Zydowsky, Thomas M.; Derby, Nina; Teleshova, Natalia; Fernandez-Romero, Jose A.] Populat Council, 1230 York Ave, New York, NY 10021 USA.
[O'Keefe, Barry R.] NCI, Mol Targets Lab, Ctr Canc Res, Frederick, MD 21701 USA.
Borough Manhattan Community Coll, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P01.35LB
BP 149
EP 149
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600264
ER
PT J
AU Teigler, JE
Eller, MA
Bolton, D
Marovich, M
Robb, ML
Martin, JN
Deeks, SG
Michael, NL
Streeck, H
AF Teigler, Jeffrey E.
Eller, Michael A.
Bolton, Diane
Marovich, Mary
Robb, Merlin L.
Martin, Jeffrey N.
Deeks, Steven G.
Michael, Nelson L.
Streeck, Hendrik
TI Differential Impact of Inhibitory Receptors and Inhibitory Receptor
Blockade on Cytokine-producing CD4 T Cell Subsets
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Teigler, Jeffrey E.; Eller, Michael A.; Bolton, Diane; Robb, Merlin L.; Michael, Nelson L.; Streeck, Hendrik] Henry M Jackson Fdn Advancement Mil Med, Bethesda, MD USA.
[Teigler, Jeffrey E.; Eller, Michael A.; Bolton, Diane; Robb, Merlin L.; Michael, Nelson L.; Streeck, Hendrik] Walter Reed Army Inst Res, US Mil HIV Res Program, Silver Spring, MD USA.
[Marovich, Mary] NIAID, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Martin, Jeffrey N.] Dept Epidemiol & Biostat, Bethesda, MD USA.
[Deeks, Steven G.] Univ Calif San Francisco, Sch Med, San Francisco, CA 94143 USA.
[Streeck, Hendrik] Inst HIV Res, Essen, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P03.08
BP 169
EP 169
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600303
ER
PT J
AU Hu, XT
Valentin, A
Dayton, F
Kulkarni, V
Alicea, C
Rosati, M
Chowdhury, B
Gautam, R
Broderick, KE
Sardesai, NY
Martin, MA
Mullins, JI
Pavlakis, GN
Felber, BK
AF Hu, Xintao
Valentin, Antonio
Dayton, Frances
Kulkarni, Viraj
Alicea, Candido
Rosati, Margherita
Chowdhury, Bhabadeb
Gautam, Rajeev
Broderick, Kate E.
Sardesai, Niranjan Y.
Martin, Malcolm A.
Mullins, James I.
Pavlakis, George N.
Felber, Barbara K.
TI Novel pDNA Prime-boost Vaccine Regimen to Augment Magnitude, Breadth,
and Cytotoxicity of Cellular Immunity to Subdominant Gag Epitope of HIV
and SIV
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Hu, Xintao; Valentin, Antonio; Dayton, Frances; Kulkarni, Viraj; Alicea, Candido; Rosati, Margherita; Chowdhury, Bhabadeb; Pavlakis, George N.; Felber, Barbara K.] NCI, Frederick, MD 21701 USA.
[Gautam, Rajeev; Martin, Malcolm A.] NIAID, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Broderick, Kate E.; Sardesai, Niranjan Y.] Inovio Pharmaceut, Plymouth Meeting, PA USA.
[Mullins, James I.] Univ Washington, Seattle, WA 98195 USA.
RI bebarta, vikhyat/K-3476-2015
NR 0
TC 0
Z9 0
U1 1
U2 1
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P03.13
BP 172
EP 172
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600308
ER
PT J
AU Mhlanga, F
Singh, D
Kamira, B
Bunge, K
Harkoo, I
Chappell, C
Mukaka, S
Palanee-Phillips, T
Crida, D
Nakabiito, C
Szydlo, D
Kachipapa, E
Pather, A
Baeten, J
Mvelase, S
Mdlala, B
Piper, J
Balkus, J
Hillier, S
AF Mhlanga, Felix
Singh, Devika
Kamira, Betty
Bunge, Katherine
Harkoo, Ishana
Chappell, Catherine
Mukaka, Shorai
Palanee-Phillips, Thesla
Crida, Danielle
Nakabiito, Clemensia
Szydlo, Danny
Kachipapa, Emma
Pather, Aren
Baeten, Jared
Mvelase, Samkelisiwe
Mdlala, Bernadette
Piper, Jeanna
Balkus, Jen
Hillier, Sharon
TI Uptake of Non-hormonal Intrauterine Contraceptive Devices (IUDs) among
Women Participating in MTN-020, a Clinical Trial for HIV Prevention in
Africa
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Mhlanga, Felix] Univ Zimbabwe, Coll Hlth Sci, Harare, Zimbabwe.
[Singh, Devika; Bunge, Katherine; Hillier, Sharon] Microbicides Trials Network, Durham, NC USA.
[Kamira, Betty; Nakabiito, Clemensia] Makerere Univ Johns Hopkins Univ, Kampala, Uganda.
[Harkoo, Ishana] CAPRISA, Durban, South Africa.
[Chappell, Catherine] Magee Womens Res Inst, Pittsburgh, PA USA.
[Mukaka, Shorai] Univ Zimbabwe Univ Calif, San Francisco Collaborat Res Program, Harare, Zimbabwe.
[Palanee-Phillips, Thesla] Wits Reprod Hlth & HIV Inst, Johannesburg, South Africa.
[Crida, Danielle] Desmond Tutu HIV Ctr, Cape Town, South Africa.
[Szydlo, Danny; Balkus, Jen] Fred Hutchinson Canc Res Ctr, 1124 Columbia St, Seattle, WA 98104 USA.
[Kachipapa, Emma] UNC Project, Lilongwe, Malawi.
[Pather, Aren; Mvelase, Samkelisiwe; Mdlala, Bernadette] Med Res Council South Africa, Tygerberg, South Africa.
[Baeten, Jared] Global Hlth Univ Washington, Seattle, WA USA.
[Piper, Jeanna] NIAID, Div Aids, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P05.06
BP 190
EP 190
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600345
ER
PT J
AU Lowry, A
Walker, CM
O'Neill, CI
Swartz, GM
Turpin, JA
Cummins, JE
AF Lowry, Anabel
Walker, Cattlena M.
O'Neill, Cynthia I.
Swartz, Glenn M.
Turpin, Jim A.
Cummins, James E., Jr.
TI Best Practices for Use of the Rabbit Rectal Irritation (RRI) Model for
Assessing the Safety and Systemic Exposure of Rectal Gel Microbicides
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Lowry, Anabel; Turpin, Jim A.; Cummins, James E., Jr.] NIAID, Div Aids, NIH, Bethesda, MD 20892 USA.
[Walker, Cattlena M.; O'Neill, Cynthia I.; Swartz, Glenn M.] Adv BioSci Labs Inc, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P06.01
BP 199
EP 199
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600361
ER
PT J
AU Marshall, LJ
O'Neill, CI
Desai, R
Goykhman, D
Madsen, TJ
Polsky-Fisher, S
Sanchez, RI
Strizki, J
Turpin, JA
van Laarhoven, H
Veronese, F
Swartz, GM
Cummins, JE
AF Marshall, Leslie J.
O'Neill, Cynthia I.
Desai, Rajesh
Goykhman, Dina
Madsen, Timothy J.
Polsky-Fisher, Stacey
Sanchez, Rosa I.
Strizki, Julie
Turpin, Jim A.
van Laarhoven, Hans
Veronese, Fulvia
Swartz, Glenn M.
Cummins, James E.
TI Utility of the Sheep Model for Testing the 28-day MK-2048A Intravaginal
Ring and Determining the Correlates of Exposure for Vicriviroc and
MK-2048
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Marshall, Leslie J.; Turpin, Jim A.; Veronese, Fulvia; Cummins, James E.] NIAID, Div Aids, NIH, Bethesda, MD 20892 USA.
[O'Neill, Cynthia I.; Swartz, Glenn M.] Adv Biosci Labs Inc, Rockville, MD USA.
[Desai, Rajesh; Goykhman, Dina; Polsky-Fisher, Stacey; Sanchez, Rosa I.; Strizki, Julie] Merck & Co Inc, Merck Res Labs, Kenilworth, NJ USA.
[Madsen, Timothy J.] Sinclair Res Ctr LLC, Auxvasse, MO USA.
[van Laarhoven, Hans] Merck & Co Inc, Schiphol Rijk, Netherlands.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P06.07
BP 202
EP 202
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600367
ER
PT J
AU Spreen, W
Lowry, A
Pal, R
Yueh, YL
Ford, S
Richardson-Harman, N
Turpin, JA
Veronese, F
Cummins, J
AF Spreen, William
Lowry, Anabel
Pal, Ranajit
Yueh, Yun Lan
Ford, Susan
Richardson-Harman, Nicola
Turpin, Jim A.
Veronese, Fulvia
Cummins, James
CA ABL BIOQUAL NHP Team
TI Use of a "Lead-in" Pharmacokinetic (PK) Study to Predict the Tissue
Concentration of Cabotegravir that Protects Macaques against SIV
Infection
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Spreen, William; Yueh, Yun Lan; Ford, Susan] GlaxoSmithKline, Philadelphia, PA USA.
[Lowry, Anabel; Turpin, Jim A.; Veronese, Fulvia; Cummins, James] NIAID, Div Aids, NIH, Bethesda, MD 20892 USA.
[Pal, Ranajit] Adv BioSci Labs Inc, Rockville, MD USA.
[Richardson-Harman, Nicola] Alpha StatConsult LLC, Damascus, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P06.13
BP 205
EP 205
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600373
ER
PT J
AU Patamawenu, AA
Connors, M
AF Patamawenu, Apisit A.
Connors, Mark
TI Truncated HIV Envelope Expressed by Synthetic Recombinant
Replication-competent (SRRC) Human Ad4 Recognized by
Conformation-dependent Antibodies
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Patamawenu, Apisit A.; Connors, Mark] NIH, Bldg 10, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P07.04
BP 209
EP 209
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600381
ER
PT J
AU Calenda, G
Barnable, P
Levendosky, K
Kleinbeck, K
Fernandez-Romero, JA
Keefe, BO
Zydowsky, TM
Teleshova, N
AF Calenda, Giulia
Barnable, Patrick
Levendosky, Keith
Kleinbeck, Kyle
Fernandez-Romero, Jose A.
Keefe, Barry O.
Zydowsky, Thomas M.
Teleshova, Natalia
TI GRFT/Carrageenan Gel Inhibits HIV and HSV-2 in Human Cervical Mucosa
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Calenda, Giulia; Barnable, Patrick; Levendosky, Keith; Kleinbeck, Kyle; Fernandez-Romero, Jose A.; Zydowsky, Thomas M.; Teleshova, Natalia] Populat Council, 1230 York Ave, New York, NY 10021 USA.
[Keefe, Barry O.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P07.19
BP 217
EP 217
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600396
ER
PT J
AU Francica, J
Lynn, G
Laga, R
Aussedat, B
Meyerhoff, R
Alam, M
Danishefsky, S
Haynes, B
Seder, R
AF Francica, Joseph
Lynn, Geoffrey
Laga, Richard
Aussedat, Baptiste
Meyerhoff, Ryan
Alam, Munir
Danishefsky, Samuel
Haynes, Barton
Seder, Robert
TI Synthetic Biocompatible Polymers Are an Effective Delivery Platform That
Elicits Potent Antibody Responses Against HIV-1 Glycopeptide Immunogens
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Francica, Joseph; Lynn, Geoffrey; Seder, Robert] NIH, Bldg 10, Bethesda, MD 20892 USA.
[Laga, Richard] Inst Macromol Chem, Prague, Czech Republic.
[Aussedat, Baptiste; Danishefsky, Samuel] Mem Sloan Kettering Canc Ctr, 1275 York Ave, New York, NY 10021 USA.
[Meyerhoff, Ryan; Alam, Munir; Haynes, Barton] Duke Human Vaccine Inst, Durham, NC USA.
RI Laga, Richard/G-3627-2014
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P07.27
BP 221
EP 221
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600404
ER
PT J
AU Jhunjhunwala, K
Sant, V
Wang, L
Graebing, P
Marshall, L
Cummins, J
Walker, C
Swartz, G
Rohan, L
AF Jhunjhunwala, Kunal
Sant, Vinayak
Wang, Lin
Graebing, Phil
Marshall, Leslie
Cummins, James, Jr.
Walker, Cattlena
Swartz, Glenn
Rohan, Lisa
TI Development of a Suppository Dosage Form for the Integrase Inhibitor,
MK-2048
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Jhunjhunwala, Kunal; Sant, Vinayak; Rohan, Lisa] Univ Pittsburgh, Sch Pharm, Pittsburgh, PA 15260 USA.
[Jhunjhunwala, Kunal; Wang, Lin; Graebing, Phil; Rohan, Lisa] Univ Pittsburgh, Magee Womens Res Inst, Pittsburgh, PA 15260 USA.
[Marshall, Leslie; Cummins, James, Jr.] NIAID, Div Aids, NIH, Bethesda, MD 20892 USA.
[Walker, Cattlena; Swartz, Glenn] Adv Biosci Labs Inc, Rockville, MD USA.
[Rohan, Lisa] Univ Pittsburgh, Sch Med, Pittsburgh, PA 15260 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P07.33
BP 224
EP 224
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600410
ER
PT J
AU Lai, YT
Pancera, M
Stewart-Jones, G
Druz, A
Kwong, P
AF Lai, Yen-Ting
Pancera, Marie
Stewart-Jones, Guillaume
Druz, Alex
Kwong, Peter
TI Improving Structural Accuracy of HIV-1 env Trimeric Structure by Crystal
Lattice Engineering and the Potential Application in Drug Discovery
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Lai, Yen-Ting; Pancera, Marie; Stewart-Jones, Guillaume; Druz, Alex; Kwong, Peter] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P08.07
BP 235
EP 235
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600431
ER
PT J
AU Chambers, MJ
Narpala, SR
Prabhakaran, MS
Acharya, P
Pancera, M
Kwon, YD
Cheng, C
Zhou, TQ
Gorman, J
Joyce, GM
Georgiev, IS
Zhang, BS
Mascola, JR
Koup, RA
Kwong, PD
McDermott, AB
AF Chambers, Michael J.
Narpala, Sandeep R.
Prabhakaran, Madhu S.
Acharya, Priyamvada
Pancera, Marie
Kwon, Young D.
Cheng, Cheng
Zhou, Tongqing
Gorman, Jason
Joyce, Gordon M.
Georgiev, Ivelin S.
Zhang, Baoshan
Mascola, John R.
Koup, Richard A.
Kwong, Peter D.
McDermott, Adrian B.
TI Antigenic Characterization of HIV-1 Trimers Using Meso Scale Discovery
ECLIA
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Chambers, Michael J.; Narpala, Sandeep R.; Prabhakaran, Madhu S.; Acharya, Priyamvada; Pancera, Marie; Kwon, Young D.; Cheng, Cheng; Zhou, Tongqing; Gorman, Jason; Joyce, Gordon M.; Georgiev, Ivelin S.; Zhang, Baoshan; Mascola, John R.; Koup, Richard A.; Kwong, Peter D.; McDermott, Adrian B.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD USA.
[Pancera, Marie] Fred Hutchinson Canc Res Ctr, 1124 Columbia St, Seattle, WA 98104 USA.
Vanderbilt Univ, Sch Med, Nashville, TN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P08.11
BP 237
EP 237
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600435
ER
PT J
AU Kleinbeck, K
Bonnaire, T
Kizima, L
Rodriguez, A
Grecky, S
Levendosky, K
Katzen, L
O'Keefe, BR
Makovec, T
Peet, M
Creasy, G
Zydowsky, TM
Fernandez-Romero, JA
AF Kleinbeck, Kyle
Bonnaire, Thierry
Kizima, Larisa
Rodriguez, Aixa
Grecky, Susanna
Levendosky, Keith
Katzen, Lauren
O'Keefe, Barry R.
Makovec, Tracy
Peet, Melissa
Creasy, George
Zydowsky, Thomas M.
Fernandez-Romero, Jose A.
TI Toxicology Profile of a Topical Multipurpose Prevention Technology that
Combines Griffithsin and Carrageenan
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Kleinbeck, Kyle; Bonnaire, Thierry; Kizima, Larisa; Rodriguez, Aixa; Grecky, Susanna; Levendosky, Keith; Katzen, Lauren; Creasy, George; Zydowsky, Thomas M.; Fernandez-Romero, Jose A.] Populat Council, New York, NY USA.
[O'Keefe, Barry R.] NCI, Mol Targets Lab, Ctr Canc Res, Frederick, MD 21701 USA.
[Makovec, Tracy; Peet, Melissa] MPI Res Inc, Mattawan, MI USA.
Borough Manhattan Community Coll, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P08.18LB
BP 240
EP 240
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600442
ER
PT J
AU Levendosky, K
Mizenina, O
Aravantinou, M
Kleinbeck, K
Bonnaire, T
Derby, N
Zydowsky, TM
O'Keefe, BR
Fernandez-Romero, JA
AF Levendosky, Keith
Mizenina, Olga
Aravantinou, Meropi
Kleinbeck, Kyle
Bonnaire, Thierry
Derby, Nina
Zydowsky, Thomas M.
O'Keefe, Barry R.
Fernandez-Romero, Jose A.
TI Preclinical Evaluation of a Griffithsin/Carrageenan Formulation to
Prevent HIV Infection
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Levendosky, Keith; Mizenina, Olga; Aravantinou, Meropi; Kleinbeck, Kyle; Bonnaire, Thierry; Derby, Nina; Zydowsky, Thomas M.; Fernandez-Romero, Jose A.] Populat Council, New York, NY USA.
[O'Keefe, Barry R.] NCI, Mol Targets Lab, Ctr Canc Res, Frederick, MD USA.
Borough Manhattan Community Coll, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P08.17LB
BP 240
EP 240
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600441
ER
PT J
AU Dawson, L
AF Dawson, Liza
TI Ethical Issues in Design of Prevention Trials: Grappling with Changing
Standards of Prevention
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Dawson, Liza] NIAID, Div AIDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P10.01
BP 255
EP 255
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600469
ER
PT J
AU deCamp, AC
Rolland, M
Edlefsen, PT
Sanders-Buell, E
Hall, B
Magaret, C
Fiore-Gartland, AJ
Juraska, M
Graham, BS
Roederer, M
Michael, NL
Robb, ML
McElrath, J
Tovanabutra, S
Sobieszczyk, ME
Hammer, SM
Kim, JH
Mullins, JI
Gilbert, PB
AF deCamp, Allan C.
Rolland, Morgane
Edlefsen, Paul T.
Sanders-Buell, Eric
Hall, Breana
Magaret, Craig
Fiore-Gartland, Andrew J.
Juraska, Michal
Graham, Barney S.
Roederer, Mario
Michael, Nelson L.
Robb, Merlin L.
McElrath, Juliana
Tovanabutra, Sodsai
Sobieszczyk, Magdalena E.
Hammer, Scott M.
Kim, Jerome H.
Mullins, James I.
Gilbert, Peter B.
CA HVTN505 Sieve Anal Team
TI Sieve Pressure toward the CD4 Binding Site of Env in HVTN 505
Breakthrough Infections
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [deCamp, Allan C.; Edlefsen, Paul T.; Magaret, Craig; Fiore-Gartland, Andrew J.; Juraska, Michal; McElrath, Juliana; Gilbert, Peter B.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Rolland, Morgane; Sanders-Buell, Eric; Michael, Nelson L.; Robb, Merlin L.; Tovanabutra, Sodsai] Walter Reed Army Inst Res, US Mil HIV Res Program, Silver Spring, MD USA.
[Rolland, Morgane; Sanders-Buell, Eric; Michael, Nelson L.; Robb, Merlin L.; Tovanabutra, Sodsai] Henry M Jackson Fdn Adv Mil Med, Bethesda, MD USA.
[Edlefsen, Paul T.; Hall, Breana; Mullins, James I.; Gilbert, Peter B.] Univ Washington, Seattle, WA 98195 USA.
[Graham, Barney S.; Roederer, Mario] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Sobieszczyk, Magdalena E.; Hammer, Scott M.] Columbia Univ, Med Ctr, New York, NY 10027 USA.
[Kim, Jerome H.] Int Vaccine Inst, Seoul, South Korea.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P12.03
BP 260
EP 260
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600477
ER
PT J
AU Rolland, M
Tovanabutra, S
Krebs, S
Sanders-Buell, E
Bose, M
Kijak, G
Sullivan, AMO
Harbolick, E
Bonar, L
Owen, C
Slike, B
Dussupt, V
Doria-Rose, N
Mascola, J
Nitayaphan, S
Polonis, V
Eller, LA
Kim, J
Michael, N
Robb, M
AF Rolland, Morgane
Tovanabutra, Sodsai
Krebs, Shelly
Sanders-Buell, Eric
Bose, Meera
Kijak, Gustavo
Sullivan, Anne Marie O.
Harbolick, Elizabeth
Bonar, Lydia
Owen, Christopher
Slike, Bonnie
Dussupt, Vincent
Doria-Rose, Nicole
Mascola, John
Nitayaphan, Sorachai
Polonis, Vicky
Eller, Leigh Anne
Kim, Jerome
Michael, Nelson
Robb, Merlin
TI Super-infection and Development of MPER-specific Neutralization Breadth
in Subject 40512 from the Acute Infection Cohort RV217
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Rolland, Morgane; Tovanabutra, Sodsai; Krebs, Shelly; Sanders-Buell, Eric; Bose, Meera; Kijak, Gustavo; Sullivan, Anne Marie O.; Harbolick, Elizabeth; Bonar, Lydia; Owen, Christopher; Slike, Bonnie; Dussupt, Vincent; Eller, Leigh Anne; Robb, Merlin] Henry M Jackson Fdn Adv Mil Med, US Mil HIV Res Program, Bethesda, MD USA.
[Doria-Rose, Nicole; Mascola, John] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Nitayaphan, Sorachai] Armed Forces Res Inst Med Sci AFRIMS, Bangkok, Thailand.
[Polonis, Vicky; Michael, Nelson] Walter Reed Army Inst Res, US Mil HIV Res Program, Silver Spring, MD USA.
[Kim, Jerome] Int Vaccine Inst, Seoul, South Korea.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P12.20
BP 268
EP 268
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600494
ER
PT J
AU Houzet, L
Perez-Losada, M
Matusali, G
Deleage, C
Dereuddre-Bosquet, N
Satie, AP
Jegou, B
Le Grand, R
Keele, BF
Crandall, KA
Dejucq-Rainsford, N
AF Houzet, Laurent
Perez-Losada, Marcos
Matusali, Giulia
Deleage, Claire
Dereuddre-Bosquet, Nathalie
Satie, Anne-Pascale
Jegou, Bernard
Le Grand, Roger
Keele, Brandon F.
Crandall, Keith A.
Dejucq-Rainsford, Nathalie
TI Origin of AIDS Virus in Semen
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Houzet, Laurent; Matusali, Giulia; Deleage, Claire; Satie, Anne-Pascale; Jegou, Bernard; Dejucq-Rainsford, Nathalie] INSERM U 1085 IRSET, Rennes, France.
[Perez-Losada, Marcos; Crandall, Keith A.] George Washington Univ, Computat Biol Inst, Washington, DC 20052 USA.
[Dereuddre-Bosquet, Nathalie] CEA, DSV iMETI, Div Immunovirol, IDMIT, Fontenay Aux Roses, France.
[Keele, Brandon F.] Frederick Natl Lab Canc Res, Leidos Biomed Res Inc, AIDS & Canc Virus Program, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P12.22LB
BP 269
EP 269
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600496
ER
PT J
AU Trainor, N
Cohen, S
Vittinghoff, E
Bacon, O
Doblecki-Lewis, S
Matheson, T
Blue, RW
Estrada, Y
Coleman, ME
Elion, R
Chege, W
Philip, SS
Buchbinder, S
Kolber, MA
Liu, AY
AF Trainor, Nikole
Cohen, Stephanie
Vittinghoff, Eric
Bacon, Oliver
Doblecki-Lewis, Susanne
Matheson, Tim
Blue, Robert Wilder
Estrada, Yannine
Coleman, Megan E.
Elion, Richard
Chege, Wairimu
Philip, Susan S.
Buchbinder, Susan
Kolber, Michael A.
Liu, Albert Y.
TI Social Harms and Social Benefits among Participants Taking Prep in the
US PrEP Demo Project
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Trainor, Nikole; Cohen, Stephanie; Matheson, Tim; Blue, Robert Wilder; Philip, Susan S.; Buchbinder, Susan] San Francisco Dept Publ Hlth, San Francisco, CA USA.
[Cohen, Stephanie; Vittinghoff, Eric; Bacon, Oliver; Philip, Susan S.; Buchbinder, Susan; Liu, Albert Y.] Univ Calif San Francisco, San Francisco, CA USA.
[Doblecki-Lewis, Susanne; Estrada, Yannine; Kolber, Michael A.] Univ Miami, Miller Sch Med, Coral Gables, FL 33124 USA.
[Coleman, Megan E.] Whitman Walker Hlth, Washington, DC USA.
[Elion, Richard] George Washington Univ, Sch Med & Hlth Sci, Washington, DC 20052 USA.
[Chege, Wairimu] NIAID, Div AIDS, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P15.18
BP 291
EP 291
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600537
ER
PT J
AU Sastry, M
Xu, L
Bhattacharya, S
Nabel, GJ
Bewley, CA
Kwong, PD
AF Sastry, Mallika
Xu, Ling
Bhattacharya, Shibani
Nabel, Gary J.
Bewley, Carole A.
Kwong, Peter D.
TI NMR Assignments and Dynamics of Ligand-free HIV-1 gp120 Outer Domain
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Sastry, Mallika; Xu, Ling; Nabel, Gary J.; Kwong, Peter D.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD USA.
[Bhattacharya, Shibani] New York Struct Biol Ctr, New York, NY USA.
[Bewley, Carole A.] NIDDK, Lab Bioorgan Chem, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P16.04
BP 296
EP 296
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600547
ER
PT J
AU Arrode-Bruses, G
Goode, D
Frank, I
Kleinbeck, K
Byrareddy, S
Arthos, J
Grasperge, B
Blanchard, J
Gettie, A
Zydowsky, T
Martinelli, E
AF Arrode-Bruses, Geraldine
Goode, Diana
Frank, Ines
Kleinbeck, Kyle
Byrareddy, Siddappa
Arthos, James
Grasperge, Brooke
Blanchard, James
Gettie, Agegnehu
Zydowsky, Thomas
Martinelli, Elena
TI Inhibition of alpha(4)beta(7) Activation May be Necessary to Reduce
Susceptibility to SIV: Differential Effect of an Agonist and an
Allosteric Inhibitor
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Arrode-Bruses, Geraldine; Goode, Diana; Frank, Ines; Kleinbeck, Kyle; Zydowsky, Thomas; Martinelli, Elena] Populat Council, New York, NY USA.
[Byrareddy, Siddappa] Univ Nebraska Med Ctr, Omaha, NE USA.
[Arthos, James] NIAID, NIH, Bethesda, MD USA.
[Grasperge, Brooke; Blanchard, James] Tulane Natl Primate Res Ctr, Covington, LA USA.
[Gettie, Agegnehu] Aaron Diamond AIDS Res Ctr, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P18.12
BP 310
EP 310
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600574
ER
PT J
AU Soto, C
Lemmin, T
Stewart-Jones, GBE
Kwong, PD
AF Soto, Cinque
Lemmin, Thomas
Stewart-Jones, Guillaume B. E.
Kwong, Peter D.
TI Dynamics of the HIV-1 Glycan Shield
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Soto, Cinque; Stewart-Jones, Guillaume B. E.; Kwong, Peter D.] NIAID, Vaccine Res Ctr, NIH, Rockville, MD USA.
[Lemmin, Thomas] Univ Calif San Francisco, San Francisco, CA 94143 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P19.09
BP 326
EP 326
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600605
ER
PT J
AU Matyas, GR
Torres, OB
Jalah, R
Antoline, JFG
Peachman, KK
Beck, Z
Rao, M
Jacobson, AE
Michael, NL
Rice, KC
Alving, CR
AF Matyas, Gary R.
Torres, Oscar B.
Jalah, Rashmi
Antoline, Joshua F. G.
Peachman, Kristina K.
Beck, Zoltan
Rao, Mangala
Jacobson, Arthur E.
Michael, Nelson L.
Rice, Kenner C.
Alving, Carl R.
TI Development of a Combination HIV-heroin Vaccine
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Matyas, Gary R.; Rao, Mangala; Michael, Nelson L.; Alving, Carl R.] Walter Reed Army Inst Res, US Mil HIV Res Program, Silver Spring, MD USA.
[Torres, Oscar B.; Jalah, Rashmi; Peachman, Kristina K.; Beck, Zoltan] Henry M Jackson Fdn Adv Mil Med, Bethesda, MD USA.
[Antoline, Joshua F. G.; Jacobson, Arthur E.; Rice, Kenner C.] NIDA, NIH, Bethesda, MD 20892 USA.
[Antoline, Joshua F. G.; Jacobson, Arthur E.; Rice, Kenner C.] NIAAA, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P19.13
BP 328
EP 328
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600608
ER
PT J
AU Chuang, GY
Geng, H
Pancera, M
Acharya, P
Chambers, M
Druz, A
Tsybovsky, Y
Yang, YP
Georgiev, I
Gorman, J
Joyce, MG
McDermott, A
Mascola, JR
Kwong, PD
AF Chuang, Gwo-Yu
Geng, Hui
Pancera, Marie
Acharya, Priyamvada
Chambers, Michael
Druz, Aliaksandr
Tsybovsky, Yaroslav
Yang, Yongping
Georgiev, Ivelin
Gorman, Jason
Joyce, M. Gordon
McDermott, Adrian
Mascola, John R.
Kwong, Peter D.
TI Increased Thermostability and Reduced CD4 Affinity of Structure-based
Stabilized Prefusion Closed HIV-1 Env Trimer
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Chuang, Gwo-Yu; Geng, Hui; Pancera, Marie; Acharya, Priyamvada; Chambers, Michael; Druz, Aliaksandr; Tsybovsky, Yaroslav; Yang, Yongping; Georgiev, Ivelin; Gorman, Jason; Joyce, M. Gordon; McDermott, Adrian; Mascola, John R.; Kwong, Peter D.] NIAID, Vaccine Res Ctr, NIH, Rockville, MD USA.
[Georgiev, Ivelin] Vanderbilt Univ, 221 Kirkland Hall, Nashville, TN 37235 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P19.16
BP 329
EP 329
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600611
ER
PT J
AU Stewart-Jones, GBE
Soto, C
Zhou, TQ
Kwong, PD
AF Stewart-Jones, Guillaume B. E.
Soto, Cinque
Zhou, Tongqing
Kwong, Peter D.
TI Identification of Dispersed Glycans on HIV-1 Env Trimer and Design of
Related Immunogens
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Stewart-Jones, Guillaume B. E.; Soto, Cinque; Zhou, Tongqing; Kwong, Peter D.] NIAID, Vaccine Res Ctr, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P19.15
BP 329
EP 329
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600610
ER
PT J
AU Lagenaur, L
Marcobal, A
Nilsen, T
Parks, T
AF Lagenaur, Laurel
Marcobal, Angela
Nilsen, Trine
Parks, Thomas
TI Safety Evaluation of Live Biotherapeutics for Prevention of BV and HIV-1
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Lagenaur, Laurel; Marcobal, Angela; Nilsen, Trine; Parks, Thomas] Osel Inc, Mountain View, CA USA.
[Lagenaur, Laurel] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P19.27
BP 335
EP 335
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600622
ER
PT J
AU Joyce, MG
Georgiev, I
Yang, YP
Sastry, M
Zhang, BS
Cheng, C
Chambers, M
Tsybovsky, Y
Aliaksandr, D
Xu, K
Zhou, TQ
Chuang, GY
Gorman, J
Pancera, M
Geng, H
Kwon, YD
Stewart-Jones, G
Mc Dermott, A
Mascola, J
Kwong, P
AF Joyce, M. Gordon
Georgiev, Ivelin
Yang, Yongping
Sastry, Mallika
Zhang Baoshan
Cheng, Cheng
Chambers, Michael
Tsybovsky, Yaroslav
Aliaksandr, Druz
Xu, Kai
Zhou, Tongqing
Chuang Gwo-Yu
Gorman, Jason
Pancera, Marie
Geng, Hui
Kwon, Young-Do
Stewart-Jones, Guillaume
Mc Dermott, Adrian
Mascola, John
Kwong, Peter
TI Designed HIV-1 Env Molecules from Multiple Clades That Display
Structural and Antigenic Characteristics of the Mature Prefusion HIV-1
Env
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Joyce, M. Gordon; Georgiev, Ivelin; Yang, Yongping; Sastry, Mallika; Zhang Baoshan; Cheng, Cheng; Chambers, Michael; Tsybovsky, Yaroslav; Aliaksandr, Druz; Xu, Kai; Zhou, Tongqing; Chuang Gwo-Yu; Gorman, Jason; Pancera, Marie; Geng, Hui; Kwon, Young-Do; Stewart-Jones, Guillaume; Mc Dermott, Adrian; Mascola, John; Kwong, Peter] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P19.30
BP 336
EP 336
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600625
ER
PT J
AU Galkin, A
Chen, YJ
Guenaga, J
O'Dell, S
Chiang, CI
Doria-Rose, N
Mascola, JR
Li, YX
AF Galkin, Andrey
Chen, Yajing
Guenaga, Javier
O'Dell, Sijy
Chiang, Chi-I
Doria-Rose, Nicole
Mascola, John R.
Li, Yuxing
TI gp120-CD4i Antibody Complex as Immunogen
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Galkin, Andrey] Univ Maryland, Inst Biosci & Biotechnol Res, College Pk, MD 20742 USA.
[Chen, Yajing] Scripps Res Inst, Dept Immunol & Microbial Sci, La Jolla, CA 92037 USA.
[Guenaga, Javier] Scripps Res Inst, IAVI Neutralizing Antibody Ctr, La Jolla, CA 92037 USA.
[O'Dell, Sijy; Doria-Rose, Nicole; Mascola, John R.] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Chiang, Chi-I; Li, Yuxing] Univ Maryland, Inst Biosci & Biotechnol Res, College Pk, MD 20742 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P19.47LB
BP 345
EP 345
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600642
ER
PT J
AU Welles, H
Bailer, R
Mason, R
Doria-Rose, N
Nguyen, R
O'Dell, S
Hoxie, J
Mascola, J
Roederer, M
AF Welles, Hugh
Bailer, Robert
Mason, Rosemarie
Doria-Rose, Nicole
Nguyen, Richard
O'Dell, Siji
Hoxie, James
Mascola, John
Roederer, Mario
TI Isolation of SIV Env-specific Tier 2 Neutralizing Antibody from
iMac-Delta D Immunized Macaque
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Welles, Hugh; Mason, Rosemarie; Doria-Rose, Nicole; Nguyen, Richard; O'Dell, Siji; Mascola, John; Roederer, Mario] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
George Washington Univ, Washington, DC 20052 USA.
[Bailer, Robert] NIAID, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Hoxie, James] Univ Penn, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P19.50LB
BP 346
EP 346
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600645
ER
PT J
AU Cheng, C
Wanninger, T
Joyce, MG
Georgiev, I
Chen, R
Yang, YP
Kong, WP
Kwong, P
Mascola, J
AF Cheng, Cheng
Wanninger, Timothy
Joyce, M. Gordon
Georgiev, Ivelin
Chen, Rita
Yang, Yongping
Kong, Wing-Pui
Kwong, Peter
Mascola, John
TI Membrane-anchored HIV-1 Envelope Immunogens with Native Trimer
Antigenicity for DNA Vaccine
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Cheng, Cheng; Wanninger, Timothy; Joyce, M. Gordon; Georgiev, Ivelin; Chen, Rita; Yang, Yongping; Kong, Wing-Pui; Kwong, Peter; Mascola, John] NIAID, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P19.52LB
BP 347
EP 347
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600647
ER
PT J
AU Acharya, P
Liu, QB
Lusso, P
Chuang, GY
Druz, A
Zhou, TQ
Rice, WJ
Wigge, C
Carragher, B
Potter, CS
Kwong, PD
AF Acharya, Priyamvada
Liu, Qingbo
Lusso, Paolo
Chuang, Gwo-Yu
Druz, Aliaksandr
Zhou, Tongqing
Rice, William J.
Wigge, Christoph
Carragher, Bridget
Potter, Clinton S.
Kwong, Peter D.
TI Cryo-EM Structure of the First Contact of CD4 Receptor with HIV-1 Env
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Acharya, Priyamvada; Liu, Qingbo; Lusso, Paolo; Chuang, Gwo-Yu; Druz, Aliaksandr; Zhou, Tongqing; Kwong, Peter D.] NIH, Bldg 10, Bethesda, MD 20892 USA.
[Acharya, Priyamvada; Rice, William J.; Wigge, Christoph; Carragher, Bridget; Potter, Clinton S.] New York Struct Biol Ctr, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P19.54LB
BP 348
EP 348
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600649
ER
PT J
AU Xu, K
Liu, K
Acharya, P
Kong, R
Druz, A
Carragher, B
Potter, CS
Mascola, JR
Kwong, PD
AF Xu, Kai
Liu, Kevin
Acharya, Priyamvada
Kong, Rui
Druz, Alex
Carragher, Bridget
Potter, Clinton S.
Mascola, John R.
Kwong, Peter D.
TI Study of Vaccine-Elicited HIV-1 Fusion Peptide-Targeting Antibody
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Xu, Kai; Liu, Kevin; Acharya, Priyamvada; Kong, Rui; Druz, Alex; Mascola, John R.; Kwong, Peter D.] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Carragher, Bridget; Potter, Clinton S.] Simons Electron Microscopy Ctr, Natl Resource Automated Mol Microscopy, New York, NY USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P19.55LB
BP 349
EP 349
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600650
ER
PT J
AU van der Straten, A
Cheng, H
Brown, ER
Reddy, K
Scheckter, R
Soto-Torres, L
Phillips-Palanee, T
Baeten, J
Mensch, B
AF van der Straten, Ariane
Cheng, Helen
Brown, Elizabeth R.
Reddy, Krishnaveni
Scheckter, Rachel
Soto-Torres, Lydia
Phillips-Palanee, Thesla
Baeten, Jared
Mensch, Barbara
CA MTN-020 ASPIRE Study Team
TI Are Ring Worries Affecting Use? Findings from the MTN-020/ASPIRE Phase
III Dapivirine Ring Trial
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [van der Straten, Ariane; Cheng, Helen] RTI Int, Womens Global Hlth Imperat, Res Triangle Pk, NC USA.
[van der Straten, Ariane] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Brown, Elizabeth R.] Fred Hutchinson Canc Res Ctr, 1124 Columbia St, Seattle, WA 98104 USA.
[Reddy, Krishnaveni; Phillips-Palanee, Thesla] Univ Witwatersrand, ZA-2050 Johannesburg, South Africa.
[Scheckter, Rachel] FHI 360, Durham, NC USA.
[Soto-Torres, Lydia] NIAID, Div Aids, NIH, Bethesda, MD 20892 USA.
[Baeten, Jared] Univ Washington, Seattle, WA 98195 USA.
[Mensch, Barbara] Populat Council, 1230 York Ave, New York, NY 10021 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P24.03
BP 376
EP 376
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600700
ER
PT J
AU Scheckter, R
McKinstry, L
Balkus, J
Beigi, R
Kabwigu, S
Noguchi, L
Ndase, P
Panchia, R
Kintu, K
Taljaard, M
Mhlanga, F
Nair, G
Palanee-Phillips, T
Moodley, J
Piper, J
Watts, H
Pan, J
Torjesen, K
AF Scheckter, Rachel
McKinstry, Laura
Balkus, Jennifer
Beigi, Rich
Kabwigu, Samuel
Noguchi, Lisa
Ndase, Patrick
Panchia, Ravindre
Kintu, Kenneth
Taljaard, Marthinette
Mhlanga, Felix
Nair, Gonasagrie
Palanee-Phillips, Thesla
Moodley, Jothi
Piper, Jeanna
Watts, Heather
Pan, Jason
Torjesen, Kristine
TI Growth and Development of Infants Born to Women Enrolled in a Clinical
Trial of Tenofovir-based Pre-exposure Prophylaxis for HIV Prevention
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Scheckter, Rachel; Torjesen, Kristine] FHI 360, Durham, NC USA.
[McKinstry, Laura; Balkus, Jennifer; Pan, Jason] Fred Hutchinson Canc Res Ctr, 1124 Columbia St, Seattle, WA 98104 USA.
[Beigi, Rich] Univ Pittsburgh, Pittsburgh, PA 15260 USA.
[Kabwigu, Samuel; Kintu, Kenneth] MU JHU, Kampala, Uganda.
[Noguchi, Lisa] Johns Hopkins Univ, Baltimore, MD 21218 USA.
[Ndase, Patrick] PSI, Washington, DC USA.
[Panchia, Ravindre] Perinatal HIV Res Unit, Soweto, South Africa.
[Taljaard, Marthinette] Aurum Inst, Johannesburg, South Africa.
[Mhlanga, Felix] UZ UCSF, Harare, Zimbabwe.
[Nair, Gonasagrie] CAPRISA, Durban, South Africa.
[Palanee-Phillips, Thesla] Wits Reprod Hlth & HIV Inst, Johannesburg, South Africa.
[Moodley, Jothi] South African Med Res Council, Cape Town, South Africa.
[Piper, Jeanna] NIH, Bldg 10, Bethesda, MD 20892 USA.
[Watts, Heather] US Dept State, Washington, DC 20520 USA.
NR 0
TC 0
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U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P25.13
BP 395
EP 395
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600738
ER
PT J
AU Yang, YP
Kwong, PD
AF Yang, Yongping
Kwong, Peter D.
TI Throughput Screening of HIV-1 Broad Neutralizing Antibodies and Env
Immunogens
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on HIV Research for Prevention (HIV R4P)
CY OCT 17-20, 2016
CL Chicago, IL
C1 [Yang, Yongping; Kwong, Peter D.] NIH, Bldg 10, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2016
VL 32
SU 1
MA P26.02
BP 400
EP 400
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA EA6YH
UT WOS:000386774600748
ER
PT J
AU Perkins, NJ
Schisterman, EF
AF Perkins, Neil J.
Schisterman, Enrique F.
TI RE: "RECEIVER OPERATING CHARACTERISTIC CURVE INFERENCE FROM A SAMPLE
WITH A LIMIT OF DETECTION" Reply
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Letter
C1 [Perkins, Neil J.; Schisterman, Enrique F.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, NIH, Bethesda, MD 20892 USA.
RP Schisterman, EF (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, NIH, Bethesda, MD 20892 USA.
EM schistee@mail.nih.gov
NR 5
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
EI 1476-6256
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD OCT 1
PY 2016
VL 184
IS 7
BP 554
EP 554
DI 10.1093/aje/kww092
PG 1
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA EA4AY
UT WOS:000386552000009
PM 27620451
ER
PT J
AU Yoon, SS
Dillon, CF
Illoh, K
Carroll, M
AF Yoon, Sung Sug (Sarah)
Dillon, Charles F.
Illoh, Kachi
Carroll, Margaret
TI Trends in the Prevalence of Coronary Heart Disease in the US National
Health and Nutrition Examination Survey, 2001-2012
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID UNITED-STATES; BLOOD-PRESSURE; SELF-REPORTS; HYPERTENSION; ADULTS;
MORTALITY; RISK; LIPOPROTEINS; POPULATION; VALIDITY
AB Introduction: This study evaluated recent trends in the prevalence of coronary heart disease in the U.S. population aged >= 40 years.
Methods: A total of 21,472 adults aged >= 40 years from the 2001-2012 National Health and Nutrition Examination Survey were included in the analysis. The analysis was conducted in 2015. Coronary heart disease included myocardial infarction, angina, and any other type of coronary heart disease, which were defined as a history of medical diagnosis of these specific conditions. Angina was also defined as currently taking anti-angina medication or having Rose Angina Questionnaire responses that scored with a Grade >= 1. Trends from 2001 to 2012 were analyzed overall, within demographic subgroups, and by major coronary heart disease risk factors.
Results: Between 2001 and 2012, the overall prevalence of coronary heart disease significantly decreased from 10.3% to 8.0% (p-trend<0.05). The prevalence of angina significantly decreased from 7.8% to 5.5% and myocardial infarction prevalence decreased from 5.5% to 4.7% (p-trend <0.05 for both groups). Overall coronary heart disease prevalence significantly decreased among women, adults aged >60 years, non-Hispanic whites, non-Hispanic blacks, adults who did not complete high school, adults with more than a high school education, and adults who had health insurance (p-trend <0.05 for all groups).
Conclusions: The overall prevalence of coronary heart disease including angina and myocardial infarction decreased significantly over the 12-year survey period. However, this reduction was seen mainly among persons without established coronary heart disease risk factors. There was no change in coronary heart disease prevalence among those with specific coronary heart disease risk factors. Published by Elsevier Inc. on behalf of American Journal of Preventive Medicine
C1 [Yoon, Sung Sug (Sarah)] NIH, Healthcare Delivery & Methodol IRG, Div AIDS Behav & Populat Sci, Ctr Sci Review, 6701 Rockledge Dr,Room 3152,MSC 7770, Bethesda, MD 20892 USA.
[Dillon, Charles F.] CDC, Natl Ctr Hlth Stat, Hyattsville, MD USA.
[Illoh, Kachi] US FDA, Off New Drugs Immediate Off, Ctr Drug Evaluat & Res, Silver Spring, MD USA.
[Carroll, Margaret] CDC, Div Hlth & Nutr Examinat Surveys, Natl Ctr Hlth Stat, Hyattsville, MD USA.
RP Yoon, SS (reprint author), NIH, Healthcare Delivery & Methodol IRG, Div AIDS Behav & Populat Sci, Ctr Sci Review, 6701 Rockledge Dr,Room 3152,MSC 7770, Bethesda, MD 20892 USA.
EM sarah.yoon@nih.gov
NR 39
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Z9 2
U1 3
U2 3
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 2016
VL 51
IS 4
BP 437
EP 445
DI 10.1016/j.amepre.2016.02.023
PG 9
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA EA7BX
UT WOS:000386784200008
PM 27113539
ER
PT J
AU Choi, K
Bernat, D
AF Choi, Kelvin
Bernat, Debra
TI E-Cigarette Use Among Florida Youth With and Without Asthma
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID BRAIN-DEVELOPMENT; SMOKING; NICOTINE; TOBACCO
AB Introduction: Although prevalence of youth e-cigarette use has increased dramatically, little is known about e-cigarette use among youth with asthma and how it differs by metropolitan status. This study assessed the prevalence of e-cigarette use among youth by asthma and metropolitan status and examined the associations between e-cigarette use, susceptibility to cigarette smoking, and asthma attack.
Methods: High school student participants from the 2012 Florida Youth Tobacco Survey were included (N=36,085). Information on demographics, asthma status, ever and past 30-day use of e-cigarettes, cigarette smoking susceptibility, and having asthma attacks in the past 12 months were collected. Data were weighted to be representative of Florida high school students. Analyses were conducted in 2015.
Results: Overall, prevalence of ever and past 30-day e-cigarette use among students who reported having asthma were 10.4% and 5.3%, respectively, higher than those without asthma (7.2% and 2.5%, respectively, p<0.01). Among students with asthma, e-cigarette use was more common among those in non-metropolitan and rural counties than those in metropolitan counties (p<0.05). Ever and past 30-day e-cigarette use was associated with cigarette smoking susceptibility among participants with asthma and those who never tried cigarettes (n=2,410; ever use, AOR=3.96, 95% CI=1.49, 10.56; past 30-day use, AOR=422.10, 95% CI=50.29, > 999.99). Past 30-day e-cigarette use was associated with having an asthma attack in the past 12 months among participants with asthma (n=5,865, p<0.01).
Conclusions: E-cigarette use is more common among Florida high school youth with asthma and is associated with susceptibility to cigarette smoking. Published by Elsevier Inc. on behalf of American Journal of Preventive Medicine
C1 [Choi, Kelvin] Natl Inst Minor Hlth & Hlth Dispar, Div Intramural Res, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Bernat, Debra] Univ Maryland, Sch Publ Hlth, Dept Behav & Community Hlth, College Pk, MD 20742 USA.
RP Choi, K (reprint author), Natl Inst Minor Hlth & Hlth Dispar, Div Intramural Res, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM kelvin.choi@nih.gov
FU Division of Intramural Research, National Institute on Minority Health
and Health Disparities, NIH; National Cancer Institute [R03 CA168411]
FX Dr. Choi's effort is funded by the Division of Intramural Research,
National Institute on Minority Health and Health Disparities, NIH. Dr.
Bernat's effort is supported with a grant from the National Cancer
Institute (R03 CA168411; D. Bernat, Principal Investigator).
NR 26
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U1 4
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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 2016
VL 51
IS 4
BP 446
EP 453
DI 10.1016/j.amepre.2016.03.010
PG 8
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA EA7BX
UT WOS:000386784200009
PM 27085691
ER
PT J
AU McCarthy, AM
Kim, JJ
Beaber, EF
Zheng, YY
Burnett-Hartman, A
Chubak, J
Ghai, NR
McLerran, D
Breen, N
Conant, EF
Geller, BM
Green, BB
Klabunde, CN
Inrig, S
Skinner, CS
Quinn, VP
Haas, JS
Schnall, M
Rutter, CM
Barlow, WE
Corley, DA
Armstrong, K
Doubeni, CA
AF McCarthy, Anne Marie
Kim, Jane J.
Beaber, Elisabeth F.
Zheng, Yingye
Burnett-Hartman, Andrea
Chubak, Jessica
Ghai, Nirupa R.
McLerran, Dale
Breen, Nancy
Conant, Emily F.
Geller, Berta M.
Green, Beverly B.
Klabunde, Carrie N.
Inrig, Stephen
Skinner, Celette Sugg
Quinn, Virginia P.
Haas, Jennifer S.
Schnall, Mitchell
Rutter, Carolyn M.
Barlow, William E.
Corley, Douglas A.
Armstrong, Katrina
Doubeni, Chyke A.
CA PROSPR Consortium
TI Follow-Up of Abnormal Breast and Colorectal Cancer Screening by
Race/Ethnicity
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID OCCULT BLOOD-TEST; LOW-INCOME WOMEN; UNITED-STATES; CARE; MAMMOGRAPHY;
DIAGNOSIS; QUALITY; PREDICTORS; TIME; IMPROVEMENT
AB Introduction: Timely follow-up of abnormal tests is critical to the effectiveness of cancer screening, but may vary by screening test, healthcare system, and sociodemographic group.
Methods: Timely follow-up of abnormal mammogram and fecal occult blood testing or fecal immunochemical tests (FOBT/FIT) were compared by race/ethnicity using Population-Based Research Optimizing Screening through Personalized Regimens consortium data. Participants were women with an abnormal mammogram (aged 40-75 years) or FOBT/FIT (aged 50-75 years) in 2010-2012. Analyses were performed in 2015. Timely follow-up was defined as colonoscopy <= 3 months following positive FOBT/ FIT; additional imaging or biopsy <= 3 months following Breast Imaging Reporting and Data System Category 0, 4, or 5 mammograms; or <= 9 months following Category 3 mammograms. Logistic regression was used to model receipt of timely follow-up adjusting for study site, age, year, insurance, and income.
Results: Among 166,602 mammograms, 10.7% were abnormal; among 566,781 FOBT/FITs, 4.3% were abnormal. Nearly 96% of patients with abnormal mammograms received timely follow-up versus 68% with abnormal FOBT/FIT. There was greater variability in receipt of follow-up across healthcare systems for positive FOBT/FIT than for abnormal mammograms. For mammography, black women were less likely than whites to receive timely follow-up (91.8% vs 96.0%, OR=0.71, 95% CI=0.51, 0.97). For FOBT/FIT, Hispanics were more likely than whites to receive timely follow-up than whites (70.0% vs 67.6%, OR=1.12, 95% CI=1.04, 1.21).
Conclusions: Timely follow-up among women was more likely for abnormal mammograms than FOBT/FITs, with small variations in follow-up rates by race/ethnicity and larger variation across healthcare systems. (C) 2016 American Journal of Preventive Medicine. Published by Elsevier Inc. All rights reserved.
C1 [McCarthy, Anne Marie; Armstrong, Katrina] Massachusetts Gen Hosp, Dept Med, 50 Staniford St,940F, Boston, MA 02114 USA.
[Kim, Jane J.] Harvard TH Chan Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA USA.
[Beaber, Elisabeth F.; McLerran, Dale] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, 1124 Columbia St, Seattle, WA 98104 USA.
[Zheng, Yingye] Fred Hutchinson Canc Res Ctr, Dept Biostat, 1124 Columbia St, Seattle, WA 98104 USA.
[Burnett-Hartman, Andrea] Fred Hutchinson Canc Res Ctr, Div Epidemiol, 1124 Columbia St, Seattle, WA 98104 USA.
[Burnett-Hartman, Andrea] Kaiser Permanente Colorado, Inst Hlth Res, Denver, CO USA.
[Chubak, Jessica; Green, Beverly B.] Grp Hlth Res Inst, Seattle, WA USA.
[Ghai, Nirupa R.; Quinn, Virginia P.] Kaiser Permanente Southern Calif, Dept Res & Evaluat, Pasadena, CA USA.
[Breen, Nancy] NCI, Hlth Syst & Intervent Res Branch, Bethesda, MD 20892 USA.
[Conant, Emily F.; Schnall, Mitchell] Univ Penn, Dept Radiol, Philadelphia, PA 19104 USA.
[Geller, Berta M.] Univ Vermont, Dept Family Med, Burlington, VT USA.
[Klabunde, Carrie N.] NIH, Off Dis Prevent, Bldg 10, Bethesda, MD 20892 USA.
[Inrig, Stephen] Univ Texas Southwestern Med Ctr Dallas, Dept Hlth Policy & Hist Med, Dallas, TX 75390 USA.
[Inrig, Stephen] Mt St Marys Univ, Dept Hlth Policy & Management, Los Angeles, CA USA.
[Skinner, Celette Sugg] Univ Texas Southwestern Med Ctr Dallas, Dept Clin Sci, Dallas, TX 75390 USA.
[Skinner, Celette Sugg] Univ Texas Southwestern Med Ctr Dallas, Simmons Comprehens Canc Ctr, Dallas, TX 75390 USA.
[Haas, Jennifer S.] Brigham & Womens Hosp, Dept Med, 75 Francis St, Boston, MA 02115 USA.
[Rutter, Carolyn M.] RAND Corp, Santa Monica, CA USA.
[Barlow, William E.] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Corley, Douglas A.] Kaiser Permanente Northern Calif, Dept Gastroenterol, Oakland, CA USA.
[Doubeni, Chyke A.] Univ Penn, Dept Family Med & Community Hlth, Philadelphia, PA 19104 USA.
RP McCarthy, AM (reprint author), Massachusetts Gen Hosp, Dept Med, 50 Staniford St,940F, Boston, MA 02114 USA.
EM amccarthy8@partners.org
OI Inrig, Stephen/0000-0003-2091-5841
FU NIH/National Cancer Institute PROSPR program [U54CA163262, U54CA163261,
U54CA163308, U54CA163313, U54CA163303, U54CA163307, U54CA164336,
U01CA163304]
FX This work was funded by the NIH/National Cancer Institute PROSPR
program, grant numbers: Kaiser Foundation Research Institute
U54CA163262, Group Health Research Institute U54CA163261, Parkland UT
Southwestern U54CA163308, University of Pennsylvania U54CA163313,
University of Vermont U54CA163303, Geisel School of Medicine at
Dartmouth and Brigham and Women's Hospital U54CA163307, University of
New Mexico U54CA164336, Fred Hutchinson Cancer Research Center
U01CA163304.
NR 32
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U1 8
U2 8
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 2016
VL 51
IS 4
BP 507
EP 512
DI 10.1016/j.amepre.2016.03.017
PG 6
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA EA7BX
UT WOS:000386784200016
PM 27132628
ER
PT J
AU Sandhu, PK
Elder, R
Patel, M
Saraiya, M
Holman, DM
Perna, F
Smith, RA
Buller, D
Sinclair, C
Reeder, A
Makin, J
McNoe, B
Glanz, K
AF Sandhu, Paramjit K.
Elder, Randy
Patel, Mona
Saraiya, Mona
Holman, Dawn M.
Perna, Frank
Smith, Robert A.
Buller, David
Sinclair, Craig
Reeder, Anthony
Makin, Jennifer
McNoe, Bronwen
Glanz, Karen
CA Community Preventive Serv
TI Community-wide Interventions to Prevent Skin Cancer Two Community Guide
Systematic
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID PROMOTE SUN PROTECTION; MALIGNANT-MELANOMA; CUTANEOUS MELANOMA;
ULTRAVIOLET-RADIATION; DYSPLASTIC NEVI; UNITED-STATES; RISK-FACTORS;
AUSTRALIA; METAANALYSIS; PREVALENCE
AB Context: Skin cancer is a preventable and commonly diagnosed cancer in the U.S. Excessive ultraviolet radiation exposure is a known cause of skin cancer. This article presents updated results of two types of interventions evaluated in a previously published Community Guide systematic review: multicomponent community-wide interventions and mass media interventions when used alone.
Evidence acquisition: Studies assessing multicomponent community-wide and mass media interventions to prevent skin cancer by reducing ultraviolet radiation exposure were evaluated using Community Guide systematic review methods. Relevant studies published between 1966 and 2013 were included and analyzed for this review.
Evidence synthesis: Seven studies evaluating the effectiveness of multicomponent community-wide interventions showed a median increase in sunscreen use of 10.8 (interquartile interval=7.3, 23.2) percentage points, a small decrease in ultraviolet radiation exposure, a decrease in indoor tanning device use of 4.0 (95% CI=2.5, 5.5) percentage points, and mixed results for other protective behaviors. Four studies evaluating the effectiveness of mass media interventions found that they generally led to improved ultraviolet protection behaviors among children and adults.
Conclusions: The available evidence showed that multicomponent community-wide interventions are effective in reducing the deleterious effects of ultraviolet radiation exposure by increasing sunscreen use. There was, however, insufficient evidence to determine the effectiveness of mass media interventions alone in reducing ultraviolet radiation exposure and increasing ultraviolet protection behaviors, indicating a continuing need for more research in this field to improve assessment of effectiveness. Published by Elsevier Inc. on behalf of American Journal of Preventive Medicine.
C1 [Sandhu, Paramjit K.; Elder, Randy; Patel, Mona] Ctr Dis Control & Prevent CDC, Community Guide Branch, Div Publ Hlth Informat Disseminat, Atlanta, GA USA.
[Saraiya, Mona; Holman, Dawn M.] CDC, Div Canc Prevent & Control, Atlanta, GA 30333 USA.
[Perna, Frank] NCI, NIH, Bethesda, MD 20892 USA.
[Smith, Robert A.] Amer Canc Soc, Atlanta, GA 30329 USA.
[Buller, David] Klein Buendel, Lakewood, CO USA.
[Sinclair, Craig] Canc Council Victoria, Ctr Behav Res Canc, Melbourne, Vic, Australia.
[Reeder, Anthony; McNoe, Bronwen] Univ Otago, Dept Prevent & Social Med, Canc Soc Social & Behav Res Unit, Dunedin, New Zealand.
[Makin, Jennifer] Univ Tasmania, Menzies Res Inst, Hobart, Tas 7001, Australia.
[Glanz, Karen] Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Glanz, Karen] Univ Penn, Sch Nursing, Philadelphia, PA 19104 USA.
RP Sandhu, PK (reprint author), Ctr Dis Control & Prevent CDC, Lab Res & Evaluat Branch, 1600 Clifton Rd,Mailstop E-69, Atlanta, GA 30329 USA.
EM psandhu@cdc.gov
FU Intramural CDC HHS [CC999999]
NR 43
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U1 5
U2 5
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 2016
VL 51
IS 4
BP 531
EP 539
DI 10.1016/j.amepre.2016.03.020
PG 9
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA EA7BX
UT WOS:000386784200021
PM 27647053
ER
PT J
AU Rigotti, NA
Stoney, CM
AF Rigotti, Nancy A.
Stoney, Catherine M.
TI CHARTing the Future Course of Tobacco-Cessation Interventions for
Hospitalized Smokers
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
C1 [Rigotti, Nancy A.] Massachusetts Gen Hosp, Dept Med, Div Gen Internal Med, Tobacco Res & Treatment Ctr, Boston, MA 02114 USA.
[Rigotti, Nancy A.] Harvard Med Sch, Boston, MA USA.
[Stoney, Catherine M.] NHLBI, Div Cardiovasc Sci, NIH, Bldg 10, Bethesda, MD 20892 USA.
RP Rigotti, NA (reprint author), Massachusetts Gen Hosp, 50 Staniford St,914, Boston, MA 02114 USA.
EM nrigotti@partners.org
FU NIH/National Heart, Lung, and Blood Institute [R01-HL11821]
FX Dr. Rigotti was supported by NIH/National Heart, Lung, and Blood
Institute grant number R01-HL11821, receives royalties from UpToDate,
Inc., and has received travel expenses from Pfizer, Inc., to attend
consultant meetings for which she received no honorarium. No other
financial disclosures were reported by the authors of this paper. The
content is solely the responsibility of the authors and does not
necessarily represent the official views of NIH or the U.S. Government.
NR 10
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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 2016
VL 51
IS 4
BP 549
EP 550
DI 10.1016/j.amepre.2016.07.012
PG 2
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA EA7BX
UT WOS:000386784200024
PM 27647055
ER
PT J
AU Fellows, JL
Mularski, RA
Leo, MC
Bentz, CJ
Waiwaiole, LA
Francisco, MC
Funkhouser, K
Stoney, CM
AF Fellows, Jeffrey L.
Mularski, Richard A.
Leo, Michael C.
Bentz, Charles J.
Waiwaiole, Lisa A.
Francisco, Melanie C.
Funkhouser, Kimberly
Stoney, Catherine M.
TI Referring Hospitalized Smokers to Outpatient Quit Services A Randomized
Trial
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID SMOKING-CESSATION INTERVENTION; CIGARETTE-SMOKING; HEART-DISEASE;
SYSTEM; CARE; PERFORMANCE; MODEL
AB Introduction: Linking outpatient cessation services to bedside counseling for hospitalized smokers can improve long-run quit rates. Adding an assisted referral (AR) offer to a tobacco treatment specialist consult service fits the team approach to care in U.S. hospitals.
Design: A two-arm patient-randomized trial tested the effectiveness of adding an AR offer to outpatient smoking-cessation services and interactive voice recognition (AR+IVR) follow-up to a usual care (UC) tobacco-cessation consult for hospitalized smokers.
Setting/participants: Over 24 months (November 2011-November 2013), 898 hospitalized adult smokers interested in quitting smoking were recruited from three large hospitals in the Portland, Oregon, area: an integrated group model HMO (n=622), a community hospital (n=195), and an academic health center (n=81).
Intervention: Tobacco treatment specialists identified smokers and provided an intensive bedside tobacco use assessment and cessation consultation (UC). AR+IVR recipients also received proactive ARs to available outpatient counseling programs and medications, and linked patients to a tailored IVR telephone follow-up system.
Main outcome measures: The primary outcome was self-reported 30-day abstinence at 6-month follow-up. Secondary outcomes included self-reported and continuous abstinence and biochemically confirmed 7-day abstinence at 6 months. Follow-up was completed in September 2014; data were analyzed in 2015.
Results: A total of 597 and 301 hospitalized smokers were randomized to AR+IVR and UC, respectively. AR+IVR and UC recipients received 19.3 and 17.0 minutes of bedside counseling (p=0.372), respectively. Most (58%) AR+IVR patients accepted referrals for counseling, 43% accepted medications, and 28% accepted both. Self-reported 30-day abstinence for AR+IVR (17.9%) and UC (17.3%) were not statistically significant (p=0.569). Differences in 7-day, continuous, and biochemically confirmed abstinence by treatment group also were insignificant, overall and adjusting for site.
Conclusions: Adding an AR to outpatient counseling and medications did not increase cigarette abstinence at 6 months compared to UC alone. (C) 2016 American Journal of Preventive Medicine. Published by Elsevier Inc. All rights reserved.
C1 [Fellows, Jeffrey L.; Mularski, Richard A.; Leo, Michael C.; Waiwaiole, Lisa A.; Francisco, Melanie C.; Funkhouser, Kimberly] Kaiser Permanente Ctr Hlth Res, Portland, OR USA.
[Bentz, Charles J.] Legacy Hlth Syst, Tobacco Cessat & Prevent, Portland, OR USA.
[Stoney, Catherine M.] NHLBI, Div Cardiovasc Sci, NIH, Bldg 10, Bethesda, MD 20892 USA.
RP Fellows, JL (reprint author), Kaiser Permanente Northwest, Ctr Hlth Res, 3800 N Interstate Ave, Portland, OR 97227 USA.
EM jeffrey.fellows@kpchr.org
FU National Heart, Lung, and Blood Institute [U01 HL105231, NCT01236079]
FX Funding was provided by the National Heart, Lung, and Blood Institute
(U01 HL105231; clinical trials registration, NCT01236079). The content
is solely the responsibility of the authors and does not necessarily
represent the official views of NIH or the U.S. Government.
NR 35
TC 1
Z9 1
U1 0
U2 0
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 2016
VL 51
IS 4
BP 609
EP 619
DI 10.1016/j.amepre.2016.06.014
PG 11
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA EA7BX
UT WOS:000386784200030
PM 27647061
ER
PT J
AU Cruvinel, E
Richter, KP
Stoney, C
Duffy, S
Fellows, J
Harrington, KF
Rigotti, NA
Sherman, S
Tindle, HA
Shireman, TI
Shelley, D
Waiwaiole, L
Cummins, S
AF Cruvinel, Erica
Richter, Kimber P.
Stoney, Catherine
Duffy, Sonia
Fellows, Jeffrey
Harrington, Kathleen F.
Rigotti, Nancy A.
Sherman, Scott
Tindle, Hilary A.
Shireman, Theresa I.
Shelley, Donna
Waiwaiole, Lisa
Cummins, Sharon
TI CHARTing a Path to Pragmatic Tobacco Treatment Research
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID TRIALS; PRECIS
AB Introduction: It is important to consider the degree to which studies are explanatory versus pragmatic to understand the implications of their findings for patients, healthcare professionals, and policymakers. Pragmatic trials test the effectiveness of interventions in real-world conditions; explanatory trials test for efficacy under ideal conditions. The Consortium of Hospitals Advancing Research on Tobacco (CHART) is a network of seven NIH-funded trials designed to identify effective programs that can be widely implemented in routine clinical practice.
Methods: A cross-sectional analysis of CHART trial study designs was conducted to place each study on the pragmatic-explanatory continuum. After reliability training, six raters independently scored each CHART study according to ten PRagmatic Explanatory Continuum Indicator Summary (PRECIS) dimensions, which covered participant eligibility criteria, intervention flexibility, practitioner expertise, follow-up procedures, participant compliance, practitioner adherence, and outcome analyses. Means and SDs were calculated for each dimension of each study, with lower scores representing more pragmatic elements. Results were plotted on "spoke and wheel" diagrams. The rating process and analyses were performed in October 2014 to September 2015.
Results: All seven CHART trials tended toward the pragmatic end of the spectrum, although there was a range from 0.76 (SD = 0.23) to 1.85 (SD = 0.58). Most studies included some explanatory design elements.
Conclusions: CHART findings should be relatively applicable to clinical practice. Funders and reviewers could integrate PRECIS criteria into their guidelines to better facilitate pragmatic research. CHART study protocols, coupled with scores reported here, may help readers improve the design of their own pragmatic trials. (C) 2016 American Journal of Preventive Medicine. Published by Elsevier Inc. All rights reserved.
C1 [Cruvinel, Erica] Univ Fed Juiz de Fora, Dept Psychol, Juiz De Fora, MG, Brazil.
[Richter, Kimber P.] Univ Kansas, Med Ctr, Dept Prevent Med & Publ Hlth, Kansas City, KS 66103 USA.
[Richter, Kimber P.] Univ Kansas, Med Ctr, Ctr Canc, Kansas City, KS 66103 USA.
[Stoney, Catherine] NHLBI, NIH, Bldg 10, Bethesda, MD 20892 USA.
[Duffy, Sonia] Ohio State Univ, Coll Nursing, Columbus, OH 43210 USA.
[Duffy, Sonia] Dept Vet Affairs Ann Arbor Healthcare Syst, Ann Arbor, MI USA.
[Fellows, Jeffrey; Waiwaiole, Lisa] Kaiser Permanente Ctr Hlth Res, Portland, OR USA.
[Harrington, Kathleen F.] Univ Alabama Birmingham, Dept Med, Div Pulm Allergy & Crit Care Med, Birmingham, AL 35294 USA.
[Rigotti, Nancy A.] Harvard Med Sch, Massachusetts Gen Hosp, Dept Med, Boston, MA USA.
[Rigotti, Nancy A.] Harvard Med Sch, Massachusetts Gen Hosp, Tobacco Res & Treatment Ctr, Boston, MA USA.
[Sherman, Scott] NYU, Sch Med, Dept Populat Hlth Med, New York, NY USA.
[Sherman, Scott] NYU, Sch Med, Dept Med, New York, NY USA.
[Sherman, Scott] NYU, Sch Med, Dept Psychiat, New York, NY USA.
[Tindle, Hilary A.] Vanderbilt Univ, Sch Med, Dept Med, Nashville, TN 37212 USA.
[Shireman, Theresa I.] Brown Univ, Dept Hlth Serv Policy & Practice, Providence, RI 02912 USA.
[Shelley, Donna] NYU, Sch Med, Dept Populat Med, New York, NY USA.
[Cummins, Sharon] Univ Calif San Diego, Dept Family Med & Publ Hlth, San Diego, CA 92103 USA.
RP Cruvinel, E (reprint author), Univ Fed Juiz de Fora, Dept Psychol, Ctr Res Intervent & Evaluat Alcohol & Other Drugs, Juiz De Fora, MG, Brazil.
EM ecruvinel@yahoo.com.br
OI Sherman, Scott/0000-0003-1752-7303
FU Foundation for Research Support of Minas Gerais (FAPEMIG); National
Council for Scientific and Technological Development (CNPq);
Coordination for the Improvement of Higher Education Personnel (CAPES)
of Brazil; National Heart, Lung, and Blood Institute [U01 HL105232-01]
FX The authors thank Niaman Nazir, MBBS, MPH, for assistance with
formatting the spoke and wheel diagrams. This work was supported by the
National Heart, Lung, and Blood Institute (U01 HL105232-01) and the
Foundation for Research Support of Minas Gerais (FAPEMIG), National
Council for Scientific and Technological Development (CNPq), and
Coordination for the Improvement of Higher Education Personnel (CAPES)
of Brazil. The content is solely the responsibility of the authors and
does not necessarily represent the official views of the National Heart,
Lung, and Blood Institute; NIH; or the government of Brazil. The study
sponsor had no role in study design; collection, analysis, or
interpretation of data; writing the report; or the decision to submit
the report for publication.
NR 18
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 0749-3797
EI 1873-2607
J9 AM J PREV MED
JI Am. J. Prev. Med.
PD OCT
PY 2016
VL 51
IS 4
BP 630
EP 636
DI 10.1016/j.amepre.2016.05.025
PG 7
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA EA7BX
UT WOS:000386784200032
PM 27647063
ER
PT J
AU Chambers, DA
Norton, WE
AF Chambers, David A.
Norton, Wynne E.
TI The Adaptome Advancing the Science of Intervention Adaptation
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID PREVENTION INTERVENTIONS; THERAPIST ADHERENCE; MENTAL-HEALTH;
IMPLEMENTATION; FIDELITY; TECHNOLOGIES; BEHAVIOR; OUTCOMES
AB In the past few decades, prevention scientists have developed and tested a range of interventions with demonstrated benefits on child and adolescent cognitive, affective, and behavioral health. These evidence-based interventions offer promise of population-level benefit if accompanied by findings of implementation science to facilitate adoption, widespread implementation, and sustainment. Though there have been notable examples of successful efforts to scale up interventions, more work is needed to optimize benefit. Although the traditional pathway from intervention development and testing to implementation has served the research community well-allowing for a systematic advance of evidence-based interventions that appear ready for implementation-progress has been limited by maintaining the hypothesis that evidence generation must be complete prior to implementation. This sets up the challenging dichotomy between fidelity and adaptation and limits the science of adaptation to findings from randomized trials of adapted interventions. The field can do better. This paper argues for the development of strategies to advance the science of adaptation in the context of implementation that would more comprehensively describe the needed fit between interventions and their settings, and embrace opportunities for ongoing learning about optimal intervention delivery over time. Efforts to build the resulting adaptome (pronounced "adapt-ohm") will include the construction of a common data platform to house systematically captured information about variations in delivery of evidence-based interventions across multiple populations and contexts, and provide feedback to intervention developers, as well as the implementation research and practice communities. Finally, the article identifies next steps to jumpstart adaptome data platform development. Published by Elsevier Inc.
C1 [Chambers, David A.; Norton, Wynne E.] NCI, Div Canc Control & Populat Sci, 9609 Med Ctr Dr, Bethesda, MD 20850 USA.
RP Chambers, DA (reprint author), NCI, Div Canc Control & Populat Sci, 9609 Med Ctr Dr, Bethesda, MD 20850 USA.
EM dchamber@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 35
TC 2
Z9 2
U1 1
U2 1
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 2016
VL 51
IS 4
SU 2
BP S124
EP S131
DI 10.1016/j.amepre.2016.05.011
PG 8
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA EA7BM
UT WOS:000386783100004
PM 27371105
ER
PT J
AU Harding, FM
Hingson, RW
Klitzner, M
Mosher, JF
Brown, J
Vincent, RM
Dahl, E
Cannon, CL
AF Harding, Frances M.
Hingson, Ralph W.
Klitzner, Michael
Mosher, James F.
Brown, Jorielle
Vincent, Robert M.
Dahl, Elizabeth
Cannon, Carol L.
TI Underage Drinking A Review of Trends and Prevention Strategies
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Review
ID ALCOHOL-RELATED MORTALITY; KEG REGISTRATION LAWS; STUDENTS AGES 18-24;
COLLEGE-STUDENTS; CONTROL POLICIES; COMMUNITY TRIAL; BINGE DRINKING;
UNITED-STATES; FATAL CRASHES; YOUTH ACCESS
AB Underage drinking and its associated problems have profound negative consequences for underage drinkers themselves, their families, their communities, and society as a whole, and contribute to a wide range of costly health and social problems. There is increased risk of negative consequences with heavy episodic or binge drinking. Alcohol is a factor related to approximately 4,300 deaths among underage youths in the U.S. every year. Since the mid-1980s, the nation has launched aggressive underage drinking prevention efforts at the federal, state, and local levels, and national epidemiologic data suggest that these efforts are having positive effects. For example, since 1982, alcohol-related traffic deaths among youth aged 16-20 years have declined by 79%. Evidence-based or promising strategies for reducing underage drinking include those that limit the physical, social, and economic availability of alcohol to youth, make it illegal for drivers aged <21 years to drive after drinking, and provide mechanisms for early identification of problem drinkers. Strategies may be implemented through a comprehensive prevention approach including policies and their enforcement, public awareness and education, action by community coalitions, and early brief alcohol intervention and referral programs. This paper focuses on underage drinking laws and their enforcement because these constitute perhaps the most fundamental component of efforts to limit youth access to and use of alcohol. Published by Elsevier Inc.
C1 [Harding, Frances M.; Brown, Jorielle; Vincent, Robert M.] SAMHSA, CSAP, Rockville, MD USA.
[Hingson, Ralph W.] NIAAA, Div Epidemiol & Prevent Res, Bethesda, MD USA.
[Klitzner, Michael; Dahl, Elizabeth; Cannon, Carol L.] CDM Grp Inc, Bethesda, MD USA.
[Mosher, James F.] Alcohol Policy Consultat, Felton, CA USA.
RP Vincent, RM (reprint author), Subst Abuse & Mental Hlth Serv Adm, CSAP, 5600 Fishers Lane, Rockville, MD 20857 USA.
EM robert.vincent@samhsa.hhs.gov
FU Substance Abuse and Mental Health Services Administration
[HHSS28320070008I/HHSS28342001T]
FX This work was funded by the Substance Abuse and Mental Health Services
Administration under Contract number HHSS28320070008I/HHSS28342001T.
NR 96
TC 1
Z9 1
U1 17
U2 17
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 2016
VL 51
IS 4
SU 2
BP S148
EP S157
DI 10.1016/j.amepre.2016.05.020
PG 10
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA EA7BM
UT WOS:000386783100007
PM 27476384
ER
PT J
AU Bissa, M
Quaglino, E
Zanotto, C
Illiano, E
Rolih, V
Pacchioni, S
Cavallo, F
Morghen, CD
Radaelli, A
AF Bissa, Massimiliano
Quaglino, Elena
Zanotto, Carlo
Illiano, Elena
Rolih, Valeria
Pacchioni, Sole
Cavallo, Federica
Morghen, Carlo De Giuli
Radaelli, Antonia
TI Protection of mice against the highly pathogenic VVIHD-J by DNA and
fowlpox recombinant vaccines, administered by electroporation and
intranasal routes, correlates with serum neutralizing activity
SO ANTIVIRAL RESEARCH
LA English
DT Article
DE Recombinant vaccines; Fowlpox virus; Prime/boost; OPXV vaccine; L1R,
A27L, A33R, B5R VV genes; Intranasal mucosal vaccination
ID PRIME-BOOST IMMUNIZATION; SMALLPOX VACCINE; ANTIBODY-RESPONSES;
NONHUMAN-PRIMATES; VIRUS CHALLENGE; T-CELLS; MONKEYPOX VIRUS; MUCOSAL;
IMMUNITY; INFECTION
AB The control of smallpox was achieved using live vaccinia virus (VV) vaccine, which successfully eradicated the disease worldwide. As the variola virus no longer exists as a natural infection agent, mass vaccination was discontinued after 1980. However, emergence of smallpox outbreaks caused by accidental or deliberate release of variola virus has stimulated new research for second-generation vaccine development based on attenuated VV strains. Considering the closely related animal poxviruses that also arise as zoonoses, and the increasing number of unvaccinated or immunocompromised people, a safer and more effective vaccine is still required. With this aim, new vectors based on avian poxviruses that cannot replicate in mammals should improve the safety of conventional vaccines, and protect from zoonotic orthopoxvirus diseases, such as cowpox and monkeypox. In this study, DNA and fowlpox (FP) recombinants that expressed the VV L1R, A27L, A33R, and B5R genes were generated (4DNAmix, 4FPmix, respectively) and tested in mice using novel administration routes. Mice were primed with 4DNAmix by electroporation, and boosted with 4FPmix applied intranasally. The lethal VVIHD-J strain was then administered by intranasal challenge. All of the mice receiving 4DNAmix followed by 4FPmix, and 20% of the mice immunized only with 4FPmix, were protected. The induction of specific humoral and cellular immune responses directly correlated with this protection. In particular, higher anti-A27 antibodies and IFN gamma-producing T lymphocytes were measured in the blood and spleen of the protected mice, as compared to controls. VVIHD-J neutralizing antibodies in sera from the protected mice suggest that the prime/boost vaccination regimen with 4DNAmix plus 4FPmix may be an effective and safe mode to induce protection against smallpox and poxvirus zoonotic infections. The electroporation/intranasal administration routes contributed to effective immune responses and mouse survival. (C) 2016 Elsevier B.V. All rights reserved.
C1 [Bissa, Massimiliano; Illiano, Elena; Pacchioni, Sole; Radaelli, Antonia] Univ Milan, Dept Pharmacol & Biomol Sci, Via Balzaretti 9, I-20133 Milan, Italy.
[Quaglino, Elena; Rolih, Valeria; Cavallo, Federica] Univ Turin, Dept Mol Biotechnol & Hlth Sci, Ctr Mol Biotechnol, Via Nizza 52, I-10126 Turin, Italy.
[Zanotto, Carlo; Morghen, Carlo De Giuli] Univ Milan, Dept Med Biotechnol & Translat Med, Via Vanvitelli 32, I-20129 Milan, Italy.
[Morghen, Carlo De Giuli] Catholic Univ Our Lady Good Counsel, Tirana, Albania.
[Radaelli, Antonia] Univ Milan, Inst Neurosci, Cellular & Mol Pharmacol Sect, CNR, Via Vanvitelli 32, I-20129 Milan, Italy.
[Bissa, Massimiliano] NCI, NIH, Basic Res Labs, Bethesda, MD 20892 USA.
RP Morghen, CD; Radaelli, A (reprint author), Univ Milan, Lab Mol Virol & Recombinant Vaccine Dev, Dept Pharmacol & Biomol Sci, Via Vanvitelli 32, I-20129 Milan, Italy.
EM massimiliano.bissa@nih.gov; elena.quaglino@unito.it;
carlo.zanotto@unimi.it; elena.illiano@unimi.it; valeria.rolih@unito.it;
sol83@libero.it; federica.cavallo@unito.it;
carlo.degiulimorghen@unimi.it; antonia.radaelli@unimi.it
RI Cavallo, Federica/C-5666-2011;
OI Cavallo, Federica/0000-0003-4571-1060; Quaglino,
Elena/0000-0002-8151-9124
FU University of Milano Transition Grant [18498, CUP G42I14001030001];
Fondazione Ricerca Molinette Onlus and Fondazione CRT, Torino, Italy
[2015-2518]
FX This work was partially founded by the University of Milano Transition
Grant, code no. 18498, CUP G42I14001030001 and by grants to FC from
Fondazione Ricerca Molinette Onlus and Fondazione CRT, Torino, Italy,
grant no. 2015-2518. The following reagents were obtained through the
NIH Biodefense and Emerging Infections Research Resources Repository,
(NIAID, NIH): vaccinia virus (WR) L1R protein with C-terminal histidine
tag, recombinant from baculovirus, NR-2625; vaccinia virus (WR) A27L
protein with C-terminal histidine tag, recombinant from baculovirus,
NR-2622; vaccinia virus (WR) A33R protein with C-terminal histidine tag,
recombinant from baculovirus, NR-545; vaccinia virus (WR) B5R protein
with N-terminal histidine tag, recombinant from baculovirus, NR-546. The
authors also thank Dr. Christopher P. Berrie for editorial assistance
with the manuscript.
NR 66
TC 0
Z9 0
U1 5
U2 5
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-3542
EI 1872-9096
J9 ANTIVIR RES
JI Antiviral Res.
PD OCT
PY 2016
VL 134
BP 182
EP 191
DI 10.1016/j.antiviral.2016.09.002
PG 10
WC Pharmacology & Pharmacy; Virology
SC Pharmacology & Pharmacy; Virology
GA EA9SA
UT WOS:000386983800021
PM 27637905
ER
PT J
AU Hartman, TL
Yang, L
Helfrick, AN
Hassink, M
Shank, NI
Rosenker, KG
Scerba, MT
Saha, M
Hughes, E
Wang, AQ
Xu, X
Gupta, P
Buckheit, RW
Appella, DH
AF Hartman, T. L.
Yang, L.
Helfrick, A. N.
Hassink, M.
Shank, N. I.
Rosenker, K. George
Scerba, M. T.
Saha, M.
Hughes, E.
Wang, A. Q.
Xu, X.
Gupta, P.
Buckheit, R. W., Jr.
Appella, D. H.
TI Preclinical evaluation of a mercaptobenzamide and its prodrug for
NCp7-targeted inhibition of human immunodeficiency virus
SO ANTIVIRAL RESEARCH
LA English
DT Article
ID TYPE-1 NUCLEOCAPSID PROTEIN; ZINC-FINGER INHIBITORS; ANTI-HIV AGENTS;
VIRAL-DNA; REPLICATION; TARGET; BINDING; NCP7; RNA; INACTIVATION
AB Although the effective use of highly active antiretroviral therapy results in the suppression of virus production in infected individuals, it does not eliminate the infection and low level virus production in cells harboring virus in sanctuary sites. Thus, the continued search for new antiretroviral agents with unique and different mechanisms of HIV inhibition remains critical, and compounds that can reduce the level of virus production from cells already infected with HIV, as opposed to preventing de novo infection, would be of great benefit. A mercaptobenzamide (MDH-1-38) and its prodrug (NS1040) are being developed as potential therapeutic compounds targeting the zinc finger of HIV nucleocapsid. In the presence of esterase enzymes, NS1040 is designed to be converted to MDH-1-38 which has antiviral activity. While we presume that NS1040 is rapidly converted to MDH-1-38 in all experiments, the two compounds were tested side-by-side to determine whether the presence of a prodrug affects the antiviral activity or mechanism of action. The two compounds were evaluated against a panel of HIV-1 clinical isolates in human PBMCs and monocyte-macrophages and yielded EC50 values ranging from 0.7 to 13 mu M with no toxicity up to 100 mu M. MDH-1-38 and NS1040 remained equally active in human PBMCs in the presence of added serum proteins as well as against HIV-1 isolates resistant to reverse transcriptase, integrase or protease inhibitors. Cell-based and biochemical mechanism of antiviral action assays demonstrated MDH-1-38 and NS1040 were virucidal at concentrations of 15 and 50 mu M, respectively. Cell to cell transmission of HIV in multiple passages was significantly reduced in CEM-SS and human PBMCs by reducing progeny virus infectivity at compound concentrations greater than 2 mu M. The combination of either MDH-1-38 or NS1040 with other FDA-approved HIV drugs yielded additive to synergistic antiviral interactions with no evidence of antiviral antagonism or synergistic toxicity. Serial dose escalation was used in attempts to select for HIV strains resistant to MDH-1-38 and NS1040. Virus at several passages failed to replicate in cells treated at increased compound concentrations, which is consistent with the proposed mechanism of action of the virus inactivating compounds. Through 14 passages, resistance to the compounds has not been achieved. Most HIV inhibitors with mechanism of antiviral action targeting a viral protein would have selected for a drug resistant virus within 14 passages. These studies indicate that these NCp7-targeted compounds represent new potent anti-HIV drug candidates which could be effectively used in combination with all approved anti-HIV drugs. (C) 2016 Published by Elsevier B.V.
C1 [Hartman, T. L.; Yang, L.; Helfrick, A. N.; Buckheit, R. W., Jr.] ImQuest Biosci Inc, 7340 Execut Way,Suite R, Frederick, MD 21704 USA.
[Hassink, M.; Shank, N. I.; Rosenker, K. George; Scerba, M. T.; Saha, M.; Gupta, P.; Appella, D. H.] NIDDK, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
[Hughes, E.; Wang, A. Q.; Xu, X.] NIH, NCATS, Bldg 10, Bethesda, MD 20892 USA.
RP Buckheit, RW (reprint author), ImQuest Biosci Inc, 7340 Execut Way,Suite R, Frederick, MD 21704 USA.; Appella, DH (reprint author), NIDDK, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
EM rbuckheit@imquestbio.com; appellad@niddk.nih.gov
FU Intramural Research Program of NIDDK, NIH [DK075135-01]
FX This work was supported in part by funding from the Intramural Research
Program of NIDDK (DK075135-01), NIH. Toxicity studies in rats were
performed under contract by Pharmaron (Irvine, CA).
NR 34
TC 0
Z9 0
U1 2
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-3542
EI 1872-9096
J9 ANTIVIR RES
JI Antiviral Res.
PD OCT
PY 2016
VL 134
BP 216
EP 225
DI 10.1016/j.antiviral.2016.08.022
PG 10
WC Pharmacology & Pharmacy; Virology
SC Pharmacology & Pharmacy; Virology
GA EA9SA
UT WOS:000386983800024
PM 27568924
ER
PT J
AU Levin, GV
Straat, PA
AF Levin, Gilbert V.
Straat, Patricia Ann
TI The Case for Extant Life on Mars and Its Possible Detection by the
Viking Labeled Release Experiment
SO ASTROBIOLOGY
LA English
DT Review
ID D-AMINO ACIDS; GALE CRATER; MARTIAN SOIL; PERCHLORATE; LANDER;
MICROORGANISMS; ENVIRONMENTS; METABOLISM; REACTIVITY; BACTERIA
AB The 1976 Viking Labeled Release (LR) experiment was positive for extant microbial life on the surface of Mars. Experiments on both Viking landers, 4000 miles apart, yielded similar, repeatable, positive responses. While the authors eventually concluded that the experiment detected martian life, this was and remains a highly controversial conclusion. Many believe that the martian environment is inimical to life and the LR responses were nonbiological, attributed to an as-yet-unidentified oxidant (or oxidants) in the martian soil. Unfortunately, no further metabolic experiments have been conducted on Mars. Instead, follow-on missions have sought to define the martian environment, mostly searching for signs of water. These missions have collected considerable data regarding Mars as a habitat, both past and present. The purpose of this article is to consider recent findings about martian water, methane, and organics that impact the case for extant life on Mars. Further, the biological explanation of the LR and recent nonbiological hypotheses are evaluated. It is concluded that extant life is a strong possibility, that abiotic interpretations of the LR data are not conclusive, and that, even setting our conclusion aside, biology should still be considered as an explanation for the LR experiment. Because of possible contamination of Mars by terrestrial microbes after Viking, we note that the LR data are the only data we will ever have on biologically pristine martian samples. Key Words: Extant life on MarsViking Labeled Release experimentAstrobiologyExtraterrestrial lifeMars. Astrobiology 16, 798-810.
C1 [Levin, Gilbert V.] Arizona State Univ, Tempe, AZ USA.
[Straat, Patricia Ann] NIH, Bldg 10, Bethesda, MD 20892 USA.
[Levin, Gilbert V.; Straat, Patricia Ann] Biospherics Inc, Rockville, MD USA.
RP Levin, GV (reprint author), 10709 Blossom Dr, Goodyear, AZ 85338 USA.
EM gilvlevin@gmail.com
FU National Aeronautics and Space Administration [NAS1-9690, NASW-3162,
NASW-3249]
FX The Viking Labeled Release results reported herein were supported by
Contracts NAS1-9690, NASW-3162, and NASW-3249 from the National
Aeronautics and Space Administration.
NR 54
TC 0
Z9 0
U1 38
U2 38
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1531-1074
EI 1557-8070
J9 ASTROBIOLOGY
JI Astrobiology
PD OCT
PY 2016
VL 16
IS 10
BP 798
EP 810
DI 10.1089/ast.2015.1464
PG 13
WC Astronomy & Astrophysics; Biology; Geosciences, Multidisciplinary
SC Astronomy & Astrophysics; Life Sciences & Biomedicine - Other Topics;
Geology
GA DZ8QR
UT WOS:000386136400007
PM 27626510
ER
PT J
AU Betsou, F
Bulla, A
Cho, SY
Clements, J
Chuaqui, R
Coppola, D
De Souza, Y
De Wilde, A
Grizzle, W
Guadagni, F
Gunter, E
Heil, S
Hodgkinson, V
Kessler, J
Kiehntopf, M
Kim, HS
Koppandi, I
Shea, K
Singh, R
Sobel, M
Somiari, S
Spyropoulos, D
Stone, M
Tybring, G
Valyi-Nagy, K
Van den Eynden, G
Wadhwa, L
AF Betsou, Fay
Bulla, Alexandre
Cho, Sang Yun
Clements, Judith
Chuaqui, Rodrigo
Coppola, Domenico
De Souza, Yvonne
De Wilde, Annemieke
Grizzle, William
Guadagni, Fiorella
Gunter, Elaine
Heil, Stacey
Hodgkinson, Verity
Kessler, Joseph
Kiehntopf, Michael
Kim, Hee Sung
Koppandi, Iren
Shea, Katheryn
Singh, Rajeev
Sobel, Marc
Somiari, Stella
Spyropoulos, Demetri
Stone, Mars
Tybring, Gunnel
Valyi-Nagy, Klara
Van den Eynden, Gert
Wadhwa, Lalita
TI Assays for Qualification and Quality Stratification of Clinical
Biospecimens Used in Research: A Technical Report from the ISBER
Biospecimen Science Working Group
SO BIOPRESERVATION AND BIOBANKING
LA English
DT Article
DE quality control; biospecimen; qualification; tissue; cells; biological
fluid
ID CEREBROSPINAL-FLUID; HUMAN PLASMA; SERUM-PROTEINS; CYSTATIN-C;
P-SELECTIN; STORAGE; STABILITY; BIOMARKER; BLOOD; EXPRESSION
AB This technical report presents quality control (QC) assays that can be performed in order to qualify clinical biospecimens that have been biobanked for use in research. Some QC assays are specific to a disease area. Some QC assays are specific to a particular downstream analytical platform. When such a qualification is not possible, QC assays are presented that can be performed to stratify clinical biospecimens according to their biomolecular quality.
C1 [Betsou, Fay] Integrated BioBank Luxemburg, 6 Rue Nicolas Ernest Barble, L-1210 Luxembourg, Luxembourg.
[Bulla, Alexandre] Univ Hosp Geneva, Biotheque SML, Div Genet & Lab Med DMGL, Geneva, Switzerland.
[Cho, Sang Yun] Natl Biobank Korea, Cheongju, South Korea.
[Clements, Judith] Queensland Univ Technol, Australian Prostate Canc Bioresource, Brisbane, Qld, Australia.
[Chuaqui, Rodrigo] NCI, Canc Diag Program, Div Canc Treatment & Diag DCTD, Rockville, MD USA.
[Coppola, Domenico] Univ S Florida, Moffitt Canc Ctr, Dept Anat Pathol, Tampa, FL USA.
[De Souza, Yvonne] Univ Calif San Francisco, AIDS Specimen Bank, San Francisco, CA 94143 USA.
[De Wilde, Annemieke] Univ Ziekenhuis Antwerpen, Edegem, Belgium.
[Grizzle, William] Univ Alabama Birmingham, Birmingham, AL USA.
[Guadagni, Fiorella] San Raffaele Rome Univ, IRCCS San Raffaele Pisana, Rome, Italy.
[Gunter, Elaine] Specimen Solut LLC, Tucker, Rep of Georgia.
[Heil, Stacey] Coriell Inst Med Res, Camden, NJ USA.
[Hodgkinson, Verity] NSW Canc Council, Canc Res Div, Woolloomooloo, NSW, Australia.
[Kessler, Joseph] Medpace Reference Labs, Cincinnati, OH USA.
[Kiehntopf, Michael] Univ Klinikum Jena, Jena, Germany.
[Kim, Hee Sung] Chung Ang Univ, Coll Med, Dept Pathol, Dongjak Gu, South Korea.
[Koppandi, Iren] Cellular Technol Ltd, Shaker Hts, OH USA.
[Shea, Katheryn] Precis Med Inc, Frederick, MD USA.
[Singh, Rajeev] Houston Methodist Res Inst, Biorepository, Houston, TX USA.
[Sobel, Marc] Amer Soc Invest Pathol, Bethesda, MD USA.
[Somiari, Stella] Windber Res Inst, Biobank & Biospecimen Sci Res, Windber, PA USA.
[Spyropoulos, Demetri] Med Univ South Carolina, Childrens Res Inst, Dept Pathol & Lab Med, Charleston, SC USA.
[Stone, Mars] Blood Syst Res Inst, San Francisco, CA USA.
[Tybring, Gunnel] Karolinska Inst, Stockholm, Sweden.
[Valyi-Nagy, Klara] Univ Illinois, Coll Med, Dept Pathol, Univ Illinois Biorepository, Chicago, IL 60612 USA.
[Van den Eynden, Gert] GZA Hosp, Dept Pathol & Cytol, Antwerp, Belgium.
[Wadhwa, Lalita] Baylor Coll Med, Houston, TX 77030 USA.
RP Betsou, F (reprint author), Integrated BioBank Luxemburg, 6 Rue Nicolas Ernest Barble, L-1210 Luxembourg, Luxembourg.
EM fay.betsou@ibbl.lu
OI Clements, Judith/0000-0001-6026-1964
FU NCI NIH HHS [UM1 CA183728]
NR 53
TC 0
Z9 0
U1 1
U2 1
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1947-5535
EI 1947-5543
J9 BIOPRESERV BIOBANK
JI Biopreserv. Biobank.
PD OCT
PY 2016
VL 14
IS 5
BP 398
EP 409
DI 10.1089/bio.2016.0018
PG 12
WC Cell Biology; Chemistry, Applied; Medical Laboratory Technology
SC Cell Biology; Chemistry; Medical Laboratory Technology
GA EA3BQ
UT WOS:000386473600007
PM 27046294
ER
PT J
AU Bledsoe, MJ
Henderson, M
Tasse, AM
Knoppers, BM
AF Bledsoe, Marianna J.
Henderson, Marianne
Tasse, Anne-Marie
Knoppers, Bartha M.
TI International Biobanking Summit V: Harmonizing Privacy Laws to Enable
International Biobank Research
SO BIOPRESERVATION AND BIOBANKING
LA English
DT Editorial Material
C1 [Bledsoe, Marianna J.] ISBER Sci Policy Comm, Silver Spring, MD 20993 USA.
[Henderson, Marianne] NCI, Ctr Global Hlth, Bethesda, MD 20892 USA.
[Tasse, Anne-Marie] Publ Populat Project Genom & Soc P3G, Montreal, PQ, Canada.
[Knoppers, Bartha M.] McGill Univ, Ctr Genom & Policy, Montreal, PQ, Canada.
RP Bledsoe, MJ (reprint author), ISBER Sci Policy Comm, Silver Spring, MD 20993 USA.
NR 3
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1947-5535
EI 1947-5543
J9 BIOPRESERV BIOBANK
JI Biopreserv. Biobank.
PD OCT
PY 2016
VL 14
IS 5
BP 452
EP 453
DI 10.1089/bio.2016.29012.mjb
PG 2
WC Cell Biology; Chemistry, Applied; Medical Laboratory Technology
SC Cell Biology; Chemistry; Medical Laboratory Technology
GA EA3BQ
UT WOS:000386473600015
PM 27749136
ER
PT J
AU Anderson, C
Milne, GL
Sandler, DP
Nichols, HB
AF Anderson, Chelsea
Milne, Ginger L.
Sandler, Dale P.
Nichols, Hazel B.
TI Oxidative stress in relation to diet and physical activity among
premenopausal women
SO BRITISH JOURNAL OF NUTRITION
LA English
DT Article
DE Oxidative stress; F-2-isoprostanes; Diet; Physical activity;
Premenopausal women
ID MAJOR URINARY METABOLITE; MASS-SPECTROMETRIC ASSAY; BREAST-CANCER RISK;
N-3 FATTY-ACIDS; PLASMA F-2-ISOPROSTANES; CARDIOVASCULAR-DISEASE;
DOCOSAHEXAENOIC ACID; ZINC SUPPLEMENTATION; ESTROGEN METABOLISM;
LIPID-PEROXIDATION
AB Higher levels of oxidative stress, as measured by F-2-isoprostanes, have been associated with chronic diseases such as CVD and some cancers. Improvements in diet and physical activity may help reduce oxidative stress; however, previous studies regarding associations between lifestyle factors and F-2-isoprostane concentrations have been inconsistent. The aim of this cross-sectional study was to investigate whether physical activity and intakes of fruits/vegetables, antioxidant nutrients, dietary fat subgroups and alcohol are associated with concentrations of F-2-isoprostane and the major F-2-isoprostane metabolite. Urinary F-2-isoprostane and its metabolite were measured in urine samples collected at enrolment from 912 premenopausal women (aged 35-54 years) participating in the Sister Study. Physical activity, alcohol consumption and dietary intakes were self-reported via questionnaires. With adjustment for potential confounders, the geometric means of F-2-isoprostane and its metabolite were calculated according to quartiles of dietary intakes, alcohol consumption and physical activity, and linear regression models were used to evaluate trends. Significant inverse associations were found between F-2-isoprostane and/or its metabolite and physical activity, vegetables, fruits, vitamin C, -carotene, vitamin E, -carotene, vitamin A, Se, lutein+zeaxanthin and long-chain n-3 fatty acids. Although trans fats were positively associated with both F-2-isoprostane and its metabolite, other dietary fat subgroups including SFA, n-6 fatty acids, n-3 fatty acids, MUFA, PUFA, short-chain n-3 fatty acids, long-chain n-3 fatty acids and total fat were not associated with either F-2-isoprostane or its metabolite. Our findings suggest that lower intake of antioxidant nutrients and higher intake of trans fats may be associated with greater oxidative stress among premenopausal women.
C1 [Anderson, Chelsea; Nichols, Hazel B.] Univ N Carolina, Gillings Sch Global Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27599 USA.
[Milne, Ginger L.] Vanderbilt Univ, Med Ctr, Div Clin Pharmacol, Nashville, TN 37232 USA.
[Sandler, Dale P.] NIEHS, Epidemiol Branch, NIH, Res Triangle Pk, NC 27709 USA.
RP Nichols, HB (reprint author), Univ N Carolina, Gillings Sch Global Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27599 USA.
EM hazel.nichols@unc.edu
RI Milne, Ginger/D-7648-2014;
OI Milne, Ginger/0000-0003-3890-151X; Sandler, Dale/0000-0002-6776-0018
FU Intramural Research Program of the National Institutes of Health,
National Institute of Environmental Health Sciences [Z01-ES044005]; Avon
Foundation [02-2012-085]; National Center for Advancing Translational
Sciences [KL2-TR001109]
FX This research was supported in part by the Intramural Research Program
of the National Institutes of Health, National Institute of
Environmental Health Sciences (Z01-ES044005), the Avon Foundation
(02-2012-085) and by the National Center for Advancing Translational
Sciences (KL2-TR001109).
NR 63
TC 0
Z9 0
U1 2
U2 2
PU CAMBRIDGE UNIV PRESS
PI CAMBRIDGE
PA EDINBURGH BLDG, SHAFTESBURY RD, CB2 8RU CAMBRIDGE, ENGLAND
SN 0007-1145
EI 1475-2662
J9 BRIT J NUTR
JI Br. J. Nutr.
PD OCT
PY 2016
VL 116
IS 8
BP 1416
EP 1424
DI 10.1017/S0007114516003226
PG 9
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA EA8TQ
UT WOS:000386912200011
PM 27725001
ER
PT J
AU Yang, XP
Sethi, A
Yanek, LR
Knapper, C
Nordestgaard, BG
Tybjaerg-Hansen, A
Becker, DM
Mathias, RA
Remaley, AT
Becker, LC
AF Yang, Xiaoping
Sethi, Amar
Yanek, Lisa R.
Knapper, Cathy
Nordestgaard, Borge G.
Tybjaerg-Hansen, Anne
Becker, Diane M.
Mathias, Rasika A.
Remaley, Alan T.
Becker, Lewis C.
TI SCARB1 Gene Variants Are Associated With the Phenotype of Combined High
High-Density Lipoprotein Cholesterol and High Lipoprotein (a)
SO CIRCULATION-CARDIOVASCULAR GENETICS
LA English
DT Article
DE Copenhagen City Heart Study; GeneSTAR; high-density lipoprotein
cholesterol; lipids and lipoproteins; lipoprotein (a); SCARB1 gene
variants; SR-B1 receptor
ID SCAVENGER RECEPTOR-BI; CORONARY-HEART-DISEASE; SR-BI; LDL RECEPTOR;
TARGETED MUTATION; SELECTIVE UPTAKE; DEFICIENT MICE; I GENE; POPULATION;
LOCUS
AB Background SR-B1 (scavenger receptor class B type 1), encoded by the gene SCARB1, is a lipoprotein receptor that binds both high-density lipoprotein (HDL) and low-density lipoprotein. We reported that SR-B1 is also a receptor for lipoprotein (a) (Lp(a)), mediating cellular uptake of Lp(a) in vitro and promoting clearance of Lp(a) in vivo. Although genetic variants in SCARB1 are associated with variations in HDL level, no SCARB1 variants affecting Lp(a) have been reported.
Methods and Results In an index subject with high levels of HDL cholesterol and Lp(a), SCARB1 was sequenced and demonstrated a missense mutation resulting in an S129L substitution in exon 3. To follow up, 2 cohorts (GeneSTAR, the family-based Genetic Study of Atherosclerosis Risk [n=543], and CCHS, the population-based Copenhagen City Heart Study [n=5835]) were screened for combined HDL cholesterol and Lp(a) elevations. Subjects with the extreme phenotype (HDL >80 mg/dL and Lp(a) >100 nmol/L in GeneSTAR, n=8, and >100 mg/dL in CCHS, n=9) underwent sequencing of SCARB1 exons; 15 of 18 from the combined population demonstrated genetic variants, including rare or uncommon missense or splice site mutations in 9 and homozygous synonymous variants in 6. Functional studies with 4 of the SCARB1 variants (c.386C>T, c.631-14T>G, c.4G>A, and c.631-53(m)C>T & c.726+55(m)CG>CA) showed decreased receptor function in vitro.
Conclusions Human SCARB1 gene variants are associated with a new lipid phenotype, characterized by high levels of both HDL cholesterol and Lp(a). SCARB1 exonic variants often result in diminished function of translated SR-B1 via reduced binding/intracellular transport of Lp(a).
C1 [Yang, Xiaoping; Yanek, Lisa R.; Becker, Diane M.; Mathias, Rasika A.; Becker, Lewis C.] Johns Hopkins Med Inst, Dept Med, Baltimore, MD 21205 USA.
[Sethi, Amar; Knapper, Cathy; Remaley, Alan T.] NHLBI, Lipoprotein Metab Sect, Pulm & Vasc Med Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
[Nordestgaard, Borge G.; Tybjaerg-Hansen, Anne] Univ Copenhagen, Copenhagen Univ Hosp, Fac Hlth Sci, DK-1168 Copenhagen, Denmark.
RP Becker, LC (reprint author), Johns Hopkins Univ Hosp, Div Cardiol, Halsted 500,600 N Wolfe St, Baltimore, MD 21287 USA.
EM lbecker@jhmi.edu
FU National Heart, Lung, and Blood Institute [HL72518, NR08153, HL59684,
HL65608]; National Heart, Lung, and Blood Institute; National Human
Genome Research Institute
FX Supported by grants HL72518 (Dr L.C. Becker), NR08153 (Dr D.M. Becker),
HL59684 (Dr L.C. Becker), and HL65608 (Dr L.C. Becker) from the National
Heart, Lung, and Blood Institute and intramural research funding of
National Heart, Lung, and Blood Institute and National Human Genome
Research Institute.
NR 50
TC 1
Z9 1
U1 5
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1942-325X
EI 1942-3268
J9 CIRC-CARDIOVASC GENE
JI Circ.-Cardiovasc. Genet.
PD OCT
PY 2016
VL 9
IS 5
BP 408
EP 418
DI 10.1161/CIRCGENETICS.116.001402
PG 11
WC Cardiac & Cardiovascular Systems; Genetics & Heredity
SC Cardiovascular System & Cardiology; Genetics & Heredity
GA EA4OY
UT WOS:000386593700004
PM 27651445
ER
PT J
AU Joehanes, R
Just, AC
Marioni, RE
Pilling, LC
Reynolds, LM
Mandaviya, PR
Guan, WH
Xu, T
Elks, CE
Aslibekyan, S
Moreno-Macias, H
Smith, JA
Brody, JA
Dhingra, R
Yousefi, P
Pankow, JS
Kunze, S
Shah, SH
McRae, AF
Lohman, K
Sha, J
Absher, DM
Ferrucci, L
Zhao, W
Demerath, EW
Bressler, J
Grove, ML
Huan, TX
Liu, CY
Mendelson, MM
Yao, C
Kiel, DP
Peters, A
Wang-Sattler, R
Visscher, PM
Wray, NR
Starr, JM
Ding, JZ
Rodriguez, CJ
Wareham, NJ
Irvin, MR
Zhi, DG
Barrdahl, M
Vineis, P
Ambatipudi, S
Uitterlinden, AG
Hofman, A
Schwartz, J
Colicino, E
Hou, LF
Vokonas, PS
Hernandez, DG
Singleton, AB
Bandinelli, S
Turner, ST
Ware, EB
Smith, AK
Klengel, T
Binder, EB
Psaty, BM
Taylor, KD
Gharib, SA
Swenson, BR
Liang, LM
DeMeo, DL
O'Connor, GT
Herceg, Z
Ressler, KJ
Conneely, KN
Sotoodehnia, N
Kardia, SLR
Melzer, D
Baccarelli, AA
van Meurs, JBJ
Romieu, I
Arnett, DK
Ong, KK
Liu, YM
Waldenberger, M
Deary, IJ
Fornage, M
Levy, D
London, SJ
AF Joehanes, Roby
Just, Allan C.
Marioni, Riccardo E.
Pilling, Luke C.
Reynolds, Lindsay M.
Mandaviya, Pooja R.
Guan, Weihua
Xu, Tao
Elks, Cathy E.
Aslibekyan, Stella
Moreno-Macias, Hortensia
Smith, Jennifer A.
Brody, Jennifer A.
Dhingra, Radhika
Yousefi, Paul
Pankow, James S.
Kunze, Sonja
Shah, Sonia H.
McRae, Allan F.
Lohman, Kurt
Sha, Jin
Absher, Devin M.
Ferrucci, Luigi
Zhao, Wei
Demerath, Ellen W.
Bressler, Jan
Grove, Megan L.
Huan, Tianxiao
Liu, Chunyu
Mendelson, Michael M.
Yao, Chen
Kiel, Douglas P.
Peters, Annette
Wang-Sattler, Rui
Visscher, Peter M.
Wray, Naomi R.
Starr, John M.
Ding, Jingzhong
Rodriguez, Carlos J.
Wareham, Nicholas J.
Irvin, Marguerite R.
Zhi, Degui
Barrdahl, Myrto
Vineis, Paolo
Ambatipudi, Srikant
Uitterlinden, Andre G.
Hofman, Albert
Schwartz, Joel
Colicino, Elena
Hou, Lifang
Vokonas, Pantel S.
Hernandez, Dena G.
Singleton, Andrew B.
Bandinelli, Stefania
Turner, Stephen T.
Ware, Erin B.
Smith, Alicia K.
Klengel, Torsten
Binder, Elisabeth B.
Psaty, Bruce M.
Taylor, Kent D.
Gharib, Sina A.
Swenson, Brenton R.
Liang, Liming
DeMeo, Dawn L.
O'Connor, George T.
Herceg, Zdenko
Ressler, Kerry J.
Conneely, Karen N.
Sotoodehnia, Nona
Kardia, Sharon L. R.
Melzer, David
Baccarelli, Andrea A.
van Meurs, Joyce B. J.
Romieu, Isabelle
Arnett, Donna K.
Ong, Ken K.
Liu, Yongmei
Waldenberger, Melanie
Deary, Ian J.
Fornage, Myriam
Levy, Daniel
London, Stephanie J.
TI Epigenetic Signatures of Cigarette Smoking
SO CIRCULATION-CARDIOVASCULAR GENETICS
LA English
DT Article
DE biomarkers; genome-wide association study; meta-analysis; methylation;
smoking
ID DIFFERENTIAL DNA METHYLATION; EPIGENOME-WIDE ASSOCIATION; F2RL3
METHYLATION; HUMAN GENOME; METAANALYSIS; NUTRITION; EXPRESSION;
BIOMARKERS; DISCOVERY; EXPOSURE
AB Background DNA methylation leaves a long-term signature of smoking exposure and is one potential mechanism by which tobacco exposure predisposes to adverse health outcomes, such as cancers, osteoporosis, lung, and cardiovascular disorders.
Methods and Results To comprehensively determine the association between cigarette smoking and DNA methylation, we conducted a meta-analysis of genome-wide DNA methylation assessed using the Illumina BeadChip 450K array on 15907 blood-derived DNA samples from participants in 16 cohorts (including 2433 current, 6518 former, and 6956 never smokers). Comparing current versus never smokers, 2623 cytosine-phosphate-guanine sites (CpGs), annotated to 1405 genes, were statistically significantly differentially methylated at Bonferroni threshold of P<1x10(-7) (18760 CpGs at false discovery rate <0.05). Genes annotated to these CpGs were enriched for associations with several smoking-related traits in genome-wide studies including pulmonary function, cancers, inflammatory diseases, and heart disease. Comparing former versus never smokers, 185 of the CpGs that differed between current and never smokers were significant P<1x10(-7) (2623 CpGs at false discovery rate <0.05), indicating a pattern of persistent altered methylation, with attenuation, after smoking cessation. Transcriptomic integration identified effects on gene expression at many differentially methylated CpGs.
Conclusions Cigarette smoking has a broad impact on genome-wide methylation that, at many loci, persists many years after smoking cessation. Many of the differentially methylated genes were novel genes with respect to biological effects of smoking and might represent therapeutic targets for prevention or treatment of tobacco-related diseases. Methylation at these sites could also serve as sensitive and stable biomarkers of lifetime exposure to tobacco smoke.
C1 [Joehanes, Roby; Kiel, Douglas P.] Hebrew SeniorLife, Inst Aging Res, Boston, MA USA.
[Joehanes, Roby; Kiel, Douglas P.] Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02215 USA.
[DeMeo, Dawn L.] Brigham & Womens Hosp, Channing Div Network Med, Boston, MA 02115 USA.
[Ressler, Kerry J.] Harvard Med Sch, Dept Psychiat, Boston, MA USA.
[Joehanes, Roby; Huan, Tianxiao; Liu, Chunyu; Mendelson, Michael M.; Yao, Chen; Levy, Daniel] NHLBI, Populat Sci Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
[Hernandez, Dena G.; Singleton, Andrew B.] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Joehanes, Roby; Huan, Tianxiao; Liu, Chunyu; Mendelson, Michael M.; Yao, Chen; Levy, Daniel] Framingham Heart Dis Epidemiol Study, Framingham, MA USA.
[Just, Allan C.] Icahn Sch Med Mt Sinai, Dept Prevent Med, New York, NY 10029 USA.
[Marioni, Riccardo E.; Visscher, Peter M.; Starr, John M.; Deary, Ian J.] Univ Edinburgh, Ctr Cognit Ageing & Cognit Epidemiol, Edinburgh, Midlothian, Scotland.
[Marioni, Riccardo E.] Univ Edinburgh, Ctr Genom & Expt Med, Inst Genet & Mol Med, Edinburgh, Midlothian, Scotland.
[Starr, John M.] Univ Edinburgh, Alzheimer Scotland Dementia Res Ctr, Edinburgh, Midlothian, Scotland.
[Deary, Ian J.] Univ Edinburgh, Dept Psychol, Edinburgh, Midlothian, Scotland.
[Marioni, Riccardo E.; Shah, Sonia H.; McRae, Allan F.; Visscher, Peter M.; Wray, Naomi R.] Univ Queensland, Queensland Brain Inst, Brisbane, Qld, Australia.
[McRae, Allan F.; Visscher, Peter M.] Univ Queensland, Diamantina Inst, Translat Res Inst, Brisbane, Qld, Australia.
[Pilling, Luke C.; Melzer, David] Univ Exeter, Sch Med, Inst Biomed & Clin Sci, Epidemiol & Publ Hlth Grp, Exeter, Devon, England.
[Reynolds, Lindsay M.; Rodriguez, Carlos J.; Liu, Yongmei] Wake Forest Sch Med, Dept Epidemiol & Prevent, Div Publ Hlth Sci, Winston Salem, NC USA.
[Lohman, Kurt] Wake Forest Sch Med, Dept Biostat Sci, Div Publ Hlth Sci, Winston Salem, NC USA.
[Ding, Jingzhong] Wake Forest Sch Med, Dept Internal Med, Winston Salem, NC USA.
[Mandaviya, Pooja R.; Uitterlinden, Andre G.; van Meurs, Joyce B. J.] Erasmus Univ, Med Ctr, Dept Internal Med, Rotterdam, Netherlands.
[Mandaviya, Pooja R.] Erasmus Univ, Med Ctr, Dept Clin Chem, Rotterdam, Netherlands.
[Hofman, Albert] Erasmus Univ, Med Ctr, Dept Epidemiol, Rotterdam, Netherlands.
[Guan, Weihua] Univ Minnesota, Sch Publ Hlth, Div Biostat, Minneapolis, MN USA.
[Pankow, James S.] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Xu, Tao; Kunze, Sonja; Peters, Annette; Wang-Sattler, Rui; Waldenberger, Melanie] Helmhotz Zentrum Muenchen, Inst Epidemiol 2, Res Unit Mol Epidemiol, Munich, Germany.
[Elks, Cathy E.; Wareham, Nicholas J.; Ong, Ken K.] Univ Cambridge, Inst Metab Sci, MRC Epidemiol Unit, Cambridge, England.
[Aslibekyan, Stella; Sha, Jin; Irvin, Marguerite R.; Arnett, Donna K.] Univ Alabama Birmingham, Dept Epidemiol, Birmingham, AL USA.
[Moreno-Macias, Hortensia] Autonomous Metropolitan Univ Iztapalapa, Mexico City, DF, Mexico.
[Moreno-Macias, Hortensia; Ambatipudi, Srikant; Herceg, Zdenko; Romieu, Isabelle] Int Agcy Res Canc, Lyon, France.
[Smith, Jennifer A.; Zhao, Wei; Ware, Erin B.; Kardia, Sharon L. R.] Univ Michigan, Sch Publ Hlth, Dept Epidemiol, Ann Arbor, MI 48109 USA.
[Ware, Erin B.] Univ Michigan, Inst Social Res, Res Ctr Grp Dynam, Ann Arbor, MI USA.
[Brody, Jennifer A.; Psaty, Bruce M.; Swenson, Brenton R.] Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA USA.
[Gharib, Sina A.] Univ Washington, Dept Med, Ctr Lung Biol, Div Pulm & Crit Care Med, Seattle, WA USA.
[Sotoodehnia, Nona] Univ Washington, Dept Epidemiol, Div Cardiol, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
[Dhingra, Radhika] Emory Univ, Rollins Sch Publ Hlth, Dept Environm Hlth, Atlanta, GA 30322 USA.
[Yousefi, Paul; Demerath, Ellen W.] Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA.
[Absher, Devin M.] HudsonAlpha Inst Biotechnol, Huntsville, AL USA.
[Ferrucci, Luigi] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
[Bressler, Jan; Grove, Megan L.; Fornage, Myriam] Univ Texas Hlth Sci Ctr Houston, Sch Publ Hlth, Ctr Human Genet, Houston, TX 77030 USA.
[Zhi, Degui] Univ Texas Hlth Sci Ctr Houston, Sch Biomed Informat, Houston, TX 77030 USA.
[Mendelson, Michael M.] Boston Childrens Hosp, Dept Cardiol, Boston, MA USA.
[Barrdahl, Myrto] German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
[Vineis, Paolo] Imperial Coll London, Sch Publ Hlth, MRC PHE Ctr Environm & Hlth, London, England.
[Vineis, Paolo] HuGeF Fdn, Turin, Italy.
[Sha, Jin; Baccarelli, Andrea A.] Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
[Baccarelli, Andrea A.] Harvard TH Chan Sch Publ Hlth, Dept Environm Hlth, Boston, MA USA.
[Hou, Lifang] Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, Chicago, IL 60611 USA.
[Hou, Lifang] Northwestern Univ, Feinberg Sch Med, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA.
[Vokonas, Pantel S.] VA Boston Healthcare Syst, VA Normat Aging Study, Boston, MA USA.
[Vokonas, Pantel S.] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
[Bandinelli, Stefania] Azienda Sanit Firenze, Geriatr Unit, Florence, Italy.
[Turner, Stephen T.] Mayo Clin, Div Nephrol & Hypertens, Rochester, MN USA.
[Smith, Alicia K.; Binder, Elisabeth B.; Ressler, Kerry J.] Emory Univ, Sch Med, Dept Psychiat & Behav Sci, Atlanta, GA USA.
[Conneely, Karen N.] Emory Univ, Sch Med, Dept Human Genet, Atlanta, GA USA.
[Klengel, Torsten; Binder, Elisabeth B.] Max Planck Inst Psychiat, Dept Translat Res Psychiat, Munich, Germany.
[Klengel, Torsten; Ressler, Kerry J.] McLean Hosp, Div Depress & Anxiety Disorders, 115 Mill St, Belmont, MA 02178 USA.
[Psaty, Bruce M.] Grp Hlth Cooperat Puget Sound, Grp Hlth Res Inst, Seattle, WA USA.
[Taylor, Kent D.] Los Angeles BioMed Res Inst, Inst Translat Genom & Populat Sci, Torrance, CA USA.
[Taylor, Kent D.] Harbor UCLA Med Ctr, Div Genom Outcomes, Dept Pediat, Torrance, CA 90509 USA.
[Taylor, Kent D.] Univ Calif Los Angeles, Dept Pediat, Los Angeles, CA 90024 USA.
[Taylor, Kent D.] Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA.
[Taylor, Kent D.] Univ Calif Los Angeles, Dept Human Genet, Los Angeles, CA USA.
[Liang, Liming] Harvard Sch Publ Hlth, Boston, MA USA.
[O'Connor, George T.] Boston Univ, Sch Med, Boston, MA 02118 USA.
[London, Stephanie J.] NIEHS, Epidemiol Branch, US Dept HHS, NIH, POB 12233,Room A306, Res Triangle Pk, NC 27709 USA.
RP London, SJ (reprint author), NIEHS, Epidemiol Branch, US Dept HHS, NIH, POB 12233,Room A306, Res Triangle Pk, NC 27709 USA.
EM london2@niehs.nih.gov
RI Shah, Sonia/N-7547-2013;
OI Mendelson, Michael/0000-0001-7590-3958; Shah, Sonia/0000-0001-5860-4526;
London, Stephanie/0000-0003-4911-5290; Colicino,
Elena/0000-0002-1875-8448; Smith, Jennifer/0000-0002-3575-5468; Just,
Allan/0000-0003-4312-5957; Pankow, James/0000-0001-7076-483X;
AMBATIPUDI, SRIKANT/0000-0003-3102-3603
FU National Heart, Lung, and Blood Institute [R01HL105756]; NIH; National
Institute of Environmental Health Sciences; National Heart Lung and
Blood Institute
FX Infrastructure for the CHARGE consortium is provided by the National
Heart, Lung, and Blood Institute grant R01HL105756. This work was
supported in part by the Intramural Research Program of the NIH;
National Institute of Environmental Health Sciences; and the National
Heart Lung and Blood Institute. Additional funding sources for each
cohort can be found in the Data Supplement.
NR 43
TC 6
Z9 6
U1 9
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1942-325X
EI 1942-3268
J9 CIRC-CARDIOVASC GENE
JI Circ.-Cardiovasc. Genet.
PD OCT
PY 2016
VL 9
IS 5
BP 436
EP 447
DI 10.1161/CIRCGENETICS.116.001506
PG 12
WC Cardiac & Cardiovascular Systems; Genetics & Heredity
SC Cardiovascular System & Cardiology; Genetics & Heredity
GA EA4OY
UT WOS:000386593700007
PM 27651444
ER
PT J
AU Mital, S
Musunuru, K
Garg, V
Russell, MW
Lanfear, DE
Gupta, RM
Hickey, KT
Ackerman, MJ
Perez, MV
Roden, DM
Woo, D
Fox, CS
Ware, S
AF Mital, Seema
Musunuru, Kiran
Garg, Vidu
Russell, Mark W.
Lanfear, David E.
Gupta, Rajat M.
Hickey, Kathleen T.
Ackerman, Michael J.
Perez, Marco V.
Roden, Dan M.
Woo, Daniel
Fox, Caroline S.
Ware, Stephanie
TI Enhancing Literacy in Cardiovascular Genetics: A Scientific Statement
From the American Heart Association
SO CIRCULATION-CARDIOVASCULAR GENETICS
LA English
DT Article
DE AHA Scientific Statements; aneurysm; arrhythmia; cardiomyopathy;
channelopathy; congenital heart defects; genetic testing; genetics;
pharmacogenetics; pharmacology
ID LONG QT SYNDROME; OF-FUNCTION POLYMORPHISM; PRIMARY-CARE; MEDICAL
GENETICS; DILATED CARDIOMYOPATHY; MUSCULAR-DYSTROPHIES; CLINICAL
MANAGEMENT; CONSENSUS STATEMENT; PRACTICE GUIDELINES; INCIDENTAL
FINDINGS
AB Advances in genomics are enhancing our understanding of the genetic basis of cardiovascular diseases, both congenital and acquired, and stroke. These advances include finding genes that cause or increase the risk for childhood and adult-onset diseases, finding genes that influence how patients respond to medications, and the development of genetics-guided therapies for diseases. However, the ability of cardiovascular and stroke clinicians to fully understand and apply this knowledge to the care of their patients has lagged. This statement addresses what the specialist caring for patients with cardiovascular diseases and stroke should know about genetics; how they can gain this knowledge; how they can keep up-to-date with advances in genetics, genomics, and pharmacogenetics; and how they can apply this knowledge to improve the care of patients and families with cardiovascular diseases and stroke.
C1 [Mital, Seema] Hosp Sick Children, 555 Univ Ave, Toronto, ON M5G 1X8, Canada.
[Musunuru, Kiran] Univ Penn, Cardiovasc Inst, Philadelphia, PA 19104 USA.
[Ackerman, Michael J.] Mayo Clin, Rochester, MN USA.
[Fox, Caroline S.] NHLBI, Bldg 10, Bethesda, MD 20892 USA.
[Garg, Vidu] Ohio State Univ, Nationwide Childrens Hosp, Columbus, OH 43210 USA.
[Gupta, Rajat M.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Hickey, Kathleen T.] Columbia Univ, Med Ctr, New York, NY 10027 USA.
[Lanfear, David E.] Henry Ford Hosp, Detroit, MI 48202 USA.
[Perez, Marco V.] Stanford Univ, Stanford, CA 94305 USA.
[Roden, Dan M.] Vanderbilt Univ, Sch Med, 221 Kirkland Hall, Nashville, TN 37235 USA.
[Russell, Mark W.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Ware, Stephanie] Indiana Univ Sch Med, Indianapolis, IN 46202 USA.
[Woo, Daniel] Univ Cincinnati, Cincinnati, OH 45221 USA.
RP Mital, S (reprint author), Hosp Sick Children, 555 Univ Ave, Toronto, ON M5G 1X8, Canada.
RI Garg, Vidu/D-8240-2012
OI Garg, Vidu/0000-0002-3778-5927
FU NIH; Janssen; Portola; HeartWare; BioControl; Amgen; AHA; Burroughs
Wellcome; March of Dimes
FX David E. Lanfear Henry Ford Hospital NIH dagger; Janssen dagger;
Portolastar; HeartWare dagger; BioControlstar;
Amgen dagger; Stephanie Ware Indiana University School of Medicine AHA
dagger; Burroughs Wellcome dagger; March of Dimes dagger; NIH dagger
NR 126
TC 2
Z9 2
U1 4
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1942-325X
EI 1942-3268
J9 CIRC-CARDIOVASC GENE
JI Circ.-Cardiovasc. Genet.
PD OCT
PY 2016
VL 9
IS 5
BP 448
EP 467
DI 10.1161/HCG.0000000000000031
PG 20
WC Cardiac & Cardiovascular Systems; Genetics & Heredity
SC Cardiovascular System & Cardiology; Genetics & Heredity
GA EA4OY
UT WOS:000386593700008
PM 27672144
ER
PT J
AU Kendall, BJ
Rubenstein, JH
Cook, MB
Vaughan, TL
Anderson, LA
Murray, LJ
Shaheen, NJ
Corley, DA
Chandar, AK
Li, L
Greer, KB
Chak, A
El-Serag, HB
Whiteman, DC
Thrift, AP
AF Kendall, Bradley J.
Rubenstein, Joel H.
Cook, Michael B.
Vaughan, Thomas L.
Anderson, Lesley A.
Murray, Liam J.
Shaheen, Nicholas J.
Corley, Douglas A.
Chandar, Apoorva K.
Li, Li
Greer, Katarina B.
Chak, Amitabh
El-Serag, Hashem B.
Whiteman, David C.
Thrift, Aaron P.
TI Inverse Association Between Gluteofemoral Obesity and Risk of Barrett's
Esophagus in a Pooled Analysis
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE BEACON; Obesity; Esophageal Cancer; Epidemiology; Risk Factors
ID BODY-MASS INDEX; ABDOMINAL OBESITY; GASTROESOPHAGEAL-REFLUX; CENTRAL
ADIPOSITY; ADENOCARCINOMA; DISEASE; CANCER; SEX; METAANALYSIS; INSULIN
AB BACKGROUND & AIMS: Gluteofemoral obesity (determined by measurement of subcutaneous fat in the hip and thigh regions) could reduce risks of cardiovascular and diabetic disorders associated with abdominal obesity. We evaluated whether gluteofemoral obesity also reduces the risk of Barrett's esophagus (BE), a premalignant lesion associated with abdominal obesity.
METHODS: We collected data from non-Hispanic white participants in 8 studies in the Barrett's and Esophageal Adenocarcinoma Consortium. We compared measures of hip circumference (as a proxy for gluteofemoral obesity) from cases of BE (n = 1559) separately with 2 control groups: 2557 population-based controls and 2064 individuals with gastroesophageal reflux disease (GERD controls). Study-specific odds ratios (ORs) and 95% confidence intervals (95% CIs) were estimated using individual participant data and multivariable logistic regression and combined using a random-effects meta-analysis.
RESULTS: We found an inverse relationship between hip circumference and BE (OR per 5-cmincrease, 0.88; 95% CI, 0.81-0.96), compared with population-based controls in a multivariable model that included waist circumference. This association was not observed in models that did not include waist circumference. Similar results were observed in analyses stratified by frequency of GERD symptoms. The inverse association with hip circumference was statistically significant only among men (vs population-based controls: OR, 0.85; 95% CI, 0.76-0.96 for men; OR, 0.93; 95% CI, 0.74-1.16 for women). For men, within each category of waist circumference, a larger hip circumference was associated with a decreased risk of BE. Increasing waist circumference was associated with an increased risk of BE in the mutually adjusted population-based and GERD control models.
CONCLUSIONS: Although abdominal obesity is associated with an increased risk of BE, there is an inverse association between gluteofemoral obesity and BE, particularly among men.
C1 [Kendall, Bradley J.; Whiteman, David C.] QIMR Berghofer Med Res Inst, Brisbane, Qld, Australia.
[Kendall, Bradley J.] Univ Queensland, Sch Med, Brisbane, Qld, Australia.
[Rubenstein, Joel H.] Ann Arbor Vet Affairs Med Ctr, Ctr Clin Management Res, Ann Arbor, MI USA.
[Rubenstein, Joel H.] Univ Michigan, Sch Med, Dept Internal Med, Barretts Esophagus Program,Div Gastroenterol, Ann Arbor, MI USA.
[Cook, Michael B.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Vaughan, Thomas L.] Fred Hutchinson Canc Res Ctr, Program Epidemiol, Seattle, WA 98104 USA.
[Anderson, Lesley A.; Murray, Liam J.] Queens Univ Belfast, Ctr Publ Hlth, Belfast, Antrim, North Ireland.
[Shaheen, Nicholas J.] Univ N Carolina, Sch Med, Div Gastroenterol & Hepatol, Chapel Hill, NC USA.
[Corley, Douglas A.] Kaiser Permanente, Div Res, Oakland, CA USA.
[Corley, Douglas A.] San Francisco Med Ctr, San Francisco, CA USA.
[Chandar, Apoorva K.; Greer, Katarina B.; Chak, Amitabh] Case Western Reserve Univ, Div Gastroenterol & Liver Dis, Cleveland, OH 44106 USA.
[Li, Li] Case Western Reserve Univ, Swetland Ctr Environm Hlth, Dept Family Med, Cleveland, OH 44106 USA.
[El-Serag, Hashem B.] Michael E DeBakey VA Med Ctr, Ctr Innovat Qual Effectiveness & Safety, Houston VA Hlth Serv Res & Dev, Dept Med, Houston, TX USA.
[Whiteman, David C.; Thrift, Aaron P.] Baylor Coll Med, Dept Med, Sect Gastroenterol & Hepatol, Houston, TX 77030 USA.
[Thrift, Aaron P.] Baylor Coll Med, Dan L Duncan Comprehens Canc Ctr, One Baylor Plaza,MS BCM305, Houston, TX 77030 USA.
RP Thrift, AP (reprint author), Baylor Coll Med, Dept Med, Sect Gastroenterol & Hepatol, Houston, TX 77030 USA.; Thrift, AP (reprint author), Baylor Coll Med, Dan L Duncan Comprehens Canc Ctr, One Baylor Plaza,MS BCM305, Houston, TX 77030 USA.
EM aaron.thrift@bcm.edu
OI Anderson, Lesley/0000-0002-1000-3649; Whiteman,
David/0000-0003-2563-9559
FU National Institutes of Health [RO1 DK63616, 1R21DK077742, K23DK59311,
R03 DK75842, K23DK079291, R01 CA116845, K24-04-107]; NCI [U54CA163060];
Intramural Program of the National Institutes of Health;
Ireland-Northern Ireland cooperation research project grant - Northern
Ireland Research and Development Office; Health Research Board, Ireland
[RES/1699/01N/S]; Study of Digestive Health grant [NCI RO1 CA 001833];
Study of Reflux Disease grant [NCI R01 CA72866]; Established
Investigator Award in Cancer Prevention and Control grant [K05
CA124911]; US Department of Veterans Affairs [I01-CX000899]; US Public
Health Service [R21 CA135692]
FX This work was supported by the National Institutes of Health RO1 DK63616
(D.A.C.), 1R21DK077742 (N.J.S. and D.A.C.), K23DK59311 (N.J.S.), R03
DK75842 (N.J.S.), K23DK079291 (J.H.R.), R01 CA116845 (H.B.E.-S.),
K24-04-107 (H.B.E.-S.); NCI grant U54CA163060 (A.C.); the Intramural
Program of the National Institutes of Health (M.B.C.); an
Ireland-Northern Ireland cooperation research project grant sponsored by
the Northern Ireland Research and Development Office and the Health
Research Board, Ireland (Factors Influencing the
Barrett's/Adenocarcinoma Relationship) (RES/1699/01N/S to L.J.M.); the
Study of Digestive Health grant NCI RO1 CA 001833 (D.C.W.); the Study of
Reflux Disease grant NCI R01 CA72866 (T.L.V.); the Established
Investigator Award in Cancer Prevention and Control grant K05 CA124911
(T.L.V.); the US Department of Veterans Affairs grant CSRD Merit
I01-CX000899 (J.H.R.); and US Public Health Service research grant R21
CA135692 (A.C.).
NR 37
TC 3
Z9 3
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD OCT
PY 2016
VL 14
IS 10
BP 1412
EP +
DI 10.1016/j.cgh.2016.05.032
PG 11
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA EA6SO
UT WOS:000386759500011
PM 27264393
ER
PT J
AU Papadakis, GZ
Millo, C
Stratakis, CA
AF Papadakis, Georgios Z.
Millo, Corina
Stratakis, Constantine A.
TI Benign hormone-secreting adenoma within a larger adrenocortical mass
showing intensely increased activity on F-18-FDG PET/CT
SO ENDOCRINE
LA English
DT Article
DE F-18-FDG PET/CT; Computed Tomography (CT); Adrenal glands; Adenoma(s)
ID LESIONS
AB Adrenal adenomas usually show F-18-FDG activity less than that of the liver parenchyma. However, lipid-poor and hormone-secreting adenomas have been reported to show mild F-18-FDG avidity. We report on a 51-year-old female with clinical symptoms of hypercortisolemia and a large right adrenal mass detected on CT. Post-contrast CT images showed an enhancing focus in the lower pole of the mass, with corresponding markedly increased activity on F-18-FDG PET/CT. Right adrenalectomy was performed and histology revealed a benign adenoma, indicating that functioning benign adenomas can show intensely increased metabolic activity on F-18-FDG mimicking malignancy.
C1 [Papadakis, Georgios Z.] NIH, Radiol & Imaging Sci, Warren Grant Magnuson Clin Ctr CC, Bldg 10, Bethesda, MD 20892 USA.
[Millo, Corina] RAD&IS, Div Nucl Med, Bethesda, MD 20892 USA.
[Millo, Corina] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Stratakis, Constantine A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Endocrinol & Genet, CRC, Bldg 10,Room 1-3330,MSC1103, Bethesda, MD 20892 USA.
RP Stratakis, CA (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Endocrinol & Genet, CRC, Bldg 10,Room 1-3330,MSC1103, Bethesda, MD 20892 USA.
EM stratakc@mail.nih.gov
FU Intramural NIH HHS [ZIA HD008920-04]
NR 3
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-008X
EI 1559-0100
J9 ENDOCRINE
JI Endocrine
PD OCT
PY 2016
VL 54
IS 1
BP 269
EP 270
DI 10.1007/s12020-016-0969-7
PG 2
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA EA4WL
UT WOS:000386616300031
PM 27154873
ER
PT J
AU Chang, FE
Beall, SA
Cox, JM
Richter, KS
DeCherney, AH
Levy, MJ
AF Chang, Frank E.
Beall, Stephanie A.
Cox, Jeris M.
Richter, Kevin S.
DeCherney, Alan H.
Levy, Michael J.
TI Assessing the adequacy of gonadotropin-releasing hormone agonist
leuprolide to trigger oocyte maturation and management of inadequate
response
SO FERTILITY AND STERILITY
LA English
DT Article
DE Gonadotropin-releasing hormone (GnRH) agonist; leuprolide acetate; human
chorionic gonadotropin (hCG); retrigger; in vitro fertilization (IVF)
ID OVARIAN HYPERSTIMULATION SYNDROME; IN-VITRO FERTILIZATION; HIGH-RISK
PATIENTS; GNRH AGONIST; PREGNANCY RATES; LUTEAL SUPPORT; HCG;
ANTAGONIST; MULTICENTER; COTREATMENT
AB Objective: To compare outcomes of in vitro fertilization (IVF) cycles with adequate versus inadequate response to the gonadotropin-releasing hormone (GnRH) agonist trigger rescued with the use of human chorionic gonadotropin (hCG) retrigger, and to identify risk factors associated with an inadequate trigger.
Design: Retrospective cohort study.
Setting: Private practice.
Patient(s): Women at high risk for ovarian hyperstimulation syndrome who underwent an autologous IVF cycle and used GnRH agonist to trigger oocyte maturation before oocyte retrieval.
Intervention(s): Patients were triggered with GnRH agonist for final oocyte maturation before retrieval. Patients with an inadequate response, defined by low post-trigger serum LH and P concentrations or failure to recover oocytes after aspiration of several follicles, were retriggered with hCG.
Main Outcome Measure(s): Number of oocytes retrieved, fertilization rate, clinical pregnancy, and live birth.
Result(s): Two percent of patients triggered with GnRH agonist had an inadequate response and were retriggered with hCG. There was no statistically significant difference in clinical outcomes between the cycles that were retriggered with hCG and successful GnRH agonist triggers. Low body mass index, low baseline LH, and higher total dosage of gonadotropins required for stimulation were associated with an increased risk of having an inadequate response to the GnRH agonist trigger.
Conclusion(s): A small minority of patients triggered with GnRH agonist had an inadequate response. Rescheduling of oocyte retrieval after hCG retrigger yielded similar IVF outcomes. Evaluation of trigger response based on serum LH and P concentrations is time dependent. Patient characteristics suggestive of hypothalamic hypofunction were predictive of an inadequate response to the GnRH agonist trigger. (C) 2016 by American Society for Reproductive Medicine.
C1 [Chang, Frank E.; Beall, Stephanie A.; Richter, Kevin S.; Levy, Michael J.] Shady Grove Fertil Reprod Sci Ctr, 15001 Shady Grove Rd, Rockville, MD 20850 USA.
[Beall, Stephanie A.; Cox, Jeris M.; DeCherney, Alan H.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
RP Chang, FE (reprint author), Shady Grove Fertil Reprod Sci Ctr, 15001 Shady Grove Rd, Rockville, MD 20850 USA.
EM frank.chang@integramed.com
NR 21
TC 0
Z9 0
U1 3
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2016
VL 106
IS 5
BP 1093
EP +
DI 10.1016/j.fertnstert.2016.06.013
PG 11
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA EA7RG
UT WOS:000386828800022
PM 27341988
ER
PT J
AU Owen, CM
Pal, L
Mumford, SL
Freeman, R
Isaac, B
McDonald, L
Santoro, N
Taylor, HS
Wolff, EF
AF Owen, Carter M.
Pal, Lubna
Mumford, Sunni L.
Freeman, Ruth
Isaac, Barbara
McDonald, Linda
Santoro, Nanette
Taylor, Hugh S.
Wolff, Erin F.
TI Effects of hormones on skin wrinkles and rigidity vary by
race/ethnicity: four-year follow-up from the ancillary skin study of the
Kronos Early Estrogen Prevention Study
SO FERTILITY AND STERILITY
LA English
DT Article
DE Menopause; hormone therapy; skin wrinkles; skin rigidity; race
ID POSTMENOPAUSAL WOMEN; ETHNIC-DIFFERENCES; COLLAGEN CONTENT; THERAPY;
ESTRADIOL
AB Objective: To measure skin wrinkles and rigidity in menopausal women of varying race/ethnicity with or without hormone therapy (HT) for up to four years.
Design: Randomized, double-blind, placebo-controlled trial.
Setting: Academic medical centers.
Patient(s): Women (42-58 years of age) within 36 months of last menstrual period and enrolled in the Kronos Early Estrogen Prevention Study (KEEPS).
Intervention(s): Treatment with 0.45 mg oral conjugated equine estrogens (CEE), transdermal E-2 (50 mu g/d) with micronized P (200 mg daily), or placebo for 4 years.
Main Outcome Measure(s): Skin wrinkles were assessed at 11 locations on the face and neck, and skin rigidity was assessed at the forehead and cheek at baseline and yearly for 4 years.
Result(s): Neither total wrinkle score nor total rigidity score was significantly different at baseline or over the 4-year follow-up among patients randomized to CEE, E-2, or placebo. Skin wrinkle and rigidity scores were primarily affected by race/ethnicity, with scores being significantly different between races for almost all of the wrinkle parameters and for all of the rigidity measures. There was no association between race and response to HT for total wrinkle or rigidity scores. Black women had the lowest wrinkle scores compared with white women across all 4 years. In general, skin rigidity decreased in all groups over time, but black women had significantly reduced total facial rigidity compared with white women after 4 years.
Conclusion(s): Race is the strongest predictor of the advancement of skin aging in the 4 years following menopause. HT does not appear to affect skin wrinkles or rigidity at most facial locations. Clinical Trial Registration Number: NCT00154180. (Fertil Steril (R) 2016;106:1170-5. (C) 2016 by American Society for Reproductive Medicine.)
C1 [Owen, Carter M.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
[Pal, Lubna; McDonald, Linda; Taylor, Hugh S.] Yale Univ, Dept Obstet Gynecol & Reprod Sci, New Haven, CT USA.
[Mumford, Sunni L.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, NIH, Bethesda, MD USA.
[Freeman, Ruth; Isaac, Barbara] Albert Einstein Coll Med, Obstet & Gynecol & Womens Hlth, Div Reprod Endocrinol & Infertil, Bronx, NY 10467 USA.
[Santoro, Nanette] Univ Colorado, Dept Obstet & Gynecol & Womens Hlth, Denver Sch Med, Aurora, CO USA.
[Wolff, Erin F.] Celmatix, New York, NY USA.
RP Owen, CM (reprint author), Program Reprod & Adult Endocrinol, 10 CRC,Room 1E-3140,10 Ctr Dr,MSC 1109, Bethesda, MD 20892 USA.
EM carter.owen@mail.nih.gov
FU Bayer Women's Healthcare; Pfizer; Bayer; Abbvie; Euroscreen; Kronos
Longevity Research Institute Reproductive Scientist Development Program
[NIH K12HD00849]; Berlex Foundation; National Institutes of Health [U54
HD052668]; Intramural Research Program of the Eunice Kennedy Shriver
National Institute of Child Health and Human Development, National
Institutes of Health, Bethesda, Maryland
FX C.M.O. has nothing to disclose. L.P. has nothing to disclose. S.L.M. has
nothing to disclose. R.F. has nothing to disclose. B.I. has nothing to
disclose. L.M. has nothing to disclose. N.S. reports stock options in
Menogenix and investigator-initiated grant support from Bayer Women's
Healthcare. H.S.T. reports grants and personal fees from Pfizer, Bayer,
and Abbvie and personal fees from Euroscreen. E.F.W. has nothing to
disclose.; Supported by the Kronos Longevity Research Institute
Reproductive Scientist Development Program (NIH K12HD00849) and the
Berlex Foundation (E.F.W.), the National Institutes of Health (U54
HD052668, H.S.T.), and the Intramural Research Program of the Eunice
Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health, Bethesda, Maryland.
NR 17
TC 0
Z9 0
U1 2
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2016
VL 106
IS 5
BP 1170
EP +
DI 10.1016/j.fertnstert.2016.06.023
PG 9
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA EA7RG
UT WOS:000386828800033
PM 27393520
ER
PT J
AU Rupert, CB
Heltzel, JMH
Taylor, DJ
Rusche, LN
AF Rupert, Christopher B.
Heltzel, Justin M. H.
Taylor, Derek J.
Rusche, Laura N.
TI Sporadic Gene Loss After Duplication Is Associated with Functional
Divergence of Sirtuin Deacetylases Among Candida Yeast Species
SO G3-GENES GENOMES GENETICS
LA English
DT Article
DE Sir2; Hst1; specifically retained ancestral gene; CTG clade
ID SACCHAROMYCES-CEREVISIAE; PHYLOGENETIC ANALYSIS; ALBICANS; EXPRESSION;
SIR2; DNA; HETEROCHROMATIN; BIODIVERSITY; SELECTION; GENOMICS
AB Gene duplication promotes the diversification of protein functions in several ways. Ancestral functions can be partitioned between the paralogs, or a new function can arise in one paralog. These processes are generally viewed as unidirectional. However, paralogous proteins often retain related functions and can substitute for one another. Moreover, in the event of gene loss, the remaining paralog might regain ancestral functions that had been shed. To explore this possibility, we focused on the sirtuin deacetylase SIR2 and its homolog HST1 in the CTG clade of yeasts. HST1 has been consistently retained throughout the clade, whereas SIR2 is only present in a subset of species. These NAD(+)-dependent deacetylases generate condensed chromatin that represses transcription and stabilizes tandemly repeated sequences. By analyzing phylogenetic trees and gene order, we found that a single duplication of the SIR2/HST1 gene occurred, likely prior to the emergence of the CTG clade. This ancient duplication was followed by at least two independent losses of SIR2. Functional characterization of Sir2 and Hst1 in three species revealed that these proteins have not maintained consistent functions since the duplication. In particular, the rDNA locus is deacetylated by Sir2 in Candida albicans, by Hst1 in C. lusitaniae, and by neither paralog in C. parapsilosis. In addition, the subtelomeres in C. albicans are deacetylated by Sir2 rather than by Hst1, which is orthologous to the sirtuin associated with Saccharomyces cerevisiae subtelomeres. These differences in function support the model that sirtuin deacetylases can regain ancestral functions to compensate for gene loss.
C1 [Rupert, Christopher B.; Heltzel, Justin M. H.; Taylor, Derek J.; Rusche, Laura N.] SUNY Buffalo, Dept Biol Sci, 109 Cooke Hall, Buffalo, NY 14260 USA.
[Heltzel, Justin M. H.] NIA, Lab Mol Biol & Immunol, NIH, Baltimore, MD 21224 USA.
RP Rusche, LN (reprint author), SUNY Buffalo, Dept Biol Sci, 109 Cooke Hall, Buffalo, NY 14260 USA.
EM lrusche@buffalo.edu
FU National Science Foundation [MCB-1121569, ARC-1023334]
FX We thank G. Butler and S. Noble for strains and plasmids, and the
members of the Rusche lab for helpful discussion. This research was
supported by grants from the National Science Foundation to L.N.R.
(MCB-1121569) and D.J.T. (ARC-1023334).
NR 48
TC 0
Z9 0
U1 0
U2 0
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
PY 2016
VL 6
IS 10
BP 3297
EP 3305
DI 10.1534/g3.116.033845
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA EA4KM
UT WOS:000386581200023
PM 27543294
ER
PT J
AU Bolte, FJ
O'Keefe, A
Serti, E
Rivera, E
Liang, TJ
Ghany, MG
Rehermann, B
AF Bolte, Fabian J.
O'Keefe, Ashley
Serti, Elisavet
Rivera, Elenita
Liang, T. Jake
Ghany, Marc G.
Rehermann, Barbara
TI Monocyte-dependent activation of intrahepatic mucosal associated
invariant T cells resolves within weeks of antiviral therapy for
hepatitis C
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Bolte, Fabian J.; O'Keefe, Ashley; Serti, Elisavet; Rivera, Elenita; Liang, T. Jake; Ghany, Marc G.; Rehermann, Barbara] NIDDK, Liver Dis Branch, NIH, DHHS, 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 10
BP 5A
EP 5A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493800011
ER
PT J
AU Uchida, T
Walsh, K
Hiraga, N
Imamura, M
Koh, C
Glenn, J
Uprichard, SL
Heller, T
Dahari, H
Chayama, K
AF Uchida, Takuro
Walsh, Kevin
Hiraga, Nobuhiko
Imamura, Michio
Koh, Christopher
Glenn, Jeffrey
Uprichard, Susan L.
Heller, Theo
Dahari, Harel
Chayama, Kazuaki
TI Characterization of HDV and HBV kinetics during acute co-infection and
interferon-alpha treatment in uPA/SCID chimeric mice with humanized
livers
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Walsh, Kevin; Uprichard, Susan L.; Dahari, Harel] Loyola Univ, Med Ctr, Program Expt & Theoret Modeling, Div Hepatol,Dept Med, 2160 S 1st Ave, Maywood, IL 60153 USA.
[Uchida, Takuro; Hiraga, Nobuhiko; Imamura, Michio; Chayama, Kazuaki] Hiroshima Univ, Inst Biomed & Hlth Sci, Dept Gastroenterol & Metab, Appl Life Sci, Hiroshima, Japan.
[Koh, Christopher; Heller, Theo] NIDDK, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
[Glenn, Jeffrey] Stanford Univ, Sch Med, Div Gastroenterol & Hepatol, Stanford, CA USA.
[Uprichard, Susan L.] Loyola Univ, Med Ctr, Dept Microbiol & Immunol, 2160 S 1st Ave, Maywood, IL 60153 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 18
BP 9A
EP 10A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493800019
ER
PT J
AU Emmanuel, B
Gross, C
Masur, H
Kottilil, S
Kattakuzhy, S
AF Emmanuel, Benjamin
Gross, Chloe
Masur, Henry
Kottilil, Shyam
Kattakuzhy, Sarah
TI High Efficacy in Real-World Treatment of Cirrhotic Patients by
Non-Specialist Providers
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Emmanuel, Benjamin; Gross, Chloe; Kottilil, Shyam; Kattakuzhy, Sarah] Univ Maryland, Sch Med, Inst Human Virol, Div Clin Care & Res, Baltimore, MD 21201 USA.
[Masur, Henry] NIH, Crit Care, Bldg 10, 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 22
BP 11A
EP 12A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493800023
ER
PT J
AU Ajmera, VH
Belt, PH
Wilson, L
Gill, RM
Loomba, R
Kleiner, DE
Tetri, BA
Terrault, N
AF Ajmera, Veeral H.
Belt, Patricia H.
Wilson, Laura
Gill, Ryan M.
Loomba, Rohit
Kleiner, David E.
Tetri, Brent A.
Terrault, Norah
TI No Benefit from Modest Alcohol Use in Nonalcoholic Fatty Liver Disease
(NAFLD)
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Ajmera, Veeral H.; Terrault, Norah] UCSF, Gastroenterol, San Francisco, CA USA.
[Belt, Patricia H.; Wilson, Laura] Johns Hopkins Univ, Baltimore, MD USA.
[Gill, Ryan M.] UCSF, Pathol, San Francisco, CA USA.
[Loomba, Rohit] Univ Calif San Diego, San Diego, CA USA.
[Kleiner, David E.] NCI, Pathol, Bethesda, MD 20892 USA.
[Tetri, Brent A.] St Luis Univ, St Louis, MO 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 31
BP 16A
EP 16A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493800032
ER
PT J
AU Kleiner, DE
Brunt, EM
Belt, PH
Wilson, L
Guy, CD
Yeh, MM
Gill, RM
Kowdley, KV
Tetri, BA
Sanyal, AJ
AF Kleiner, David E.
Brunt, Elizabeth M.
Belt, Patricia H.
Wilson, Laura
Guy, Cynthia D.
Yeh, Matthew M.
Gill, Ryan M.
Kowdley, Kris V.
Tetri, Brent A.
Sanyal, Arun J.
TI Diagnostic Pattern and Disease Activity Are Related To Disease
Progression and Regression in Nonalcoholic Fatty Liver Disease
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Sanyal, Arun J.] Virginia Commonwealth Univ, Richmond, VA USA.
[Kleiner, David E.] NIH, Bldg 10, Bethesda, MD 20892 USA.
[Brunt, Elizabeth M.] Washington Univ, St Louis, MO USA.
[Belt, Patricia H.; Wilson, Laura] Johns Hopkins Sch Publ Hlth, Baltimore, MD USA.
[Guy, Cynthia D.] Duke Univ, Durham, NC USA.
[Yeh, Matthew M.] Univ Washington, Seattle, WA USA.
[Gill, Ryan M.] Univ Calif San Francisco, San Francisco, CA USA.
[Kowdley, Kris V.] Swedish Med Ctr, Seattle, WA USA.
[Tetri, Brent A.] St Louis Univ, St Louis, MO 63103 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
BP 19A
EP 19A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493800038
ER
PT J
AU Puri, P
Mirshahi, F
Daita, K
Vincent, R
Liangpunsakul, S
Chalasani, NP
Crabb, DW
Shah, V
Kamath, PS
Gores, GJ
Katz, BP
Radaeva, S
Sanyal, AJ
AF Puri, Puneet
Mirshahi, Faridoddin
Daita, Kalyani
Vincent, Robert
Liangpunsakul, Suthat
Chalasani, Naga P.
Crabb, David W.
Shah, Vijay
Kamath, Patrick S.
Gores, Gregory J.
Katz, Barry P.
Radaeva, Svetlana
Sanyal, Arun J.
TI Quantitative and Qualitative Changes in the Circulating Microbiome Are
Associated With the Development and Severity of Alcoholic Hepatitis
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Puri, Puneet; Mirshahi, Faridoddin; Daita, Kalyani; Vincent, Robert; Sanyal, Arun J.] Virginia Commonwealth Univ, Richmond, VA USA.
[Liangpunsakul, Suthat; Chalasani, Naga P.; Crabb, David W.; Katz, Barry P.] Indiana Univ Sch Med, Indianapolis, IN 46202 USA.
[Shah, Vijay; Kamath, Patrick S.; Gores, Gregory J.] Mayo Clin, Rochester, MN USA.
[Radaeva, Svetlana] NIAAA, 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 48
BP 25A
EP 25A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493800049
ER
PT J
AU Alao, H
Cam, M
Zhang, F
Suarez, DF
Henderson, WA
Fourie, NI
Li, QS
Liang, TJ
Ghany, MG
AF Alao, Hawwa
Cam, Margaret
Zhang, Fang
Suarez, Daniel F.
Henderson, Wendy A.
Fourie, N. I.
Li, Qisheng
Liang, T. Jake
Ghany, Marc G.
TI Role Of MiRNAs In Hepatitis C Virus Clearance In Prior Non-Responders
During Therapy With DAAs
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Alao, Hawwa; Zhang, Fang; Suarez, Daniel F.; Li, Qisheng; Liang, T. Jake; Ghany, Marc G.] NIDDK, NIH, Baltimore, MD USA.
[Cam, Margaret] NCI, NIH, Bethesda, MD 20892 USA.
[Henderson, Wendy A.; Fourie, N. I.] NINR, 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 66
BP 34A
EP 35A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493800067
ER
PT J
AU Asselah, T
Shiha, G
Feld, JJ
Abergel, A
Kohli, A
Kottilil, S
Ruane, PJ
Naggie, S
Letterio, C
Hahambis, TA
Llewellyn, J
Natha, M
Kersey, K
McNally, J
Brainard, DM
Esmat, GE
AF Asselah, Tarik
Shiha, Gamal
Feld, Jordan J.
Abergel, Armando
Kohli, Anita
Kottilil, Shyam
Ruane, Peter J.
Naggie, Susanna
Letterio, Cathleen
Hahambis, Thomas A.
Llewellyn, Joseph
Natha, Macky
Kersey, Kathryn
McNally, John
Brainard, Diana M.
Esmat, Gamal E.
TI Integrated Analysis of SOF plus RBV, LDV/SOF or SOF/VEL for the
Treatment of Genotype 4 Chronic HCV Infection
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Letterio, Cathleen; Hahambis, Thomas A.; Llewellyn, Joseph; Natha, Macky; Kersey, Kathryn; McNally, John; Brainard, Diana M.] Gilead Sci, Foster City, CA USA.
[Kohli, Anita] Creighton Univ, Sch Med, Phoenix, AZ USA.
[Feld, Jordan J.] Toronto Western Hosp, Toronto, ON, Canada.
[Ruane, Peter J.] Ruane Med & Liver Hlth Inst, Los Angeles, CA USA.
[Shiha, Gamal] Almansoura Univ Hosp, Mansoura, Egypt.
[Abergel, Armando] Beaujon Hosp, Clermont Ferrand, France.
[Asselah, Tarik] Hop Beaujon, Serv Hepatol, Clichy, France.
[Asselah, Tarik] Hop Beaujon, INSERM, U773, CRB3, Clichy, France.
[Naggie, Susanna] Duke Clin Res Inst, Durham, NC USA.
[Kottilil, Shyam] NIAID, Baltimore, MD USA.
[Esmat, Gamal E.] Cairo Univ, Cairo, Egypt.
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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 75
BP 40A
EP 41A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493800076
ER
PT J
AU Alonso, EM
Ye, W
Hawthorne, K
Venkat, VL
Loomes, KM
Mack, CL
Hertel, PM
Karpen, SJ
Kerkar, N
Molleston, JP
Murray, KF
Romero, R
Rosenthal, P
Schwarz, KB
Shneider, B
Suchy, FJ
Turmelle, YP
Wang, KS
Whitington, PF
Sherker, AH
Sokol, RJ
Bezerra, JA
Magee, JC
AF Alonso, Estella M.
Ye, Wen
Hawthorne, Kieran
Venkat, Veena L.
Loomes, Kathleen M.
Mack, Cara L.
Hertel, Paula M.
Karpen, Saul J.
Kerkar, Nanda
Molleston, Jean P.
Murray, Karen F.
Romero, Rene
Rosenthal, Phil
Schwarz, Kathleen B.
Shneider, Benjamin
Suchy, Frederick J.
Turmelle, Yumirle P.
Wang, Kasper S.
Whitington, Peter F.
Sherker, Averell H.
Sokol, Ronald J.
Bezerra, Jorge A.
Magee, John C.
TI Impact of Steroid Therapy on Early Growth in Infants with Biliary
Atresia
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Alonso, Estella M.; Whitington, Peter F.] Ann & Robert H Lurie Childrens Hosp, Div Pediat Gastroenterol Hepatol & Nutr, Chicago, IL USA.
[Ye, Wen] Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.
[Hawthorne, Kieran] Arbor Res Collaborat Hlth, Ann Arbor, MI USA.
[Venkat, Veena L.] Childrens Hosp Pittsburgh, Pittsburgh, PA 15213 USA.
[Loomes, Kathleen M.] Childrens Hosp Philadelphia, Pediat Gastroenterol Hepatol & Nutr, Philadelphia, PA 19104 USA.
[Mack, Cara L.; Suchy, Frederick J.; Sokol, Ronald J.] Univ Colorado, Sch Med, Sect Pediat Gastroenterol Hepatol & Nutr, Aurora, CO USA.
[Hertel, Paula M.; Shneider, Benjamin] Baylor Coll Med, Pediat Gastroenterol Hepatol & Nutr, Houston, TX 77030 USA.
[Karpen, Saul J.; Romero, Rene] Emory Univ, Sch Med, Childrens Healthcare Atlanta, Pediat Gastroenterol Hepatol & Nutr, Atlanta, GA USA.
[Kerkar, Nanda; Wang, Kasper S.] Childrens Hosp Los Angeles, Div Pediat Surg, Los Angeles, CA 90027 USA.
[Molleston, Jean P.] Indiana Univ Sch Med, Riley Hosp Children, Pediat Gastroenterol Hepatol & Nutr, Indianapolis, IN 46202 USA.
[Murray, Karen F.] Univ Washington, Med Ctr, Seattle Childrens, Div Gastroenterol & Hepatol, Seattle, WA 98195 USA.
[Rosenthal, Phil] Univ Calif San Francisco, Dept Pediat, Div Gastroenterol Hepatol & Nutr, San Francisco, CA USA.
[Schwarz, Kathleen B.] Johns Hopkins Sch Med, Baltimore, MD USA.
[Turmelle, Yumirle P.] Washington Univ, Sch Med, St Louis, MO USA.
[Sherker, Averell H.] NIDDKD, NIH, Bethesda, MD USA.
[Bezerra, Jorge A.] Cincinnati Childrens Hosp Med, Div Pediat Gastroenterol Hepatol & Nutr, Cincinnati, OH USA.
[Magee, John C.] Univ Michigan, Sch Med, Ann Arbor, MI USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 79
BP 43A
EP 43A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493800080
ER
PT J
AU Murray, KF
Rodriguez-Baez, N
Kleiner, DE
Shaffer, M
Cooper, KL
Ling, SC
Rosenthal, P
Schwarz, KB
Schwarzenberg, SJ
AF Murray, Karen F.
Rodriguez-Baez, Norberto
Kleiner, David E.
Shaffer, Michele
Cooper, Kara L.
Ling, Simon C.
Rosenthal, Philip
Schwarz, Kathleen B.
Schwarzenberg, Sarah J.
TI Liver Histology in North American Children with Immune-active Chronic
Hepatitis B Infection
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Murray, Karen F.; Shaffer, Michele; Cooper, Kara L.] Univ Washington, Med Ctr, Div Pediat GI & Hepatol, Seattle, WA 98195 USA.
[Rodriguez-Baez, Norberto] Univ Texas Dallas, Pediatr Gastroenterol, Dallas, TX USA.
[Kleiner, David E.] NCI, Pathol, Washington, DC USA.
[Ling, Simon C.] Hosp Sick Kids, Pediat Gastroenterol & Hepatol, Toronto, ON, Canada.
[Rosenthal, Philip] Univ Calif San Fransisco, Pediat Gastroenterol, San Francisco, CA USA.
[Schwarz, Kathleen B.] Johns Hopkins Sch Med, Pediat Gastroenterol, Baltimore, MD USA.
[Schwarzenberg, Sarah J.] Univ Minnesota, Pediat Gastroenterol, Minneapolis, MN 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 105
BP 57A
EP 57A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493800106
ER
PT J
AU Chalasani, NP
Ghabril, M
Fontana, RJ
Barnhart, HX
Hayashi, PH
Ahmad, J
Stolz, A
Navarro, VJ
Hoofnagle, JH
AF Chalasani, Naga P.
Ghabril, Marwan
Fontana, Robert J.
Barnhart, Huiman X.
Hayashi, Paul H.
Ahmad, Jawad
Stolz, Andrew
Navarro, Victor J.
Hoofnagle, Jay H.
TI Idiosyncratic drug induced liver injury in African Americans: Causes,
Clinical Features and Outcomes
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Chalasani, Naga P.; Ghabril, Marwan] Indiana Univ Sch Med, Indianapolis, IN 46202 USA.
[Fontana, Robert J.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Barnhart, Huiman X.] Duke Univ, Med Ctr, Durham, NC USA.
[Hayashi, Paul H.] Univ N Carolina, Chapel Hill, NC USA.
[Ahmad, Jawad] Icahn Sch Med Mt Sinai, Med Ctr, New York, NY 10029 USA.
[Stolz, Andrew] Univ Southern Calif, Los Angeles, CA USA.
[Navarro, Victor J.] Einstein Healthcare Network, Philadelphia, PA USA.
[Hoofnagle, Jay H.] NIDDK, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 116
BP 64A
EP 64A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493800117
ER
PT J
AU Ahmad, J
Rossi, S
Rodgers, SK
Fontana, RJ
Chalasani, NP
Stolz, A
Hayashi, PH
Barnhart, HX
Kleiner, DE
Bjornsson, E
AF Ahmad, Jawad
Rossi, Simona
Rodgers, Shuchi K.
Fontana, Robert J.
Chalasani, Naga P.
Stolz, Andrew
Hayashi, Paul H.
Barnhart, Huiman X.
Kleiner, David E.
Bjornsson, Einar
TI Drug Induced Liver Injury Associated with Sclerosing Cholangitis Like
Changes on Magnetic Resonance Cholangiography Imaging
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Ahmad, Jawad] Icahn Sch Med Mt Sinai, Div Liver Dis, New York, NY 10029 USA.
[Rossi, Simona] Einstein Med Ctr, Philadelphia, PA USA.
[Rodgers, Shuchi K.] Einstein Med Ctr, Dept Radiol, Philadelphia, PA USA.
[Fontana, Robert J.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Chalasani, Naga P.] Indiana Univ, Indianapolis, IN 46204 USA.
[Stolz, Andrew] Univ Southern Calif, Los Angeles, CA USA.
[Hayashi, Paul H.] Univ N Carolina, Chapel Hill, NC USA.
[Barnhart, Huiman X.] Duke Univ, Durham, NC USA.
[Kleiner, David E.] NCI, Bethesda, MD 20892 USA.
[Bjornsson, Einar] Landspitali Univ Hosp, Reykjavik, Iceland.
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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 118
BP 65A
EP 65A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493800119
ER
PT J
AU Chalasani, NP
Xu, YF
de Boer, YS
Raman, I
Lian, Y
Eckert, G
Li, QZ
Hoofnagle, JH
AF Chalasani, Naga P.
Xu, Yuanfang
de Boer, Ynto S.
Raman, Indu
Lian, Yun
Eckert, George
Li, Quanzhen
Hoofnagle, Jay H.
TI Serum Ig M autoantibody profiling using autoantigen arrays identifies
Histone H4 Ig M antibody as highly specific to patients with autoimmune
like drug induced liver injury
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Chalasani, Naga P.; Xu, Yuanfang; Eckert, George] Indiana Univ Sch Med, Indianapolis, IN 46202 USA.
[Raman, Indu; Lian, Yun; Li, Quanzhen] Univ Texas Southwestern Med Ctr Dallas, Dallas, TX 75390 USA.
[de Boer, Ynto S.] Vrije Univ Amsterdam, Med Ctr, Amsterdam, Netherlands.
[Hoofnagle, Jay H.] NIDDK, 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 119
BP 65A
EP 66A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493800120
ER
PT J
AU Gawrieh, S
Karns, R
Kleiner, DE
Goldblatt, MI
Olivier, M
Chalasani, NP
Xanthakos, S
AF Gawrieh, Samer
Karns, Rebekah
Kleiner, David E.
Goldblatt, Matthew I.
Olivier, Michael
Chalasani, Naga P.
Xanthakos, Stavra
TI Comparative analysis of global hepatic gene expression profiles in
adolescents and adults with NAFLD
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Gawrieh, Samer; Chalasani, Naga P.] Indiana Univ Sch Med, Div Gastroenterol & Hepatol, Indianapolis, IN 46202 USA.
[Olivier, Michael] Texax Biomed Inst, Genet, San Antonio, TX USA.
[Karns, Rebekah] Cincinnati Children Hosp, Bioinformat, Cincinnati, OH USA.
[Kleiner, David E.] NCI, Pathol Lab, Bldg 10, Bethesda, MD 20892 USA.
[Goldblatt, Matthew I.] Med Coll Wisconsin, Surg, Milwaukee, WI 53226 USA.
[Xanthakos, Stavra] Cincinnati Children Hosp, Div Gastroenterol & Hepatol, 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 199
BP 105A
EP 105A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493800200
ER
PT J
AU Chen, JG
Odena, G
Xu, MJ
Rodrigo, D
Altamirano, J
Massey, VL
Affo, S
Cabezas, J
Gines, P
Caballeria, J
Sancho-Bru, P
Gao, B
Bataller, R
AF Chen, Jiegen
Odena, Gemma
Xu, Ming-Jiang
Rodrigo, Daniel
Altamirano, Jose
Massey, Veronica L.
Affo, Silvia
Cabezas, Joaquin
Gines, Pere
Caballeria, Juan
Sancho-Bru, Pau
Gao, Bin
Bataller, Ramon
TI Lipocalin-2 overexpression is mediated by LPS-TL4 pathway and mediates
liver fibrosis in alcoholic hepatitis
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Chen, Jiegen; Odena, Gemma; Massey, Veronica L.; Cabezas, Joaquin; Bataller, Ramon] Univ N Carolina, Dept Med, Chapel Hill, NC USA.
[Chen, Jiegen; Odena, Gemma; Massey, Veronica L.; Cabezas, Joaquin; Bataller, Ramon] Univ N Carolina, Dept Nutr, Chapel Hill, NC USA.
[Chen, Jiegen; Odena, Gemma; Massey, Veronica L.; Cabezas, Joaquin; Bataller, Ramon] Univ N Carolina, Div Gastroenterol & Hepatol, Chapel Hill, NC USA.
[Xu, Ming-Jiang; Gao, Bin] NIAAA, Lab Liver Dis, NIH, Bethesda, MD USA.
[Rodrigo, Daniel; Affo, Silvia; Gines, Pere; Caballeria, Juan; Sancho-Bru, Pau] CIBER Enfermedades Hepat & Digest CIBERehd, Inst INvest Biomed August Pi & Sunyer IDIBAPS, Hosp Clin, Barcelona, Spain.
[Altamirano, Jose] Univ Autonoma Barcelona, Vall dHebron Hosp, Dept Internal Med, Liver Unit, Barcelona, Spain.
[Altamirano, Jose] Univ Autonoma Barcelona, Vall dHebron Inst Recerca VHIR, Barcelona, Spain.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 219
BP 116A
EP 116A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493800220
ER
PT J
AU Han, MAT
Samala, N
Rizvi, BS
Etzion, O
Wright, EC
Patel, R
Samala-Venkata, V
Kleiner, DE
Koh, C
Pavletic, S
Williams, K
Heller, T
AF Han, Ma Ai Thanda
Samala, Niharika
Rizvi, Bisharah S.
Etzion, Ohad
Wright, Elizabeth C.
Patel, Ruchi
Samala-Venkata, Vikramaditya
Kleiner, David E.
Koh, Christopher
Pavletic, Steven
Williams, Kirsten
Heller, Theo
TI Abnormal Liver Tests Are Inaccurate For Diagnosis Of Chronic Hepatic
Graft Versus Host Disease In Critically Ill Patients
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Han, Ma Ai Thanda; Samala, Niharika; Rizvi, Bisharah S.; Etzion, Ohad; Patel, Ruchi; Samala-Venkata, Vikramaditya; Koh, Christopher; Heller, Theo] NIDDK, Liver Dis Branch, NIH, Rockville, MD USA.
[Wright, Elizabeth C.] NIDDK, NIH, Bethesda, MD 20892 USA.
[Kleiner, David E.; Pavletic, Steven; Williams, Kirsten] NCI, 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 356
BP 182A
EP 182A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493801098
ER
PT J
AU Bae, H
Hodge, D
Yang, GX
Leung, PS
Valencia, J
Tsuneyama, K
Gershwin, ME
Young, HA
AF Bae, Heekyong
Hodge, Deborah
Yang, Guo-Xiang
Leung, Patrick S.
Valencia, Julio
Tsuneyama, Koichi
Gershwin, M. Eric
Young, Howard A.
TI The interplay of type I and type II interferons in murine autoimmune
cholangitis as a basis for sex-biased autoimmunity
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Bae, Heekyong; Hodge, Deborah; Valencia, Julio; Young, Howard A.] NCI, Canc & Inflammat Program, Frederick, MD 21701 USA.
[Yang, Guo-Xiang; Leung, Patrick S.; Gershwin, M. Eric] Univ Calif Davis, Sch Med, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
[Tsuneyama, Koichi] Univ Tokushima, Grad Sch, Dept Pathol & Lab Med, Tokushima, Japan.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 364
BP 186A
EP 186A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493801106
ER
PT J
AU Roberts, LR
Farshidfar, F
Zheng, SY
Gingras, MC
Newton, Y
Shih, J
Robertson, AG
Hinoue, T
Hoadley, KA
Gibbs, R
Roszik, J
Covington, K
Wu, CC
Shinbrot, E
Stransky, N
Hegde, AM
Yang, JD
Reznik, E
Sadeghi, S
Pedamallu, CS
Ojesina, AI
Hess, J
Auman, JT
Rhie, SK
Bowlby, R
Borad, MJ
Stuart, J
Sander, C
Akbani, R
Cherniack, AD
Laird, PW
Deshpande, V
Mounajjed, T
Foo, WC
Torbenson, M
Kleiner, DE
Wheeler, DA
Mcree, AJ
Bathe, OF
Andersen, JB
Bardeesy, N
Kwong, LN
AF Roberts, Lewis R.
Farshidfar, Farshad
Zheng, Siyuan
Gingras, Marie-Claude
Newton, Yulia
Shih, Juliann
Robertson, A. Gordon
Hinoue, Toshinori
Hoadley, Katherine A.
Gibbs, Richard
Roszik, Jason
Covington, Kyle
Wu, Chia-Chin
Shinbrot, Eve
Stransky, Nicolas
Hegde, Apurva M.
Yang, Ju Dong
Reznik, Ed
Sadeghi, Sara
Pedamallu, Chandra Sekhar
Ojesina, Akinyemi I.
Hess, Julian
Auman, J. Todd
Rhie, Suhn K.
Bowlby, Reanne
Borad, Mitesh J.
Stuart, Josh
Sander, Chris
Akbani, Rehan
Cherniack, Andrew D.
Laird, Peter W.
Deshpande, Vikram
Mounajjed, Taofic
Foo, Wai Chin
Torbenson, Michael
Kleiner, David E.
Wheeler, David A.
Mcree, Autumn J.
Bathe, Oliver F.
Andersen, Jesper B.
Bardeesy, Nabeel
Kwong, Lawrence N.
TI Integrative Genomic Analysis of Cholangiocarcinoma Identifies Distinct
IDH-Mutant Molecular Profiles
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Roberts, Lewis R.; Yang, Ju Dong; Mounajjed, Taofic; Torbenson, Michael] Mayo Clin, Coll Med, Rochester, MN USA.
[Farshidfar, Farshad] Univ Calgary, Calgary, AB, Canada.
[Zheng, Siyuan; Roszik, Jason; Wu, Chia-Chin; Hegde, Apurva M.; Akbani, Rehan; Foo, Wai Chin; Kwong, Lawrence N.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Gingras, Marie-Claude; Gibbs, Richard; Covington, Kyle; Shinbrot, Eve; Wheeler, David A.] Baylor Coll Med, Houston, TX 77030 USA.
[Newton, Yulia; Stuart, Josh] Univ Calif Santa Cruz, Santa Cruz, CA 95064 USA.
[Shih, Juliann; Cherniack, Andrew D.] Eli & Edythe L Broad Inst Massachusetts Inst Tech, Cambridge, MA USA.
[Robertson, A. Gordon; Sadeghi, Sara; Bowlby, Reanne] BC Canc Agcy, Canadas Michael Smith Genome Sci Ctr, Vancouver, BC, Canada.
[Hinoue, Toshinori; Laird, Peter W.] Van Andel Res Inst, Grand Rapids, MI USA.
[Hoadley, Katherine A.; Auman, J. Todd; Mcree, Autumn J.] Univ North Carolina Chapel Hill, Chapel Hill, NC USA.
[Stransky, Nicolas] Blueprint Med, Cambridge, MA USA.
[Reznik, Ed] Mem Sloan Kettering Canc Ctr, 1275 York Ave, New York, NY 10021 USA.
[Pedamallu, Chandra Sekhar; Sander, Chris] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Ojesina, Akinyemi I.] Univ Alabama Birmingham, Birmingham, AL USA.
[Rhie, Suhn K.] Univ Southern Calif, Los Angeles, CA USA.
[Borad, Mitesh J.] Mayo Clin, Scottsdale, AZ USA.
[Kleiner, David E.] NCI, Bethesda, MD 20892 USA.
[Bathe, Oliver F.] Tom Baker Canc Clin, Calgary, AB, Canada.
[Andersen, Jesper B.] Univ Copenhagen, DK-1168 Copenhagen, Denmark.
[Bardeesy, Nabeel] Harvard Med Sch, Ctr Canc, Gen Hosp 1Massachusetts, Boston, MA USA.
[Hess, Julian] Broad Inst, Cambridge, MA USA.
[Deshpande, Vikram] Massachusetts Gen Hosp, Boston, MA 02114 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 447
BP 227A
EP 227A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493801189
ER
PT J
AU Castven, D
Czauderna, C
Becker, D
Worns, MA
Grimminger, P
Lang, H
Thorgeirsson, SS
Galle, PR
Marquardt, JU
AF Castven, Darko
Czauderna, Carolin
Becker, Diana
Worns, Marcus A.
Grimminger, Peter
Lang, Hauke
Thorgeirsson, Snorri S.
Galle, Peter R.
Marquardt, Jens U.
TI Importance of Stem-like Tumor-initiating Cells for the Development of
Chemoresistance During Anti-angiogenic Therapies in Hepatocellular
Carcinoma
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Castven, Darko; Czauderna, Carolin; Becker, Diana; Worns, Marcus A.; Galle, Peter R.; Marquardt, Jens U.] Johannes Gutenberg Univ Mainz, Dept Internal Med, Mainz, Germany.
[Thorgeirsson, Snorri S.] NCI, CCR, NIH, Bethesda, MD 20892 USA.
[Grimminger, Peter] Johannes Gutenberg Univ Mainz, Dept Surg, Mainz, Germany.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 494
BP 250A
EP 250A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493801236
ER
PT J
AU An, P
Zeng, Z
Winkler, CA
AF An, Ping
Zeng, Zheng
Winkler, Cheryl A.
TI The loss-of-function S267F variant in the HBV receptor NTCP reduces
human risk to HBV infection
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [An, Ping; Winkler, Cheryl A.] NCI, Basic Res Lab, Leidos Biomed Res Inc, Frederick Natl Lab Canc Res, Frederick, MD 21701 USA.
[Zeng, Zheng] Peking Univ, Dept Infect Dis, Hosp 1, Beijing, Peoples R China.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 602
BP 300A
EP 300A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493801342
ER
PT J
AU Zhang, Q
Matsuura, K
Kleiner, DE
Zamboni, F
Alter, HJ
Farci, P
AF Zhang, Quan
Matsuura, Kentaro
Kleiner, David E.
Zamboni, Fausto
Alter, Harvey J.
Farci, Patrizia
TI Identification of Long Noncoding RNA Associated with Hepatocellular
Carcinoma of Different Viral Etiology
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Zhang, Quan; Farci, Patrizia] NIH, Infect Dis Lab, Bldg 10, Bethesda, MD 20892 USA.
[Matsuura, Kentaro; Alter, Harvey J.] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
[Kleiner, David E.] NCI, Pathol Lab, NIH, Bldg 10, Bethesda, MD 20892 USA.
[Zamboni, Fausto] Brotzu Hosp, Liver Transplantat Ctr, Cagliari, Italy.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 609
BP 303A
EP 304A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493801349
ER
PT J
AU Townsend, EC
Moon, MS
Zhang, G
Firke, M
Han, MAT
Kleiner, DE
Koh, C
Heller, T
AF Townsend, Elizabeth C.
Moon, Mi Sun
Zhang, Grace
Firke, Marian
Han, Ma Ai Thanda
Kleiner, David E.
Koh, Christopher
Heller, Theo
TI Microbial Translocation in the Context of Hepatitis B and Hepatitis D
infection
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Townsend, Elizabeth C.; Moon, Mi Sun; Zhang, Grace; Firke, Marian; Han, Ma Ai Thanda; Koh, Christopher; Heller, Theo] NIH, Liver Dis Branch, Bldg 10, Bethesda, MD 20892 USA.
[Kleiner, David E.] NCI, 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 627
BP 312A
EP 313A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493801367
ER
PT J
AU Tillmann, HL
Barnhart, HX
Serrano, J
Rockey, DC
AF Tillmann, Hans L.
Barnhart, Huiman X.
Serrano, Jose
Rockey, Don C.
TI A Novel Computerized Drug Induced Liver Injury Causality Assessment Tool
(DILI-CAT)
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Tillmann, Hans L.] East Carolina Univ, Dept Med, Div Gastroenterol Hepatol & Nutr, Greenville, NC USA.
[Barnhart, Huiman X.] Duke Univ, Duke Clin Res Inst, Durham, NC USA.
[Serrano, Jose] NIDDK, Digest Dis Branch, Bethesda, DC USA.
[Rockey, Don C.] Med Univ South Carolina, Med, Charleston, SC 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 645
BP 320A
EP 321A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493801385
ER
PT J
AU Amet, T
Li, W
Yang, D
Liangpunsakul, S
Puri, P
Kamath, PS
Sanyal, AJ
Shah, V
Radaeva, S
Crabb, DW
Chalasani, NP
Yu, QA
AF Amet, Tohti
Li, Wei
Yang, Dennis
Liangpunsakul, Suthat
Puri, Puneet
Kamath, Patrick S.
Sanyal, Arun J.
Shah, Vijay
Radaeva, Svetlana
Crabb, David W.
Chalasani, Naga P.
Yu, Qigui A.
TI Profiles of inflammatory cytokines/chemokines and immune cell activation
in patients with alcoholic hepatitis
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Amet, Tohti; Li, Wei; Yang, Dennis; Yu, Qigui A.] Indiana Univ Sch Med, Microbiol & Immunol, Indianapolis, IN 46202 USA.
[Liangpunsakul, Suthat; Crabb, David W.; Chalasani, Naga P.] Indiana Univ Sch Med, Dept Med, Indianapolis, IN 46202 USA.
[Puri, Puneet; Sanyal, Arun J.] Virginia Commonwealth Univ, Richmond, VA USA.
[Kamath, Patrick S.; Shah, Vijay] Mayo Clin, Rochester, MN USA.
[Radaeva, Svetlana] NIAAA, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 689
BP 341A
EP 342A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493801429
ER
PT J
AU Vatsalya, V
Song, M
Schwandt, M
Cave, M
Barve, S
George, D
Ramchandani, VA
McClain, C
AF Vatsalya, Vatsalya
Song, Ming
Schwandt, Melanie
Cave, Matthew
Barve, Shirish
George, David
Ramchandani, Vijay A.
McClain, Craig
TI Effects of sex, drinking history and omega-3 and omega-6 fatty acids
dysregulation on the onset of liver injury in very heavy drinking
alcohol dependent patients
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Vatsalya, Vatsalya; Song, Ming; Cave, Matthew; Barve, Shirish; McClain, Craig] Univ Louisville, Med, Louisville, KY 40292 USA.
[Schwandt, Melanie; George, David; Ramchandani, Vijay A.] NIAAA, DICBR LCTS, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 688
BP 341A
EP 341A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493801428
ER
PT J
AU Li, W
Amet, T
Yang, K
Liangpunsakul, S
Puri, P
Kamath, PS
Sanyal, AJ
Shah, V
Radaeva, S
Crabb, DW
Chalasani, NP
Yu, QA
AF Li, Wei
Amet, Tohti
Yang, Kai
Liangpunsakul, Suthat
Puri, Puneet
Kamath, Patrick S.
Sanyal, Arun J.
Shah, Vijay
Radaeva, Svetlana
Crabb, David W.
Chalasani, Naga P.
Yu, Qigui A.
TI Monocyte/macrophage activation and IL-22 dysregulation in patients with
alcoholic hepatitis
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Li, Wei; Amet, Tohti; Yang, Kai; Yu, Qigui A.] Indiana Univ Sch Med, Microbiol & Immunol, Indianapolis, IN 46202 USA.
[Liangpunsakul, Suthat; Crabb, David W.; Chalasani, Naga P.] Indiana Univ Sch Med, Dept Med, Indianapolis, IN 46202 USA.
[Puri, Puneet; Sanyal, Arun J.] Virginia Commonwealth Univ, Richmond, VA USA.
[Kamath, Patrick S.; Shah, Vijay] Mayo Clin, Rochester, MN USA.
[Radaeva, Svetlana] NIAAA, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 3
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 696
BP 344A
EP 345A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493801436
ER
PT J
AU Etzion, O
Ali, R
Koh, C
Levy, E
Kleiner, DE
Rampertaap, S
Rosenzweig, S
Takyar, VK
Han, MAT
Lingala, S
Fryzek, N
Haynes-Williams, V
Heller, T
AF Etzion, Ohad
Ali, Rabab
Koh, Christopher
Levy, Elliot
Kleiner, David E.
Rampertaap, Shakuntala
Rosenzweig, Sergio
Takyar, Varun K.
Han, Ma Ai Thanda
Lingala, Shilpa
Fryzek, Nancy
Haynes-Williams, Vanessa
Heller, Theo
TI Disparate Changes in Adaptive Immunity in Systemic vs. Portal Venous
Circulation, Across the Spectrum of HCV Associated Liver Disease
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Kleiner, David E.] NCI, Pathol Lab, Bldg 10, Bethesda, MD 20892 USA.
[Etzion, Ohad; Ali, Rabab; Koh, Christopher; Levy, Elliot; Kleiner, David E.; Rampertaap, Shakuntala; Rosenzweig, Sergio; Takyar, Varun K.; Han, Ma Ai Thanda; Lingala, Shilpa; Fryzek, Nancy; Haynes-Williams, Vanessa; Heller, Theo] NIH, Bldg 10, Bethesda, MD 20892 USA.
[Etzion, Ohad; Ali, Rabab; Koh, Christopher; Takyar, Varun K.; Han, Ma Ai Thanda; Lingala, Shilpa; Fryzek, Nancy; Haynes-Williams, Vanessa; Heller, Theo] NIDDK, Liver Dis Branch, Bethesda, MD 20892 USA.
[Levy, Elliot] Ctr Clin, Intervent Radiol, Bethesda, MD USA.
[Rampertaap, Shakuntala; Rosenzweig, Sergio] Ctr Clin, Immunol Serv, 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 731
BP 362A
EP 362A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493802003
ER
PT J
AU Unalp-Arida, A
Ruhl, CE
AF Unalp-Arida, Aynur
Ruhl, Constance E.
TI The Burden of Viral Hepatitis B and C Infection in the United States
Population
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Unalp-Arida, Aynur] NIDDK, Bethesda, MD 20892 USA.
[Ruhl, Constance E.] Social & Sci Syst Inc, Silver Spring, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 793
BP 391A
EP 391A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493802062
ER
PT J
AU Naggie, S
Rosenthal, E
Kattakuzhy, S
McGinnis, J
Naik, S
Natha, M
Llewellyn, J
Haubrich, R
Osinusi, AO
Stamm, LM
Cooper, C
Dieterich, DT
Sulkowski, MS
AF Naggie, Susanna
Rosenthal, Eric
Kattakuzhy, Sarah
McGinnis, Justin
Naik, Sarjita
Natha, Macky
Llewellyn, Joseph
Haubrich, Richard
Osinusi, Anu O.
Stamm, Luisa M.
Cooper, Curtis
Dieterich, Douglas T.
Sulkowski, Mark S.
TI Real World Effectiveness of Ledipasvir/Sofosbuvir (LDV/SOF) in Patients
Coinfected With HCV and HIV-1: A Comparative Analysis of Clinical Trials
with Four Real World Cohorts
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Naggie, Susanna] Duke Univ, Durham, NC USA.
[Rosenthal, Eric] Univ Hosp Archet, Nice, France.
[Kattakuzhy, Sarah] NIH, Rockville, MD USA.
[McGinnis, Justin] Univ Southern Calif, Los Angeles, CA USA.
[Naik, Sarjita; Natha, Macky; Llewellyn, Joseph; Haubrich, Richard; Osinusi, Anu O.; Stamm, Luisa M.] Gilead Sci, Foster City, CA USA.
[Cooper, Curtis] Ottawa Hosp, Ottawa, ON, Canada.
[Dieterich, Douglas T.] Mt Sinai Sch Med, New York, NY USA.
[Sulkowski, Mark S.] 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 892
BP 445A
EP 445A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493802159
ER
PT J
AU Tran, NJQ
Kovalic, AJ
Kleiner, DE
Bridges, D
Satapathy, SK
AF Tran, Nhu Josephine Q.
Kovalic, Alexander J.
Kleiner, David E.
Bridges, Dave
Satapathy, Sanjaya K.
TI The use of calcineurin inhibitors post-liver transplantation and the
donor SOD2 C47T polymorphism influence recurrent NAFLD after liver
transplantation
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Tran, Nhu Josephine Q.] Univ Tennessee, Ctr Hlth Sci, Prevent Med, Memphis, TN 38163 USA.
[Bridges, Dave] Univ Tennessee, Ctr Hlth Sci, Physiol, Memphis, TN 38163 USA.
[Satapathy, Sanjaya K.] Univ Tennessee, Ctr Hlth Sci, Surg, Memphis, TN 38163 USA.
[Satapathy, Sanjaya K.] Methodist Univ Hosp, Transplant Inst, Memphis, TN USA.
[Kovalic, Alexander J.] Univ Tennessee, Ctr Hlth Sci, Med, Memphis, TN 38163 USA.
[Kleiner, David E.] NIH, 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 990
BP 502A
EP 502A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493802257
ER
PT J
AU Bolte, FJ
O'Keefe, A
Etzion, O
Ali, R
Serti, E
Liang, TJ
Heller, T
Rehermann, B
AF Bolte, Fabian J.
O'Keefe, Ashley
Etzion, Ohad
Ali, Rabab
Serti, Elisavet
Liang, T. Jake
Heller, Theo
Rehermann, Barbara
TI Innate immune cell phenotype and function in different compartments of
the gut-liver-axis in chronic liver diseas
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Bolte, Fabian J.; O'Keefe, Ashley; Etzion, Ohad; Ali, Rabab; Serti, Elisavet; Liang, T. Jake; Heller, Theo; Rehermann, Barbara] NIDDK, Liver Dis Branch, NIH, DHHS, 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 1029
BP 520A
EP 520A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493802296
ER
PT J
AU Ouyang, XS
Han, SN
Lau, G
Feng, DC
Cardone, R
Cai, SY
Hoque, R
Chen, YL
Yang, WH
Garcia-Martinez, I
Wang, FS
Gao, B
Torok, NJ
Kibbey, R
Mehal, WZ
AF Ouyang, Xinshou
Han, Sheng-Na
Lau, George
Feng, Dechun
Cardone, Rebecca
Cai, Shi-Ying
Hoque, Rafaz
Chen, Yonglin
Yang, Wei-Hong
Garcia-Martinez, Irma
Wang, Fu-Sheng
Gao, Bin
Torok, Natalie J.
Kibbey, Richard
Mehal, Wajahat Z.
TI Digoxin protects from sterile inflammation in the liver by targeting
pyruvate kinase M2 (PKM2) promoted HIF-1 alpha transactivation
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Ouyang, Xinshou; Han, Sheng-Na; Lau, George; Cardone, Rebecca; Cai, Shi-Ying; Hoque, Rafaz; Chen, Yonglin; Yang, Wei-Hong; Garcia-Martinez, Irma; Kibbey, Richard; Mehal, Wajahat Z.] Yale Univ, New Haven, CT USA.
[Feng, Dechun; Gao, Bin] NIAAA, NIH, Bethesda, MD USA.
[Wang, Fu-Sheng] Beijing 302 Hosp, Inst Translat Hepatol, Beijing, Peoples R China.
[Torok, Natalie J.] Univ Calif Davis, Dept Med, Sacramento, CA USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 1035
BP 522A
EP 523A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493802302
ER
PT J
AU Samala, N
Hallinan, EK
Kleiner, DE
Hoofnagle, JH
Loomba, R
AF Samala, Niharika
Hallinan, Erin K.
Kleiner, David E.
Hoofnagle, Jay H.
Loomba, Rohit
TI Race and Ethnicity in Patients with Nonalcoholic Fatty Liver Disease
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Hoofnagle, Jay H.] NIDDK, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
[Samala, Niharika] Indiana Univ Sch Med, Med, Indianapolis, IN 46202 USA.
[Hallinan, Erin K.] John Hopkins Univ Bloomberg Sch Publ Hlth, Stat, Indianapolis, IN USA.
[Kleiner, David E.] NCI, Pathol, NIH, Indianapolis, IN USA.
[Loomba, Rohit] Univ Calif San Diego, Med, Indianapolis, IN 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 1055
BP 532A
EP 532A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493802322
ER
PT J
AU Unalp-Arida, A
Ruhl, CE
AF Unalp-Arida, Aynur
Ruhl, Constance E.
TI The US Fatty Liver Index and Fatty Liver Index as Potential Steatosis
Markers Predict Liver Disease Mortality in the US Population
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Unalp-Arida, Aynur] NIDDK, Bethesda, MD 20892 USA.
[Ruhl, Constance E.] Social & Sci Syst Inc, Silver Spring, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 1059
BP 533A
EP 534A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493802326
ER
PT J
AU Unalp-Arida, A
Ruhl, CE
AF Unalp-Arida, Aynur
Ruhl, Constance E.
TI The Burden of Liver Disease in the United States Population
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Unalp-Arida, Aynur] NIDDK, Bethesda, MD 20892 USA.
[Ruhl, Constance E.] Social & Sci Syst Inc, Silver Spring, 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 1115
BP 563A
EP 563A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493802382
ER
PT J
AU Rotman, Y
Lingala, S
Morris, N
AF Rotman, Yaron
Lingala, Shilpa
Morris, Nevitt
TI Subtle Iron Deficiency is Common During Vitamin E Treatment For NAFLD
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Rotman, Yaron; Lingala, Shilpa; Morris, Nevitt] NIDDK, Liver & Energy Metab Unit, Liver Dis Branch, 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 1133
BP 571A
EP 572A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493802400
ER
PT J
AU Takyar, VK
Nath, A
Beri, A
Rotman, Y
AF Takyar, Varun K.
Nath, Anand
Beri, Andrea
Rotman, Yaron
TI How Healthy are "Healthy Volunteers"? Prevalence and Potential Impact of
Fatty Liver Disease in Volunteers to Clinical Trials
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Takyar, Varun K.; Nath, Anand; Rotman, Yaron] NIDDK, Liver & Energy Metab Unit, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
[Nath, Anand] Georgetown Univ, Sch Med, Medstar Washington Hosp Ctr, Dept Internal Med, Washington, DC USA.
[Beri, Andrea] NIH, BTRIS, Lab Informat Dev, Ctr Clin, Bldg 10, 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 1157
BP 583A
EP 583A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493802424
ER
PT J
AU Serti, E
Werner, JM
Keane, M
Bolte, FJ
Lingala, S
Morris, N
Liang, TJ
Rotman, Y
Rehermann, B
AF Serti, Elisavet
Werner, Jens M.
Keane, Meghan
Bolte, Fabian J.
Lingala, Shilpa
Morris, Nevitt
Liang, T. Jake
Rotman, Yaron
Rehermann, Barbara
TI Natural killer T cells and mucosal associated invariant T cells share
phenotypic and functional alterations in patients with non-alcoholic
fatty liver disease
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Serti, Elisavet; Werner, Jens M.; Keane, Meghan; Bolte, Fabian J.; Lingala, Shilpa; Morris, Nevitt; Liang, T. Jake; Rotman, Yaron; Rehermann, Barbara] NIDDK, Liver Dis Branch, NIH, DHHS, 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 1160
BP 584A
EP 584A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493802427
ER
PT J
AU Sampaziotis, F
de Brito, MC
Sawiak, S
Gomez-Vazquez, MJ
Berntsen, NL
Tysoe, OC
Ortmann, D
Bertero, A
Bargehr, J
Zonneveld, MC
Pedersen, MT
Pawlowski, M
Georgakopoulos, N
Yiangou, L
Godfrey, EM
Upponi, SS
Gieseck, R
Rimland, C
Simonic, I
Davies, S
Jensen, KB
Sinha, S
Gelson, W
Alexander, GJ
Melum, E
Hannan, NR
Saeb-Parsy, K
Vallier, L
AF Sampaziotis, Fotios
de Brito, Miguel Cardoso
Sawiak, Steve
Gomez-Vazquez, Maria J.
Berntsen, Natalie L.
Tysoe, Olivia C.
Ortmann, Daniel
Bertero, Alessandro
Bargehr, Johannes
Zonneveld, Marielle C.
Pedersen, Marianne T.
Pawlowski, Matthias
Georgakopoulos, Nikitas
Yiangou, Loukia
Godfrey, Edmund M.
Upponi, Sara S.
Gieseck, Richard
Rimland, Casey
Simonic, Ingrid
Davies, Susan
Jensen, Kim B.
Sinha, Sanjay
Gelson, William
Alexander, Graeme J.
Melum, Espen
Hannan, Nicholas R.
Saeb-Parsy, Kourosh
Vallier, Ludovic
TI Reconstruction of the biliary tree using primary in vitro propagated
extra-hepatic cholangiocytes and biode-gradable scaffolds
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Sampaziotis, Fotios] Cambridge Univ Hosp NHS Fdn Trust, Hepatol, Hitchin, England.
[Sampaziotis, Fotios; de Brito, Miguel Cardoso; Tysoe, Olivia C.; Ortmann, Daniel; Bertero, Alessandro; Zonneveld, Marielle C.; Georgakopoulos, Nikitas; Yiangou, Loukia; Rimland, Casey; Saeb-Parsy, Kourosh; Vallier, Ludovic] Univ Cambridge, Surg, Cambridge, England.
[Sawiak, Steve] Univ Cambridge, Clin Neurosci, Cambridge, England.
[Gomez-Vazquez, Maria J.] Univ Cambridge, Pathol, Cambridge, England.
[Bargehr, Johannes; Pawlowski, Matthias; Sinha, Sanjay; Alexander, Graeme J.] Univ Cambridge, Med, Cambridge, England.
[Pedersen, Marianne T.; Jensen, Kim B.] Univ Copenhagen, Biotech Res & Innovat Ctr, Copenhagen, Denmark.
[Godfrey, Edmund M.; Upponi, Sara S.] Cambridge Univ Hosp NHS Fdn Trust, Radiol, Cambridge, England.
[Gieseck, Richard] NIAID, Parasit Dis Lab, Bethesda, MD USA.
[Simonic, Ingrid] Cambridge Univ Hosp NHS Fdn Trust, Med Genet Labs, Cambridge, England.
[Davies, Susan] Cambridge Univ Hosp NHS Fdn Trust, Histopathol, Cambridge, England.
[Gelson, William] Cambridge Univ Hosp NHS Fdn Trust, Hepatol, Cambridge, England.
[Melum, Espen] Natl Hosp Norway, Oslo Univ Hosp, Clin Specialized Med & Surg, Norwegian PSC Res Ctr, Oslo, Norway.
[Hannan, Nicholas R.] Univ Nottingham, Ctr Biomol Sci, Nottingham, England.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 1187
BP 597A
EP 598A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493802454
ER
PT J
AU Puri, P
Daita, K
Mirshahi, F
Liangpunsakul, S
Chalasani, NP
Crabb, DW
Shah, V
Kamath, PS
Gores, GJ
Katz, BP
Sikaroodi, M
Radaeva, S
Gillevet, PM
Sanyal, AJ
AF Puri, Puneet
Daita, Kalyani
Mirshahi, Faridoddin
Liangpunsakul, Suthat
Chalasani, Naga P.
Crabb, David W.
Shah, Vijay
Kamath, Patrick S.
Gores, Gregory J.
Katz, Barry P.
Sikaroodi, Masoumeh
Radaeva, Svetlana
Gillevet, Patrick M.
Sanyal, Arun J.
TI Alcoholic Hepatitis and Disease Severity Are Associated With Distinct
Shifts in Fecal Microbial Ecology
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Puri, Puneet; Daita, Kalyani; Mirshahi, Faridoddin; Sanyal, Arun J.] Virginia Commonwealth Univ, Richmond, VA USA.
[Liangpunsakul, Suthat; Chalasani, Naga P.; Crabb, David W.; Katz, Barry P.] Indiana Univ Sch Med, Indianapolis, IN 46202 USA.
[Shah, Vijay; Kamath, Patrick S.; Gores, Gregory J.] Mayo Clin, Rochester, MN USA.
[Sikaroodi, Masoumeh; Gillevet, Patrick M.] George Mason Univ, Manassas, VA USA.
[Radaeva, Svetlana] NIAAA, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 1212
BP 609A
EP 609A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493803019
ER
PT J
AU Unalp-Arida, A
Ruhl, CE
AF Unalp-Arida, Aynur
Ruhl, Constance E.
TI The Burden of Liver Cancer in the United States Population
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Unalp-Arida, Aynur] NIDDK, Bethesda, MD 20892 USA.
[Ruhl, Constance E.] Social & Sci Syst Inc, Silver Spring, 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 1278
BP 641A
EP 642A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493803085
ER
PT J
AU Tang, MM
Alao, H
Morris, N
Walter, M
Rolman, Y
AF Tang, Michele M.
Alao, Hawwa
Morris, Nevitt
Walter, Mary
Rolman, Yaron
TI The Fatigue of Chronic Liver Disease is Associated with Altered
Circadian Rhythm of Cortisol
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Tang, Michele M.; Alao, Hawwa; Morris, Nevitt; Rolman, Yaron] NIDDK, Liver & Energy Metab Unit, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
[Tang, Michele M.] Univ Calif San Francisco, Dept Med, Div Gastroenterol, San Francisco, CA USA.
[Tang, Michele M.] Univ Calif San Francisco, UCSF Liver Transplant Ctr, San Francisco, CA 94143 USA.
[Walter, Mary] NIDDK, Clin Res Core Lab, 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 1446
BP 723A
EP 724A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493803253
ER
PT J
AU Ramirez, T
Lie, YM
Yin, S
Xu, MJ
Feng, DC
Zang, MW
Pacher, P
Gao, B
Wang, H
AF Ramirez, Teresa
Lie, Yongmei
Yin, Shi
Xu, Ming-Jiang
Feng, Dechun
Zang, Mengwei
Pacher, Pal
Gao, Bin
Wang, Hua
TI Aging aggravates alcoholic liver injury and fibrosis in mice by
downregulating Sirtuin 1 expressionin the liver
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Wang, Hua] Anhui Med Univ, Affiliated Prov Hosp, Dept Oncol, Hefei, Anhui, Peoples R China.
[Ramirez, Teresa; Lie, Yongmei; Yin, Shi; Xu, Ming-Jiang; Feng, Dechun; Gao, Bin; Wang, Hua] NIAAA, Lab Liver Dis, NIH, Rockville, MD 20852 USA.
[Zang, Mengwei] Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, Barshop Inst Longev & Aging Studies, San Antonio, TX 78229 USA.
[Pacher, Pal] NIAAA, Lab Cardiovasc Physiol & Tissue Injury, Rockville, MD 20852 USA.
RI Zhou, Zhou/R-7788-2016
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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 1513
BP 755A
EP 755A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493803320
ER
PT J
AU Chen, HQ
Li, Y
Sherban, A
Nocon, A
Luo, T
Wang, H
Bin Gao,
Zang, MW
AF Chen, Hanqing
Li, Yu
Sherban, Alex
Nocon, Allison
Luo, Ting
Wang, Hua
Bin Gao
Zang, Mengwei
TI Pharmacological and Molecular inhibition of mTORC1 Activation Reduces
Ethanol-Induced ER Stress and Ameliorates Alcoholic Liver Injury in Mice
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Chen, Hanqing; Li, Yu; Sherban, Alex; Nocon, Allison; Luo, Ting] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
[Wang, Hua; Bin Gao] NIAAA, Lab Liver Dis, NIH, Bethesda, MD USA.
[Chen, Hanqing; Zang, Mengwei] Univ Texas Hlth Sci Ctr San Antonio, Barshop Inst Longev & Aging Studies, Ctr Hlth Aging, San Antonio, TX 78229 USA.
[Chen, Hanqing; Zang, Mengwei] Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78229 USA.
[Zang, Mengwei] South Texas Vet Hlth Care Syst, Geriatr Res Educ & Clin Ctr, San Antonio, TX 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 1515
BP 756A
EP 756A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493803322
ER
PT J
AU Abdelmegeed, M
Choi, YS
Song, BJ
AF Abdelmegeed, Mohamed
Choi, Youngshim
Song, Byoung-Joon
TI The role of cytochrome P450-2E1 in fast food-induced hepatic fibrosis
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Abdelmegeed, Mohamed; Choi, Youngshim; Song, Byoung-Joon] NIH, Membrane Biochem & Biophys, 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 1546
BP 769A
EP 770A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493803353
ER
PT J
AU Naguib, G
Morris, N
Bernstein, S
Rotman, Y
AF Naguib, Gihan
Morris, Nevitt
Bernstein, Shanna
Rotman, Yaron
TI NAFLD is Associated with Decreased Oxidation of Orally-Delivered Fatty
Acids - a Palmitate Breath Test Study
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Naguib, Gihan; Morris, Nevitt; Rotman, Yaron] NIDDK, Liver & Energy Metab Unit, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
[Naguib, Gihan] Univ Maryland, Pediat Gastroenterol, Baltimore, MD 21201 USA.
[Bernstein, Shanna] NIH, Dept Nutr, Ctr Clin, Bldg 10, 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 1562
BP 776A
EP 776A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493803369
ER
PT J
AU Samala, N
Ted, H
Maloney, D
Nadler, JL
Chalasani, NP
Mirmira, R
Anderson, R
AF Samala, Niharika
Ted, Holman
Maloney, David
Nadler, Jerry L.
Chalasani, Naga P.
Mirmira, Raghavendra
Anderson, Ryan
TI Role of 12-Lipoxygenase in a Zebrafish Model of Non Alcoholic Fatty
Liver Disease (NAFLD)
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Samala, Niharika; Chalasani, Naga P.; Mirmira, Raghavendra] Indiana Univ Sch Med, Med, Indianapolis, IN 46202 USA.
[Ted, Holman] Univ Calif Santa Cruz, PBSci Chem & Biochem, Santa Cruz, CA 95064 USA.
[Maloney, David] NIH, Natl Ctr Adv Translat Sci, Bldg 10, Bethesda, MD 20892 USA.
[Anderson, Ryan] Indiana Univ Sch Med, Pediat, Indianapolis, IN 46202 USA.
[Nadler, Jerry L.] Eastern Virginia Med Sch, Internal Med, Norfolk, VA 23501 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 1566
BP 778A
EP 778A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493803373
ER
PT J
AU Suarez, DF
Loria, A
Ferreira, M
Raziuddin, A
Ghany, MG
AF Suarez, Daniel F.
Loria, Anthony
Ferreira, Michelle
Raziuddin, Arati
Ghany, Marc G.
TI Proportion of Pre-Core Mutation Determines HBV Phenotype after HBeAg
Seroconversion
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Suarez, Daniel F.; Loria, Anthony; Ferreira, Michelle; Ghany, Marc G.] NIH, Liver Dis Branch, Bldg 10, Bethesda, MD 20892 USA.
[Raziuddin, Arati] NCI, 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 1831
BP 903A
EP 903A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493804192
ER
PT J
AU Yurdaydin, C
Idilman, R
Kalkan, C
Karakaya, F
Kartal, AC
Keskin, O
Karatayli, E
Karatayli, SC
Bozdayi, AM
Koh, C
Heller, T
Glenn, J
AF Yurdaydin, Cihan
Idilman, Ramazan
Kalkan, Cagdas
Karakaya, Fatih
Kartal, Aysun Caliskan
Keskin, Onur
Karatayli, Ersin
Karatayli, Senem C.
Bozdayi, A. Mithat
Koh, Christopher
Heller, Theo
Glenn, Jeffrey
TI Exploring Optimal Dosing Of Lonafarnib With Ritonavir For The Treatment
Of Chronic Delta Hepatitis-Interim Results From The Lowr Hdv-2 Study
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Yurdaydin, Cihan; Idilman, Ramazan; Kalkan, Cagdas; Karakaya, Fatih; Kartal, Aysun Caliskan; Keskin, Onur; Karatayli, Ersin; Karatayli, Senem C.; Bozdayi, A. Mithat] Ankara Univ, Sch Med, Gastroenterol Sect, Ankara, Turkey.
[Koh, Christopher; Heller, Theo] NIDDK, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
[Glenn, Jeffrey] Stanford Univ, Sch Med, Div Gastroenterol & Hepatol, Stanford, CA 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 1845
BP 910A
EP 911A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493804206
ER
PT J
AU Li, Y
Xia, YC
Han, MF
Chen, G
Zhang, DK
Thasler, WE
Protzer, U
Ning, Q
AF Li, Yong
Xia, Yuchen
Han, Meifang
Chen, Guang
Zhang, Dake
Thasler, Wolfgang E.
Protzer, Ulrike
Ning, Qin
TI IFN-alpha-mediated Base Excision Repair Pathway Correlates with
Antiviral Response Against Hepatitis B Virus Infection
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Li, Yong; Han, Meifang; Chen, Guang; Ning, Qin] Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Wuhan, Peoples R China.
[Xia, Yuchen; Protzer, Ulrike] Tech Univ Munich, Helmholtz Zentrum Munchen, Inst Virol, D-81675 Munich, Germany.
[Xia, Yuchen] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
[Zhang, Dake] Chinese Acad Sci, Beijing Inst Genom, Key Lab Genom & Precis Med, Beijing, Peoples R China.
[Thasler, Wolfgang E.] Univ Munich, Dept Gen Visceral Transplantat Vasc Surg Grossula, Munich, Germany.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 1864
BP 921A
EP 921A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493804225
ER
PT J
AU Yurdaydin, C
Idilman, R
Kalkan, C
Karakaya, F
Kartal, AC
Keskin, O
Karatayli, E
Karatayli, SC
Bozdayi, AM
Koh, C
Heller, T
Glenn, J
AF Yurdaydin, Cihan
Idilman, Ramazan
Kalkan, Cagdas
Karakaya, Fatih
Kartal, Aysun Caliskan
Keskin, Onur
Karatayli, Ersin
Karatayli, Senem C.
Bozdayi, A. Mithat
Koh, Christopher
Heller, Theo
Glenn, Jeffrey
TI The Prenylation Inhibitor Lonafarnib Can Induce Post-Treatment Alt
Flares With Viral Clearance In Patients With Chronic Delta Hepatitis
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 67th Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 11-15, 2016
CL Boston, MA
SP Amer Assoc Study Liver Dis
C1 [Yurdaydin, Cihan; Idilman, Ramazan; Kalkan, Cagdas; Karakaya, Fatih; Kartal, Aysun Caliskan; Keskin, Onur; Karatayli, Ersin; Karatayli, Senem C.; Bozdayi, A. Mithat] Ankara Univ, Sch Med, Gastroenterol Sect, Ankara, Turkey.
[Koh, Christopher; Heller, Theo] NIDDK, Liver Dis Branch, Bethesda, MD USA.
[Glenn, Jeffrey] Stanford Univ, Sch Med, Div Gastroenterol & Hepatol, Stanford, CA 94305 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 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
SU 1
MA 1875
BP 927A
EP 927A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DY9YT
UT WOS:000385493804236
ER
PT J
AU Haut, LH
Gill, AL
Kurupati, RK
Bian, A
Li, Y
Giles-Davis, W
Xiang, ZQ
Zhou, XY
Ertl, HCJ
AF Haut, Larissa H.
Gill, Amanda L.
Kurupati, Raj K.
Bian, Ang
Li, Yan
Giles-Davis, Wynetta
Xiang, Zhiquan
Zhou, Xiang Yang
Ertl, Hildegund C. J.
TI A Partial E3 Deletion in Replication-Defective Adenoviral Vectors Allows
for Stable Expression of Potentially Toxic Transgene Products
SO HUMAN GENE THERAPY METHODS
LA English
DT Article
DE HIV-1; vaccine; genetic stability; immune responses
ID CD8(+) T-CELLS; CHIMPANZEE ADENOVIRUS; PROTECTIVE EFFICACY;
TRANSCRIPTION UNIT; NONHUMAN-PRIMATES; RHESUS MACAQUES; FUSION PROTEIN;
DOUBLE-BLIND; VACCINE; HIV-1
AB Adenovirus (Ad) is used extensively for construction of viral vectors, most commonly with deletion in its E1 and/or E3 genomic regions. Previously, our attempts to insert envelope proteins (Env) of HIV-1 into such vectors based on chimpanzee-derived Ad (AdC) viruses were thwarted. Here, we describe that genetic instability of an E1- and E3-deleted AdC vector of serotype C6 expressing Env of HIV-1 can be overcome by reinsertion of E3 sequences with anti-apoptotic activities. This partial E3 deletion presumably delays premature death of HEK-293 packaging cell lines due to Env-induced cell apoptosis. The same partial E3 deletion also allows for the generation of stable glycoprotein 140 (gp140)- and gp160-expressing Ad vectors based on AdC7, a distinct AdC serotype. Env-expressing AdC vectors containing the partial E3 deletion are genetically stable upon serial cell culture passaging, produce yields comparable to those of other AdC vectors, and induce transgene product-specific antibody responses in mice. A partial E3 deletion thereby allows expansion of the repertoire of transgenes that can be expressed by Ad vectors.
C1 [Haut, Larissa H.; Gill, Amanda L.; Kurupati, Raj K.; Bian, Ang; Li, Yan; Giles-Davis, Wynetta; Xiang, Zhiquan; Zhou, Xiang Yang; Ertl, Hildegund C. J.] Wistar Inst Anat & Biol, 3601 Spruce St, Philadelphia, PA 19104 USA.
[Gill, Amanda L.] NIAID, Clin Mol Regulat Sect, Immunoregulat Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
RP Ertl, HCJ (reprint author), Wistar Inst Anat & Biol, Dept Immunol, 3601 Spruce St,Room 283, Philadelphia, PA 19104 USA.
EM ertl@wistar.upenn.edu
FU NIAID/IPCAVD [U19 AI074078]
FX We wish to thank C. Cole for help with preparing the manuscript. Funding
for this project was provided by the NIAID/IPCAVD U19 AI074078.
NR 44
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1946-6536
EI 1946-6544
J9 HUM GENE THER METHOD
JI Hum. Gene Ther. Methods
PD OCT
PY 2016
VL 27
IS 5
BP 187
EP 196
DI 10.1089/hgtb.2016.044
PG 10
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA EA6YT
UT WOS:000386775800003
PM 27604324
ER
PT J
AU Teratani-Ota, Y
Yamamizu, K
Piao, Y
Sharova, L
Amano, M
Yu, H
Schlessinger, D
Ko, MSH
Sharov, AA
AF Teratani-Ota, Yusuke
Yamamizu, Kohei
Piao, Yulan
Sharova, Lioudmila
Amano, Misa
Yu, Hong
Schlessinger, David
Ko, Minoru S. H.
Sharov, Alexei A.
TI Induction of specific neuron types by overexpression of single
transcription factors
SO IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL
LA English
DT Article
DE GABAergic neurons; Dopaminergic neurons; Cholinergic neurons; Ascl1;
ESCs; Gene expression profiling; miRNA
ID EMBRYONIC STEM-CELLS; DOPAMINERGIC-NEURONS; HUMAN FIBROBLASTS; IN-VIVO;
CORTICOFUGAL NEURONS; PARKINSONS-DISEASE; TISSUE-SPECIFICITY;
FUNCTIONAL-NEURONS; GABAERGIC NEURONS; DIRECT CONVERSION
AB Specific neuronal types derived from embryonic stem cells (ESCs) can facilitate mechanistic studies and potentially aid in regenerative medicine. Existing induction methods, however, mostly rely on the effects of the combined action of multiple added growth factors, which generally tend to result in mixed populations of neurons. Here, we report that overexpression of specific transcription factors (TFs) in ESCs can rather guide the differentiation of ESCs towards specific neuron lineages. Analysis of data on gene expression changes 2 d after induction of each of 185 TFs implicated candidate TFs for further ESC differentiation studies. Induction of 23 TFs (out of 49 TFs tested) for 6 d facilitated neural differentiation of ESCs as inferred from increased proportion of cells with neural progenitor marker PSA-NCAM. We identified early activation of the Notch signaling pathway as a common feature of most potent inducers of neural differentiation. The majority of neuron-like cells generated by induction of Ascl1, Smad7, Nr2f1, Dlx2, Dlx4, Nr2f2, Barhl2, and Lhx1 were GABA-positive and expressed other markers of GABAergic neurons. In the same way, we identified Lmx1a and Nr4a2 as inducers for neurons bearing dopaminergic markers and Isl1, Fezf2, and St18 for cholinergic motor neurons. A time-course experiment with induction of Ascl1 showed early upregulation of most neural-specific messenger RNA (mRNA) and microRNAs (miRNAs). Sets of Ascl1-induced mRNAs and miRNAs were enriched in Ascl1 targets. In further studies, enrichment of cells obtained with the induction of Ascl1, Smad7, and Nr2f1 using microbeads resulted in essentially pure population of neuron-like cells with expression profiles similar to neural tissues and expressed markers of GABAergic neurons. In summary, this study indicates that induction of transcription factors is a promising approach to generate cultures that show the transcription profiles characteristic of specific neural cell types.
C1 [Teratani-Ota, Yusuke; Yamamizu, Kohei; Piao, Yulan; Sharova, Lioudmila; Amano, Misa; Yu, Hong; Schlessinger, David; Sharov, Alexei A.] NIA, Genet Lab, NIH, Baltimore, MD 21224 USA.
[Teratani-Ota, Yusuke] Univ Calif Davis, Dept Psychol, Ctr Neurosci, Davis, CA 95616 USA.
[Yamamizu, Kohei] Kyoto Univ, Ctr iPS Cell Res & Applicat CiRA, Lab Stem Cell Differentiat, Kyoto 6068507, Japan.
[Amano, Misa; Yu, Hong] Elixirgen LLC, Baltimore, MD 21205 USA.
[Ko, Minoru S. H.] Keio Univ, Dept Syst Med, Sakaguchi Lab, Sch Med, Tokyo 1608582, Japan.
RP Sharov, AA (reprint author), NIA, Genet Lab, NIH, Baltimore, MD 21224 USA.
EM sharoval@mail.nih.gov
FU Intramural Research Program of the NIH, National Institute on Aging [Z01
AG000656-09]; Post-Baccalaureate Intramural Research Training Award;
Kanae Foundation, Japan; Uehara Memorial Foundation, Japan; Naito
Foundation, Japan; Japan Society for Promotion of Science (JSPS); Japan
Science and Technology Agency (JST), CREST program
FX This research was supported in part by the Intramural Research Program
of the NIH, National Institute on Aging, project Z01 AG000656-09. Y.T-O.
was funded by Post-Baccalaureate Intramural Research Training Award.
K.Y. was supported by the postdoctoral fellowships from the Kanae
Foundation, Japan, Uehara Memorial Foundation, Japan, Naito Foundation,
Japan, and the Japan Society for Promotion of Science (JSPS). This
research was also supported in part by the Japan Science and Technology
Agency (JST), CREST program. The authors declare no competing financial
interests. Y.T-O., K.Y., Y.P., and L.S. performed experiments; M.A. made
new ES clones; H.Y. carried out vector construction for ES clones and
synthetic mRNA; D.S. and M.S.H.K supervised the project and edited the
manuscript; and A.A.S. performed statistical analysis and wrote the
manuscript.
NR 74
TC 0
Z9 0
U1 2
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1071-2690
EI 1543-706X
J9 IN VITRO CELL DEV-AN
JI In Vitro Cell. Dev. Biol.-Anim.
PD OCT
PY 2016
VL 52
IS 9
BP 961
EP 973
DI 10.1007/s11626-016-0056-7
PG 13
WC Cell Biology; Developmental Biology
SC Cell Biology; Developmental Biology
GA EA5KE
UT WOS:000386658200008
PM 27251161
ER
PT J
AU Park, YM
Steck, SE
Fung, TT
Zhang, J
Hazlett, LJ
Han, K
Merchant, AT
AF Park, Y-M
Steck, S. E.
Fung, T. T.
Zhang, J.
Hazlett, L. J.
Han, K.
Merchant, A. T.
TI Mediterranean diet and mortality risk in metabolically healthy obese and
metabolically unhealthy obese phenotypes
SO INTERNATIONAL JOURNAL OF OBESITY
LA English
DT Article
ID NUTRITION EXAMINATION SURVEY; CORONARY-HEART-DISEASE; KOREA
NATIONAL-HEALTH; CARDIOVASCULAR-DISEASE; RECOVERY BIOMARKERS;
ALCOHOL-CONSUMPTION; PHYSICAL-ACTIVITY; ADIPOSE-TISSUE; US POPULATION;
WEIGHT-LOSS
AB BACKGROUND: The Mediterranean diet has been consistently associated with reduced mortality risk. Few prospective studies have examined whether the benefits from a Mediterranean diet are equally shared by obese individuals with varying metabolic health.
OBJECTIVE: The objective of this study was to investigate the association between Mediterranean diet, metabolic phenotypes and mortality risk in a representative obese US population.
METHODS: Data from 1739 adults aged 20-88 years were analyzed from participants of the National Health and Nutrition Examination Survey III, 1988-1994 followed up for deaths until 31 December 2011 in a prospective cohort analysis. Mediterranean Diet Scores (MDS) were created to assess the adherence to Mediterranean diet. Participants were classified as metabolically healthy obese (MHO) phenotype (0 or 1 metabolic abnormality) or metabolically unhealthy obese (MUO) phenotype (two or more metabolic abnormalities), based on high glucose, insulin resistance, blood pressure, triglycerides, C-reactive protein and low high-density lipoprotein cholesterol.
RESULTS: The MHO phenotype (n = 598) was observed in 34.8% (s.e., 1.7%) of those who were obese (mean body mass index was 33.4 and 34.8 in MHO and MUO phenotypes, respectively). During a median follow-up of 18.5 years, there were 77 (12.9%) and 309 (27.1%) deaths in MHO and MUO individuals, respectively. In MHO individuals, the multivariable-adjusted hazard ratio (HR) of all-cause mortality in the highest tertile compared with the first tertile of MDS was 0.44 (95% confidence interval (CI), 0.26-0.75; P for trend < 0.001), after adjustment for potential confounders. A five-point (1 s.d.) increment in the adherence to MDS was associated with a 41% reduction in the risk of all-cause mortality (HR, 0.59; 95% CI, 0.37-0.94). Similar findings were obtained when we restricted our analyses to those with or without prevalent diabetes mellitus and hypertension. We did not observe mortality risk reduction in either individuals with MUO phenotype or all obese participants combined.
CONCLUSIONS: Adherence to a Mediterranean dietary pattern appears to reduce mortality in the MHO phenotype, but not among the MUO phenotype in an obese population.
C1 [Park, Y-M; Steck, S. E.; Zhang, J.; Hazlett, L. J.; Merchant, A. T.] Univ South Carolina, Arnold Sch Publ Hlth, Dept Epidemiol & Biostat, 915 Greene St, Columbia, SC 29208 USA.
[Park, Y-M] NIEHS, Epidemiol Branch, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
[Fung, T. T.] Simmons Coll, Dept Nutr, Boston, MA 02115 USA.
[Fung, T. T.] Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA.
[Han, K.] Catholic Univ Korea, Coll Med, Dept Biostat, Seoul, South Korea.
RP Merchant, AT (reprint author), Univ South Carolina, Arnold Sch Publ Hlth, Dept Epidemiol & Biostat, 915 Greene St, Columbia, SC 29208 USA.
EM merchant@mailbox.sc.edu
OI PARK, YONG-MOON/0000-0002-5879-6879
NR 54
TC 1
Z9 1
U1 3
U2 3
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 2016
VL 40
IS 10
BP 1541
EP 1549
DI 10.1038/ijo.2016.114
PG 9
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA EA4JZ
UT WOS:000386579500011
PM 27339604
ER
PT J
AU Zhang, Y
Ji, G
Xu, M
Cai, W
Zhu, Q
Qian, L
Zhang, YE
Yuan, K
Liu, J
Li, Q
Cui, G
Wang, H
Zhao, Q
Wu, K
Fan, D
Gold, MS
Tian, J
Tomasi, D
Liu, Y
Nie, Y
Wang, GJ
AF Zhang, Y.
Ji, G.
Xu, M.
Cai, W.
Zhu, Q.
Qian, L.
Zhang, Y. E.
Yuan, K.
Liu, J.
Li, Q.
Cui, G.
Wang, H.
Zhao, Q.
Wu, K.
Fan, D.
Gold, M. S.
Tian, J.
Tomasi, D.
Liu, Y.
Nie, Y.
Wang, G-J
TI Recovery of brain structural abnormalities in morbidly obese patients
after bariatric surgery
SO INTERNATIONAL JOURNAL OF OBESITY
LA English
DT Article
ID GASTRIC BYPASS-SURGERY; FOOD ADDICTION SCALE; HIGH-CALORIE FOODS;
BODY-MASS INDEX; WEIGHT-LOSS; COGNITIVE CONTROL; FUTURE INCREASES;
NETWORK; MRI; ACTIVATION
AB BACKGROUND/OBJECTIVES: Obesity-related brain structural abnormalities have been reported extensively, and bariatric surgery (BS) is currently the most effective intervention to produce sustained weight reduction in overtly obese (OB) people. It is unknown whether BS can repair the brain circuitry abnormalities concomitantly with long-term weight loss.
SUBJECTS/ METHODS: In order to investigate whether BS promotes neuroplastic structural recovery in morbidly OB patients, we quantified fractional anisotropy (FA), mean diffusivity (MD) and gray (GM) and white (WM) matter densities in 15 morbidly OB patients and in 18 normal weight (NW) individuals. OB patients were studied at baseline and also 1 month after laparoscopic sleeve gastrectomy surgery.
RESULTS: Two-sample t-test between OB (baseline) and NW groups showed decreased FA values, GM/WM densities and increased MD value in brain regions associated with food intake control (that is, caudate, orbitofrontal cortex, body and genu of corpus callosum) and cognitive-emotion regulation (that is, inferior frontal gyrus, hippocampus, insula, external capsule) (P < 0.05, familywise error correction). Paired t-test in the OB group between before and after surgery showed that BS generated partial neuroplastic structural recovery in the OB group, but the differences had relative less strength and smaller volume (P < 0.001).
CONCLUSIONS: This study provides the first anatomical evidence for BS-induced acute neuroplastic recovery that might in part mediate the long-term benefit of BS in weight reduction. It also highlights the importance of this line of gut-brain axis research employing the combined BS and neuroimaging model for identifying longitudinal changes in brain structure that correlated with obesity status.
C1 [Zhang, Y.; Cai, W.; Zhu, Q.; Yuan, K.; Liu, J.; Tian, J.] Xidian Univ, Sch Life Sci & Technol, Ctr Brain Imaging, Xian 710071, Shaanxi, Peoples R China.
[Zhang, Y.; Zhang, Y. E.; Gold, M. S.; Liu, Y.] Univ Florida, Dept Psychiat, Gainesville, FL 32611 USA.
[Zhang, Y.; Zhang, Y. E.; Gold, M. S.; Liu, Y.] Univ Florida, McKnight Brain Inst, Gainesville, FL USA.
[Ji, G.; Zhao, Q.; Wu, K.; Fan, D.; Nie, Y.] Fourth Mil Med Univ, Xijing Gastrointestinal Hosp, 127 Changle West Rd, Xian 710032, Shaanxi, Peoples R China.
[Xu, M.; Qian, L.; Liu, Y.] Peking Univ, Dept Biomed Engn, Beijing, Peoples R China.
[Zhang, Y. E.] Malcom Randall Vet Affairs Med Ctr, Gainesville, FL USA.
[Li, Q.; Cui, G.] Fourth Mil Med Univ, Tangdu Hosp, Dept Radiol, Xian, Peoples R China.
[Wang, H.] Fourth Mil Med Univ, Xijing Hosp, Dept Psychiat, Xian, Peoples R China.
[Tian, J.] Chinese Acad Sci, Inst Automat, Beijing, Peoples R China.
[Tomasi, D.; Wang, G-J] NIAAA, Lab Neuroimaging, 10 Ctr Dr,MSC1013,Bldg 10,Room B2L304, Bethesda, MD 20892 USA.
RP Zhang, Y (reprint author), Xidian Univ, Sch Life Sci & Technol, Ctr Brain Imaging, Xian 710071, Shaanxi, Peoples R China.; Nie, Y (reprint author), Fourth Mil Med Univ, Xijing Gastrointestinal Hosp, 127 Changle West Rd, Xian 710032, Shaanxi, Peoples R China.; Wang, GJ (reprint author), NIAAA, Lab Neuroimaging, 10 Ctr Dr,MSC1013,Bldg 10,Room B2L304, Bethesda, MD 20892 USA.
EM zhangyiuf@gmail.com; yongznie@fmmu.edu.cn; gene-jack.wang@nih.gov
FU National Natural Science Foundation of China [81271549, 81470816,
61131003, 61431013, 81201081, 81227901, 81120108005, 81501543, 81371530,
81571751, 81571753]; Shaanxi Provincial Natural Science Foundation
[2015JM3117]; Project for the National Key Basic Research and
Development Program (973) [2011CB707700]
FX This work is supported by the National Natural Science Foundation of
China under Grant Nos. 81271549, 81470816, 61131003, 61431013, 81201081,
81227901, 81120108005, 81501543, 81371530, 81571751 and 81571753; the
Shaanxi Provincial Natural Science Foundation under Grant No.
2015JM3117; and the Project for the National Key Basic Research and
Development Program (973) under Grant No. 2011CB707700. We thank Dr
Samantha Cunningham of NIAAA and Dr Jiayu Liu of Yale University for
proofreading.
NR 46
TC 0
Z9 0
U1 4
U2 4
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 2016
VL 40
IS 10
BP 1558
EP 1565
DI 10.1038/ijo.2016.98
PG 8
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA EA4JZ
UT WOS:000386579500013
PM 27200505
ER
PT J
AU Wu, J
Peters, BA
Dominianni, C
Zhang, YL
Pei, ZH
Yang, LY
Ma, YF
Purdue, MP
Jacobs, EJ
Gapstur, SM
Li, HL
Alekseyenko, AV
Hayes, RB
Ahn, JY
AF Wu, Jing
Peters, Brandilyn A.
Dominianni, Christine
Zhang, Yilong
Pei, Zhiheng
Yang, Liying
Ma, Yingfei
Purdue, Mark P.
Jacobs, Eric J.
Gapstur, Susan M.
Li, Huilin
Alekseyenko, Alexander V.
Hayes, Richard B.
Ahn, Jiyoung
TI Cigarette smoking and the oral microbiome in a large study of American
adults
SO ISME JOURNAL
LA English
DT Article
ID CANCER SCREENING TRIAL; POLYMORPHONUCLEAR LEUKOCYTES; TOBACCO SMOKING;
PERIODONTITIS; CESSATION; BACTERIA; SMOKERS; SALIVA; LUNG; METAANALYSIS
AB Oral microbiome dysbiosis is associated with oral disease and potentially with systemic diseases; however, the determinants of these microbial imbalances are largely unknown. In a study of 1204 US adults, we assessed the relationship of cigarette smoking with the oral microbiome. 16S rRNA gene sequencing was performed on DNA from oral wash samples, sequences were clustered into operational taxonomic units (OTUs) using QIIME and metagenomic content was inferred using PICRUSt. Overall oral microbiome composition differed between current and non-current (former and never) smokers (Po0.001). Current smokers had lower relative abundance of the phylum Proteobacteria (4.6%) compared with never smokers (11.7%) (false discovery rate q= 5.2 x 10(-7)), with no difference between former and never smokers; the depletion of Proteobacteria in current smokers was also observed at class, genus and OTU levels. Taxa not belonging to Proteobacteria were also associated with smoking: the genera Capnocytophaga, Peptostreptococcus and Leptotrichia were depleted, while Atopobium and Streptococcus were enriched, in current compared with never smokers. Functional analysis from inferred metagenomes showed that bacterial genera depleted by smoking were related to carbohydrate and energy metabolism, and to xenobiotic metabolism. Our findings demonstrate that smoking alters the oral microbiome, potentially leading to shifts in functional pathways with implications for smoking-related diseases.
C1 [Wu, Jing; Peters, Brandilyn A.; Dominianni, Christine; Hayes, Richard B.; Ahn, Jiyoung] NYU, Sch Med, Dept Populat Hlth, Div Epidemiol, New York, NY USA.
[Wu, Jing; Pei, Zhiheng; Hayes, Richard B.; Ahn, Jiyoung] NYU, Perlmutter Canc Ctr, New York, NY USA.
[Zhang, Yilong; Li, Huilin] NYU, Sch Med, Dept Populat Hlth, Div Biostat, New York, NY USA.
[Pei, Zhiheng; Ma, Yingfei] NYU, Sch Med, Dept Pathol, New York, NY USA.
[Pei, Zhiheng] New York Harbor Healthcare Syst, Dept Vet Affairs, New York, NY USA.
[Yang, Liying] NYU, Sch Med, Dept Med, Div Translat Med, New York, NY USA.
[Purdue, Mark P.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Purdue, Mark P.] Ontario Inst Canc Res, Toronto, ON, Canada.
[Jacobs, Eric J.; Gapstur, Susan M.] Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA.
[Alekseyenko, Alexander V.] Med Univ South Carolina, Biomed Informat Ctr, Charleston, SC 29425 USA.
[Alekseyenko, Alexander V.] Med Univ South Carolina, Dept Publ Hlth Sci, Charleston, SC 29425 USA.
[Alekseyenko, Alexander V.] Med Univ South Carolina, Dept Oral Hlth Sci, Charleston, SC 29425 USA.
RP Ahn, JY (reprint author), NYU, Sch Med, Dept Populat Hlth, 650 Ist Ave,5th Floor, New York, NY 10016 USA.
EM Jiyoung.Ahn@nyumc.org
OI Alekseyenko, Alexander/0000-0002-5748-2085; Yang,
Liying/0000-0003-1442-4915; Peters, Brandilyn/0000-0002-1534-2578; Pei,
Zhiheng/0000-0001-8570-6747; Hayes, Richard/0000-0002-0918-661X
FU US National Cancer Institute [R01CA159036, U01CA182370,
U01CA170948-01A1, R01CA164964, R03CA159414, P30CA016087, R21CA183887];
AACR/Pancreas Cancer Action Network Career Development Award; American
Cancer Society (ACS)
FX Research reported in this publication was supported in part by the US
National Cancer Institute under award numbers R01CA159036, U01CA182370,
U01CA170948-01A1, R01CA164964, R03CA159414, P30CA016087, R21CA183887,
and by AACR/Pancreas Cancer Action Network Career Development Award. ZP
is a Staff Physician at the Department of Veterans Affairs New York
Harbor Healthcare System. The American Cancer Society (ACS) funds the
creation, maintenance and updating of the Cancer Prevention Study II
cohort. The content is solely the responsibility of the authors and does
not necessarily represent the official views of the National Institutes
of Health, the US Department of Veterans Affairs or the United States
Government.
NR 55
TC 3
Z9 3
U1 17
U2 17
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1751-7362
EI 1751-7370
J9 ISME J
JI ISME J.
PD OCT
PY 2016
VL 10
IS 10
BP 2435
EP 2446
DI 10.1038/ismej.2016.37
PG 12
WC Ecology; Microbiology
SC Environmental Sciences & Ecology; Microbiology
GA EB0LN
UT WOS:000387035400008
PM 27015003
ER
PT J
AU Maas, P
Barrdahl, M
Joshi, AD
Auer, PL
Gaudet, MM
Milne, RL
Schumacher, FR
Anderson, WF
Check, D
Chattopadhyay, S
Baglietto, L
Berg, CD
Chanock, SJ
Cox, DG
Figueroa, JD
Gail, MH
Graubard, BI
Haiman, CA
Hankinson, SE
Hoover, RN
Isaacs, C
Kolonel, LN
Le Marchand, L
Lee, IM
Lindstrom, S
Overvad, K
Romieu, I
Sanchez, MJ
Southey, MC
Stram, DO
Tumino, R
VanderWeele, TJ
Willett, WC
Zhang, SM
Buring, JE
Canzian, F
Gapstur, SM
Henderson, BE
Hunter, DJ
Giles, GG
Prentice, RL
Ziegler, RG
Kraft, P
Garcia-Closas, M
Chatterjee, N
AF Maas, Paige
Barrdahl, Myrto
Joshi, Amit D.
Auer, Paul L.
Gaudet, Mia M.
Milne, Roger L.
Schumacher, Fredrick R.
Anderson, William F.
Check, David
Chattopadhyay, Subham
Baglietto, Laura
Berg, Christine D.
Chanock, Stephen J.
Cox, David G.
Figueroa, Jonine D.
Gail, Mitchell H.
Graubard, Barry I.
Haiman, Christopher A.
Hankinson, Susan E.
Hoover, Robert N.
Isaacs, Claudine
Kolonel, Laurence N.
Le Marchand, Loic
Lee, I-Min
Lindstrom, Sara
Overvad, Kim
Romieu, Isabelle
Sanchez, Maria-Jose
Southey, Melissa C.
Stram, Daniel O.
Tumino, Rosario
VanderWeele, Tyler J.
Willett, Walter C.
Zhang, Shumin
Buring, Julie E.
Canzian, Federico
Gapstur, Susan M.
Henderson, Brian E.
Hunter, David J.
Giles, Graham G.
Prentice, Ross L.
Ziegler, Regina G.
Kraft, Peter
Garcia-Closas, Montse
Chatterjee, Nilanjan
TI Breast Cancer Risk From Modifiable and Nonmodifiable Risk Factors Among
White Women in the United States
SO JAMA ONCOLOGY
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; SINGLE-NUCLEOTIDE POLYMORPHISMS;
GENE-ENVIRONMENT INTERACTIONS; SUSCEPTIBILITY LOCI; COHORT CONSORTIUM;
MODELS; PREDICTION; INDIVIDUALS; INFORMATION; VARIANTS
AB IMPORTANCE An improved model for risk stratification can be useful for guiding public health strategies of breast cancer prevention.
OBJECTIVE To evaluate combined risk stratification utility of common low penetrant single nucleotide polymorphisms (SNPs) and epidemiologic risk factors.
DESIGN, SETTING, AND PARTICIPANTS Using a total of 17 171 cases and 19 862 controls sampled from the Breast and Prostate Cancer Cohort Consortium (BPC3) and 5879 women participating in the 2010 National Health Interview Survey, a model for predicting absolute risk of breast cancer was developed combining information on individual level data on epidemiologic risk factors and 24 genotyped SNPs from prospective cohort studies, published estimate of odds ratios for 68 additional SNPs, population incidence rate from the National Cancer Institute-Surveillance, Epidemiology, and End Results Program cancer registry and data on risk factor distribution from nationally representative health survey. The model is used to project the distribution of absolute risk for the population of white women in the United States after adjustment for competing cause of mortality.
EXPOSURES Single nucleotide polymorphisms, family history, anthropometric factors, menstrual and/ or reproductive factors, and lifestyle factors.
MAIN OUTCOMES AND MEASURES Degree of stratification of absolute risk owing to nonmodifiable (SNPs, family history, height, and some components of menstrual and/ or reproductive history) and modifiable factors (body mass index [BMI; calculated as weight in kilograms divided by height in meters squared], menopausal hormone therapy [MHT], alcohol, and smoking).
RESULTS The average absolute risk for a 30-year-old white woman in the United States developing invasive breast cancer by age 80 years is 11.3%. A model that includes all risk factors provided a range of average absolute risk from 4.4% to 23.5% for women in the bottom and top deciles of the risk distribution, respectively. For women who were at the lowest and highest deciles of nonmodifiable risks, the 5th and 95th percentile range of the risk distribution associated with 4 modifiable factors was 2.9% to 5.0% and 15.5% to 25.0%, respectively. For women in the highest decile of risk owing to nonmodifiable factors, those who had low BMI, did not drink or smoke, and did not use MHT had risks comparable to an average woman in the general population.
CONCLUSIONS AND RELEVANCE This model for absolute risk of breast cancer including SNPs can provide stratification for the population of white women in the United States. The model can also identify subsets of the population at an elevated risk that would benefit most from risk-reduction strategies based on altering modifiable factors. The effectiveness of this model for individual risk communication needs further investigation.
C1 [Maas, Paige; Anderson, William F.; Check, David; Chattopadhyay, Subham; Chanock, Stephen J.; Figueroa, Jonine D.; Gail, Mitchell H.; Graubard, Barry I.; Hoover, Robert N.; Ziegler, Regina G.; Garcia-Closas, Montse; Chatterjee, Nilanjan] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Barrdahl, Myrto] German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
[Joshi, Amit D.; Lindstrom, Sara; Hunter, David J.; Kraft, Peter] Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Program Genet Epidemiol & Stat Genet, Boston, MA USA.
[Auer, Paul L.; Prentice, Ross L.] Fred Hutchinson Canc Res Ctr, 1124 Columbia St, Seattle, WA 98104 USA.
[Auer, Paul L.] Univ Wisconsin, Sch Publ Hlth, Milwaukee, WI 53201 USA.
[Gaudet, Mia M.; Gapstur, Susan M.] Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA.
[Milne, Roger L.; Baglietto, Laura; Giles, Graham G.] Canc Council Victoria, Canc Epidemiol Ctr, Melbourne, Vic, Australia.
[Milne, Roger L.; Baglietto, Laura; Giles, Graham G.] Univ Melbourne, Melbourne Sch Populat & Global Hlth, Ctr Epidemiol & Biostat, Melbourne, Vic, Australia.
[Schumacher, Fredrick R.; Haiman, Christopher A.; Stram, Daniel O.; Henderson, Brian E.] Univ Southern Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA USA.
[Berg, Christine D.] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
[Cox, David G.] Ctr Leon Berard, INSERM, U1052, Canc Res Ctr Lyon, Lyon, France.
[Cox, David G.] Imperial Coll London, Sch Publ Hlth, Dept Epidemiol & Biostat, London, England.
[Hankinson, Susan E.] Univ Massachusetts, Sch Publ Hlth & Hlth Sci, Dept Biostat & Epidemiol, Amherst, MA 01003 USA.
[Hankinson, Susan E.] Brigham & Womens Hosp, Dept Med, Channing Div Network Med, 75 Francis St, Boston, MA 02115 USA.
[Hankinson, Susan E.; Lee, I-Min; Zhang, Shumin; Buring, Julie E.] Harvard Med Sch, Boston, MA USA.
[Isaacs, Claudine] Georgetown Univ, Lombardi Comprehens Canc Ctr, Washington, DC USA.
[Kolonel, Laurence N.] Univ Hawaii, Canc Res Ctr, Program Epidemiol, Honolulu, HI 96813 USA.
[Le Marchand, Loic] Univ Hawaii, Ctr Canc, Honolulu, HI 96822 USA.
[Lee, I-Min; Zhang, Shumin; Buring, Julie E.] Brigham & Womens Hosp, Div Prevent Med, 75 Francis St, Boston, MA 02115 USA.
[Overvad, Kim] Aarhus Univ, Dept Publ Hlth, Aarhus, Denmark.
[Romieu, Isabelle] Int Agcy Res Canc, Nutr & Metab Sect, Lyon, France.
[Sanchez, Maria-Jose] Univ Granada, Hosp Univ Granada, Inst Invest Biosanitaria Ibs GRANADA, Escuela Andaluza Salud Publ, Granada, Spain.
[Sanchez, Maria-Jose] CIBER Epidemiol & Salud Publ CIBERESP, Madrid, Spain.
[Southey, Melissa C.] Univ Melbourne, Dept Pathol, Genet Epidemiol Lab, Melbourne, Vic, Australia.
[Tumino, Rosario] Civ MP Arezzo Hosp, ASP Ragusa, Canc Registry & Histopathol Unit, Ragusa, Italy.
[VanderWeele, Tyler J.] Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
[VanderWeele, Tyler J.] Harvard TH Chan Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Willett, Walter C.] Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA.
[Canzian, Federico] German Canc Res Ctr, Heidelberg, Germany.
[Giles, Graham G.] Monash Univ, Dept Epidemiol & Prevent Med, Melbourne, Vic, Australia.
[Prentice, Ross L.] Univ Washington, Sch Publ Hlth & Community Med, Seattle, WA 98195 USA.
[Garcia-Closas, Montse] Inst Canc Res, Breakthrough Breast Canc Res Ctr, Div Genet & Epidemiol, London, England.
[Chatterjee, Nilanjan] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Biostat, 615 N Wolfe St, Baltimore, MD 21205 USA.
[Chatterjee, Nilanjan] Johns Hopkins Univ, Sch Med, Dept Oncol, 615 N Wolfe St, Baltimore, MD 21205 USA.
RP Chatterjee, N (reprint author), Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Biostat, 615 N Wolfe St, Baltimore, MD 21205 USA.
EM nilanjan@jhu.edu
FU US National Institutes of Health, National Cancer Institute
[U01-CA98233-07, U01-CA98710-06, U01-CA98216-06, U01-CA98758-07];
Intramural Research Program, Division of Cancer Epidemiology and
Genetics, National Cancer Institute, National Institutes of Health,
Department of Health and Human Services; National Heart, Lung, and Blood
Institute, National Institutes of Health, US Department of Health and
Human Services [HHSN268201100046C, HHSN268201100001C, HHSN268201100002C,
HHSN268201100003C, HHSN268201100004C, HHSN271201100004C]; Hellenic
Health Association; Stavros Niarchos Foundation
FX Design and conduct of the study; collection, management, analysis and
interpretation of the data; preparation, review, or approval of the
manuscript; and decision to submit the manuscript for publication was
supported by US National Institutes of Health, National Cancer Institute
(cooperative agreements U01-CA98233-07 to Dr Hunter, U01-CA98710-06 to
M.J.T., U01-CA98216-06 to E.R. and R.K., and U01-CA98758-07 to Dr
Henderson) and Intramural Research Program, Division of Cancer
Epidemiology and Genetics, National Cancer Institute, National
Institutes of Health, Department of Health and Human Services. The WHI
program is funded by the National Heart, Lung, and Blood Institute,
National Institutes of Health, US Department of Health and Human
Services through contracts HHSN268201100046C, HHSN268201100001C,
HHSN268201100002C, HHSN268201100003C, HHSN268201100004C, and
HHSN271201100004C. EPIC Greece is funded by the Hellenic Health
Association and the Stavros Niarchos Foundation.
NR 37
TC 6
Z9 6
U1 9
U2 9
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
EI 2374-2445
J9 JAMA ONCOL
JI JAMA Oncol.
PD OCT 1
PY 2016
VL 2
IS 10
BP 1295
EP 1302
DI 10.1001/jamaoncol.2016.1025
PG 8
WC Oncology
SC Oncology
GA EA3GB
UT WOS:000386488600012
PM 27228256
ER
PT J
AU Journy, NMY
Morton, LM
Kleinerman, RA
Bekelman, JE
de Gonzalez, AB
AF Journy, Neige M. Y.
Morton, Lindsay M.
Kleinerman, Ruth A.
Bekelman, Justin E.
de Gonzalez, Amy Berrington
TI Second Primary Cancers After Intensity-Modulated vs 3-Dimensional
Conformal Radiation Therapy for Prostate Cancer
SO JAMA ONCOLOGY
LA English
DT Letter
C1 [Journy, Neige M. Y.; Morton, Lindsay M.; Kleinerman, Ruth A.; de Gonzalez, Amy Berrington] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Room 7E556,MSC 9778,9609 Med Ctr Dr, Bethesda, MD 20892 USA.
[Bekelman, Justin E.] Abramson Canc Ctr, Dept Radiat Oncol, Philadelphia, PA USA.
[Bekelman, Justin E.] Univ Penn, Dept Biostat & Epidemiol, Ctr Clin Epidemiol & Biostat, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Bekelman, Justin E.] Univ Penn, Leonard Davis Inst Hlth Econ, Philadelphia, PA 19104 USA.
RP Journy, NMY (reprint author), NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Room 7E556,MSC 9778,9609 Med Ctr Dr, Bethesda, MD 20892 USA.
EM neige.journy@nih.gov
NR 6
TC 0
Z9 0
U1 2
U2 2
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
EI 2374-2445
J9 JAMA ONCOL
JI JAMA Oncol.
PD OCT 1
PY 2016
VL 2
IS 10
BP 1368
EP 1370
DI 10.1001/jamaoncol.2016.1368
PG 3
WC Oncology
SC Oncology
GA EA3GB
UT WOS:000386488600024
PM 27415446
ER
PT J
AU Quinn, GE
Ying, GS
Repka, MX
Siatkowski, RM
Hoffman, R
Mills, MD
Morrison, D
Daniel, E
Baumritter, A
Hildebrand, PL
Schron, EB
Ells, AL
Wade, K
Kemper, AR
AF Quinn, Graham E.
Ying, Gui-shuang
Repka, Michael X.
Siatkowski, R. Michael
Hoffman, Robert
Mills, Monte D.
Morrison, David
Daniel, Ebenezer
Baumritter, Agnieshka
Hildebrand, P. Lloyd
Schron, Eleanor B.
Ells, Anna L.
Wade, Kelly
Kemper, Alex R.
TI Timely implementation of a retinopathy of prematurity telemedicine
system
SO JOURNAL OF AAPOS
LA English
DT Article
ID ACUTE-PHASE RETINOPATHY; INFANTS; CARE; ROP
AB PURPOSE To examine the feasibility of a retinopathy of prematurity (ROP) telemedicine evaluation system of providing timely feedback to a neonatal intensive care unit (NICU) with at-risk premature infants.
METHODS This was a prospective observational study of premature infants with birth weights of <1251 g in five NICUs in the United States. Infants scheduled for clinically indicated ROP evaluations underwent indirect ophthalmoscopic examinations and digital imaging on the same day. Imaging was performed by nonphysician retinal imagers. Times required were determined from obtaining digital images of both eyes to submission via web-based system to a secure server for grading by trained readers at a central reading center to sending back grading results to the clinical center.
RESULTS A total of 1,642 image sets of eyes of 292 infants were obtained, from 823 imaging sessions. The mean turnaround time from submission of image sets of both eyes to return of the grading results to the clinical center was 10.1 +/- 11.3 hours (standard deviation), with a median of 12.0 hours (1st quartile, 0.9 hours; 3rd quartile, 16 hours). Overall, 95.5% of gradings (95% CI, 93.9%-96.7%) were returned within 24 hours. Subgroup analyses found, for image sets submitted to the reading center before 2 p.m. Eastern Standard Time, median time to report was 1.7 hours (1st quartile, 0.7 hours; 3rd quartile, 15.5 hours) compared with those submitted after 2pm (median, 14.1 hours; 1st quartile, 11.2, hours; 3rd quartile, 16.3 hours).
CONCLUSIONS An ROP telemedicine approach can provide timely feedback to the NICU regarding the detection of potentially serious ROP and thus referral to an ophthalmologist for examination and consideration of treatment.
C1 [Quinn, Graham E.; Ying, Gui-shuang; Mills, Monte D.; Daniel, Ebenezer; Wade, Kelly] Univ Penn, Dept Ophthalmol, Philadelphia, PA 19104 USA.
[Quinn, Graham E.; Mills, Monte D.; Baumritter, Agnieshka; Wade, Kelly] Childrens Hosp Philadelphia, Div Pediat Ophthalmol, Philadelphia, PA 19104 USA.
[Repka, Michael X.; Hildebrand, P. Lloyd] Johns Hopkins Univ, Wilmer Eye Inst, Baltimore, MD 21218 USA.
[Siatkowski, R. Michael] Univ Oklahoma, Dean McGee Eye Inst, Oklahoma City, OK USA.
[Hoffman, Robert] Univ Utah, Dept Ophthalmol, Salt Lake City, UT USA.
[Morrison, David] Vanderbilt Univ, Dept Ophthalmol, 221 Kirkland Hall, Nashville, TN 37235 USA.
[Schron, Eleanor B.] NEI, Bethesda, MD 20892 USA.
[Ells, Anna L.] Univ Calgary, Dept Ophthalmol, Calgary, AB T2N 1N4, Canada.
[Kemper, Alex R.] Duke Univ, Dept Pediat, Sch Med, Durham, NC 27706 USA.
RP Quinn, GE (reprint author), Childrens Hosp Philadelphia, Div Ophthalmol, Wood Ctr, 1st Floor, Philadelphia, PA 19104 USA.
EM quinn@email.chop.edu
FU National Eye Institute of the National Institutes of Health, Department
of Health and Human Services [U10 EY017014]
FX Funded by National Eye Institute of the National Institutes of Health,
Department of Health and Human Services. U10 EY017014.
NR 13
TC 0
Z9 0
U1 2
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1091-8531
EI 1528-3933
J9 J AAPOS
JI J. AAPOS
PD OCT
PY 2016
VL 20
IS 5
BP 425
EP 430
DI 10.1016/j.jaapos.2016.06.007
PG 6
WC Ophthalmology; Pediatrics
SC Ophthalmology; Pediatrics
GA EA5FL
UT WOS:000386644700010
PM 27651231
ER
PT J
AU Revell, AD
Wang, DC
Wood, R
Morrow, C
Tempelman, H
Hamers, RL
Reiss, P
van Sighem, AI
Nelson, M
Montaner, JSG
Lane, HC
Larder, BA
AF Revell, Andrew D.
Wang, Dechao
Wood, Robin
Morrow, Carl
Tempelman, Hugo
Hamers, Raph L.
Reiss, Peter
van Sighem, Ard I.
Nelson, Mark
Montaner, Julio S. G.
Lane, H. Clifford
Larder, Brendan A.
CA RDI Data Study Grp
TI An update to the HIV-TRePS system: the development and evaluation of new
global and local computational models to predict HIV treatment outcomes,
with or without a genotype
SO JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY
LA English
DT Article
ID RESOURCE-LIMITED SETTINGS; ANTIRETROVIRAL THERAPY; GUIDELINES;
RESISTANCE; ADULTS
AB Optimizing antiretroviral drug combination on an individual basis in resource-limited settings is challenging because of the limited availability of drugs and genotypic resistance testing. Here, we describe our latest computational models to predict treatment responses, with or without a genotype, and compare the potential utility of global and local models as a treatment tool for South Africa.
Global random forest models were trained to predict the probability of virological response to therapy following virological failure using 29aEuroS574 treatment change episodes (TCEs) without a genotype, 3179 of which were from South Africa and were used to develop local models. In addition, 15aEuroS130 TCEs including genotypes were used to develop another set of models. The 'no-genotype' models were tested with an independent global test set (naEuroS=aEuroS1700) plus a subset from South Africa (naEuroS=aEuroS222). The genotype models were tested with 750 independent cases.
The global no-genotype models achieved area under the receiver-operating characteristic curve (AUC) values of 0.82 and 0.79 with the global and South African tests sets, respectively, and the South African models achieved AUCs of 0.70 and 0.79. The genotype models achieved an AUC of 0.84. The global no-genotype models identified more alternative, locally available regimens that were predicted to be effective for cases that failed their new regimen in the South African clinics than the local models. Both sets of models were significantly more accurate predictors of outcomes than genotyping with rules-based interpretation.
These latest global models predict treatment responses accurately even without a genotype, out-performed the local South African models and have the potential to help optimize therapy, particularly in resource-limited settings.
C1 [Revell, Andrew D.; Wang, Dechao; Larder, Brendan A.] HIV Resistance Response Database Initiat RDI, London, England.
[Wood, Robin; Morrow, Carl] Univ Cape Town, Desmond Tutu HIV Ctr, Cape Town, South Africa.
[Tempelman, Hugo] Ndlovu Care Grp, Elandsdoorn, South Africa.
[Hamers, Raph L.; Reiss, Peter] Univ Amsterdam, Amsterdam Inst Global Hlth & Dev, Acad Med Ctr, Dept Internal Med, Amsterdam, Netherlands.
[Hamers, Raph L.; Reiss, Peter] Univ Amsterdam, Amsterdam Inst Global Hlth & Dev, Acad Med Ctr, Dept Global Hlth, Amsterdam, Netherlands.
[Reiss, Peter; van Sighem, Ard I.] Stichting HIV Monitoring, Amsterdam, Netherlands.
[Nelson, Mark] Chelsea & Westminster Hosp, London, England.
[Montaner, Julio S. G.] BC Ctr Excellence HIV AIDS, Vancouver, BC, Canada.
[Lane, H. Clifford] NIAID, 9000 Rockville Pike, Bethesda, MD 20892 USA.
RP Revell, AD (reprint author), HIV Resistance Response Database Initiat RDI, London, England.
EM andrewrevell@hivrdi.org
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; National Institute of Allergy and Infectious
Diseases
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. This research was supported by the
National Institute of Allergy and Infectious Diseases.
NR 14
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-7453
EI 1460-2091
J9 J ANTIMICROB CHEMOTH
JI J. Antimicrob. Chemother.
PD OCT
PY 2016
VL 71
IS 10
BP 2928
EP 2937
DI 10.1093/jac/dkw217
PG 10
WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy
SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy
GA EA2VO
UT WOS:000386453900030
PM 27330070
ER
PT J
AU Aresh, W
Liu, Y
Sine, J
Thayer, D
Puri, A
Huang, YK
Wang, Y
Nieh, MP
AF Aresh, Wafa
Liu, Ying
Sine, Jessica
Thayer, Derek
Puri, Anu
Huang, Yike
Wang, Yong
Nieh, Mu-Ping
TI The Morphology of Self-Assembled Lipid-Based Nanoparticles Affects Their
Uptake by Cancer Cells
SO JOURNAL OF BIOMEDICAL NANOTECHNOLOGY
LA English
DT Article
DE Cancer Cellular Internalization; Spontaneous Formation;
Morphology-Targeting; Bicelles; Vesicles; SANS
ID FORMED UNILAMELLAR VESICLES; CELLULAR UPTAKE; ENGINEERED NANOPARTICLES;
MAMMALIAN-CELLS; DRUG-DELIVERY; SIZE; SHAPE; LIPOSOMES; NANODISCS;
INTERNALIZATION
AB The morphology of nanoparticles (NPs) has been presumed to play an important role in cellular uptake and in vivo stability. This report experimentally demonstrates such dependence by using two types of uniform-sized self-assembled lipid-based NPs, namely nanodiscs and nanovesicles, composed of identical lipid composition. The morphology is characterized by small angle neutron scattering, dynamic light scattering and transmission electron microscopy. Both NPs have similar bio-stability in serum and cellular cytotoxicity. However, cellular uptake of the nanodiscs at 37 degrees C is consistently and significantly higher than that of the vesicles according to the uptake results of several human cancer cell lines, i.e., CCRF-CEM, KB, and OVCAR-8, indicating a strong morphological dependence of cellular internalization. Further studies on such morphological dependence using CCRF-CEM reveals that vesicles only use Clathrin-and caveolae-mediated endocytic pathways, while nanodiscs also take the additional routes of macropinocytosis and microtubule-mediated endocytosis.
C1 [Aresh, Wafa; Nieh, Mu-Ping] Univ Connecticut, Dept Biomed Engn, Storrs, CT 06269 USA.
[Liu, Ying; Nieh, Mu-Ping] Univ Connecticut, Dept Chem & Biomol Engn, Storrs, CT 06269 USA.
[Sine, Jessica; Thayer, Derek; Puri, Anu] NCI, Basic Res Lab, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
[Huang, Yike; Wang, Yong] Penn State Univ, Dept Biomed Engn, University Pk, PA 16802 USA.
[Nieh, Mu-Ping] Univ Connecticut, Inst Mat Sci, Polymer Program, Storrs, CT 06269 USA.
RP Nieh, MP (reprint author), Univ Connecticut, Dept Biomed Engn, Storrs, CT 06269 USA.; Nieh, MP (reprint author), Univ Connecticut, Dept Chem & Biomol Engn, Storrs, CT 06269 USA.; Nieh, MP (reprint author), Univ Connecticut, Inst Mat Sci, Polymer Program, Storrs, CT 06269 USA.
EM mu-ping.nieh@uconn.edu
FU Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research; [NSF-CMMI 1131587]
FX Mu-Ping Nieh, Yong Wang, Ying Liu, and Yike Huang would like to
acknowledge the financial support by NSF-CMMI 1131587 and the assistance
from the staff and scientist at the Spallation Neutron Source at the Oak
Ridge National Laboratory. This research was also supported in part by
the Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research. We would like to thank Mr. Patrick Hall and
Mr. Joseph Bergman for their assistance in the stability of the
nanoparticles. We also thank Dr. Carol Norris for the training and her
assistance in the use of Flow Cytometry/Confocal Microscope at the UConn
Biotechnology-Bioservice Center as well as Dr. William Heller for his
help with the experiment on EQ-SANS.
NR 42
TC 0
Z9 0
U1 8
U2 8
PU AMER SCIENTIFIC PUBLISHERS
PI VALENCIA
PA 26650 THE OLD RD, STE 208, VALENCIA, CA 91381-0751 USA
SN 1550-7033
EI 1550-7041
J9 J BIOMED NANOTECHNOL
JI J. Biomed. Nanotechnol.
PD OCT
PY 2016
VL 12
IS 10
BP 1852
EP 1863
DI 10.1166/jbn.2016.2292
PG 12
WC Nanoscience & Nanotechnology; Materials Science, Biomaterials
SC Science & Technology - Other Topics; Materials Science
GA EA3FN
UT WOS:000386486800002
ER
PT J
AU Ostrom, QT
Gittleman, H
Kruchko, C
Louis, DN
Brat, DJ
Gilbert, MR
Petkov, VI
Barnholtz-Sloan, JS
AF Ostrom, Quinn T.
Gittleman, Haley
Kruchko, Carol
Louis, David N.
Brat, Daniel J.
Gilbert, Mark R.
Petkov, Valentina I.
Barnholtz-Sloan, Jill S.
TI Completeness of required site-specific factors for brain and CNS tumors
in the Surveillance, Epidemiology and End Results (SEER) 18 database
(2004-2012, varying)
SO JOURNAL OF NEURO-ONCOLOGY
LA English
DT Article
DE WHO grade; Brain tumors; Cancer registration; MGMT methylation; 1p/19q
codeletion
ID MGMT PROMOTER METHYLATION; CENTRAL-NERVOUS-SYSTEM; DNA-REPAIR GENE;
O-6-METHYLGUANINE-DNA METHYLTRANSFERASE; ANAPLASTIC OLIGODENDROGLIOMAS;
GRADE GLIOMAS; TEMOZOLOMIDE; MUTATIONS; CLASSIFICATION; TRIAL
AB Cancer registries are an important source of population-level information on brain tumor incidence and survival. Surveillance, Epidemiology, and End Results (SEER) registries currently collect data on specific required factors related to brain tumors as defined by the American Joint Commission on Cancer, including World Health Organization (WHO) grade, MGMT methylation and 1p/19q codeletion status. We assessed 'completeness', defined as having valid values over the time periods that they have been collected, overall, by year, histology, and registry. Data were obtained through a SEER custom data request for four factors related to brain tumors for the years 2004-2012 (3/4 factors were collected only from 2010 to 2012). SEER*Stat was used to generate frequencies of 'completeness' for each factor overall, and by year, histology and registry. The four factors varied in completeness, but increased over time. WHO grade has been collected the longest, and showed significant increases in completeness. Completeness of MGMT and 1p/19q codeletion was highest for glioma subtypes for which testing is recommended by clinical practice guidelines. Completeness of all factors varied by histology and cancer registry. Overall, several of the factors had high completeness, and all increased in completeness over time. With increasing focus on 'precision medicine' and the incorporation of molecular parameters into the 2016 WHO CNS tumor classification, it is critical that the data are complete, and factors collected at the population level are fully integrated into cancer reporting. It is critical that cancer registries continue to collect established and emerging prognostic and predictive factors.
C1 [Ostrom, Quinn T.; Gittleman, Haley; Barnholtz-Sloan, Jill S.] Case Western Reserve Univ, Case Comprehens Canc Ctr, Sch Med, 11100 Euclid Ave,Wearn 152, Cleveland, OH 44106 USA.
[Ostrom, Quinn T.; Gittleman, Haley; Kruchko, Carol; Barnholtz-Sloan, Jill S.] CBTRUS, Hinsdale, IL 60521 USA.
[Louis, David N.] Harvard Med Sch, Massachusetts Gen Hosp, Dept Pathol, Boston, MA USA.
[Brat, Daniel J.] Emory Univ, Dept Pathol & Lab Med, Winship Canc Inst, Atlanta, GA 30322 USA.
[Gilbert, Mark R.] NIH, Neurooncol Branch, Bldg 10, Bethesda, MD 20892 USA.
[Petkov, Valentina I.] NCI, Surveillance Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Barnholtz-Sloan, JS (reprint author), Case Western Reserve Univ, Case Comprehens Canc Ctr, Sch Med, 11100 Euclid Ave,Wearn 152, Cleveland, OH 44106 USA.; Barnholtz-Sloan, JS (reprint author), CBTRUS, Hinsdale, IL 60521 USA.
EM jsb42@case.edu
FU National Cancer Institute Case Comprehensive Cancer Center
[P30CA043703]; CBTRUS database: the Centers for Disease Control and
Prevention (CDC) [5U58DP00383]; Sontag Foundation, Genentech, Novocure,
Inc; Celldex Therapeutics, Inc; AbbVie, Inc; Musella Foundation; Voices
Against Brain Cancer, Elekta
FX QTO, HG, and JSB-S were supported by the National Cancer Institute Case
Comprehensive Cancer Center Support Grant (P30CA043703). CBTRUS is
honored to be included among the research grant recipients of the
following organizations, which have contributed to the maintenance of
the CBTRUS database: the Centers for Disease Control and Prevention
(CDC) under Agreement 5U58DP00383, the Sontag Foundation, Genentech,
Novocure, Inc., Celldex Therapeutics, Inc., AbbVie, Inc., along with the
Musella Foundation, Voices Against Brain Cancer, Elekta, the Zelda Dorin
Memorial Fund, as well as private and in kind donations.
NR 42
TC 0
Z9 0
U1 3
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-594X
EI 1573-7373
J9 J NEURO-ONCOL
JI J. Neuro-Oncol.
PD OCT
PY 2016
VL 130
IS 1
BP 31
EP 42
DI 10.1007/s11060-016-2217-7
PG 12
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA EA4FH
UT WOS:000386565200004
PM 27418206
ER
PT J
AU Nesvick, CL
Zhang, C
Edwards, NA
Montgomery, BK
Lee, M
Yang, CZ
Wang, HR
Zhu, DW
Heiss, JD
Merrill, MJ
Ray-Chaudhury, A
Zhuang, ZP
AF Nesvick, Cody L.
Zhang, Chao
Edwards, Nancy A.
Montgomery, Blake K.
Lee, Michaela
Yang, Chunzhang
Wang, Herui
Zhu, Dongwang
Heiss, John D.
Merrill, Marsha J.
Ray-Chaudhury, Abhik
Zhuang, Zhengping
TI ZEB1 expression is increased in IDH1-mutant lower-grade gliomas
SO JOURNAL OF NEURO-ONCOLOGY
LA English
DT Article
DE IDH; Lower-grade glioma; Epithelial-mesenchymal transition; ZEB1
ID EPITHELIAL-MESENCHYMAL TRANSITION; INTEGRATED GENOMIC ANALYSIS;
GENE-EXPRESSION; GLIOBLASTOMA-MULTIFORME; TUMOR INITIATION; STEM-CELLS;
MUTATIONS; INVASION; IDH1; TRANSCRIPTION
AB Transcription factors that induce epithelial-mesenchymal transition (EMT) promote invasion, chemoresistance and a stem-cell phenotype in epithelial tumors, but their roles in central nervous system tumors are not well-understood. We hypothesized these transcription factors have a functional impact in grades II-III gliomas. Using the National Cancer Institute (NCI) Repository for Molecular Brain Neoplasia Data (REMBRANDT) and the Cancer Genome Atlas (TCGA) Lower-Grade Glioma (LGG) data, we determined the impact of EMT-promoting transcription factors (EMT-TFs) on overall survival in grades II-III gliomas, compared their expression across common genetic subtypes and subsequently validated these findings in a set of 31 tumors using quantitative real-time polymerase chain reaction (PCR) and immunohistochemistry. Increased expression of the gene coding for the transcriptional repressor Zinc Finger E box-binding Homeobox 1 (ZEB1) was associated with a significant increase in overall survival (OS) on Kaplan-Meier analysis. Genetic subtype analysis revealed that ZEB1 expression was relatively increased in IDH1/2-mutant gliomas, and IDH1/2-mutant gliomas expressed significantly lower levels of many ZEB1 transcriptional targets. Similarly, IDH1/2-mutant tumors expressed significantly higher levels of targets of microRNA 200C (MIR200C), a key regulator of ZEB1. In a validation study, ZEB1 mRNA was significantly increased in IDH1-mutant grades II-III gliomas, and ZEB1 protein expression was more pronounced in these tumors. Our findings demonstrate a novel relationship between IDH1/2 mutations and expression of ZEB1 and its transcriptional targets. Therapy targeting ZEB1-associated pathways may represent a novel therapeutic avenue for this class of tumors.
C1 [Nesvick, Cody L.; Zhang, Chao; Edwards, Nancy A.; Montgomery, Blake K.; Lee, Michaela; Yang, Chunzhang; Wang, Herui; Zhu, Dongwang; Heiss, John D.; Merrill, Marsha J.; Ray-Chaudhury, Abhik; Zhuang, Zhengping] NINDS, Surg Neurol Branch, 9000 Rockville Pike,Bldg 10 Room 3D17, Bethesda, MD 20892 USA.
[Nesvick, Cody L.] Mayo Clin, Dept Neurol Surg, 200 1st St SW, Rochester, MN 55905 USA.
[Montgomery, Blake K.] Stanford Univ, Dept Orthopaed Surg, 450 Broadway St,Pavil C,4th Floor, Redwood City, CA 94063 USA.
[Lee, Michaela] George Washington Univ, Dept Neurol Surg, 2150 Penn Ave NW,Suite 7-420, Washington, DC 20037 USA.
[Yang, Chunzhang] NCI, Neurooncol Branch, Bldg 37,Room 1142E, Bethesda, MD 20892 USA.
RP Nesvick, CL; Zhuang, ZP (reprint author), NINDS, Surg Neurol Branch, 9000 Rockville Pike,Bldg 10 Room 3D17, Bethesda, MD 20892 USA.; Nesvick, CL (reprint author), Mayo Clin, Dept Neurol Surg, 200 1st St SW, Rochester, MN 55905 USA.
EM Cody.Nesvick@gmail.com; ZhuangP@ninds.nih.gov
FU Intramural Research Program at the National Institute of Neurological
Disorders and Stroke; National Institutes of Health Medical Research
Scholars Program
FX This research was supported by the Intramural Research Program at the
National Institute of Neurological Disorders and Stroke and the National
Institutes of Health Medical Research Scholars Program.
NR 56
TC 1
Z9 1
U1 3
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-594X
EI 1573-7373
J9 J NEURO-ONCOL
JI J. Neuro-Oncol.
PD OCT
PY 2016
VL 130
IS 1
BP 111
EP 122
DI 10.1007/s11060-016-2240-8
PG 12
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA EA4FH
UT WOS:000386565200012
PM 27568035
ER
PT J
AU Jacobson, KA
Civan, MM
AF Jacobson, Kenneth A.
Civan, Mortimer M.
TI Ocular Purine Receptors as Drug Targets in the Eye
SO JOURNAL OF OCULAR PHARMACOLOGY AND THERAPEUTICS
LA English
DT Review
DE adenosine receptor; P2Y receptor; P2X receptor; ATP
ID RETINAL GANGLION-CELLS; DIQUAFOSOL OPHTHALMIC SOLUTION; A(3) ADENOSINE
RECEPTOR; MOUSE INTRAOCULAR-PRESSURE; TRAUMATIC OPTIC NEUROPATHY;
TRABECULAR MESHWORK CELLS; AQUEOUS-HUMOR; DRY-EYE; A(2A) RECEPTOR;
GLAUCOMA TREATMENT
AB Agonists and antagonists of various subtypes of G protein coupled adenosine receptors (ARs), P2Y receptors (P2YRs), and ATP-gated P2X receptor ion channels (P2XRs) are under consideration as agents for the treatment of ocular diseases, including glaucoma and dry eye. Numerous nucleoside and nonnucleoside modulators of the receptors are available as research tools and potential therapeutic molecules. Three of the 4 subtypes of ARs have been exploited with clinical candidate molecules for treatment of the eye: A(1), A(2A), and A(3). An A(1)AR agonist is in clinical trials for glaucoma, A(2A)AR reduces neuroinflammation, A(3)AR protects retinal ganglion cells from apoptosis, and both A(3)AR agonists and antagonists had been reported to lower intraocular pressure (IOP). Extracellular concentrations of endogenous nucleotides, including dinucleoside polyphosphates, are increased in pathological states, activating P2Y and P2XRs throughout the eye. P2YR agonists, including P2Y(2) and P2Y(6), lower IOP. Antagonists of the P2X7R prevent the ATP-induced neuronal apoptosis in the retina. Thus, modulators of the purinome in the eye might be a source of new therapies for ocular diseases.
C1 [Jacobson, Kenneth A.] NIDDK, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
[Civan, Mortimer M.] Univ Penn, Dept Physiol, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Civan, Mortimer M.] Univ Penn, Dept Med, Perelman Sch Med, Philadelphia, PA 19104 USA.
RP Jacobson, KA (reprint author), NIDDK, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
EM kennethj@helix.nih.gov
FU NIDDK, NIH Intramural Research Program
FX K.A.J. thanks the NIDDK, NIH Intramural Research Program for support.
NR 123
TC 0
Z9 0
U1 4
U2 4
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1080-7683
EI 1557-7732
J9 J OCUL PHARMACOL TH
JI J. Ocular Pharmacol. Ther.
PD OCT
PY 2016
VL 32
IS 8
SI SI
BP 534
EP 547
DI 10.1089/jop.2016.0090
PG 14
WC Ophthalmology; Pharmacology & Pharmacy
SC Ophthalmology; Pharmacology & Pharmacy
GA EA4NJ
UT WOS:000386589200011
PM 27574786
ER
PT J
AU Louis, GMB
Backonja, U
Schliep, KC
Sun, LP
Peterson, CM
Chen, Z
AF Louis, Germaine M. Buck
Backonja, Uba
Schliep, Karen C.
Sun, Liping
Peterson, C. Matthew
Chen, Zhen
TI Women's Reproductive History Before the Diagnosis of Incident
Endometriosis
SO JOURNAL OF WOMENS HEALTH
LA English
DT Article
DE endometriosis; epidemiology; fertility
ID PREDICTIVE-VALUE; INFERTILE WOMEN; BODY-SIZE; PREGNANCY; POPULATION;
RISK; RECURRENCE; CLASSIFICATION; ASSOCIATION; PERFORMANCE
AB Background: Endometriosis is a gynecologic disease reported to be associated with infertility and, possibly, adverse pregnancy outcomes. While considerable research focuses on pregnancy outcomes following diagnosis and/or treatment, few data actually describe women's reproductive history before diagnosis for a more complete understanding of endometriosis and reproduction. Materials and Methods: The study sample comprised 473 women (aged 18-44 years) undergoing laparoscopies or laparotomies, irrespective of surgical indication at 14 clinical sites, during the period 2007-2009. Upon enrollment and before surgery, women were queried about pregnancy intentions and the time required to become pregnant for planned pregnancies. Endometriosis was defined as surgically visualized disease. Using discrete time survival analysis, we estimated fecundability odds ratios (FORs) and 95% confidence intervals (CIs) to assess time to pregnancy (TTP) after adjusting for potential confounders (age, body composition, cigarette smoking, site). Generalized estimating equations accounted for multiple pregnancy attempts per woman. FORs <1.0 denote a longer TTP or diminished fecundity. Results: Approximately 66% and 69% of women with and without endometriosis, respectively, reported having a planned pregnancy before surgery, respectively. After adjustment, an endometriosis diagnosis was associated with approximate to 29% reduction in fecundity or a longer TTP across all pregnancy-trying attempts (adjusted FOR=0.71; 95% CI 0.46-1.10). While FORs were consistently <1.0, irrespective of endometriosis staging, CIs included 1. Conclusions: Women with endometriosis had a longer TTP than unaffected women, irrespective of disease severity, although the findings did not achieve significance. Prior reproductive history may be informative for predicting fecundity and pregnancy outcomes following diagnosis/treatment.
C1 [Louis, Germaine M. Buck; Backonja, Uba] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth, Rockville, MD USA.
[Backonja, Uba] Univ Washington, Sch Med, Dept Biomed Informat & Med Educ, Div Biomed & Hlth Informat, Seattle, WA USA.
[Schliep, Karen C.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Epidemiol Branch, Div Intramural Populat Hlth, Rockville, MD USA.
[Schliep, Karen C.] Univ Utah, Sch Med, Dept Family & Prevent Med, Div Publ Hlth, Salt Lake City, UT 84112 USA.
[Sun, Liping] Glotech Corp, Rockville, MD USA.
[Peterson, C. Matthew] Univ Utah, Sch Med, Dept Obstet & Gynecol, Div Reprod Endocrinol & Infertil, Salt Lake City, UT 84132 USA.
[Chen, Zhen] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Biostat & Bioinformat Branch, Div Intramural Populat Hlth, Rockville, MD USA.
RP Louis, GMB (reprint author), 6710B Rockledge Blvd, Rockville, MD 20852 USA.
EM louisg@mail.nih.gov
OI Buck Louis, Germaine/0000-0002-1774-4490
FU Intramural Research Program, Eunice Kennedy Shriver National Institute
of Child Health and Human Development [NO1-DK-6-3428, NO1-DK-6-3427,
10001406-02]; National Institutes of Health, National Library of
Medicine (NLM) Biomedical and Health Informatics Training Program at the
University of Washington [T15LM007442]
FX This research was supported by the Intramural Research Program, Eunice
Kennedy Shriver National Institute of Child Health and Human Development
(contracts NO1-DK-6-3428; NO1-DK-6-3427; 10001406-02). Dr. U.B. was
supported as a predoctoral fellow by the National Institute for Nursing
Research's Graduate Partnership Program during the course of this
research and is now supported, in part, by the National Institutes of
Health, National Library of Medicine (NLM) Biomedical and Health
Informatics Training Program at the University of Washington (Grant Nr.
T15LM007442).
NR 52
TC 0
Z9 0
U1 3
U2 3
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1540-9996
EI 1931-843X
J9 J WOMENS HEALTH
JI J. Womens Health
PD OCT
PY 2016
VL 25
IS 10
BP 1021
EP 1029
DI 10.1089/jwh.2015.5712
PG 9
WC Public, Environmental & Occupational Health; Medicine, General &
Internal; Obstetrics & Gynecology; Women's Studies
SC Public, Environmental & Occupational Health; General & Internal
Medicine; Obstetrics & Gynecology; Women's Studies
GA EA3BH
UT WOS:000386472300008
ER
PT J
AU Lerin, C
Goldfine, AB
Boes, T
Liu, M
Kasif, S
Dreyfuss, JM
De Sousa-Coelho, AL
Daher, G
Manoli, I
Sysol, JR
Isganaitis, E
Jessen, N
Goodyear, LJ
Beebe, K
Gall, W
Venditti, CP
Patti, ME
AF Lerin, Carles
Goldfine, Allison B.
Boes, Tanner
Liu, Manway
Kasif, Simon
Dreyfuss, Jonathan M.
De Sousa-Coelho, Ana Luisa
Daher, Grace
Manoli, Irini
Sysol, Justin R.
Isganaitis, Elvira
Jessen, Niels
Goodyear, Laurie J.
Beebe, Kirk
Gall, Walt
Venditti, Charles P.
Patti, Mary-Elizabeth
TI Defects in muscle branched-chain amino acid oxidation contribute to
impaired lipid metabolism
SO MOLECULAR METABOLISM
LA English
DT Article
DE Insulin sensitivity; BCAA; Fatty acid oxidation; TCA cycle
ID TYPE-2 DIABETES-MELLITUS; VISCERAL ADIPOSE-TISSUE; CIRCULATING BCAA
LEVELS; INSULIN-RESISTANCE; SKELETAL-MUSCLE; METHYLMALONIC ACIDEMIA;
GENE-EXPRESSION; ENZYME-ACTIVITY; WEIGHT-LOSS; OBESITY
AB Objective: Plasma levels of branched-chain amino acids (BCAA) are consistently elevated in obesity and type 2 diabetes (T2D) and can also prospectively predict T2D. However, the role of BCAA in the pathogenesis of insulin resistance and T2D remains unclear.
Methods: To identify pathways related to insulin resistance, we performed comprehensive gene expression and metabolomics analyses in skeletal muscle from 41 humans with normal glucose tolerance and 11 with T2D across a range of insulin sensitivity (SI, 0.49 to 14.28). We studied both cultured cells and mice heterozygous for the BCAA enzyme methylmalonyl-CoA mutase (Mut) and assessed the effects of altered BCAA flux on lipid and glucose homeostasis.
Results: Our data demonstrate perturbed BCAA metabolism and fatty acid oxidation in muscle from insulin resistant humans. Experimental alterations in BCAA flux in cultured cells similarly modulate fatty acid oxidation. Mut heterozygosity in mice alters muscle lipid metabolism in vivo, resulting in increased muscle triglyceride accumulation, increased plasma glucose, hyperinsulinemia, and increased body weight after high-fat feeding.
Conclusions: Our data indicate that impaired muscle BCAA catabolism may contribute to the development of insulin resistance by perturbing both amino acid and fatty acid metabolism and suggest that targeting BCAA metabolism may hold promise for prevention or treatment of T2D. (C) 2016 The Authors. Published by Elsevier GmbH.
C1 [Lerin, Carles; Goldfine, Allison B.; Boes, Tanner; Dreyfuss, Jonathan M.; De Sousa-Coelho, Ana Luisa; Daher, Grace; Isganaitis, Elvira; Jessen, Niels; Goodyear, Laurie J.; Patti, Mary-Elizabeth] Joslin Diabet Ctr, Res Div, Boston, MA 02215 USA.
[Lerin, Carles; Goldfine, Allison B.; De Sousa-Coelho, Ana Luisa; Isganaitis, Elvira; Patti, Mary-Elizabeth] Harvard Med Sch, Boston, MA 02215 USA.
[Lerin, Carles] Hosp St Joan Deu, Inst Recerca Pediat, Endocrinol Dept, Barcelona 08950, Spain.
[Liu, Manway; Kasif, Simon; Dreyfuss, Jonathan M.] Boston Univ, Dept Biomed Engn, Boston, MA 02215 USA.
[Manoli, Irini; Sysol, Justin R.; Venditti, Charles P.] NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
[Beebe, Kirk; Gall, Walt] Metabolon Inc, Durham, NC 27723 USA.
[Gall, Walt] Saffron Technol, Cary, NC 27513 USA.
RP Patti, ME (reprint author), Joslin Diabet Ctr, One Joslin Pl, Boston, MA 02215 USA.; Lerin, C (reprint author), Hosp St Joan Deu, Inst Recerca Pediat, Barcelona 08950, Spain.
EM clerin@fsjd.org; mary.elizabeth.patti@joslin.harvard.edu
OI Jessen, Niels/0000-0001-5613-7274
FU NICHD NIH HHS [K99 HD064793]; NIDDK NIH HHS [K23 DK002795, P30 DK036836,
R01 DK101043]; NLM NIH HHS [U54 LM008748]
NR 64
TC 0
Z9 0
U1 10
U2 10
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 2212-8778
J9 MOL METAB
JI Mol. Metab.
PD OCT
PY 2016
VL 5
IS 10
BP 926
EP 936
DI 10.1016/j.molmet.2016.08.001
PG 11
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA EA8KC
UT WOS:000386882700012
PM 27689005
ER
PT J
AU Bachis, A
Wenzel, E
Boelk, A
Becker, J
Mocchetti, I
AF Bachis, Alessia
Wenzel, Erin
Boelk, Allyssia
Becker, Jodi
Mocchetti, Italo
TI The neurotrophin receptor p75 mediates gp120-induced loss of synaptic
spines in aging mice
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE Aging; Hippocampus; HIV; p75NTR; proBDNF; TrkB
ID HUMAN-IMMUNODEFICIENCY-VIRUS; CENTRAL-NERVOUS-SYSTEM; ENVELOPE PROTEIN
GP120; LONG-TERM POTENTIATION; ANTIRETROVIRAL THERAPY;
HIPPOCAMPAL-NEURONS; ALZHEIMERS-DISEASE; HIV-1 ENCEPHALITIS;
AXONAL-TRANSPORT; DENDRITIC GROWTH
AB Human immunodeficiency virus 1 and its envelope protein gp120 reduce synaptodendritic complexity. However, the mechanisms contributing to this pathological feature are still not understood. The proneurotrophin brain-derived neurotrophic factor promotes synaptic simplification through the activation of the p75 neurotrophin receptor (p75NTR). Here, we have used gp120 transgenic (gp120tg) mice to investigate whether p75NTR has a role in gp120-mediated neurotoxicity. Old (similar to 10 months) gp120tg mice exhibited an increase in proneurotrophin brain-derived neurotrophic factor levels in the hippocampus as well as a decrease in the number of dendritic spines when compared to age-matched wild type. These effects were not observed in 3-or 6-month-old mice. To test if the reduction in spine density and morphology is caused by the activation of p75NTR, we crossed gp120tg mice with p75NTR null mice. We found that deletion of only 1 copy of the p75NTR gene in gp120tg mice is sufficient to normalize the number of hippocampal spines, strongly suggesting that the neurotoxic effect of gp120 is mediated by p75NTR. These data indicate that p75NTR antagonists could provide an adjunct therapy against synaptic simplification caused by human immunodeficiency virus 1. (C) 2016 Elsevier Inc. All rights reserved.
C1 [Bachis, Alessia; Wenzel, Erin; Boelk, Allyssia; Mocchetti, Italo] Georgetown Univ, Med Ctr, Dept Neurosci, Lab Preclin Neurobiol, Washington, DC 20007 USA.
[Wenzel, Erin] Georgetown Univ, Med Ctr, Dept Pharmacol, Washington, DC 20007 USA.
[Becker, Jodi] NCI, Ctr Canc Res, Frederick, MD 21701 USA.
RP Mocchetti, I (reprint author), Georgetown Univ, Med Ctr, EP09 New Res Bldg,3970 Reservoir Rd NW, Washington, DC 20057 USA.
EM moccheti@georgetown.edu
FU HHS [NS079172, NS074916]
FX This work was supported by HHS grants NS079172 and NS074916. Special
thanks to Dr. Eliezer Masliah (University of California San Diego, San
Diego, CA) for the breading pairs of gp120tg mice, to Dr. Bruce Carter
(Vanderbilt University, Nashville, TE) for the gift of the p75NTR
antibody, and Lino Tessarollo (NCI-Frederick, MD) for discussions and
advice with the animal studies. The authors are grateful to the National
NeuroAIDS Tissue Consortium for providing human brain tissues.
NR 57
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U1 2
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0197-4580
EI 1558-1497
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD OCT
PY 2016
VL 46
BP 160
EP 168
DI 10.1016/j.neurobiolaging.2016.07.001
PG 9
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA EA9OP
UT WOS:000386973900017
PM 27498053
ER
PT J
AU Bras, J
Djaldetti, R
Alves, AM
Mead, S
Darwent, L
Lleo, A
Molinuevo, JL
Blesa, R
Singleton, A
Hardy, J
Clarimon, J
Guerreiro, R
AF Bras, Jose
Djaldetti, Ruth
Alves, Ana Margarida
Mead, Simon
Darwent, Lee
Lleo, Alberto
Luis Molinuevo, Jose
Blesa, Rafael
Singleton, Andrew
Hardy, John
Clarimon, Jordi
Guerreiro, Rita
TI Exome sequencing in a consanguineous family clinically diagnosed with
early-onset Alzheimer's disease identifies a homozygous CTSF mutation
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE Early onset Alzheimer's disease; Kufs disease; Recessive; Exome
sequencing; Homozygosity; CTSF
ID NEURONAL CEROID-LIPOFUSCINOSIS; B KUFS-DISEASE; EXTENDED TRACTS;
CANDIDATE GENES; GENOME ANALYSIS; FRAMEWORK; DEMENTIA
AB We have previously reported the whole genome genotyping analysis of 2 consanguineous siblings clinically diagnosed with early onset Alzheimer's disease (AD). In this analysis, we identified several large regions of homozygosity shared between both affected siblings, which we suggested could be candidate loci for a recessive genetic lesion underlying the early onset AD in these cases. We have now performed exome sequencing in one of these siblings and identified the potential cause of disease: the CTSF c.1243G>A:p. Gly415Arg mutation in homozygosity. Biallelic mutations in this gene have been shown to cause Type B Kufs disease, an adult-onset neuronal ceroid lipofuscinosis with some cases resembling the impairment seen in AD. (C) 2016 Elsevier Inc. All rights reserved.
C1 [Bras, Jose; Alves, Ana Margarida; Darwent, Lee; Hardy, John; Guerreiro, Rita] UCL, Inst Neurol, Dept Mol Neurosci, 1 Wakefield St 1st Floor, London WC1N 1PJ, England.
[Bras, Jose; Guerreiro, Rita] Univ Aveiro, Dept Med Sci, Aveiro, Portugal.
[Bras, Jose; Guerreiro, Rita] Univ Aveiro, Inst Biomed iBiMED, Aveiro, Portugal.
[Djaldetti, Ruth] Rabin Med Ctr, Dept Neurol, Beilinson Campus, Petah Tiqwa, Israel.
[Djaldetti, Ruth] Felsenstein Res Ctr, Petah Tiqwa, Israel.
[Djaldetti, Ruth] Tel Aviv Univ, Sackler Sch Med, Tel Aviv, Israel.
[Mead, Simon] UCL, Inst Neurol, Dept Neurodegenerat Dis, MRC Prion Unit, London, England.
[Lleo, Alberto; Blesa, Rafael; Clarimon, Jordi] Univ Autonoma Barcelona, Hosp Santa Creu & St Pau, Dept Neurol, Memory Unit, Barcelona, Spain.
[Lleo, Alberto; Blesa, Rafael; Clarimon, Jordi] Univ Autonoma Barcelona, Hosp Santa Creu & St Pau, St Pau Biomed Res Inst, Barcelona, Spain.
[Lleo, Alberto] Ctr Networked Biomed Res Neurodegenerat Dis, CIBERNED, Madrid, Spain.
[Luis Molinuevo, Jose] Hosp Clin Barcelona, Inst Neurosci, Dept Neurol, Alzheimers Dis & Other Cognit Disorders Unit, Barcelona, Spain.
[Luis Molinuevo, Jose] Univ Barcelona, IDIBAPS, Barcelona, Spain.
[Singleton, Andrew] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
RP Guerreiro, R (reprint author), UCL, Inst Neurol, Dept Mol Neurosci, 1 Wakefield St 1st Floor, London WC1N 1PJ, England.
EM r.guerreiro@ucl.ac.uk
RI Hardy, John/C-2451-2009
FU Medical Research Council (UK); National Institute of Health Research's
Biomedical Research Centre and Biomedical Research Unit (Dementia) at
UCL Hospitals NHS Foundation Trust; Alzheimer's Society; European Grand
Prix for Young Researcher-SCOR - Fondation pour la Recherche sur
Alzheimer
FX This work was supported in part by an anonymous donor; the Medical
Research Council (UK) and by the National Institute of Health Research's
Biomedical Research Centre and Biomedical Research Unit (Dementia) at
UCL Hospitals NHS Foundation Trust; fellowships from the Alzheimer's
Society to Jose Bras and Rita Guerreiro, and by the 2014 European Grand
Prix for Young Researcher-SCOR awarded by the Fondation pour la
Recherche sur Alzheimer to Rita Guerreiro. The authors would like to
thank the Exome Aggregation Consortium and the groups that provided
exome variant data for comparison. A full list of contributing groups
can be found at http://exac.broadinstitute.org/about.
NR 22
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 0197-4580
EI 1558-1497
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD OCT
PY 2016
VL 46
AR 236.e1
DI 10.1016/j.neurobiolaging.2016.06.018
PG 6
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA EA9OP
UT WOS:000386973900025
PM 27524508
ER
PT J
AU Sassi, C
Nalls, MA
Ridge, PG
Gibbs, JR
Ding, JH
Lupton, MK
Troakes, C
Lunnon, K
Al-Sarraj, S
Brown, KS
Medway, C
Clement, N
Lord, J
Turton, J
Bras, J
Almeida, MR
Holstege, H
Louwersheimer, E
Van Der Flier, WM
Scheltens, P
Van Swieten, JC
Santana, I
Oliveira, C
Morgan, K
Powell, JF
Kauwe, JS
Cruchaga, C
Goate, AM
Singleton, AB
Guerreiro, R
Hardy, J
AF Sassi, Celeste
Nalls, Michael A.
Ridge, Perry G.
Gibbs, Jesse R.
Ding, Jinhui
Lupton, Michelle K.
Troakes, Claire
Lunnon, Katie
Al-Sarraj, Safa
Brown, Kristelle S.
Medway, Christopher
Clement, Naomi
Lord, Jenny
Turton, James
Bras, Jose
Almeida, Maria R.
Holstege, Henne
Louwersheimer, Eva
van der Flier, Wiesje M.
Scheltens, Philip
Van Swieten, John C.
Santana, Isabel
Oliveira, Catarina
Morgan, Kevin
Powell, John F.
Kauwe, John S.
Cruchaga, Carlos
Goate, Alison M.
Singleton, Andrew B.
Guerreiro, Rita
Hardy, John
CA ARUK Consortium
TI ABCA7 p.G215S as potential protective factor for Alzheimer's disease
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE Alzheimer's disease (AD); Genome-wide association studies (GWASs);
ABCA7; Whole exome sequencing (WES); Whole genome sequencing (WGS);
Protective variant
ID GENOME-WIDE ASSOCIATION; IDENTIFIES VARIANTS; APOLIPOPROTEIN-E; COMMON
VARIANTS; SEQUENCING DATA; RARE VARIANTS; RISK; LOCI; EXPRESSION;
SUSCEPTIBILITY
AB Genome-wide association studies (GWASs) have been effective approaches to dissect common genetic variability underlying complex diseases in a systematic and unbiased way. Recently, GWASs have led to the discovery of over 20 susceptibility loci for Alzheimer's disease (AD). Despite the evidence showing the contribution of these loci to AD pathogenesis, their genetic architecture has not been extensively investigated, leaving the possibility that low frequency and rare coding variants may also occur and contribute to the risk of disease. We have used exome and genome sequencing data to analyze the single independent and joint effect of rare and low-frequency protein coding variants in 9 AD GWAS loci with the strongest effect sizes after APOE (BIN1, CLU, CR1, PICALM, MS4A6A, ABCA7, EPHA1, CD33, and CD2AP) in a cohort of 332 sporadic AD cases and 676 elderly controls of British and North-American ancestry. We identified coding variability in ABCA7 as contributing to AD risk. This locus harbors a low-frequency coding variant (p. G215S, rs72973581, minor allele frequency = 4.3%) conferring a modest but statistically significant protection against AD (p-value = 0.024, odds ratio = 0.57, 95% confidence interval = 0.41-0.80). Notably, our results are not driven by an enrichment of loss of function variants in ABCA7, recently reported as main pathogenic factor underlying AD risk at this locus. In summary, our study confirms the role of ABCA7 in AD and provides new insights that should address functional studies. (C) 2016 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY license.
C1 [Sassi, Celeste; Bras, Jose; Guerreiro, Rita; Hardy, John] UCL Inst Neurol, Dept Mol Neurosci, Weston Res Labs, Reta Lila, London, England.
[Sassi, Celeste; Nalls, Michael A.; Gibbs, Jesse R.; Ding, Jinhui; Singleton, Andrew B.] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Sassi, Celeste] Charite, Ctr Stroke Res Berlin CSB, Dept Expt Neurol, Berlin, Germany.
[Sassi, Celeste] German Ctr Neurodegenerat Dis DZNE, Berlin Site, Germany.
[Ridge, Perry G.; Kauwe, John S.] Brigham Young Univ, Dept Biol, Provo, UT 84602 USA.
[Lupton, Michelle K.; Troakes, Claire; Lunnon, Katie; Al-Sarraj, Safa; Powell, John F.] Kings Coll London, Inst Psychiat Psychol & Neurosci, London, England.
[Lupton, Michelle K.] QIMR Berghofer Med Res Inst, Brisbane, Qld, Australia.
[Lunnon, Katie] Univ Exeter, Sch Med, Inst Biomed & Clin Sci, Exeter, Devon, England.
[Brown, Kristelle S.; Medway, Christopher; Clement, Naomi; Lord, Jenny; Turton, James; Morgan, Kevin] Univ Nottingham, Queens Med Ctr, Sch Life Sci, Translat Cell Sci Human Genet, Nottingham, England.
[Almeida, Maria R.] Univ Coimbra, Ctr Neurosci & Cell Biol, Neurogenet Lab, Coimbra, Portugal.
[Holstege, Henne; Louwersheimer, Eva; van der Flier, Wiesje M.; Scheltens, Philip; Van Swieten, John C.] Vrije Univ Amsterdam, Med Ctr, Alzheimer Ctr, Dept Neurol, Neurosci Campus Amsterdam, Amsterdam, Netherlands.
[Van Swieten, John C.] Erasmus MC, Dept Neurol, Rotterdam, Netherlands.
[Santana, Isabel] Ctr Hosp & Univ Coimbra, Neurol Dept, Coimbra, Portugal.
[Santana, Isabel] Univ Coimbra, Fac Med, Coimbra, Portugal.
[Oliveira, Catarina] Univ Coimbra, CNC Ctr Neurosci & Cell Biol, Coimbra, Portugal.
[Oliveira, Catarina] Univ Coimbra, Fac Med, Biochem Lab, Coimbra, Portugal.
[Powell, John F.] Brigham Young Univ, Dept Neurosci, Provo, UT 84602 USA.
[Cruchaga, Carlos] Washington Univ, Div Biol & Biomed Sci, St Louis, MO USA.
[Goate, Alison M.] Icahn Sch Med Mt Sinai, Icahn Med Inst, New York, NY 10029 USA.
RP Hardy, J (reprint author), UCL Inst Neurol, Dept Mol Neurosci, Weston Res Labs, Reta Lila, London, England.
EM j.hardy@ucl.ac.uk
RI Powell, John/G-4412-2011; Hardy, John/C-2451-2009;
OI Powell, John/0000-0001-6124-439X; Todd, Stephen/0000-0002-2312-9195
FU Alzheimer's Research UK; Medical Research Council (MRC); Wellcome
Trust/MRC Joint Call in Neurodegeneration award [WT089698]; National
Institute for Health Research Biomedical Research Unit in Dementia at
University College London Hospitals, University College London;
Intramural Research Programs of the National Institute on Aging;
National Institute of Neurological Disease and Stroke; National
Institutes of Health (Department of Health and Human Services) [ZO1
AG000950-10]; ARUK; AS; Intramural Research Program of the National
Institute on Aging; National Institutes of Health; Department of Health
and Human Services [ZO1 AG000950-10]; National Institute on Aging (NIA)
[U24 AG21886]; NIH [R01 AG042611]; [P50 AG016574]; [U01 AG006786];
[R01 AG18023]
FX This study was supported by the Alzheimer's Research UK, the Medical
Research Council (MRC), the Wellcome Trust/MRC Joint Call in
Neurodegeneration award (WT089698) to the UK Parkinson's Disease
Consortium (whose members are from the University College London
Institute of Neurology, the University of Sheffield, and the MRC Protein
Phosphorylation Unit at the University of Dundee), grants (P50 AG016574,
U01 AG006786, and R01 AG18023), the National Institute for Health
Research Biomedical Research Unit in Dementia at University College
London Hospitals, University College London; an anonymous donor, the Big
Lottery (to Dr. Morgan); a fellowship from Alzheimer's Research UK (to
Dr. Guerreiro); and the Intramural Research Programs of the National
Institute on Aging and the National Institute of Neurological Disease
and Stroke, National Institutes of Health (Department of Health and
Human Services Project number, ZO1 AG000950-10). The MRC London
Neurodegenerative Diseases Brain Bank and the Manchester Brain Bank from
Brains for Dementia Research are jointly funded from ARUK and AS. This
work was supported in part by the Intramural Research Program of the
National Institute on Aging, National Institutes of Health, Department
of Health and Human Services, project number ZO1 AG000950-10. Samples
from the National Cell Repository for Alzheimer's Disease (NCRAD), which
receives government support under a cooperative agreement grant (U24
AG21886) awarded by the National Institute on Aging (NIA), were used in
this study. NIH grant R01 AG042611 to Kauwe J.
NR 37
TC 0
Z9 0
U1 4
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0197-4580
EI 1558-1497
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD OCT
PY 2016
VL 46
AR 235.e1
DI 10.1016/j.neurobiolaging.2016.04.004
PG 9
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA EA9OP
UT WOS:000386973900023
PM 27289440
ER
PT J
AU Knittel, G
Liedgens, P
Korovkina, D
Seeger, JM
Al-Baldawi, Y
Al-Maarri, M
Fritz, C
Vlantis, K
Bezhanova, S
Scheel, AH
Wolz, OO
Reimann, M
Moller, P
Lopez, C
Staudt, LM
Ortmann, M
Pasparakis, M
Siebert, R
Schmitt, CA
Klatt, AR
Wunderlich, FT
Schafer, SC
Persigehl, T
Montesinos-Rongen, M
Odenthal, M
Buttner, R
Frenzel, LP
Kashkar, H
Reinhardt, HC
AF Knittel, G.
Liedgens, P.
Korovkina, D.
Seeger, J. M.
Al-Baldawi, Y.
Al-Maarri, M.
Fritz, C.
Vlantis, K.
Bezhanova, S.
Scheel, A. H.
Wolz, O. -O.
Reimann, M.
Moeller, P.
Lopez, C.
Staudt, L. M.
Ortmann, M.
Pasparakis, M.
Siebert, R.
Schmitt, C. A.
Klatt, A. R.
Wunderlich, F. T.
Schaefer, S. C.
Persigehl, T.
Montesinos-Rongen, M.
Odenthal, M.
Buettner, R.
Frenzel, L. P.
Kashkar, H.
Reinhardt, H. C.
TI B cell-specific conditional expression of Myd88 p.L252P leads to the
development of diffuse large B cell lymphoma in mice
SO ONCOLOGY RESEARCH AND TREATMENT
LA English
DT Meeting Abstract
C1 [Knittel, G.; Liedgens, P.; Korovkina, D.; Fritz, C.; Frenzel, L. P.; Reinhardt, H. C.] Univ Hosp Cologne, Dept Internal Med 1, Cologne, Germany.
[Seeger, J. M.; Kashkar, H.] Univ Hosp Cologne, Inst Microbiol & Hyg, Cologne, Germany.
[Al-Baldawi, Y.; Persigehl, T.] Univ Hosp Cologne, Dept Radiol, Cologne, Germany.
[Al-Maarri, M.; Wunderlich, F. T.] Max Planck Inst Metab Res, Cologne, Germany.
[Vlantis, K.; Pasparakis, M.] Univ Cologne, Cologne Excellence Cluster Cellular Stress Respon, Cologne, Germany.
[Bezhanova, S.] NN Blokhin Russian Canc Res Ctr, Moscow, Russia.
[Scheel, A. H.; Ortmann, M.; Schaefer, S. C.; Odenthal, M.; Buettner, R.] Univ Hosp Cologne, Inst Pathol, Cologne, Germany.
[Wolz, O. -O.] Univ Tubingen, Interfac Inst Cell Biol, Dept Immunol, Tubingen, Germany.
[Reimann, M.; Schmitt, C. A.] Charite Univ Med Ctr, Dept Hematol Oncol, Berlin, Germany.
[Moeller, P.] Univ Ulm, Fac Med, Inst Pathol, Ulm, Germany.
[Lopez, C.; Siebert, R.] Univ Kiel, Kiel, Germany.
[Lopez, C.; Siebert, R.] Univ Hosp Schleswig Holstein, Inst Human Genet, Kiel, Germany.
[Staudt, L. M.] NCI, NIH, Metab Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Klatt, A. R.] Univ Hosp Cologne, Inst Clin Chem, Cologne, Germany.
[Montesinos-Rongen, M.] Univ Hosp Cologne, Inst Neuropathol, Cologne, Germany.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 2296-5270
EI 2296-5262
J9 ONCOL RES TREAT
JI Oncol. Res. Treat.
PD OCT
PY 2016
VL 39
SU 3
MA V717
BP 218
EP 219
PG 2
WC Oncology
SC Oncology
GA DZ2SK
UT WOS:000385691300538
ER
PT J
AU Smit, RAJ
Postmus, I
Trompet, S
Barnes, MR
Warren, H
Arsenault, BJ
Chasman, DI
Cupples, LA
Hitman, GA
Krauss, RM
Li, XH
Psaty, BM
Stein, CM
Rotter, JI
Jukema, JW
AF Smit, Roelof A. J.
Postmus, Iris
Trompet, Stella
Barnes, Michael R.
Warren, Helen
Arsenault, Benoit J.
Chasman, Daniel I.
Cupples, L. Adrienne
Hitman, Graham A.
Krauss, Ronald M.
Li, Xiaohui
Psaty, Bruce M.
Stein, Charles M.
Rotter, Jerome I.
Jukema, J. Wouter
TI Rooted in risk: genetic predisposition for low-density lipoprotein
cholesterol level associates with diminished low-density lipoprotein
cholesterol response to statin treatment
SO PHARMACOGENOMICS
LA English
DT Article
DE MR-Egger; pharmacogenetics; statin therapy
ID MENDELIAN RANDOMIZATION; LDL-CHOLESTEROL; HEART-DISEASE; NPC1L1;
METAANALYSIS; EZETIMIBE; THERAPY; BIAS
AB Aims: To utilize previously reported lead SNPs for low-density lipoprotein cholesterol (LDL-c) levels to find additional loci of importance to statin response, and examine whether genetic predisposition to LDL-c levels associates with differential statin response. Methods: We investigated effects on statin response of 59 LDL-c SNPs, by combining summary level statistics from the Global Lipids Genetics and Genomic Investigation of Statin Therapy consortia. Results: Lead SNPs for APOE, SORT1 and NPC1L1 were associated with a decreased LDL-c response to statin treatment, as was overall genetic predisposition for increased LDL-c levels as quantified with 59 SNPs, with a 5.4% smaller statin response per standard deviation increase in genetically raised LDL-c levels. Conclusion: Genetic predisposition for increased LDL-c level may decrease efficacy of statin therapy.
C1 [Smit, Roelof A. J.; Trompet, Stella; Jukema, J. Wouter] Leiden Univ, Med Ctr, Dept Cardiol, Leiden, Netherlands.
[Smit, Roelof A. J.; Postmus, Iris; Trompet, Stella] Leiden Univ, Med Ctr, Dept Internal Med, Sect Gerontol & Geriatr, Leiden, Netherlands.
[Barnes, Michael R.; Warren, Helen] Queen Mary Univ London, William Harvey Res Inst, Barts & London Sch Med, London EC1M 6BQ, England.
[Barnes, Michael R.; Warren, Helen] Queen Mary Univ London, Barts & London Sch Med, NIHR Barts Cardiovasc Biomed Res Unit, London EC1M 6BQ, England.
[Arsenault, Benoit J.] Inst Univ Cardiol & Pneumol Quebec, Ctr Rech, Quebec City, PQ, Canada.
[Chasman, Daniel I.] Brigham & Womens Hosp, Div Prevent Med, 75 Francis St, Boston, MA 02115 USA.
[Chasman, Daniel I.] Harvard Univ, Harvard Med Sch, Boston, MA 02115 USA.
[Cupples, L. Adrienne] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02118 USA.
[Cupples, L. Adrienne] NHLBI, Framingham Heart Study, Framingham, MA 01702 USA.
[Hitman, Graham A.] Queen Mary Univ London, Blizard Inst, Barts & London Sch Med & Dent, London EC1M 6BQ, England.
[Krauss, Ronald M.] Childrens Hosp Oakland, Res Inst, Dept Atherosclerosis Res, Oakland, CA 94609 USA.
[Li, Xiaohui; Rotter, Jerome I.] Harbor UCLA Med Ctr, Los Angeles Biomed Res Inst, Inst Translat Genom & Populat Sci, Torrance, CA 90502 USA.
[Psaty, Bruce M.] Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA 98101 USA.
[Psaty, Bruce M.] Univ Washington, Dept Epidemiol, Seattle, WA 98101 USA.
[Psaty, Bruce M.] Univ Washington, Dept Hlth Serv, Seattle, WA 98101 USA.
[Psaty, Bruce M.] Grp Hlth Res Inst, Grp Hlth Cooperat, Seattle, WA 98101 USA.
[Stein, Charles M.] Vanderbilt Univ, Dept Med, Nashville, TN 37232 USA.
[Stein, Charles M.] Vanderbilt Univ, Dept Pharmacol, Nashville, TN 37232 USA.
[Jukema, J. Wouter] Leiden Univ, Med Ctr, Einthoven Lab Expt Vasc Med, Leiden, Netherlands.
[Jukema, J. Wouter] Interuniv Cardiol Inst Netherlands, Utrecht, Netherlands.
RP Smit, RAJ (reprint author), Leiden Univ, Med Ctr, Dept Cardiol, Leiden, Netherlands.; Smit, RAJ (reprint author), Leiden Univ, Med Ctr, Dept Internal Med, Sect Gerontol & Geriatr, Leiden, Netherlands.
EM r.a.j.smit@lumc.nl
FU Steering Committee of the Yale Open Data Access Project by Johnson
Johnson; JUPITER from AstraZeneca; Netherlands Heart Foundation [2001 D
032]
FX BM Psaty serves on the Data and Safety Monitoring Board of a clinical
trial funded by the manufacturer, and on the Steering Committee of the
Yale Open Data Access Project funded by Johnson & Johnson. DI Chasman
received research support for independent genetic analysis in JUPITER
from AstraZeneca. JW Jukema is an Established Clinical Investigator of
The Netherlands Heart Foundation (grant no. 2001 D 032). RM Krauss
serves on the Merck Global Atherosclerosis Advisory Board. 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 26
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U1 0
U2 0
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1462-2416
EI 1744-8042
J9 PHARMACOGENOMICS
JI Pharmacogenomics
PD OCT
PY 2016
VL 17
IS 15
BP 1621
EP 1628
DI 10.2217/pgs-2016-0091
PG 8
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA EA3UD
UT WOS:000386529900003
PM 27648687
ER
PT J
AU Pereira, TA
Syn, WK
Amancio, FF
Cunha, PHD
Caporali, JFM
Trindade, GVD
Santos, ET
Souza, MM
Andrade, ZA
Witek, RP
Secor, WE
Pereira, FEL
Lambertucci, JR
Diehl, AM
AF Pereira, Thiago Almeida
Syn, Wing-Kin
Amancio, Frederico Figueiredo
Diniz Cunha, Pedro Henrique
Morais Caporali, Julia Fonseca
de Melo Trindade, Guilherme Vaz
Santos, Elisangela Trindade
Souza, Marcia Maria
Andrade, Zilton Araujo
Witek, Rafal P.
Secor, William Evan
Lima Pereira, Fausto Edmundo
Lambertucci, Jose Roberto
Diehl, Anna Mae
TI Osteopontin Is Upregulated in Human and Murine Acute Schistosomiasis
Mansoni
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID GRANULOMA-FORMATION; LIVER; INFLAMMATION; INFECTION; RESPONSES;
FIBROSIS; INJURY; CELLS
AB Background
Symptomatic acute schistosomiasis mansoni is a systemic hypersensitivity reaction against the migrating schistosomula and mature eggs after a primary infection. The mechanisms involved in the pathogenesis of acute schistosomiasis are not fully elucidated. Osteopontin has been implicated in granulomatous reactions and in acute hepatic injury. Our aims were to evaluate if osteopontin plays a role in acute Schistosoma mansoni infection in both human and experimentally infected mice and if circulating OPN levels could be a novel biomarker of this infection.
Methodology/Principal Findings
Serum/plasma osteopontin levels were measured by ELISA in patients with acute (n = 28), hepatointestinal (n = 26), hepatosplenic (n = 39) schistosomiasis and in uninfected controls (n = 21). Liver osteopontin was assessed by immunohistochemistry in needle biopsies of 5 patients. Sera and hepatic osteopontin were quantified in the murine model of schistosomiasis mansoni during acute (7 and 8 weeks post infection, n = 10) and chronic (30 weeks post infection, n = 8) phase. Circulating osteopontin levels are increased in patients with acute schistosomiasis (p = 0.0001). The highest levels of OPN were observed during the peak of clinical symptoms (7-11 weeks post infection), returning to baseline level once the granulomas were modulated (>12 weeks post infection). The plasma levels in acute schistosomiasis were even higher than in hepatosplenic patients. The murine model mirrored the human disease. Macrophages were the major source of OPN in human and murine acute schistosomiasis, while the ductular reaction maintains OPN production in hepatosplenic disease. Soluble egg antigens from S. mansoni induced OPN expression in primary human kupffer cells.
Conclusions/Significance
S. mansoni egg antigens induce the production of OPN by macrophages in the necroticexudative granulomas characteristic of acute schistosomiasis mansoni. Circulating OPN levels are upregulated in human and murine acute schistosomiasis and could be a noninvasive biomarker of this form of disease.
C1 [Pereira, Thiago Almeida; Diehl, Anna Mae] Duke Univ, Med Ctr, Dept Med, Div Gastroenterol, Durham, NC 27710 USA.
[Pereira, Thiago Almeida; Amancio, Frederico Figueiredo; Diniz Cunha, Pedro Henrique; Morais Caporali, Julia Fonseca; de Melo Trindade, Guilherme Vaz; Lambertucci, Jose Roberto] Univ Fed Minas Gerais, Fac Med, Dept Clin Med, Lab Doencas Infecciosas & Parasitarias, Belo Horizonte, MG, Brazil.
[Pereira, Thiago Almeida; Santos, Elisangela Trindade; Souza, Marcia Maria; Andrade, Zilton Araujo] Fundacao Oswaldo Cruz, Ctr Pesquisas Goncalo Moniz, Lab Patol Expt, Salvador, BA, Brazil.
[Pereira, Thiago Almeida] NIAID, Immunopathogesis Sect, Parasit Dis Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Syn, Wing-Kin] Ralph H Johnson Vet Affairs Med Ctr, Gastroenterol Sect, Charleston, SC USA.
[Syn, Wing-Kin] Med Univ South Carolina, Div Gastroenterol & Hepatol, Charleston, SC USA.
[Syn, Wing-Kin] Fdn Liver Res, Inst Hepatol, Liver Regenerat & Repair Res Grp, London, England.
[de Melo Trindade, Guilherme Vaz] Natl Univ Ireland, Sch Med, Dept Physiol, Galway, Ireland.
[Witek, Rafal P.] Thermo Fisher Sci, Frederick, MD USA.
[Secor, William Evan] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Lima Pereira, Fausto Edmundo] Univ Fed Espirito Santo, Nucleo Doencas Infecciosas, Vitoria, ES, Brazil.
RP Diehl, AM (reprint author), Duke Univ, Med Ctr, Dept Med, Div Gastroenterol, Durham, NC 27710 USA.; Lambertucci, JR (reprint author), Univ Fed Minas Gerais, Fac Med, Dept Clin Med, Lab Doencas Infecciosas & Parasitarias, Belo Horizonte, MG, Brazil.
EM jrlambertu@gmail.com; annamae.diehl@duke.edu
FU National Institutes of Health [R01-DK-077794]; National Institutes of
Health (Division of Intramural Research, NIAID, NIH); Duke University;
Conselho Nacional de Desenvolvimento Cientifico e Tecnologico, Ministry
of Science, Technology and Innovation of Brazil (CNPq); Fundacao de
Amparo a Pesquisa do Estado de Minas Gerais (FAPEMIG)
FX This work was supported by National Institutes of Health (grant number
R01-DK-077794 (to AMD); Division of Intramural Research, NIAID, NIH (to
TAP)); the Duke University Endowment (the Florence McAlister
Professorship) (to AMD), the Conselho Nacional de Desenvolvimento
Cientifico e Tecnologico, Ministry of Science, Technology and Innovation
of Brazil (CNPq) (to TAP, FELP, JRL and ZAA); and Fundacao de Amparo a
Pesquisa do Estado de Minas Gerais (FAPEMIG) (to JRL). The funders had
no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 29
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U1 0
U2 0
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1935-2735
J9 PLOS NEGLECT TROP D
JI Plos Neglect. Trop. Dis.
PD OCT
PY 2016
VL 10
IS 10
AR e0005057
DI 10.1371/journal.pntd.0005057
PG 13
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA EA5QH
UT WOS:000386676200038
PM 27755536
ER
PT J
AU Tomashek, KM
Rivera, A
Torres-Velasquez, B
Hunsperger, EA
Munoz-Jordan, JL
Sharp, TM
Rivera, I
Sanabria, D
Blau, DM
Galloway, R
Torres, J
Rodriguez, R
Serrano, J
Chavez, C
Davila, F
Perez-Padilla, J
Ellis, EM
Caballero, G
Wright, L
Zaki, SR
Deseda, C
Rodriguez, E
Margolis, HS
AF Tomashek, Kay M.
Rivera, Aidsa
Torres-Velasquez, Brenda
Hunsperger, Elizabeth A.
Munoz-Jordan, Jorge L.
Sharp, Tyler M.
Rivera, Irma
Sanabria, Dario
Blau, Dianna M.
Galloway, Renee
Torres, Jose
Rodriguez, Rosa
Serrano, Javier
Chavez, Carlos
Davila, Francisco
Perez-Padilla, Janice
Ellis, Esther M.
Caballero, Gladys
Wright, Laura
Zaki, Sherif R.
Deseda, Carmen
Rodriguez, Edda
Margolis, Harold S.
TI Enhanced Surveillance for Fatal Dengue-Like Acute Febrile Illness in
Puerto Rico, 2010-2012
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID LINKED-IMMUNOSORBENT-ASSAY; CONSENSUS CONFERENCE; HEMORRHAGIC-FEVER;
CASE-MANAGEMENT; SHOCK SYNDROME; PCR ASSAY; RT-PCR; DIAGNOSIS; VIRUS;
EPIDEMIC
AB Background
Dengue is a leading cause of morbidity throughout the tropics; however, accurate population- based estimates of mortality rates are not available.
Methods/Principal Findings
We established the Enhanced Fatal Acute Febrile Illness Surveillance System (EFASS) to estimate dengue mortality rates in Puerto Rico. Healthcare professionals submitted serum and tissue specimens from patients who died from a dengue-like acute febrile illness, and death certificates were reviewed to identify additional cases. Specimens were tested for markers of dengue virus (DENV) infection by molecular, immunologic, and immunohistochemical methods, and were also tested for West Nile virus, Leptospira spp., and other pathogens based on histopathologic findings. Medical records were reviewed and clinical data abstracted. A total of 311 deaths were identified, of which 58 (19%) were DENV laboratory-positive. Dengue mortality rates were 1.05 per 100,000 population in 2010, 0.16 in 2011 and 0.36 in 2012. Dengue mortality was highest among adults 19-64 years and seniors >= 65 years (1.17 and 1.66 deaths per 100,000, respectively). Other pathogens identified included 34 Leptospira spp. cases and one case of Burkholderia pseudomallei and Neisseria meningitidis.
Conclusions/Significance
EFASS showed that dengue mortality rates among adults were higher than reported for influenza, and identified a leptospirosis outbreak and index cases of melioidosis and meningitis.
C1 [Tomashek, Kay M.; Rivera, Aidsa; Torres-Velasquez, Brenda; Hunsperger, Elizabeth A.; Munoz-Jordan, Jorge L.; Sharp, Tyler M.; Perez-Padilla, Janice; Ellis, Esther M.; Margolis, Harold S.] Ctr Dis Control & Prevent CDC, Dengue Branch, Div Vector Borne Dis, San Juan, PR 00920 USA.
[Rivera, Irma; Sanabria, Dario; Torres, Jose; Rodriguez, Rosa; Serrano, Javier; Chavez, Carlos; Davila, Francisco; Rodriguez, Edda] Puerto Rico Inst Forens Sci, San Juan, PR USA.
[Blau, Dianna M.; Zaki, Sherif R.] CDC, Infect Dis Pathol Branch, Div High Consequence Pathogens & Pathol, Atlanta, GA 30333 USA.
[Galloway, Renee] CDC, Bacterial Special Pathogens Branch, Div High Consequence Pathogens, Atlanta, GA 30333 USA.
[Caballero, Gladys] Demog Registry Puerto Rico, San Juan, PR USA.
[Wright, Laura] ATSDR, Geospatial Res Anal & Serv Program, Div Toxicol & Human Hlth Sci, Atlanta, GA USA.
[Deseda, Carmen] Puerto Rico Dept Hlth, San Juan, PR USA.
[Tomashek, Kay M.] NIAID, Off Clin Res Resources, Div Microbiol & Infect Dis, NIH, Rockville, MD USA.
RP Tomashek, KM (reprint author), Ctr Dis Control & Prevent CDC, Dengue Branch, Div Vector Borne Dis, San Juan, PR 00920 USA.; Tomashek, KM (reprint author), NIAID, Off Clin Res Resources, Div Microbiol & Infect Dis, NIH, Rockville, MD USA.
EM kay.tomashek@nih.gov
FU CDC Dengue Branch programmatic
FX The authors received CDC Dengue Branch programmatic funding for this
project. No additional sources of funding were received. The funders had
no role in the system design, data collection and analysis, decision to
publish or preparation of the manuscript.
NR 61
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U1 3
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1935-2735
J9 PLOS NEGLECT TROP D
JI Plos Neglect. Trop. Dis.
PD OCT
PY 2016
VL 10
IS 10
AR e0005025
DI 10.1371/journal.pntd.0005025
PG 19
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA EA5QH
UT WOS:000386676200018
PM 27727271
ER
PT J
AU Meacham, E
Orem, J
Nakigudde, G
Zujewski, JA
Rao, D
AF Meacham, Elizabeth
Orem, Jackson
Nakigudde, Gertrude
Zujewski, Jo Anne
Rao, Deepa
TI Exploring stigma as a barrier to cancer service engagement with breast
cancer survivors in Kampala, Uganda
SO PSYCHO-ONCOLOGY
LA English
DT Article
DE cancer; oncology; qualitative; stigma; Uganda
AB ObjectiveTo understand the role of stigma in the delay of cancer service engagement by women with breast cancer in Kampala, Uganda.
BackgroundWomen in Sub-Saharan African countries are twice as likely to die from cancer as women in high-income countries, which is largely attributable to late diagnosis. While breast cancer-related stigma has been identified in Sub-Saharan Africa, limited research focuses on how stigma impacts the behavior of breast cancer patients in Uganda.
MethodsThis qualitative study used a grounded theory approach to examine illness narratives from 20 breast cancer survivors in Uganda, gathered through semistructured interviews.
ResultsThematic analysis showed that perceived and internalized stigma associated with breast cancer influenced care engagement throughout illness, delaying engagement and inhibiting treatment completion. Women identified key factors for overcoming stigma including acceptance of diagnosis, social support, and understanding of breast cancer.
ConclusionThe growing burden of mortality associated with breast cancer in Uganda can be mitigated by improving early detection and treatment engagement through interventions which account for key psychosocial barriers such as stigma.
C1 [Meacham, Elizabeth] Univ Washington, Dept Global Hlth, Seattle, WA USA.
[Orem, Jackson] Uganda Canc Inst, Kampala, Uganda.
[Nakigudde, Gertrude] Uganda Womens Canc Support Org UWOCASO, Kampala, Uganda.
[Zujewski, Jo Anne] NCI, Rockville, MD USA.
[Rao, Deepa] Univ Washington, Dept Global Hlth, Dept Psychiat & Behav Sci, Seattle, WA USA.
RP Meacham, E (reprint author), Univ Washington, Dept Global Hlth, Seattle, WA USA.
EM elizabeth.meacham@gmail.com
FU National Cancer Institute - Center for Global Health
FX We are indebted to all of the breast cancer survivors in Uganda who were
willing to share their illness experiences. This project was funded
through a contract from the National Cancer Institute - Center for
Global Health.
NR 13
TC 1
Z9 1
U1 3
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1057-9249
EI 1099-1611
J9 PSYCHO-ONCOLOGY
JI Psycho-Oncol.
PD OCT
PY 2016
VL 25
IS 10
SI SI
BP 1206
EP 1211
DI 10.1002/pon.4215
PG 6
WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences,
Biomedical
SC Oncology; Psychology; Biomedical Social Sciences
GA DZ3CA
UT WOS:000385720300011
PM 27421234
ER
PT J
AU Blair, KS
Otero, M
Teng, C
Geraci, M
Lewis, E
Hollon, N
Blair, RJR
Ernst, M
Grillon, C
Pine, DS
AF Blair, K. S.
Otero, M.
Teng, C.
Geraci, M.
Lewis, E.
Hollon, N.
Blair, R. J. R.
Ernst, Monique
Grillon, C.
Pine, D. S.
TI Learning from other people's fear: amygdala-based social reference
learning in social anxiety disorder
SO PSYCHOLOGICAL MEDICINE
LA English
DT Article
DE Amygdala; emotions; imaging; medial prefrontal cortex; social anxiety
ID EMOTIONAL EXPRESSIONS; FACIAL EXPRESSIONS; FRONTAL-CORTEX; PHOBIA;
FACES; BRAIN; ACTIVATION; ANGRY; SELF; MECHANISMS
AB Background Social anxiety disorder involves fear of social objects or situations. Social referencing may play an important role in the acquisition of this fear and could be a key determinant in future biomarkers and treatment pathways. However, the neural underpinnings mediating such learning in social anxiety are unknown. Using event-related functional magnetic resonance imaging, we examined social reference learning in social anxiety disorder. Specifically, would patients with the disorder show increased amygdala activity during social reference learning, and further, following social reference learning, show particularly increased response to objects associated with other people's negative reactions?
Method A total of 32 unmedicated patients with social anxiety disorder and 22 age-, intelligence quotient- and gender-matched healthy individuals responded to objects that had become associated with others' fearful, angry, happy or neutral reactions.
Results During the social reference learning phase, a significant group x social context interaction revealed that, relative to the comparison group, the social anxiety group showed a significantly greater response in the amygdala, as well as rostral, dorsomedial and lateral frontal and parietal cortices during the social, relative to non-social, referencing trials. In addition, during the object test phase, relative to the comparison group, the social anxiety group showed increased bilateral amygdala activation to objects associated with others' fearful reactions, and a trend towards decreased amygdala activation to objects associated with others' happy and neutral reactions.
Conclusions These results suggest perturbed observational learning in social anxiety disorder. In addition, they further implicate the amygdala and dorsomedial prefrontal cortex in the disorder, and underscore their importance in future biomarker developments.
C1 [Blair, K. S.; Otero, M.; Teng, C.; Geraci, M.; Lewis, E.; Hollon, N.; Blair, R. J. R.; Ernst, Monique; Grillon, C.; Pine, D. S.] NIMH, Dept Hlth & Human Serv, NIH, 15K North Dr,Room 115A,MSC 2670, Bethesda, MD 20892 USA.
RP Blair, KS (reprint author), NIMH, Dept Hlth & Human Serv, NIH, 15K North Dr,Room 115A,MSC 2670, Bethesda, MD 20892 USA.
EM peschark@mail.nih.gov
FU National Institutes of Health, National Institute of Mental Health
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Mental Health. The
authors have no financial disclosures to report. Further, the authors
assert that all procedures contributing to this work comply with the
ethical standards of the relevant national and institutional committees
on human experimentation and with the Helsinki Declaration of 1975, as
revised in 2008.
NR 35
TC 0
Z9 0
U1 4
U2 4
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0033-2917
EI 1469-8978
J9 PSYCHOL MED
JI Psychol. Med.
PD OCT
PY 2016
VL 46
IS 14
BP 2943
EP 2953
DI 10.1017/S0033291716001537
PG 11
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA EA5DN
UT WOS:000386639700006
PM 27476529
ER
PT J
AU Carlson, BA
Tobe, R
Yefremova, E
Tsuji, PA
Hoffmann, VJ
Schweizer, U
Gladyshev, VN
Hatfield, DL
Conrad, M
AF Carlson, Bradley A.
Tobe, Ryuta
Yefremova, Elena
Tsuji, Petra A.
Hoffmann, Victoria J.
Schweizer, Ulrich
Gladyshev, Vadim N.
Hatfield, Dolph L.
Conrad, Marcus
TI Glutathione peroxidase 4 and vitamin E cooperatively prevent
hepatocellular degeneration
SO REDOX BIOLOGY
LA English
DT Article
DE Selenoprotein; Ferroptosis; Lipid peroxidation
ID THIOREDOXIN REDUCTASE; CELL-DEATH; TARGETED DISRUPTION; EMBRYONIC
LETHALITY; MOUSE DEVELOPMENT; OXIDATIVE STRESS; ALPHA-TOCOPHEROL;
GENE-EXPRESSION; UGA CODONS; SELENOCYSTEINE
AB The selenoenzyme glutathione peroxidase 4 (Gpx4) is an essential mammalian glutathione peroxidase, which protects cells against detrimental lipid peroxidation and governs a novel form of regulated necrotic cell death, called ferroptosis. To study the relevance of Gpx4 and of another vitally important selenoprotein, cytosolic thioredoxin reductase (Txnrd1), for liver function, mice with conditional deletion of Gpx4 in hepatocytes were studied, along with those lacking Txnrd1 and selenocysteine (Sec) tRNA (Trsp) in hepatocytes. Unlike Txnrd1- and Trsp-deficient mice, Gpx4(-/-) mice died shortly after birth and presented extensive hepatocyte degeneration. Similar to Txnrd1-deficient livers, Gpx4(-/-) livers manifested upregulation of nuclear factor (erythroid-derived)-like 2 (Nrf2) response genes. Remarkably, Gpx4(-/-) pups born from mothers fed a vitamin E-enriched diet survived, yet this protection was reversible as subsequent vitamin E deprivation caused death of Gpx4-deficient mice similar to 4 weeks thereafter. Abrogation of selenoprotein expression in Gpx4(-/-) mice did not result in viable mice, indicating that the combined deficiency aggravated the loss of Gpx4 in liver. By contrast, combined Trsp/Txnrd1-deficient mice were born, but had significantly shorter lifespans than either single knockout, suggesting that Txnrd1 plays an important role in supporting liver function of mice lacking Trsp. In sum our study demonstrates that the ferroptosis regulator Gpx4 is critical for hepatocyte survival and proper liver function, and that vitamin E can compensate for its loss by protecting cells against deleterious lipid peroxidation. Published by Elsevier B.V.
C1 [Carlson, Bradley A.; Tobe, Ryuta; Hatfield, Dolph L.] NCI, Mol Biol Selenium Sect, Mouse Canc Genet Program, NIH, 37 Convent Dr,Bldg 37,Room 5016, Bethesda, MD 20892 USA.
[Yefremova, Elena; Conrad, Marcus] Helmholtz Zentrum Munchen, Inst Dev Genet, Neuherberg, Germany.
[Tsuji, Petra A.] Towson Univ, Dept Biol Sci, Towson, MD USA.
[Hoffmann, Victoria J.] NIH, Off Director Diagnost & Res Serv Branch, Bldg 10, Bethesda, MD 20892 USA.
[Schweizer, Ulrich] Univ Bonn, Inst Biochem & Mol Biol, Bonn, Germany.
[Gladyshev, Vadim N.] Harvard Med Sch, Dept Med, Div Genet, Brigham & Womens Hosp, Boston, MA USA.
RP Hatfield, DL (reprint author), NCI, Mol Biol Selenium Sect, Mouse Canc Genet Program, NIH, 37 Convent Dr,Bldg 37,Room 5016, Bethesda, MD 20892 USA.; Conrad, M (reprint author), Helmholtz Zentrum Munchen, Inst Dev Genet, Neuherberg, Germany.
EM hatfield@mail.nih.gov; marcus.conrad@helmholtz-muenchen.de
OI Conrad, Marcus/0000-0003-1140-5612; Schweizer,
Ulrich/0000-0003-1380-4780
FU Intramural Research Program of the National Institutes of Health,
National Cancer Institute, Center for Cancer Research; Deutsche
Forschungsgemeinschaft [CO 291/2-3, CO 291/5-1]; Human Frontier Science
Program [RGP0013/14]
FX We are grateful to Jose Pedro Friedmann Angeli for critical reading of
the manuscript. DLH was funded by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute, Center for
Cancer Research. MC received funding from the Deutsche
Forschungsgemeinschaft (CO 291/2-3; CO 291/5-1) and the Human Frontier
Science Program (RGP0013/14).
NR 39
TC 6
Z9 6
U1 10
U2 10
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 2213-2317
J9 REDOX BIOL
JI Redox Biol.
PD OCT
PY 2016
VL 9
BP 22
EP 31
DI 10.1016/j.redox.2016.05.003
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA EA6RQ
UT WOS:000386757000003
PM 27262435
ER
PT J
AU Childs, R
Blaise, D
AF Childs, Richard
Blaise, Didier
TI Alternative Donor Allogeneic Transplants: Introduction
SO SEMINARS IN HEMATOLOGY
LA English
DT Editorial Material
C1 [Childs, Richard] NHLBI, NIH, Bldg 10, Bethesda, MD 20892 USA.
[Blaise, Didier] Ctr Rech Cancerol Marseille, Marseille, France.
RP Childs, R (reprint author), NHLBI, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM childsr@nhlbi.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0037-1963
EI 1532-8686
J9 SEMIN HEMATOL
JI Semin. Hematol.
PD OCT
PY 2016
VL 53
IS 4
BP 219
EP 220
DI 10.1053/j.seminhematol.2016.08.003
PG 2
WC Hematology
SC Hematology
GA EB1FL
UT WOS:000387094900001
PM 27788758
ER
PT J
AU van Besien, K
Childs, R
AF van Besien, Koen
Childs, Richard
TI Haploidentical cord transplantation-The best of both worlds
SO SEMINARS IN HEMATOLOGY
LA English
DT Article
DE Alternative donor transplant; Umbilical cord blood; Third-party
progenitors
ID HEMATOPOIETIC-CELL TRANSPLANTATION; ACUTE MYELOID-LEUKEMIA; ALTERNATIVE
DONOR TRANSPLANTATION; RELAPSE-FREE SURVIVAL; HOST DISEASE-FREE; BLOOD
TRANSPLANTATION; BONE-MARROW; OUTCOMES; UNIT; ENGRAFTMENT
AB Haploidentical (haplo)-cord transplantation combines infusion of an umbilical cord blood (UCB) unit with CD34-selected cells usually from human leukocyte antigen (HLA) mismatched donors. Initial rapid count recovery from the haplo-hematopoietic progenitors, is gradually replaced by durable engraftment from UCB progenitors. UCB grafts used for haplo-cord are smaller, but better matched than those required for single or double UCB stem cell transplant (SCT). More than 200 patients with hematological malignancies have been transplanted. Median age was 54 years (range 17-74) and 77 were over age 60. One-year survival was 64% for patients with intermediate- and low-risk disease, with no deaths beyond 2 years. In high-risk disease, 1-year survival was 44%. In a comparison with patients undergoing double UCB SCT, haplo-cord transplant resulted in faster hematopoietic recovery, lower rates of acute and chronic graft-versus-host disease (GVHD), lower rates of disease recurrence, and improved GVHD- and relapse-free survival (GRFS). Excellent results were also reported for patients with aplastic anemia where 18 of 21 patients had sustained cord blood engraftment. Rates of GVHD and of disease recurrence after haplo-cord are encouraging. However, in the approximately 10% of patients with failure of the UCB graft disease recurrence is high, supporting the important role of UCB-mediated graft-versus-leukemia (GVL). Ongoing efforts are aimed at identifying determinants of UCB engraftment, at reducing rates of disease recurrence in high risk patients and at optimizing dose and schedule of ATG -necessary to avoid early haplo-graft rejection, but also contributing to early post-transplant immunocompromise. For those lacking haploidentical donors, unrelated donors have been successfully utilized. (C) 2016 Elsevier Inc. All rights reserved.
C1 [van Besien, Koen] Weill Cornell Med, Div Hematol Oncol, 520 E 70th St, New York, NY 10021 USA.
[Childs, Richard] NHLBI, NIH, Bldg 10, Bethesda, MD 20892 USA.
RP van Besien, K (reprint author), Weill Cornell Med, Div Hematol Oncol, 520 E 70th St, New York, NY 10021 USA.
EM kov9001@med.cornell.edu
FU Miltenyi Biotec (Germany)
FX Dr. van Besien's research was supported by an unrestricted grant from
Miltenyi Biotec (Germany).
NR 38
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U1 2
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 0037-1963
EI 1532-8686
J9 SEMIN HEMATOL
JI Semin. Hematol.
PD OCT
PY 2016
VL 53
IS 4
BP 257
EP 266
DI 10.1053/j.seminhematol.2016.07.004
PG 10
WC Hematology
SC Hematology
GA EB1FL
UT WOS:000387094900007
PM 27788764
ER
PT J
AU Truog, WE
Higgins, RD
AF Truog, William E.
Higgins, Rosemary D.
TI The Neonatal Research Network Introduction
SO SEMINARS IN PERINATOLOGY
LA English
DT Editorial Material
C1 [Truog, William E.] Univ Missouri, Sch Med, Childrens Mercy Hosp, Kansas City, MO 64108 USA.
[Higgins, Rosemary D.] Eunice Kennedy Shriner Natl Inst Child Hlth, Human Dev, NIH, Bethesda, MD USA.
RP Truog, WE (reprint author), Univ Missouri, Sch Med, Childrens Mercy Hosp, Kansas City, MO 64108 USA.
NR 2
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0146-0005
EI 1558-075X
J9 SEMIN PERINATOL
JI Semin. Perinatol.
PD OCT
PY 2016
VL 40
IS 6
BP 335
EP 336
DI 10.1053/j.semperi.2016.05.001
PG 2
WC Obstetrics & Gynecology; Pediatrics
SC Obstetrics & Gynecology; Pediatrics
GA EA3XX
UT WOS:000386543700001
PM 27344191
ER
PT J
AU Higgins, RD
Shankaran, S
AF Higgins, Rosemary D.
Shankaran, Seetha
TI The Neonatal Research Network: History since 2003, future directions and
challenges
SO SEMINARS IN PERINATOLOGY
LA English
DT Review
DE Neonatal; Research; Infant; Trial; Study
ID EXTREMELY PRETERM INFANTS; NEURODEVELOPMENTAL OUTCOMES; EARLY CPAP;
ENCEPHALOPATHY; HYPOTHERMIA; MORTALITY; DISEASE; GROWTH; AGE
AB The Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) Neontal Research Network (NRN) was established in 1986 in response to the need for rigorous studies to guide care and management of sick and premature newborns. The network is comprise of clinical centers that perform clinical protocols to investigate the safety and efficay of treatment and management strategies for newborn infants as well as a data cordinating center. Infrastructure is set up for observational and interventional studies as well as neurodevelopmental follow-up of patients. The network has conducted trials and observational studies on major neonatal problems including pulmonary disease, neuroprotection, sepsis and infection, necrotizing enterocolitis, vaccine administration to preterm infants, retinopathy of prematurity, cardiovascular issues including blood pressure, human milk, growth and nutrition, hematologic issues, resuscitation, pulmonary hypertension, and neurodevelopmental outcome. This mechanism of clinical research for newborns has led to changes in care practices leading to improved outcomes for high-risk infants. Published by Elsevier Inc.
C1 [Higgins, Rosemary D.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pregnancy & Perinatol Branch, NIH, 6710B Rockledge Dr,Room 2233,MSC 7002, Bethesda, MD 20892 USA.
[Shankaran, Seetha] Wayne State Univ, Sch Med, Dept Pediat, Div Neonatal Perinatal Med, Detroit, MI 48201 USA.
RP Higgins, RD (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pregnancy & Perinatol Branch, NIH, 6710B Rockledge Dr,Room 2233,MSC 7002, Bethesda, MD 20892 USA.
EM higginsr@mail.nih.gov
FU Intramural NIH HHS [Z99 HD999999]; NICHD NIH HHS [U10 HD021385, UG1
HD027853]
NR 18
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0146-0005
EI 1558-075X
J9 SEMIN PERINATOL
JI Semin. Perinatol.
PD OCT
PY 2016
VL 40
IS 6
BP 337
EP 340
DI 10.1053/j.semperi.2016.05.002
PG 4
WC Obstetrics & Gynecology; Pediatrics
SC Obstetrics & Gynecology; Pediatrics
GA EA3XX
UT WOS:000386543700002
PM 27371959
ER
PT J
AU Das, A
Tyson, J
Pedroza, C
Schmidt, B
Gantz, M
Wallace, D
Truog, WE
Higgins, RD
AF Das, Abhik
Tyson, Jon
Pedroza, Claudia
Schmidt, Barbara
Gantz, Marie
Wallace, Dennis
Truog, William E.
Higgins, Rosemary D.
TI Methodological issues in the design and analyses of neonatal research
studies: Experience of the NICHD Neonatal Research Network
SO SEMINARS IN PERINATOLOGY
LA English
DT Review
DE Statistical methodology; Trial design; Competing outcomes; Randomization
of multiples; Causal inference
ID LOW-BIRTH-WEIGHT; EXTREMELY PRETERM INFANTS; CLUSTER-RANDOMIZED-TRIAL;
SEMICOMPETING RISKS DATA; WEEKS GESTATIONAL-AGE; CLINICAL-TRIALS;
MULTIPLE BIRTHS; NEURODEVELOPMENTAL OUTCOMES; BRONCHOPULMONARY
DYSPLASIA; PROPENSITY SCORE
AB Impressive advances in neonatology have occurred over the 30 years of life of The Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network (NRN). However, substantial room for improvement remains in investigating and further developing the evidence base for improving outcomes among the extremely premature. We discuss some of the specific methodological challenges in the statistical design and analysis of randomized trials and observational studies in this population. Challenges faced by the NRN include designing trials for unusual or rare outcomes, accounting for and explaining center variations, identifying other subgroup differences, and balancing safety and efficacy concerns between short-term hospital outcomes and longer-term neurodevelopmental outcomes. In conclusion, the constellation of unique patient characteristics in neonates calls for broad understanding and careful consideration of the issues identified in this article for conducting rigorous studies in this population. (C) 2016 Elsevier Inc. All rights reserved.
C1 [Das, Abhik] RTI Int, Biostat & Epidemiol Div, 6110 Execut Blvd,Suite 902, Rockville, MD 20852 USA.
[Tyson, Jon; Pedroza, Claudia] Univ Texas Hlth Sci Ctr Houston, Ctr Clin Res & Evidence Based Med, Houston, TX 77030 USA.
[Schmidt, Barbara] Univ Penn, Dept Pediat, Philadelphia, PA 19104 USA.
[Gantz, Marie; Wallace, Dennis] RTI Int, Biostat & Epidemiol Div, Res Triangle Pk, NC USA.
[Truog, William E.] Univ Missouri, Sch Med, Childrens Mercy Hosp & Clin, Kansas City, MO 64108 USA.
[Higgins, Rosemary D.] Eunice Kennedy Shriver Natl Inst Hlth & Human Dev, Pregnancy & Perinatol Branch, NIH, Bethesda, MD USA.
RP Das, A (reprint author), RTI Int, Biostat & Epidemiol Div, 6110 Execut Blvd,Suite 902, Rockville, MD 20852 USA.
EM adas@rti.org
FU NICHD NIH HHS [U10 HD021373, UG1 HD027853, U10 HD036790, UG1 HD068244,
UG1 HD068284, UG1 HD087229]
NR 80
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Z9 1
U1 1
U2 1
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0146-0005
EI 1558-075X
J9 SEMIN PERINATOL
JI Semin. Perinatol.
PD OCT
PY 2016
VL 40
IS 6
BP 374
EP 384
DI 10.1053/j.semperi.2016.05.005
PG 11
WC Obstetrics & Gynecology; Pediatrics
SC Obstetrics & Gynecology; Pediatrics
GA EA3XX
UT WOS:000386543700007
PM 27344192
ER
PT J
AU Archer, SW
Carlo, WA
Truog, WE
Stevenson, DK
Van Meurs, KP
Sanchez, PJ
Das, A
Devaskar, U
Nelin, LD
Huitema, CMP
Crawford, MM
Higgins, RD
AF Archer, Stephanie Wilson
Carlo, Waldemar A.
Truog, William E.
Stevenson, David K.
Van Meurs, Krisa P.
Sanchez, Pablo J.
Das, Abhik
Devaskar, Uday
Nelin, Leif D.
Huitema, Carolyn M. Petrie
Crawford, Margaret M.
Higgins, Rosemary D.
CA Eunice Kennedy Shriver Natl Inst
TI Improving publication rates in a collaborative clinical trials research
network
SO SEMINARS IN PERINATOLOGY
LA English
DT Review
DE Publication rates; Network collaboration; Authorship policies
AB Unpublished results can bias biomedical literature, favoring positive over negative findings, primary over secondary analyses, and can lead to duplicate studies that unnecessarily endanger subjects and waste resources. The Neonatal Research Network's (NRN) publication policies for approving, reviewing, and tracking abstracts and papers work to combat these problems. In 2003, the NRN restricted investigators with unfinished manuscripts from proposing new ones and in 2010, urged authors to complete long-outstanding manuscripts. Data from 1991 to 2015 were analyzed to determine effectiveness of these policy changes. The NRN has achieved an overall publication rate of 78% for abstracts. For 1990-2002, of 137 abstracts presented, 43 (31%) were published within 2 years; for 2003-2009, after the manuscript completion policy was instituted, of 140 abstracts presented, 68 (49%) were published within 2 years. Following the effort in 2010, the rate increased to 64%. The NRN surpassed reported rates by developing a comprehensive process, holding investigators accountable and tracking abstracts from presentation to publication. (C) 2016 Published by Elsevier Inc.
C1 [Archer, Stephanie Wilson; Higgins, Rosemary D.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, NICHD Pregnancy & Perinatol Branch, 6710B Rockledge Dr,2321B, Bethesda, MD 20817 USA.
[Carlo, Waldemar A.] Univ Alabama Birmingham, Div Neonatol, Birmingham, AL USA.
[Truog, William E.] Univ Missouri, Sch Med, Dept Pediat, Childrens Mercy Hosp, Kansas City, MO 64108 USA.
[Stevenson, David K.; Van Meurs, Krisa P.] Stanford Univ, Sch Med, Dept Pediat, Div Neonatal & Dev Med, Palo Alto, CA 94304 USA.
[Stevenson, David K.; Van Meurs, Krisa P.] Lucile Packard Childrens Hosp, Palo Alto, CA USA.
[Sanchez, Pablo J.] Univ Texas Southwestern Med Ctr Dallas, Dept Pediat, Dallas, TX USA.
[Sanchez, Pablo J.; Nelin, Leif D.] Nationwide Childrens Hosp, Div Neonatol, Columbus, OH USA.
[Das, Abhik; Huitema, Carolyn M. Petrie; Crawford, Margaret M.] RTI Int, Social Stat & Environm Sci Unit, Rockville, MD USA.
[Devaskar, Uday] Univ Calif Los Angeles, David Geffen Sch Med, Div Neonatol & Dev Biol, Los Angeles, CA 90095 USA.
RP Archer, SW (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, NICHD Pregnancy & Perinatol Branch, 6710B Rockledge Dr,2321B, Bethesda, MD 20817 USA.
EM archerst@mail.nih.gov
FU National Institutes of Health; Eunice Kennedy Shriver National Institute
of Child Health and Human Development (NICHD); National Center for
Research Resources; National Center for Advancing Translational Sciences
FX The National Institutes of Health, the Eunice Kennedy Shriver National
Institute of Child Health and Human Development (NICHD), the National
Center for Research Resources, and the National Center for Advancing
Translational Sciences provided grant support for the Neonatal Research
Network. The content of the publication is solely the responsibility of
the authors and does not necessarily represent the official views of the
National Institutes of Health.
NR 9
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PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0146-0005
EI 1558-075X
J9 SEMIN PERINATOL
JI Semin. Perinatol.
PD OCT
PY 2016
VL 40
IS 6
BP 410
EP 417
DI 10.1053/j.semperi.2016.05.003
PG 8
WC Obstetrics & Gynecology; Pediatrics
SC Obstetrics & Gynecology; Pediatrics
GA EA3XX
UT WOS:000386543700011
PM 27423510
ER
PT J
AU Ginexi, EM
Vollinger, RE
AF Ginexi, Elizabeth M.
Vollinger, Robert E., Jr.
TI National Cancer Institute's leadership role in promoting State and
Community Tobacco Control research
SO TOBACCO CONTROL
LA English
DT Editorial Material
DE Environment; Media; Prevention; Public policy; Secondhand smoke
ID UNITED-STATES; SMOKING; DISPARITIES; ADULTS; US
AB The National Cancer Institute (NCI) has been at the vanguard of funding tobacco control research for decades with major efforts such as the Community Intervention Trial for Smoking Cessation (COMMIT) in 1988 and the American Stop Smoking Intervention Study (ASSIST) in 1991, followed by the Tobacco Research Initiative for State and Community Interventions in 1999. Most recently, in 2011, the NCI launched the State and Community Tobacco Control (SCTC) Research Initiative to address gaps in secondhand smoke policies, tax and pricing policies, mass media countermeasures, community and social norms and tobacco marketing. The initiative supported large scale research projects and time-sensitive ancillary pilot studies in response to expressed needs of state and community partners. This special issue of Tobacco Control showcases exciting findings from the SCTC. In this introductory article, we provide a brief account of NCI's historical commitment to promoting research to inform tobacco control policy.
C1 [Ginexi, Elizabeth M.; Vollinger, Robert E., Jr.] NCI, Tobacco Control Res Branch, 9609 Med Ctr Dr,Room 3E564,MSC 9761, Bethesda, MD 20892 USA.
RP Ginexi, EM (reprint author), NCI, Tobacco Control Res Branch, 9609 Med Ctr Dr,Room 3E564,MSC 9761, Bethesda, MD 20892 USA.
EM LGinexi@mail.nih.gov
NR 21
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U1 1
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PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0964-4563
EI 1468-3318
J9 TOB CONTROL
JI Tob. Control
PD OCT
PY 2016
VL 25
SU 1
BP i4
EP i5
DI 10.1136/tobaccocontrol-2016-053153
PG 2
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA EA2ZF
UT WOS:000386465600002
PM 27697941
ER
PT J
AU Williams, B
Mirmonsef, P
Boucher, CA
Bushman, F
Carrington-Lawrence, S
Collman, RG
Dandekar, S
Dang, Q
Malaspina, A
Paredes, R
Stone, A
Landay, A
AF Williams, Brett
Mirmonsef, Paria
Boucher, Charles A. B.
Bushman, Frederic
Carrington-Lawrence, Stacy
Collman, Ronald G.
Dandekar, Satya
Que Dang
Malaspina, Angela
Paredes, Roger
Stone, Arthur
Landay, Alan
TI A Summary of the First HIV Microbiome Workshop 2015
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Article
DE HIV; microbiome; immune activation; microbial translocation
ID IMMUNODEFICIENCY-VIRUS-INFECTION; EPITHELIAL BARRIER DYSFUNCTION;
SYSTEMIC IMMUNE ACTIVATION; TRIMETHYLAMINE-N-OXIDE; BACTERIAL VAGINOSIS;
GUT MICROBIOTA; VAGINAL MICROBIOTA; GENITAL-TRACT; T-CELLS; MUCOSAL
AB The role of microbiota in the pathogenesis of HIV infection has become the subject of intense research in recent years. A rapidly growing amount of data suggest that microbial dysbiosisin the gut or the genital tractcan influence HIV transmission and/or disease progression; however, a deeper understanding of the mechanisms involved is lacking. To better understand the relationship between the microbiome and HIV infection, investigators from a wide variety of disciplines, including those working in basic and clinical HIV studies, cardiovascular disease, reproductive health, and bioinformatics, gathered at the first International Workshop on Microbiome in HIV Pathogenesis, Prevention and Treatment, at NIH on 7 and 8 April, 2015.
C1 [Williams, Brett] Rush Univ, Med Ctr, Div Infect Dis, 600 South Paulina Suite 143, Chicago, IL 60612 USA.
[Mirmonsef, Paria; Landay, Alan] Rush Univ, Med Ctr, Dept Immunol Microbiol, Chicago, IL 60612 USA.
[Boucher, Charles A. B.] Erasmus Univ, Dept Virosci, Erasmus Med Ctr, Rotterdam, Netherlands.
[Bushman, Frederic] Univ Penn, Dept Microbiol, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Carrington-Lawrence, Stacy] US Natl Inst Hlth, Off AIDS Res, Div Program Coordinat Planning & Strateg Initiat, Off Director,US Dept Hlth & Human Serv, Philadelphia, PA USA.
[Collman, Ronald G.] Univ Penn, Dept Med, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Dandekar, Satya] Univ Calif Davis, Dept Med Microbiol & Immunol, Davis, CA 95616 USA.
[Que Dang; Malaspina, Angela] NIAID, Vaccine Res Program, Div AIDS, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Paredes, Roger] Univ Vic, Univ Autonoma Barcelona, Inst Recerca, SIDA IrsiCaixa, Catalonia, Spain.
[Paredes, Roger] Univ Vic, Univ Autonoma Barcelona, Unitat VIH, Catalonia, Spain.
[Stone, Arthur] NIAID, HJF DAIDS, NIH, DHHS, Bethesda, MD USA.
RP Williams, B (reprint author), Rush Univ, Med Ctr, Div Infect Dis, 600 South Paulina Suite 143, Chicago, IL 60612 USA.
EM brett_williams@rush.edu
FU NHLBI NIH HHS [R01 HL113252, U01 HL098957, U01 HL112712]; NIAID NIH HHS
[P30 AI045008]; NIMH NIH HHS [R01 MH061139]
NR 56
TC 0
Z9 0
U1 2
U2 2
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT-NOV
PY 2016
VL 32
IS 10-11
BP 935
EP 941
DI 10.1089/aid.2016.0034
PG 7
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA DZ9RL
UT WOS:000386216200001
PM 27267576
ER
PT J
AU Porter, KA
Turpin, J
Begg, L
Brown, G
Chakhtoura, N
Church, E
Grossman, C
Wira, C
Veronese, F
AF Porter, Kristen A.
Turpin, Jim
Begg, Lisa
Brown, Gina
Chakhtoura, Nahida
Church, Elizabeth
Grossman, Cynthia
Wira, Charles
Veronese, Fulvia
TI Understanding the Intersection of Young Age, Mucosal Injury, and HIV
Susceptibility
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Review
DE HIV; HIV; AIDS pathogenesis; HIV transmission; HIV prevention; mucosal
ID INTIMATE PARTNER VIOLENCE; FEMALE REPRODUCTIVE-TRACT; GENITOANAL INJURY;
MENSTRUAL-CYCLE; VAGINAL TRANSMISSION; SEXUAL VIOLENCE; WOMEN;
ADOLESCENT; RISK; METAANALYSIS
AB Adolescent boys and girls are disproportionately affected in the current HIV epidemic. Numerous sociobehavioral studies have addressed the indirect drivers surrounding this vulnerabilityfor example, socioeconomic, geographical locale, and all forms of violence. However, the direct factors that may influence infection, such as the anatomical and physiological maturation of the anogenital tracts of adolescents or the trauma and wound-healing processes of injured mucosal tissue, are understudied and represent a gap within the HIV prevention field. This article reviews the epidemiology of HIV infection and violence in adolescents and the available basic science knowledge attending this research area. More importantly, this review highlights the most critical gaps that need to be addressed to design preventive interventions that are safe and effective for this population, which is key to ending the HIV pandemic.
C1 [Porter, Kristen A.; Turpin, Jim; Church, Elizabeth; Veronese, Fulvia] NIAID, Div Aids, NIH, Room 8B53,MSC9831,5601 Fishers Lane, Bethesda, MD 20852 USA.
[Begg, Lisa] NIH, Off Res Womens Hlth, Bldg 10, Bethesda, MD 20892 USA.
[Brown, Gina] NIH, Off AIDS Res, Bldg 10, Bethesda, MD 20892 USA.
[Chakhtoura, Nahida] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
[Grossman, Cynthia] NIMH, Div AIDS Res, NIH, Rockville, MD 20857 USA.
[Wira, Charles] Dartmouth Coll, Geisel Sch Med, Hanover, NH 03755 USA.
[Porter, Kristen A.] Westfield State Univ, Dept Biol, Westfield, MA USA.
[Grossman, Cynthia] FasterCures, Washington, DC USA.
RP Veronese, F (reprint author), NIAID, Div Aids, NIH, Room 8B53,MSC9831,5601 Fishers Lane, Bethesda, MD 20852 USA.
EM fv10x@nih.gov
FU NIAID NIH HHS [R01 AI117739]
NR 52
TC 0
Z9 0
U1 3
U2 3
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT-NOV
PY 2016
VL 32
IS 10-11
BP 1149
EP 1158
DI 10.1089/aid.2016.0206
PG 10
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA DZ9RL
UT WOS:000386216200026
PM 27726428
ER
PT J
AU Opitz, JM
Biesecker, LG
Hennekam, RC
AF Opitz, John M.
Biesecker, Leslie G.
Hennekam, Raoul C.
TI GAUDEAMUS IGITUR...In gratitude to John Carey for his stewardship of the
American Journal of Medical Genetics 2001-2016
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Editorial Material
C1 [Opitz, John M.] Univ Utah, Sch Med, Dept Pediat Med Genet, Salt Lake City, UT USA.
[Opitz, John M.] Univ Utah, Sch Med, Dept Human Genet, Salt Lake City, UT 84132 USA.
[Opitz, John M.] Univ Utah, Sch Med, Dept Pathol, Salt Lake City, UT USA.
[Opitz, John M.] Univ Utah, Sch Med, Dept Obstet & Gynecol, Salt Lake City, UT 84132 USA.
[Biesecker, Leslie G.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Hennekam, Raoul C.] Acad Med Ctr, Dept Pediat, Amsterdam, Netherlands.
RP Opitz, JM (reprint author), Univ Utah, Sch Med, Dept Pediat, Div Med Genet, 295 Chipeta Way, Salt Lake City, UT 84108 USA.
EM john.opitz@hsc.utah.edu
NR 1
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4825
EI 1552-4833
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD OCT
PY 2016
VL 170
IS 10
SI SI
BP 2501
EP 2502
DI 10.1002/ajmg.a.37760
PG 2
WC Genetics & Heredity
SC Genetics & Heredity
GA DW4KQ
UT WOS:000383612200003
PM 27540900
ER
PT J
AU Gripp, KW
Baker, L
Kandula, V
Conard, K
Scavina, M
Napoli, JA
Griffin, GC
Thacker, M
Knox, RG
Clark, GR
Parker, VER
Semple, R
Mirzaa, G
Keppler-Noreuil, KM
AF Gripp, Karen W.
Baker, Laura
Kandula, Vinay
Conard, Katrina
Scavina, Mena
Napoli, Joseph A.
Griffin, Gregory C.
Thacker, Mihir
Knox, Rachel G.
Clark, Graeme R.
Parker, Victoria E. R.
Semple, Robert
Mirzaa, Ghayda
Keppler-Noreuil, Kim M.
TI Nephroblastomatosis or Wilms tumor in a fourth patient with a somatic
PIK3CA mutation
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE Wilms tumor; nephroblastomatosis; PIK3CA-related overgrowth;
hemihyperplasia; hemihypertrophy; CLOVES; lipoma; somatic mutation
ID MARMORATA-TELANGIECTATICA-CONGENITA; PIK3CA-RELATED OVERGROWTH SPECTRUM;
KLIPPEL-TRENAUNAY-SYNDROME; NEVI CLOVE-SYNDROME; VASCULAR MALFORMATIONS;
LIPOMATOUS OVERGROWTH; ACTIVATING MUTATIONS; CHILDREN; RISK;
HEMIHYPERTROPHY
AB Wilms tumor and nephroblastomatosis are associated with syndromic conditions including hemihyperplasia. Hemihyperplasia is genetically heterogeneous and may be the result of genomic abnormalities seen in Beckwith-Wiedemann syndrome, mosaic chromosome or genomic abnormalities, or somatic point mutations. Somatic missense mutations affecting the PI3K-AKT-MTOR pathway result in segmental overgrowth and are present in numerous benign and malignant tumors. Here, we report a fourth patient with asymmetric overgrowth due to a somatic PIK3CA mutation who had nephroblastomatosis or Wilms tumor. Similar to two of three reported patients with a somatic PIK3CA mutation and renal tumors, he shared a PIK3CA mutation affecting codon 1047, presented at birth with asymmetric overgrowth, and had fibroadipose overgrowth. Codon 1047 is most commonly affected by somatic mutations in PIK3CA-related overgrowth spectrum (PROS). While the fibroadipose overgrowth phenotype appears to be common in individuals with PIK3CA mutations at codon 1047, individuals with a clinical diagnosis of Klippel-Trenaunay syndrome or isolated lymphatic malformation also had mutations affecting this amino acid. Screening for Wilms tumor in individuals with PROS-related hemihyperplasia may be considered and, until the natural history is fully elucidated in larger cohort studies, may follow guidelines for Beckwith-Wiedemann syndrome, or isolated hemihyperplasia. It is not known if the specific PIK3CA mutation, the mosaic distribution, or the clinical presentation affect the Wilms tumor or nephroblastomatosis risk in individuals with PROS. (c) 2016 Wiley Periodicals, Inc.
C1 [Gripp, Karen W.; Baker, Laura; Kandula, Vinay; Conard, Katrina; Scavina, Mena; Napoli, Joseph A.; Griffin, Gregory C.; Thacker, Mihir] AI du Pont Hosp Children Nemours, Wilmington, DE 19803 USA.
[Knox, Rachel G.; Clark, Graeme R.; Parker, Victoria E. R.; Semple, Robert] Univ Cambridge, Metab Res Labs, Inst Metab Sci, Cambridge, MA USA.
[Mirzaa, Ghayda] Seattle Childrens Res Inst, Ctr Integrat Brain Res, Seattle, WA USA.
[Keppler-Noreuil, Kim M.] NHGRI, NIH, Bethesda, MD 20892 USA.
RP Gripp, KW (reprint author), AI du Pont Hosp Children Nemours, Wilmington, DE 19803 USA.
EM kgripp@nemours.org
FU US National Institutes of Health under NINDS [K08NS092898]; Intramural
Research Program of the National Human Genome Research Institute;
Wellcome Trust [WT097721, WT098498]; Medical Research Council
[MRC_MC_UU_12012/5]; United Kingdom National Institute for Health
Research Rare Diseases Translational Research Collaboration
FX Grant sponsor: US National Institutes of Health under NINDS; Grant
number: K08NS092898; Grant sponsor: Intramural Research Program of the
National Human Genome Research Institute; Grant sponsor: Wellcome Trust;
Grant numbers: WT097721, WT098498; Grant sponsor: Medical Research
Council; Grant number: MRC_MC_UU_12012/5; Grant sponsor: United Kingdom
National Institute for Health Research Rare Diseases Translational
Research Collaboration.
NR 36
TC 2
Z9 2
U1 2
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4825
EI 1552-4833
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD OCT
PY 2016
VL 170
IS 10
SI SI
BP 2559
EP 2569
DI 10.1002/ajmg.a.37758
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA DW4KQ
UT WOS:000383612200009
PM 27191687
ER
PT J
AU Keppler-Noreuil, KM
Baker, EH
Sapp, JC
Lindhurst, MJ
Biesecker, LG
AF Keppler-Noreuil, Kim M.
Baker, Eva H.
Sapp, Julie C.
Lindhurst, Marjorie J.
Biesecker, Leslie G.
TI Somatic AKT1 mutations cause meningiomas colocalizing with a
characteristic pattern of cranial hyperostosis
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE AKT1 mutations; cranial hyperostosis; hemimegalencephaly; meningiomas;
Proteus syndrome
ID PROTEUS-SYNDROME; MOLECULAR-GENETICS; DIAGNOSTIC-CRITERIA; EN PLAQUE;
SECONDARY; SKULL; BASE
AB Somatic genetic mutations in meningiomas are associated with histologic subtypes, anatomical location, and grade. Concomitant hyperostosis occurs with some meningiomas and the pathogenesis is not well understood. Cranial hyperostosis and meningiomas are common in patients with Proteus syndrome, which is caused by a somatic activating mutation in AKT1 c.49G>A. This same mutation has also been found in 6-9% of sporadic non-syndromic meningiomas. Sixty-one patients with Proteus syndrome meeting clinical diagnostic criteria were evaluated at the NIH from 1997 to 2014. Of these 61, 52 had a somatic activating mutation (c.49G>A, p.Glu17Lys) in AKT1 confirmed from affected tissue samples. Photographs, physical examination and/or autopsy, X-rays, CT, and/or MRI scan of the head were reviewed in 29/52 patients. Of the 29 patients, the most common intracranial tumor was meningioma, all co-localizing with cranial hyperostosis, and diagnosed at younger ages than typical for isolated, non-syndromic meningiomas. These patients had progressive cranial overgrowth that consisted primarily of diploic space expansion, and was characterized by unilateral, parasagittal, and frontal bone involvement. We hypothesize that sporadic meningothelial and transitional subtype meningiomas are a forme fruste or microform of Proteus syndrome, and activation of the AKT/PI3K pathway drives hyperostosis in both non-syndromic, and Proteus-related meningiomas. (c) 2016 The Authors. American Journal of Medical Genetics Part A Published by Wiley Periodicals, Inc.
C1 [Keppler-Noreuil, Kim M.; Sapp, Julie C.; Lindhurst, Marjorie J.; Biesecker, Leslie G.] NHGRI, Med Genom & Metab Genet Branch, NIH, Bethesda, MD 20892 USA.
[Baker, Eva H.] NIH, Dept Radiol & Imaging Sci, Ctr Clin, Bldg 10, Bethesda, MD 20892 USA.
RP Keppler-Noreuil, KM (reprint author), NHGRI, NIH, 49 Convent Dr,4A83, Bethesda, MD 20892 USA.
EM kim.keppler-noreuil@nih.gov
FU National Human Genome Research Institute
FX Grant sponsor: National Human Genome Research Institute.
NR 22
TC 1
Z9 1
U1 2
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4825
EI 1552-4833
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD OCT
PY 2016
VL 170
IS 10
SI SI
BP 2605
EP 2610
DI 10.1002/ajmg.a.37737
PG 6
WC Genetics & Heredity
SC Genetics & Heredity
GA DW4KQ
UT WOS:000383612200017
PM 27550858
ER
PT J
AU AuYoung, M
Linke, SE
Pagoto, S
Buman, MP
Craft, LL
Richardson, CR
Hutber, A
Marcus, BH
Estabrooks, P
Gorin, SS
AF AuYoung, Mona
Linke, Sarah E.
Pagoto, Sherry
Buman, Matthew P.
Craft, Lynette L.
Richardson, Caroline R.
Hutber, Adrian
Marcus, Bess H.
Estabrooks, Paul
Gorin, Sherri Sheinfeld
TI Integrating Physical Activity in Primary Care Practice
SO AMERICAN JOURNAL OF MEDICINE
LA English
DT Review
DE Physical activity; Primary care; Socioecologic model
ID HEALTH-CARE; ACTIVITY INTERVENTIONS; ACTIVITY PROMOTION; SOCIAL ECOLOGY;
OBESITY PREVENTION; RANDOMIZED-TRIAL; ACTIVITY ADVICE; UNITED-STATES;
WEIGHT-LOSS; EXERCISE
AB Based on a collaborative symposium in 2014 hosted by the Society of Behavioral Medicine (SBM) and the American College of Sports Medicine (ACSM), this paper presents a model for physical activity counseling for primary care physicians (PCPs). Most US adults do not meet national recommendations for physical activity levels. Socioecological factors drive differences in physical activity levels by geography, sex, age, and racial/ethnic group. The recent Patient Protection and Affordable Care Act incentivizes PCPs to offer patients physical activity counseling. However, PCPs have reported socioecological barriers to physical activity counseling and also patient barriers to physical activity, spanning from the individual to the environmental (eg, lack of safe spaces for physical activity), policy (eg, reimbursement policies), and organizational (eg, electronic medical record protocols, worksite norms/policies) levels. The aims of this paper are to: 1) discuss barriers to PCP counseling for physical activity; 2) provide evidence-based strategies and techniques to help PCPs address these counseling barriers; and 3) suggest practical steps for PCPs to counsel patients on physical activity using strategies and supports from policy, the primary care team, and other support networks. (C) 2016 Elsevier Inc. All rights reserved.
C1 [AuYoung, Mona] Ann Arbor VA Ctr Clin Management Res, Ann Arbor, MI USA.
[Linke, Sarah E.; Marcus, Bess H.] Univ Calif San Diego, Dept Family Med & Publ Hlth, San Diego, CA 92103 USA.
[Pagoto, Sherry] Univ Massachusetts, Sch Med, Dept Med, Worcester, MA USA.
[Buman, Matthew P.] Arizona State Univ, Sch Nutr & Hlth Promot, Phoenix, AZ USA.
[Craft, Lynette L.] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Richardson, Caroline R.] Univ Michigan, Dept Family Med, Ann Arbor, MI 48109 USA.
[Hutber, Adrian] ACSM, Indianapolis, IN USA.
[Estabrooks, Paul] Univ Nebraska Med Ctr, Dept Hlth Promot Social & Behav Hlth, Omaha, NE USA.
[Gorin, Sherri Sheinfeld] NYPAC, New York, NY USA.
[Gorin, Sherri Sheinfeld] NIH, Leidos Biomed Res SAIC, Frederick, MD USA.
RP Gorin, SS (reprint author), NYPAC, New York, NY USA.; Gorin, SS (reprint author), NCI, Leidos Biomed Res Inc, NIH, 3167 Fairbury Ln, Fairfax, VA 22031 USA.
EM sherri.gorin@gmail.com
FU Society of Behavioral Medicine (SBM); American College of Sports
Medicine
FX This paper resulted from an American College of Sports Medicine and
Society of Behavioral Medicine (SBM) co-sponsored symposium for the SBM
Annual Meeting, April 2014.
NR 64
TC 1
Z9 1
U1 16
U2 16
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9343
EI 1555-7162
J9 AM J MED
JI Am. J. Med.
PD OCT
PY 2016
VL 129
IS 10
BP 1022
EP 1029
DI 10.1016/j.amjmed.2016.02.008
PG 8
WC Medicine, General & Internal
SC General & Internal Medicine
GA EA1EA
UT WOS:000386334100025
PM 26953063
ER
PT J
AU Gomez-Lopez, N
Romero, R
Xu, Y
Miller, D
Unkel, R
MacKenzie, TC
Frascoli, M
Hassan, SS
AF Gomez-Lopez, Nardhy
Romero, Roberto
Xu, Yi
Miller, Derek
Unkel, Ronald
MacKenzie, Tippi C.
Frascoli, Michela
Hassan, Sonia S.
TI Umbilical cord CD71+erythroid cells are reduced in neonates born to
women in spontaneous preterm labor
SO AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY
LA English
DT Article
DE cord blood; immunosuppression; neonates; parturition; placenta;
pregnancy
ID IMMATURE ERYTHROID-CELLS; INFECTION; NEWBORNS; BIRTH
AB Problem: Preterm neonates are highly susceptible to infection. Neonatal host defense against infection seems to be maintained by the temporal presence of immunosuppressive CD71+ erythroid cells. The aim of this study was to investigate whether umbilical cord CD71+ erythroid cells are reduced in neonates born to women who undergo spontaneous preterm labor/birth.
Method of study: Umbilical cord blood samples (n=155) were collected from neonates born to women who delivered preterm with (n=39) and without (n=12) spontaneous labor or at term with (n=82) and without (n=22) spontaneous labor. Time-matched maternal peripheral blood samples were also included (n=111). Mononuclear cells were isolated from these samples, and CD71+ erythroid cells were identified and quantified as CD3-CD235a+ CD71+ cells by flow cytometry.
Results: (i) The proportion of CD71+ erythroid cells was 50-fold higher in cord blood than in maternal blood; (ii) a reduced number and frequency of umbilical cord CD71+ erythroid cells were found in neonates born to women who underwent spontaneous preterm labor compared to those born to women who delivered preterm without labor; (iii) umbilical cord CD71+ erythroid cells were fewer in neonates born to term pregnancies, regardless of the process of labor, than in those born to women who delivered preterm without labor; and (iv) no differences were seen in umbilical cord CD71+ erythroid cells between neonates born to women who -underwent spontaneous preterm labor and those born to women who delivered at term with labor.
Conclusion: Umbilical cord CD71+ erythroid cells are reduced in neonates born to women who had undergone spontaneous preterm labor.
C1 [Gomez-Lopez, Nardhy; Romero, Roberto; Xu, Yi; Miller, Derek; Unkel, Ronald; Hassan, Sonia S.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, Program Perinatal Res & Obstet, Div Intramural Res,NICHD,NIH,DHHS, Bethesda, MD USA.
[Gomez-Lopez, Nardhy; Romero, Roberto; Xu, Yi; Miller, Derek; Unkel, Ronald; Hassan, Sonia S.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, Program Perinatal Res & Obstet, Div Intramural Res,NICHD,NIH,DHHS, Detroit, MI USA.
[Gomez-Lopez, Nardhy; Xu, Yi; Miller, Derek; Unkel, Ronald; Hassan, Sonia S.] Wayne State Univ, Sch Med, Dept Obstet & Gynecol, Detroit, MI 48201 USA.
[Gomez-Lopez, Nardhy; Miller, Derek] Wayne State Univ, Sch Med, Dept Immunol & Microbiol, Detroit, MI 48201 USA.
[Romero, Roberto] Univ Michigan, Dept Obstet & Gynecol, Ann Arbor, MI 48109 USA.
[Romero, Roberto] Michigan State Univ, Dept Epidemiol & Biostat, E Lansing, MI 48824 USA.
[Romero, Roberto] Wayne State Univ, Ctr Mol Med & Genet, Detroit, MI USA.
[MacKenzie, Tippi C.; Frascoli, Michela] Univ Calif San Francisco, Eli & Edythe Broad Ctr Regenerat Med, San Francisco, CA 94143 USA.
[MacKenzie, Tippi C.; Frascoli, Michela] Univ Calif San Francisco, Dept Surg, San Francisco, CA 94143 USA.
RP Gomez-Lopez, N (reprint author), Wayne State Univ, Perinatol Res Branch, Dept Obstet & Gynecol, Sch Med,NICHD,NIH,DHHS, Detroit, MI 48202 USA.; Romero, R (reprint author), Wayne State Univ, Perinatol Res Branch, NICHD, NIH,DHHS,Hutzel Womens Hosp, Detroit, MI 48202 USA.
EM nardhy.gomez-lopez@wayne.edu; romeror@mail.nih.gov
RI Gomez-Lopez, Nardhy/R-7664-2016
OI Gomez-Lopez, Nardhy/0000-0002-3406-5262
FU Perinatology Research Branch, Division of Intramural Research, Eunice
Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health, U. S. Department of Health
and Human Services (NICHD/NIH/DHHS); NICHD/NIH/DHHS [HHSN275201300006C];
Wayne State University Perinatal Initiative in Maternal, Perinatal and
Child Health
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, U. S. Department of Health and Human Services (NICHD/NIH/DHHS),
and, in part, with federal funds from the NICHD/NIH/DHHS under Contract
No. HHSN275201300006C. This research was also supported by the Wayne
State University Perinatal Initiative in Maternal, Perinatal and Child
Health. We thank the physicians and nurses from the Center for Advanced
Obstetrical Care and Research and the Intrapartum Unit, as well as the
research assistants from the PRB Clinical Laboratory, for their help in
collecting human samples. We also thank staff members of the PRB
Histology and Pathology Units for their examination of the pathological
sections and Tara Mial for her critical readings of the manuscript.
NR 19
TC 0
Z9 0
U1 0
U2 0
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 2016
VL 76
IS 4
BP 280
EP 284
DI 10.1111/aji.12556
PG 5
WC Immunology; Reproductive Biology
SC Immunology; Reproductive Biology
GA EA1CP
UT WOS:000386330400004
PM 27625200
ER
PT J
AU Olivier, KN
AF Olivier, Kenneth N.
TI Lady Windermere Dissected: More Form Than Fastidious
SO ANNALS OF THE AMERICAN THORACIC SOCIETY
LA English
DT Editorial Material
C1 [Olivier, Kenneth N.] NHLBI, Bldg 10, Bethesda, MD 20892 USA.
RP Olivier, KN (reprint author), NHLBI, Cardiovasc & Pulm Branch, 10 Ctr Dr,MSC 1454,Bldg 10 CRC,Room 6-3130, Bethesda, MD 20832 USA.
EM olivierk@nhlbi.nih.gov
FU Intramural Research Program, National Heart, Lung and Blood Institute,
National Institutes of Health
FX Supported in part by the Intramural Research Program, National Heart,
Lung and Blood Institute, National Institutes of Health.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER THORACIC SOC
PI NEW YORK
PA 25 BROADWAY, 18 FL, NEW YORK, NY 10004 USA
SN 1546-3222
EI 2325-6621
J9 ANN AM THORAC SOC
JI Ann. Am. Thoracic Society
PD OCT
PY 2016
VL 13
IS 10
BP 1674
EP 1676
DI 10.1513/AnnalsATS.201607-521ED
PG 3
WC Respiratory System
SC Respiratory System
GA DZ8KG
UT WOS:000386118700003
PM 27726444
ER
PT J
AU Labonte, ME
Kirkpatrick, SI
Bell, RC
Boucher, BA
Csizmadi, I
Koushik, A
L'Abbe, MR
Massarelli, I
Robson, PJ
Rondeau, I
Shatenstein, B
Subar, AF
Lamarche, B
AF Labonte, Marie-Eve
Kirkpatrick, Sharon I.
Bell, Rhonda C.
Boucher, Beatrice A.
Csizmadi, Ilona
Koushik, Anita
L'Abbe, Mary R.
Massarelli, Isabelle
Robson, Paula J.
Rondeau, Isabelle
Shatenstein, Bryna
Subar, Amy F.
Lamarche, Benoit
TI Dietary assessment is a critical element of health research -
Perspective from the Partnership for Advancing Nutritional and Dietary
Assessment in Canada
SO APPLIED PHYSIOLOGY NUTRITION AND METABOLISM
LA English
DT Article
DE dietary analysis; nutrition; dietary intake; diet
ID FOOD-FREQUENCY QUESTIONNAIRE; VALIDITY; WOMEN
AB Challenges and complexities associated with assessing dietary intakes are numerous, but not insurmountable. This opinion paper from Canadian researchers draws attention to the importance of building capacity and providing funding opportunities for research in dietary assessment methods in Canada and elsewhere. Such strategies would contribute to a better understanding of the roles played by diet in human health and better translation of this information into the most meaningful and effective dietary guidelines, policies, and interventions.
C1 [Labonte, Marie-Eve; Lamarche, Benoit] Univ Laval, Inst Nutr & Funct Foods, Sch Nutr, Quebec City, PQ G1V 0A6, Canada.
[Kirkpatrick, Sharon I.] Univ Waterloo, Sch Publ Hlth & Hlth Syst, Waterloo, ON N2L 3G1, Canada.
[Bell, Rhonda C.] Univ Alberta, Dept Agr Food & Nutr Sci, Div Human Nutr, Li Ka Shing Ctr Hlth Res Innovat, Edmonton, AB T6G 2E1, Canada.
[Boucher, Beatrice A.] Canc Care Ontario, Prevent & Canc Control, Toronto, ON M5G 2L7, Canada.
[Boucher, Beatrice A.] Univ Toronto, Dept Nutr Sci, Toronto, ON M5S 3E2, Canada.
[Csizmadi, Ilona] Alberta Hlth Serv, CancerControl Alberta, Canc Epidemiol & Prevent Res, Calgary, AB T2S 3C3, Canada.
[Koushik, Anita] Univ Montreal, CRCHUM, Montreal, PQ H2X 0A9, Canada.
[Koushik, Anita] Univ Montreal, Dept Social & Prevent Med, Montreal, PQ H2X 0A9, Canada.
[Labonte, Marie-Eve; L'Abbe, Mary R.] Univ Toronto, Dept Nutr Sci, Fac Med, Toronto, ON M5S 3E2, Canada.
[Massarelli, Isabelle; Rondeau, Isabelle] Hlth Canada, Bur Food Surveillance & Sci Integrat, Food Directorate, Ottawa, ON K1A 0K9, Canada.
[Robson, Paula J.] Alberta Hlth Serv, CancerControl Alberta, C MORE, Edmonton, AB T5J 3H1, Canada.
[Shatenstein, Bryna] Univ Montreal, Dept Nutr, Ctr Rech, Inst Univ Geriatrie Montreal, Montreal, PQ H3W 1W5, Canada.
[Subar, Amy F.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20814 USA.
RP Lamarche, B (reprint author), Univ Laval, Inst Nutr & Funct Foods, Sch Nutr, Quebec City, PQ G1V 0A6, Canada.; Kirkpatrick, SI (reprint author), Univ Waterloo, Sch Publ Hlth & Hlth Syst, Waterloo, ON N2L 3G1, Canada.
EM sharon.kirkpatrick@uwaterloo.ca; benoit.lamarche@fsaa.ulaval.ca
OI Koushik, Anita/0000-0001-5304-7660
FU Canadian Cancer Society Research Institute [702855]
FX B. L. and M. E. L. have developed a Web-based FFQ that is licensed for
utilization by researchers and clinicians through formal agreements with
Laval University's Research Office. User fees serve solely for the
maintenance and upgrade of the dietary assessment tool. S. I. K.
receives financial support from the Canadian Cancer Society Research
Institute (grant no. 702855). R. C. B., B. A. B., I. C., A. K., M. R.
L., I. M., P. J. R., I. R., B. S., A. F. S. report no conflicts of
interest.
NR 24
TC 3
Z9 3
U1 2
U2 2
PU CANADIAN SCIENCE PUBLISHING, NRC RESEARCH PRESS
PI OTTAWA
PA 65 AURIGA DR, SUITE 203, OTTAWA, ON K2E 7W6, CANADA
SN 1715-5312
EI 1715-5320
J9 APPL PHYSIOL NUTR ME
JI Appl. Physiol. Nutr. Metab.
PD OCT
PY 2016
VL 41
IS 10
BP 1096
EP 1099
DI 10.1139/apnm-2016-0146
PG 4
WC Nutrition & Dietetics; Physiology; Sport Sciences
SC Nutrition & Dietetics; Physiology; Sport Sciences
GA DZ8NZ
UT WOS:000386128400014
ER
PT J
AU Nakamura, Y
Mochida, A
Choyke, PL
Kobayashi, H
AF Nakamura, Yuko
Mochida, Ai
Choyke, Peter L.
Kobayashi, Hisataka
TI Nanodrug Delivery: Is the Enhanced Permeability and Retention Effect
Sufficient for Curing Cancer?
SO BIOCONJUGATE CHEMISTRY
LA English
DT Review
ID INTERSTITIAL FLUID PRESSURE; NEAR-INFRARED PHOTOIMMUNOTHERAPY;
ENDOTHELIAL GROWTH-FACTOR; TUMOR-NECROSIS-FACTOR; ISOLATED LIMB
PERFUSION; TEMPERATURE-SENSITIVE LIPOSOMES; INTENSITY FOCUSED
ULTRASOUND; ELEVATING BLOOD-PRESSURE; TARGETED DRUG-DELIVERY; SOLID
TUMORS
AB Nanotechnology offers several attractive design features that have prompted its exploration for cancer diagnosis and treatment. Nanosized drugs have a large loading capacity, the ability to protect the payload from degradation, a large surface on which to conjugate targeting ligands, and controlled or sustained release. Nanosized drugs also leak preferentially into tumor tissue through permeable tumor vessels and are then retained in the tumor bed due to reduced lymphatic drainage. This process is known as the enhanced permeability and retention (EPR) effect. However, while the EPR effect is widely held to improve delivery of nanodrugs to tumors, it in fact offers less than a 2-fold increase in nanodrug delivery compared with critical normal organs, resulting in drug concentrations that are not sufficient for curing most cancers. In this Review, we first overview various barriers for nanosized drug delivery with an emphasis on the capillary wall's resistance, the main obstacle to delivering drugs. Then, we discuss current regulatory issues facing nanomedicine. Finally, we discuss how to make the delivery of nanosized drugs to tumors more effective by building on the EPR effect.
C1 [Nakamura, Yuko; Mochida, Ai; 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, Bethesda, MD 20892 USA.
EM kobayash@mail.nih.gov
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.
NR 165
TC 4
Z9 4
U1 47
U2 47
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1043-1802
J9 BIOCONJUGATE CHEM
JI Bioconjugate Chem.
PD OCT
PY 2016
VL 27
IS 10
BP 2225
EP 2238
DI 10.1021/acs.bioconjchem.6b00437
PG 14
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Multidisciplinary; Chemistry, Organic
SC Biochemistry & Molecular Biology; Chemistry
GA DZ6SK
UT WOS:000385992000001
PM 27547843
ER
PT J
AU Jacobson, O
Kiesewetter, DO
Chen, XY
AF Jacobson, Orit
Kiesewetter, Dale O.
Chen, Xiaoyuan
TI Albumin-Binding Evans Blue Derivatives for Diagnostic Imaging and
Production of Long-Acting Therapeutics
SO BIOCONJUGATE CHEMISTRY
LA English
DT Review
ID NEONATAL FC-RECEPTOR; MRI CONTRAST AGENT; IN-VIVO; RGD PEPTIDE;
HALF-LIFE; POLYETHYLENE-GLYCOL; BOUND PACLITAXEL; SERUM-ALBUMIN;
TUMOR-THERAPY; PLASMA-VOLUME
AB One of the major design considerations for a drug is its pharmacokinetics: a drug with short blood half-life is less available at a target organ which in turn dictates treatment with either high or more frequent doses, and increases the likelihood of undesirable side effects. One method to improve drug pharmacokinetics is adding functional chemical groups to the drug molecule that can increase the half-life in the blood, hopefully, without significantly affecting its desired biological activity. Evans Blue (EB) dye reversibly binds to serum albumin with moderate affinity and has a long blood half-life. The binding of EB to albumin has been exploited to quantify protein leakage as an indicator of increased vascular permeability. Design of new chemical entities based on EB structure and coupling them to drugs, enables the usage of albumin as a reversible carrier in the blood and improves drug's half-life. This Topical Review summarizes the recent developments of various EB derivatives for molecular imaging and therapy applications.
C1 [Jacobson, Orit; Kiesewetter, Dale O.; Chen, Xiaoyuan] NIBIB, Lab Mol Imaging & Nanomed LOMIN, NIH, Bethesda, MD 20892 USA.
RP Chen, XY (reprint author), NIBIB, Lab Mol Imaging & Nanomed LOMIN, NIH, Bethesda, MD 20892 USA.
EM shawn.chen@nih.gov
NR 68
TC 0
Z9 0
U1 15
U2 15
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1043-1802
J9 BIOCONJUGATE CHEM
JI Bioconjugate Chem.
PD OCT
PY 2016
VL 27
IS 10
BP 2239
EP 2247
DI 10.1021/acs.bioconjchem.6b00487
PG 9
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Multidisciplinary; Chemistry, Organic
SC Biochemistry & Molecular Biology; Chemistry
GA DZ6SK
UT WOS:000385992000002
ER
PT J
AU Francica, JR
Lynn, GM
Laga, R
Joyce, MG
Ruckwardt, TJ
Morabito, KM
Chen, M
Chaudhuri, R
Zhang, BS
Sastry, M
Druz, A
Ko, K
Choe, M
Pechar, M
Georgiev, IS
Kueltzo, LA
Seymour, LW
Mascola, JR
Kwong, PD
Graham, BS
Seder, RA
AF Francica, Joseph R.
Lynn, Geoffrey M.
Laga, Richard
Joyce, M. Gordon
Ruckwardt, Tracy J.
Morabito, Kaitlyn M.
Chen, Man
Chaudhuri, Rajoshi
Zhang, Baoshan
Sastry, Mallika
Druz, Aliaksandr
Ko, Kiyoon
Choe, Misook
Pechar, Michal
Georgiev, Ivelin S.
Kueltzo, Lisa A.
Seymour, Leonard W.
Mascola, John R.
Kwong, Peter D.
Graham, Barney S.
Seder, Robert A.
TI Thermoresponsive Polymer Nanoparticles Co-deliver RSV F Trimers with a
TLR-7/8 Adjuvant
SO BIOCONJUGATE CHEMISTRY
LA English
DT Article
ID RESPIRATORY SYNCYTIAL VIRUS; T-CELL RESPONSES; DENDRITIC CELLS;
IMMUNE-RESPONSES; FUSION GLYCOPROTEIN; RATIONAL DESIGN; INNATE IMMUNITY;
VACCINE DEVELOPMENT; CROSS-PRESENTATION; NONHUMAN-PRIMATES
AB Structure-based vaccine design has been used to develop immunogens that display conserved neutralization sites on pathogens such as HIV-1, respiratory syncytial virus (RSV), and influenza. Improving the immunogenicity of these designed immunogens with adjuvants will require formulations that do not alter protein antigenicity. Here, we show that nanoparticle-forming thermoresponsive polymers (TRP) allow for co-delivery of RSV fusion (F) protein trimers with Toll like receptor 7 and 8 agonists (TLR-7/8a) to enhance protective immunity. Although primary amine conjugation of TLR-7/8a to F trimers severely disrupted the recognition of critical neutralizing epitopes, F trimers site-selectively coupled to TRP nanoparticles retained appropriate antigenicity and elicited high titers of prefusion-specific, T(H)1 isotype anti-RSV F antibodies following vaccination. Moreover, coupling F trimers to TRP delivering TLR-7/8a resulted in similar to 3-fold higher binding and neutralizing antibody titers than soluble F trimers admixed with TLR-7/8a and conferred protection from intranasal RSV challenge. Overall, these data show that TRP nanoparticles may provide a broadly applicable platform for eliciting neutralizing antibodies to structure-dependent epitopes on RSV, influenza, HIV-1, or other pathogens.
C1 [Francica, Joseph R.; Lynn, Geoffrey M.; Joyce, M. Gordon; Ruckwardt, Tracy J.; Morabito, Kaitlyn M.; Chen, Man; Zhang, Baoshan; Sastry, Mallika; Druz, Aliaksandr; Ko, Kiyoon; Choe, Misook; Georgiev, Ivelin S.; Mascola, John R.; Kwong, Peter D.; Graham, Barney S.; Seder, Robert A.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Laga, Richard; Pechar, Michal] Acad Sci Czech Republic, Inst Macromol Chem, CR-16206 Prague, Czech Republic.
[Chaudhuri, Rajoshi; Kueltzo, Lisa A.] NIAID, Vaccine Prod Program, Vaccine Res Ctr, NIH, Gaithersburg, MD 20878 USA.
[Seymour, Leonard W.] Univ Oxford, Dept Oncol, Oxford OX3 7DQ, England.
RP Seder, RA (reprint author), NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
EM rseder@mail.nih.gov
RI Pechar, Michal/G-6423-2014; Laga, Richard/G-3627-2014
FU Vaccine Research Center (NIAID, NIH); Czech Science Foundation
[16-14957Y]; Ministry of Education, Youth and Sports of the Czech
Republic [BIOCEV-FAR LQ1604]
FX The authors acknowledge Marlon Dillon, Kefale Wuddie, Gloria Salbador,
and Carmelo Chiedi for expert veterinary technical assistance; Azad
Kumar for generously providing untagged RSV F proteins; and April
Kilikelly, Joan Ngwuta, and Andrew Ishizuka for helpful discussion. This
work was funded in part by the intramural research program of the
Vaccine Research Center (NIAID, NIH). Further support was given by the
Czech Science Foundation (project 16-14957Y) and by the Ministry of
Education, Youth and Sports of the Czech Republic within the National
Sustainability Program II (project BIOCEV-FAR LQ1604).
NR 84
TC 0
Z9 0
U1 9
U2 9
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1043-1802
J9 BIOCONJUGATE CHEM
JI Bioconjugate Chem.
PD OCT
PY 2016
VL 27
IS 10
BP 2372
EP 2385
DI 10.1021/acs.bioconjchem.6b00370
PG 14
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Multidisciplinary; Chemistry, Organic
SC Biochemistry & Molecular Biology; Chemistry
GA DZ6SK
UT WOS:000385992000019
PM 27583777
ER
PT J
AU Lesage, E
Nailer, EL
Miall, RC
AF Lesage, Elise
Nailer, Emma L.
Miall, R. Chris
TI Cerebellar BOLD signal during the acquisition of a new lexicon predicts
its early consolidation
SO BRAIN AND LANGUAGE
LA English
DT Article
DE Cerebellum; Language; Vocabulary; Learning; Lexicon; fMRI; Word
association; Non-motor
ID WORKING-MEMORY; PREFRONTAL CORTEX; FUNCTIONAL TOPOGRAPHY; SEMANTIC
KNOWLEDGE; EPISODIC MEMORY; INTERNAL-MODELS; COGNITIVE TASKS; HUMAN
BRAIN; LANGUAGE; FMRI
AB Cerebellar contributions to language are presently poorly understood, but it has been argued that the cerebellar role in motor learning can be extended to learning in cognitive and linguistic domains. Here, we used fMRI to investigate whether the cerebellum is recruited in mapping novel words onto existing semantic concepts. On separate days, participants performed a Basque vocabulary learning task and a control English synonym task in the MRI scanner. Learning-related BOLD activity was found in left inferior frontal gyrus, bilateral insula, pre-SMA, left superior parietal cortex, right caudate, the right cerebellar vermis and right cerebellar Crus II. The extent to which the cerebellar regions, but not the cerebral areas, were recruited during learning correlated positively with participants' off-line improvement in performance after the learning task. These data provide evidence for a cerebellar role in lexical learning, and suggest that the right cerebellum may contribute toward consolidation of lexico-semantic associations in the language network. (C) 2015 The Authors. Published by Elsevier Inc.
C1 [Lesage, Elise; Nailer, Emma L.; Miall, R. Chris] Univ Birmingham, Sch Psychol, Birmingham B15 2TT, W Midlands, England.
[Lesage, Elise] NIDA, Neuroimaging Res Branch, NIH, Baltimore, MD 21224 USA.
[Nailer, Emma L.] Univ Birmingham, Sch Educ, Birmingham B15 2TT, W Midlands, England.
RP Lesage, E (reprint author), NIDA, Neuroimaging Res Branch, NIH, Baltimore, MD 21224 USA.
EM Elise.r.d.lesage@gmail.com
FU Wellcome Trust [WT087554]; Marie Curie Actions Grant [EU-FP7-ITN "C7"]
FX This work was supported by grants from the Wellcome Trust (WT087554) and
the Marie Curie Actions Grant EU-FP7-ITN "C7". We thank the staff of the
Birmingham University Imaging Centre for their help.
NR 97
TC 2
Z9 2
U1 2
U2 2
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0093-934X
EI 1090-2155
J9 BRAIN LANG
JI Brain Lang.
PD OCT
PY 2016
VL 161
SI SI
BP 33
EP 44
DI 10.1016/j.bandl.2015.07.005
PG 12
WC Audiology & Speech-Language Pathology; Linguistics; Neurosciences;
Psychology, Experimental
SC Audiology & Speech-Language Pathology; Linguistics; Neurosciences &
Neurology; Psychology
GA DZ8FA
UT WOS:000386105100005
PM 26303580
ER
PT J
AU Thomas, RM
Van Dyke, T
Merlino, G
Day, CP
AF Thomas, Renee M.
Van Dyke, Terry
Merlino, Glenn
Day, Chi-Ping
TI Concepts in Cancer Modeling: A Brief History
SO CANCER RESEARCH
LA English
DT Review
ID ANTITUMOR IMMUNITY; MELANOMA; CHEMOTHERAPY; IMMUNOTHERAPY; KINETICS;
THERAPY
AB Modeling, an experimental approach to investigate complex biological systems, has significantly contributed to our understanding of cancer. Although extensive cancer research has been conducted utilizing animal models for elucidating mechanisms and developing therapeutics, the concepts in a good model design and its application have not been well elaborated. In this review, we discuss the theory underlying biological modeling and the process of producing a valuable and relevant animal model. Several renowned examples in the history of cancer research will be used to illustrate how modeling can be translatable to clinical applications. Finally, we will also discuss how the advances in cancer genomics and cancer modeling will influence each other going forward. (C) 2016 AACR.
C1 [Thomas, Renee M.; Merlino, Glenn; Day, Chi-Ping] NCI, Lab Canc Biol & Genet, NIH, 37 Convent Dr,Room 5002, Bethesda, MD 20892 USA.
[Thomas, Renee M.] NIH, Med Res Scholars Program, Bldg 10, Bethesda, MD 20892 USA.
[Van Dyke, Terry] NCI, Ctr Adv Preclin Res, Ctr Canc Res, Frederick, MD 21701 USA.
RP Merlino, G; Day, CP (reprint author), NCI, Lab Canc Biol & Genet, NIH, 37 Convent Dr,Room 5002, Bethesda, MD 20892 USA.
EM gmerlino@helix.nih.gov; daychi@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999, ZIA BC011167-01]
NR 26
TC 0
Z9 0
U1 4
U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD OCT
PY 2016
VL 76
IS 20
BP 5921
EP 5925
DI 10.1158/0008-5472.CAN-16-1293
PG 5
WC Oncology
SC Oncology
GA DZ1UW
UT WOS:000385627600003
PM 27694601
ER
PT J
AU Campbell, PT
Newton, CC
Freedman, ND
Koshiol, J
Alavanja, MC
Freeman, LEB
Buring, JE
Chan, AT
Chong, DQ
Datta, M
Gaudet, MM
Gaziano, JM
Giovannucci, EL
Graubard, BI
Hollenbeck, AR
King, L
Lee, IM
Linet, MS
Palmer, JR
Petrick, JL
Poynter, JN
Purdue, MP
Robien, K
Rosenberg, L
Sahasrabuddhe, VV
Schairer, C
Sesso, HD
Sigurdson, AJ
Stevens, VL
Wactawski-Wende, J
Zeleniuch-Jacquotte, A
Renehan, AG
McGlynn, KA
AF Campbell, Peter T.
Newton, Christina C.
Freedman, Neal D.
Koshiol, Jill
Alavanja, Michael C.
Freeman, Laura E. Beane
Buring, Julie E.
Chan, Andrew T.
Chong, Dawn Q.
Datta, Mridul
Gaudet, Mia M.
Gaziano, J. Michael
Giovannucci, Edward L.
Graubard, Barry I.
Hollenbeck, Albert R.
King, Lindsey
Lee, I-Min
Linet, Martha S.
Palmer, Julie R.
Petrick, Jessica L.
Poynter, Jenny N.
Purdue, Mark P.
Robien, Kim
Rosenberg, Lynn
Sahasrabuddhe, Vikrant V.
Schairer, Catherine
Sesso, Howard D.
Sigurdson, Alice J.
Stevens, Victoria L.
Wactawski-Wende, Jean
Zeleniuch-Jacquotte, Anne
Renehan, Andrew G.
McGlynn, Katherine A.
TI Body Mass Index, Waist Circumference, Diabetes, and Risk of Liver Cancer
for US Adults
SO CANCER RESEARCH
LA English
DT Article
ID EPIC-OXFORD PARTICIPANTS; BILIARY-TRACT CANCER;
HEPATOCELLULAR-CARCINOMA; EUROPEAN COHORT; UNITED-STATES; MELLITUS;
OBESITY; METAANALYSIS; ASSOCIATION; WEIGHT
AB Incidence rates for liver cancer have increased 3-fold since the mid-1970s in the United States in parallel with increasing trends for obesity and type II diabetes mellitus. Weconducted an analysis of baseline body mass index (BMI), waist circumference (WC), and type II diabetes mellitus with risk of liver cancer. The Liver Cancer Pooling Project maintains harmonized data from 1.57 million adults enrolled in 14 U.S.-based prospective studies. Cox regression estimated HRs and 95% confidence intervals (CI) adjusted for age, sex, study center, alcohol, smoking, race, and BMI (for WC and type II diabetes mellitus). Stratified analyses assessed whether the BMI-liver cancer associations differed by hepatitis sera-positivity in nested analyses for a subset of cases (n = 220) and controls (n = 547). After enrollment, 2,162 incident liver cancer diagnoses were identified. BMI, per 5 kg/m(2), was associated with higher risks of liver cancer, more so for men (HR = 1.38; 95% CI, 1.30-1.46) than women (HR = 1.25; 95% CI, 1.17-1.35; P-interaction = 0.02). WC, per 5 cm, was associated with higher risks of liver cancer, approximately equally by sex (overall, HR = 1.08; 95% CI, 1.04-1.13). Type II diabetes mellitus was associated with higher risk of liver cancer (HR = 2.61; 95% CI, 2.34-2.91). In stratified analyses, there was a null association between BMI and liver cancer risk for participants who were sera-positive for hepatitis. This study suggests that high BMI, high WC, and type II diabetes mellitus are associated with higher risks of liver cancer and that the association may differ by status of viral hepatitis infection. (C) 2016 AACR.
C1 [Campbell, Peter T.; Newton, Christina C.; Gaudet, Mia M.; Stevens, Victoria L.] Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA.
[Freedman, Neal D.; Koshiol, Jill; Alavanja, Michael C.; Freeman, Laura E. Beane; Graubard, Barry I.; Linet, Martha S.; Petrick, Jessica L.; Purdue, Mark P.; Sahasrabuddhe, Vikrant V.; Schairer, Catherine; Sigurdson, Alice J.; McGlynn, Katherine A.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Buring, Julie E.; Chan, Andrew T.; Gaziano, J. Michael; King, Lindsey; Lee, I-Min; Sesso, Howard D.] Brigham & Womens Hosp, Dept Med, 75 Francis St, Boston, MA 02115 USA.
[Buring, Julie E.; Giovannucci, Edward L.; Lee, I-Min; Sesso, Howard D.] Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
[Chan, Andrew T.; King, Lindsey] Brigham & Womens Hosp, Channing Div Network Med, 75 Francis St, Boston, MA 02115 USA.
[Chan, Andrew T.; Chong, Dawn Q.; King, Lindsey] Massachusetts Gen Hosp, Div Gastroenterol, Boston, MA 02114 USA.
[Chan, Andrew T.; Chong, Dawn Q.; King, Lindsey] Harvard Med Sch, Boston, MA USA.
[Chong, Dawn Q.] Natl Canc Ctr Singapore, Div Med Oncol, Singapore, Singapore.
[Datta, Mridul] Purdue Univ, Dept Nutr Sci, W Lafayette, IN 47907 USA.
[Gaziano, J. Michael] VA Boston Healthcare Syst, Boston, MA USA.
[Giovannucci, Edward L.] Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA.
[Hollenbeck, Albert R.] AARP, Washington, DC USA.
[Palmer, Julie R.; Rosenberg, Lynn] Boston Univ, Slone Epidemiol Ctr, Boston, MA 02215 USA.
[Poynter, Jenny N.] Univ Minnesota, Div Pediat Epidemiol & Clin Res, Minneapolis, MN USA.
[Poynter, Jenny N.] Univ Minnesota, Masonic Canc Ctr, Minneapolis, MN USA.
[Robien, Kim] George Washington Univ, Milken Inst, Sch Publ Hlth, Dept Exercise & Nutr Sci, Washington, DC USA.
[Wactawski-Wende, Jean] SUNY Buffalo, Dept Epidemiol & Environm Hlth, Buffalo, NY USA.
[Zeleniuch-Jacquotte, Anne] NYU, Sch Med, Dept Populat Hlth, New York, NY USA.
[Renehan, Andrew G.] Univ Manchester, Fac Inst Canc Sci, Manchester, Lancs, England.
RP Campbell, PT (reprint author), Amer Canc Soc, 250 Williams St NW, Atlanta, GA 30303 USA.
EM peter.campbell@cancer.org
RI Beane Freeman, Laura/C-4468-2015;
OI Beane Freeman, Laura/0000-0003-1294-4124; Robien,
Kim/0000-0002-2120-2280; Zeleniuch-Jacquotte, Anne/0000-0001-9350-1303
FU Intramural NIH HHS [Z01 CP010119-12, Z01 ES049030-11]; NCI NIH HHS [UM1
CA186107, P01 CA055075, P01 CA087969, P30 CA016087, R01 CA034944, R01
CA034944-03, R01 CA039742, R01 CA040360, R01 CA047988, R01 CA049449, R01
CA058420, R01 CA097193, R01 CA098661, UM1 CA164974, UM1 CA167552]; NHLBI
NIH HHS [R01 HL026490, R01 HL026490-03, R01 HL034595, R01 HL034595-07,
R01 HL043851, R01 HL080467]; NIEHS NIH HHS [P30 ES000260, Z01 ES049030]
NR 37
TC 0
Z9 0
U1 2
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD OCT
PY 2016
VL 76
IS 20
BP 6076
EP 6083
DI 10.1158/0008-5472.CAN-16-0787
PG 8
WC Oncology
SC Oncology
GA DZ1UW
UT WOS:000385627600018
PM 27742674
ER
PT J
AU Ali, I
Hogberg, J
Hsieh, JH
Auerbach, S
Korhonen, A
Stenius, U
Silins, I
AF Ali, Imran
Hogberg, Johan
Hsieh, Jui-Hua
Auerbach, Scott
Korhonen, Anna
Stenius, Ulla
Silins, Ilona
TI Gender differences in cancer susceptibility: role of oxidative stress
SO CARCINOGENESIS
LA English
DT Article
ID HEME OXYGENASE-1; SEX DISPARITIES; CHROMOSOME Y; MOSAIC LOSS;
CARCINOGENESIS; RISK
AB Cancer statistics indicate that compared to women, men are more susceptible to cancer. In literature analysis based on about 600000 scientific references covering male- and female-specific carcinogens, estradiol and testosterone, oxidative stress emerges as one critical factor that could offer explanation for the gender disparity observed.Cancer is a leading cause of death worldwide and environmental factors, including chemicals, have been suggested as major etiological incitements. Cancer statistics indicates that men get more cancer than women. However, differences in the known risk factors including life style or occupational exposure only offer partial explanation. Using a text mining tool, we have investigated the scientific literature concerning male- and female-specific rat carcinogens that induced tumors only in one gender in NTP 2-year cancer bioassay. Our evaluation shows that oxidative stress, although frequently reported for both male- and female-specific rat carcinogens, was mentioned significantly more in literature concerning male-specific rat carcinogens. Literature analysis of testosterone and estradiol showed the same pattern. Tox21 high-throughput assay results, although showing only weak association of oxidative stress-related processes for male- and female-specific rat carcinogens, provide additional support. We also analyzed the literature concerning 26 established human carcinogens (IARC group 1). Oxidative stress was more frequently reported for the majority of these carcinogens, and the Tox21 data resembled that of male-specific rat carcinogens. Thus, our data, based on about 600000 scientific abstracts and Tox21 screening assays, suggest a link between male-specific carcinogens, testosterone and oxidative stress. This implies that a different cellular response to oxidative stress in men and women may be a critical factor in explaining the greater cancer susceptibility observed in men. Although the IARC carcinogens are classified as human carcinogens, their classification largely based on epidemiological evidence from male cohorts, which raises the question whether carcinogen classifications should be gender specific.
C1 [Ali, Imran; Hogberg, Johan; Stenius, Ulla; Silins, Ilona] Karolinska Inst, Inst Environm Med, SE-17177 Stockholm, Sweden.
[Hsieh, Jui-Hua; Auerbach, Scott] NIEHS, Div Natl Toxicol Program, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
[Korhonen, Anna] Univ Cambridge, Dept Theoret & Appl Linguist, Cambridge CB3 9DA, England.
RP Ali, I; Silins, I (reprint author), Karolinska Inst, Inst Environm Med, SE-17177 Stockholm, Sweden.
EM imran.ali@ki.se; ilona.silins@ki.se
OI Ali, Imran/0000-0001-9274-2295
FU Swedish Research Council Formas [2013-0529]; Swedish Research Council
for Health, Working Life and Welfare (FORTE) [2014-1530]; VINNOVA,
Sweden [2011-01319]
FX This work was supported by The Swedish Research Council Formas (Grant
number 2013-0529), Swedish Research Council for Health, Working Life and
Welfare (FORTE) (grant number 2014-1530) and VINNOVA (grant number
2011-01319), Sweden.
NR 35
TC 0
Z9 0
U1 1
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 2016
VL 37
IS 10
BP 985
EP 992
DI 10.1093/carcin/bgw076
PG 8
WC Oncology
SC Oncology
GA DZ7IC
UT WOS:000386037100008
PM 27481070
ER
PT J
AU Callejas-Valera, JL
Iglesias-Bartolome, R
Amornphimoltham, P
Palacios-Garcia, J
Martin, D
Califano, JA
Molinolo, AA
Gutkind, JS
AF Callejas-Valera, Juan Luis
Iglesias-Bartolome, Ramiro
Amornphimoltham, Panomwat
Palacios-Garcia, Julia
Martin, Daniel
Califano, Joseph A.
Molinolo, Alfredo A.
Gutkind, J. Silvio
TI mTOR inhibition prevents rapid-onset of carcinogen-induced malignancies
in a novel inducible HPV-16 E6/E7 mouse model
SO CARCINOGENESIS
LA English
DT Article
ID HUMAN-PAPILLOMAVIRUS TYPE-16; SQUAMOUS-CELL CARCINOMA; STEM-CELLS;
OROPHARYNGEAL CANCER; HAIR FOLLICLE; TUMOR-GROWTH; HPV16 E6/E7; SKIN;
E7; E6
AB The rising incidence of human papillomavirus (HPV)-associated malignancies, especially for oropharyngeal cancers, has highlighted the urgent need to understand how the interplay between high-risk HPV oncogenes and carcinogenic exposure results in squamous cell carcinoma (SCC) development. Here, we describe an inducible mouse model expressing high risk HPV-16 E6/E7 oncoproteins in adults, bypassing the impact of these viral genes during development. HPV-16 E6/E7 genes were targeted to the basal squamous epithelia in transgenic mice using a doxycycline inducible cytokeratin 5 promoter (cK5-rtTA) system. After doxycycline induction, both E6 and E7 were highly expressed, resulting in rapid epidermal hyperplasia with a remarkable expansion of the proliferative cell compartment to the suprabasal layers. Surprisingly, in spite of the massive growth of epithelial cells and their stem cell progenitors, HPV-E6/E7 expression was not sufficient to trigger mTOR activation, a key oncogenic driver in HPV-associated malignancies, and malignant progression to SCC. However, these mice develop SCC rapidly after a single exposure to a skin carcinogen, DMBA, which was increased by the prolonged exposure to a tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA). Thus, only few oncogenic hits may be sufficient to induce cancer in E6/E7 expressing cells. All HPV-E6/E7 expressing SCC lesions exhibited increased mTOR activation. Remarkably, rapamycin, an mTOR inhibitor, abolished tumor development when administered to HPV-E6/E7 mice prior to DMBA exposure. Our findings revealed that mTOR inhibition protects HPV-E6/E7 expressing tissues form SCC development upon carcinogen exposure, thus supporting the potential clinical use of mTOR inhibitors as a molecular targeted approach for prevention of HPV-associated malignancies.
C1 [Callejas-Valera, Juan Luis; Amornphimoltham, Panomwat; Califano, Joseph A.; Molinolo, Alfredo A.; Gutkind, J. Silvio] Moores Canc Ctr, 3855 Hlth Sci Dr, La Jolla, CA 92093 USA.
[Iglesias-Bartolome, Ramiro] NIAMS, Dev Skin Biol Sect HNB 254, NIH, Bldg 50, Bethesda, MD 20814 USA.
[Palacios-Garcia, Julia] Ctr Biol Mol Severo Ochoa CSIC UAM, Madrid 28049, Spain.
[Martin, Daniel] NIDCR, Oral & Pharyngeal Canc Branch, NIH, Bldg 30, Bethesda, MD 20892 USA.
RP Gutkind, JS (reprint author), Moores Canc Ctr, 3855 Hlth Sci Dr, La Jolla, CA 92093 USA.
EM sgutkind@ucsd.edu
NR 47
TC 0
Z9 0
U1 1
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 2016
VL 37
IS 10
BP 1014
EP 1025
DI 10.1093/carcin/bgw086
PG 97
WC Oncology
SC Oncology
GA DZ7IC
UT WOS:000386037100001
PM 27538837
ER
PT J
AU Zhang, T
Ye, YH
AF Zhang, Ting
Ye, Yihong
TI Ever HRD a ubiquitin-gated channel?
SO CELL RESEARCH
LA English
DT Editorial Material
ID ENDOPLASMIC-RETICULUM; QUALITY-CONTROL; ER PROTEINS; RETROTRANSLOCATION
AB Elimination of misfolded proteins of the endoplasmic reticulum (ER) requires their retrotranslocation from the ER to the cytosol via membrane-bound ubiquitin ligase complexes. Baldridge and Rapoport now reconstitute a key step of retrotranslocation, demonstrating a protein conduit gated by ubiquitination.
C1 [Zhang, Ting; Ye, Yihong] NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Ye, YH (reprint author), NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
EM yihongy@mail.nih.gov
NR 10
TC 0
Z9 0
U1 3
U2 3
PU INST BIOCHEMISTRY & CELL BIOLOGY
PI SHANGHAI
PA SIBS, CAS, 319 YUEYANG ROAD, SHANGHAI, 200031, PEOPLES R CHINA
SN 1001-0602
EI 1748-7838
J9 CELL RES
JI Cell Res.
PD OCT
PY 2016
VL 26
IS 10
BP 1075
EP 1076
DI 10.1038/cr.2016.92
PG 2
WC Cell Biology
SC Cell Biology
GA DZ8QF
UT WOS:000386135200003
PM 27491350
ER
PT J
AU Kadri, SS
Rhee, C
Magda, G
Strich, JR
Cai, RM
Sun, JF
Decker, BK
O'Grady, NP
AF Kadri, Sameer S.
Rhee, Chanu
Magda, Gabriela
Strich, Jeffrey R.
Cai, Rongman
Sun, Junfeng
Decker, Brooke K.
O'Grady, Naomi P.
TI Synergy, Salary, and Satisfaction: Benefits of Training in Critical Care
Medicine and Infectious Diseases Gleaned From a National Pilot Survey of
Dually Trained Physicians
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
DE critical care; infectious diseases; survey
ID UNITED-STATES; EMERGENCY PHYSICIANS; MORTALITY; CONSULTATIONS;
SUBSPECIALTY; CHALLENGES; PREVENTION; PULMONARY; EDUCATION; THERAPY
AB A survey of physicians trained in critical care medicine (CCM) and infectious diseases (ID) suggested this combination is synergistic and satisfying. However, most respondents had to train in individual specialties at separate institutions. Avenues for CCM-ID training should be considered.Methods.aEuro integral All physicians trained and/or certified in both CCM and ID to date in the United States were sent a Web-based questionnaire in 2015. Responses enabled a cross-sectional analysis of physician demographics and training and practice characteristics and satisfaction.
Results.aEuro integral Of 202 CCM-ID physicians, 196 were alive and reachable. The response rate was 79%. Forty-six percent trained and 34% practice in the northeastern United States. Only 40% received dual training at the same institution. Eighty-three percent identified as either an intensivist with ID expertise (44%) or as equally an intensivist and ID physician (38%). Median salary was $265 000 (interquartile range [IQR], $215 000-$350 000). Practice settings were split between academic (45%) and community settings (42%). Two-thirds are clinicians but 62% conduct some research and 26% practice outpatient ID. Top reasons to dually specialize included clinical synergy (70%), procedural activity (50%), and less interest in pulmonology (49%). Although 38% cited less proficiency with bronchoscopy as a disadvantage, 87% seldom need pulmonary consultation in the intensive care unit. Median career satisfaction was 4 (IQR, 4-5) out of 5, and 76% would dually train again.
Conclusions.aEuro integral CCM-ID graduates prefer the acute care setting, predominantly CCM or a combination of CCM and ID. They find combination training and practice to be synergistic and satisfying, but most have had to seek CCM and ID training independently at separate institutions. Given these findings, avenues for combined training in CCM-ID should be considered.
C1 [Kadri, Sameer S.; Cai, Rongman; Sun, Junfeng; O'Grady, Naomi P.] NIH, Dept Crit Care Med, Ctr Clin, 10 Ctr Dr,B10 2C-145, Bethesda, MD 20892 USA.
[Rhee, Chanu] Brigham & Womens Hosp, Div Infect Dis, 75 Francis St, Boston, MA 02115 USA.
[Rhee, Chanu] Harvard Med Sch, Dept Populat Med, Boston, MA USA.
[Rhee, Chanu] Harvard Pilgrim Hlth Care Inst, Boston, MA USA.
[Magda, Gabriela] Georgetown Univ Hosp, Medstar, Dept Med, Washington, DC 20007 USA.
[Strich, Jeffrey R.] NIAID, Div Clin Res, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Decker, Brooke K.] VA Pittsburgh Healthcare Syst, Infect Dis Sect, Pittsburgh, PA USA.
RP Kadri, SS (reprint author), NIH, Dept Crit Care Med, Ctr Clin, 10 Ctr Dr,B10 2C-145, Bethesda, MD 20892 USA.
EM sameer.kadri@nih.gov
FU National Institutes of Health
FX This work was supported by intramural funds from the National Institutes
of Health.
NR 34
TC 3
Z9 3
U1 1
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1058-4838
EI 1537-6591
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD OCT 1
PY 2016
VL 63
IS 7
BP 868
EP 875
DI 10.1093/cid/ciw441
PG 8
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA DZ7JL
UT WOS:000386041100009
PM 27358351
ER
PT J
AU Fwu, CW
Kimmel, PL
Eggers, PW
Abbott, KC
AF Fwu, Chyng-Wen
Kimmel, Paul L.
Eggers, Paul W.
Abbott, Kevin C.
TI Comparison of trends in colorectal cancer screening in the US end-stage
renal disease population and the US Medicare population
SO CLINICAL KIDNEY JOURNAL
LA English
DT Article
DE colorectal cancer; dialysis; screening; kidney; transplant; USRDS
ID TRANSPLANT CANDIDATES; KIDNEY-TRANSPLANT; DIALYSIS PATIENTS; GUIDELINES;
RISK; HEMODIALYSIS; COLONOSCOPY; BENEFITS; SOCIETY; INJURY
AB Background: Although patients treated with maintenance hemodialysis are at an increased risk of colorectal cancer compared with the general population, national practices for colorectal cancer screening have not been reported in this population. We assessed the performance of colorectal cancer screening in the US end-stage renal disease program in comparison with the US Medicare population.
Methods: We studied the United States Renal Data System for US prevalent hemodialysis patients between 2002 and 2011 who had Medicare as their primary insurer. We assessed procedure codes for performance of common colorectal cancer screening tests, including fecal occult blood testing, sigmoidoscopy and colonoscopy. We assessed screening sigmoidoscopy and screening colonoscopy only and excluded patients who had preexisting colon cancer or gastrointestinal hemorrhage. Because colorectal cancer screening recommendations are established for hemodialysis patients who have been listed for kidney transplantation, but no general recommendations exist for patients who are not wait-listed, we assessed colorectal cancer screening separately for the two groups.
Results: We found that 1-year performance of colonoscopy in wait-listed hemodialysis patients was similar to or higher than that in general Medicare patients of the same age, while performance of colonoscopy in non-wait-listed patients was significantly lower than among general Medicare patients of the same age.
Conclusions: Given improved survival among hemodialysis patients in the last decade, the utility of colorectal cancer screening even among non-wait-listed hemodialysis patients should be reassessed.
C1 [Fwu, Chyng-Wen] Social & Sci Syst Inc, Silver Spring, MD USA.
[Kimmel, Paul L.; Eggers, Paul W.; Abbott, Kevin C.] NIDDK, Div Kidney Urol & Hematol Dis, NIH, 6707 Democracy Blvd, Bethesda, MD 20892 USA.
RP Abbott, KC (reprint author), NIDDK, Div Kidney Urol & Hematol Dis, NIH, 6707 Democracy Blvd, Bethesda, MD 20892 USA.
EM kevin.abbott@nih.gov
OI Abbott, Kevin/0000-0003-2111-7112
NR 28
TC 0
Z9 0
U1 1
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1753-0784
EI 1753-0792
J9 CLIN KIDNEY J
JI Clin. Kidney J.
PD OCT
PY 2016
VL 9
IS 5
BP 722
EP 728
DI 10.1093/ckj/sfw053
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA DZ8OX
UT WOS:000386131400011
PM 27679719
ER
PT J
AU Yamada, KM
Mayor, R
AF Yamada, Kenneth M.
Mayor, Roberto
TI Editorial overview: Cell dynamics in development, tissue remodelling,
and cancer
SO CURRENT OPINION IN CELL BIOLOGY
LA English
DT Editorial Material
C1 [Yamada, Kenneth M.] Natl Inst Dent & Craniofacial Res, Lab Cell & Dev Biol, Cell Biol Sect, NIH, Bethesda, MD 20892 USA.
[Mayor, Roberto] UCL, Dept Cell & Dev Biol, Gower St, London WC1E 6BT, England.
RP Yamada, KM (reprint author), Natl Inst Dent & Craniofacial Res, Lab Cell & Dev Biol, Cell Biol Sect, NIH, Bethesda, MD 20892 USA.
EM kyamada@dir.nidcr.nih.gov; r.mayor@ucl.ac.uk
NR 0
TC 0
Z9 0
U1 0
U2 0
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0955-0674
EI 1879-0410
J9 CURR OPIN CELL BIOL
JI Curr. Opin. Cell Biol.
PD OCT
PY 2016
VL 42
BP IV
EP VI
DI 10.1016/j.ceb.2016.09.001
PG 3
WC Cell Biology
SC Cell Biology
GA EA1PC
UT WOS:000386363300001
PM 27725095
ER
PT J
AU Petrie, RJ
Yamada, KM
AF Petrie, Ryan J.
Yamada, Kenneth M.
TI Multiple mechanisms of 3D migration: the origins of plasticity
SO CURRENT OPINION IN CELL BIOLOGY
LA English
DT Article
ID 3-DIMENSIONAL CELL-MIGRATION; FUNDULUS DEEP CELLS; LEADING-EDGE; FOCAL
ADHESIONS; RAC ACTIVATION; STRESS FIBERS; CONTRACTILITY; MATRIX;
INVASION; DYNAMICS
AB Cells migrate through 3D environments using a surprisingly wide variety of molecular mechanisms. These distinct modes of migration often rely on the same intracellular components, which are used in different ways to achieve cell motility. Recent work reveals that how a cell moves can be dictated by the relative amounts of cell-matrix adhesion and actomyosin contractility. A current concept is that the level of difficulty in squeezing the nucleus through a confining 3D environment determines the amounts of adhesion and contractility required for cell motility. Ultimately, determining how the nucleus controls the mode of cell migration will be essential for understanding both physiological and pathological processes dependent on cell migration in the body.
C1 [Petrie, Ryan J.] Drexel Univ, Dept Biol, Philadelphia, PA 19104 USA.
[Yamada, Kenneth M.] Natl Inst Dent & Craniofacial Res, Lab Cell & Dev Biol, NIH, Bethesda, MD USA.
RP Petrie, RJ (reprint author), Drexel Univ, Dept Biol, Philadelphia, PA 19104 USA.
EM rjp336@drexel.edu
FU Department of Biology; College of Arts and Sciences of Drexel
University; National Institutes of Health, National Institute of Dental
and Craniofacial Research (NIH, NIDCR)
FX RJP is supported by startup funds from the Department of Biology and the
College of Arts and Sciences of Drexel University. Work in KMY's
laboratory is supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Dental and
Craniofacial Research (NIH, NIDCR).
NR 64
TC 4
Z9 4
U1 8
U2 8
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0955-0674
EI 1879-0410
J9 CURR OPIN CELL BIOL
JI Curr. Opin. Cell Biol.
PD OCT
PY 2016
VL 42
BP 7
EP 12
DI 10.1016/j.ceb.2016.03.025
PG 6
WC Cell Biology
SC Cell Biology
GA EA1PC
UT WOS:000386363300003
PM 27082869
ER
PT J
AU Koo, H
Yamada, KM
AF Koo, Hyun
Yamada, Kenneth M.
TI Dynamic cell-matrix interactions modulate microbial biofilm and tissue
3D microenvironments
SO CURRENT OPINION IN CELL BIOLOGY
LA English
DT Article
ID VIBRIO-CHOLERAE BIOFILMS; EXTRACELLULAR-MATRIX; STREPTOCOCCUS-MUTANS;
BACILLUS-SUBTILIS; PSEUDOMONAS-AERUGINOSA; CANDIDA-ALBICANS; IN-VIVO;
STIFFNESS; CANCER; COLLAGEN
AB Microbial biofilms and most eukaryotic tissues consist of cells embedded in a three-dimensional extracellular matrix. This matrix serves as a scaffold for cell adhesion and a dynamic milieu that provides varying chemical and physical signals to the cells. Besides a vast array of specific molecular components, an extracellular matrix can provide locally heterogeneous microenvironments differing in porosity/diffusion, stiffness, pH, oxygen and metabolites or nutrient levels. Mechanisms of matrix formation, mechanosensing, matrix remodeling, and modulation of cell-cell or cell-matrix interactions and dispersal are being revealed. This perspective article aims to identify such concepts from the fields of biofilm or eukaryotic matrix biology relevant to the other field to help stimulate new questions, approaches, and insights.
C1 [Koo, Hyun] Univ Penn, Sch Dent Med, Dept Orthodont, Biofilm Res Labs,Levy Ctr Oral Hlth, Philadelphia, PA 19104 USA.
[Koo, Hyun] Univ Penn, Sch Dent Med, Div Pediat Dent, Philadelphia, PA 19104 USA.
[Koo, Hyun] Univ Penn, Sch Dent Med, Div Community Oral Hlth, Philadelphia, PA 19104 USA.
[Yamada, Kenneth M.] Natl Inst Dent & Craniofacial Res, Lab Cell & Dev Biol, Cell Biol Sect, NIH, Bethesda, MD 20892 USA.
[Koo, Hyun] Univ Penn, Sch Dent Med, 240 South 40th St,Levy Bldg Rm 417, Philadelphia, PA 19104 USA.
RP Koo, H (reprint author), Univ Penn, Sch Dent Med, 240 South 40th St,Levy Bldg Rm 417, Philadelphia, PA 19104 USA.
EM koohy@upenn.edu
FU National Institute for Dental and Craniofacial Research (NIDCR), NIH
Intramural Research Program; NIDCR [DE16139, DE18023, DE25220]
FX The authors' research is supported by the National Institute for Dental
and Craniofacial Research (NIDCR), NIH Intramural Research Program (KMY)
and by NIDCR grants DE16139, DE18023, and DE25220 (HK). We thank Dr.
Marlise Klein (State University of Sao Paulo, Brazil) and Dr. William H.
Bowen (University of Rochester Medical Center, Rochester, NY, USA) for
helpful suggestions and comments. We are also grateful to Jill Harunaga,
Ryan Petrie, and Roumen Pankov for the fluorescence images. The diagrams
and schematics were designed by Long Do and Mirae Jang (The University
of Arts, Philadelphia, PA, USA; Instructor: Joel Katz). The authors
regret that many studies could only be cited indirectly owing to space
and reference number limitation.
NR 71
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U1 6
U2 6
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0955-0674
EI 1879-0410
J9 CURR OPIN CELL BIOL
JI Curr. Opin. Cell Biol.
PD OCT
PY 2016
VL 42
BP 102
EP 112
DI 10.1016/j.ceb.2016.05.005
PG 11
WC Cell Biology
SC Cell Biology
GA EA1PC
UT WOS:000386363300014
PM 27257751
ER
PT J
AU Deroo, LA
Wilcox, AJ
Lie, RT
Romitti, PA
Pedersen, DA
Munger, RG
Uribe, LMM
Wehby, GL
AF DeRoo, Lisa A.
Wilcox, Allen J.
Lie, Rolv T.
Romitti, Paul A.
Pedersen, Dorthe Almind
Munger, Ronald G.
Uribe, Lina M. Moreno
Wehby, George L.
TI Maternal alcohol binge-drinking in the first trimester and the risk of
orofacial clefts in offspring: a large population-based pooling study
SO EUROPEAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE Cleft lip; Cleft palate; Alcohol
ID BIRTH-DEFECTS; ORAL CLEFTS; POOLED ANALYSES; CONSUMPTION; PREGNANCY;
METAANALYSES; EPIDEMIOLOGY; NORWAY; COHORT; GENES
AB Using individual participant data from six population-based case-control studies, we conducted pooled analyses to examine maternal alcohol consumption and the risk of clefts among > 4600 infants with cleft lip only, cleft lip with cleft palate, or cleft palate only and > 10,000 unaffected controls. We examined two first-trimester alcohol measures: average number of drinks/sitting and maximum number of drinks/sitting, with five studies contributing to each analysis. Study-specific odds ratios (ORs) were estimated using logistic regression and pooled to generate adjusted summary ORs. Across studies, 0.9-3.2 % of control mothers reported drinking an average of 5+ drinks/sitting, while 1.4-23.5 % reported drinking a maximum of 5+ drinks/sitting. Compared with non-drinkers, mothers who drank an average of 5+ drinks/sitting were more likely to deliver an infant with cleft lip only (pooled OR 1.48; 95 % confidence intervals 1.01, 2.18). The estimate was higher among women who drank at this level 3+ times (pooled OR 1.95; 1.23, 3.11). Ever drinking a maximum of 5+ drinks/sitting and non-binge drinking were not associated with cleft risk. Repeated heavy maternal alcohol consumption was associated with an increased risk of cleft lip only in offspring. There was little evidence of increased risk for other cleft types or alcohol measures.
C1 [DeRoo, Lisa A.; Lie, Rolv T.] Univ Bergen, Dept Global Publ Hlth & Primary Care, Postboks 7804, N-5020 Bergen, Norway.
[DeRoo, Lisa A.; Wilcox, Allen J.] NIEHS, Epidemiol Branch, NIH, Durham, NC 27711 USA.
[Lie, Rolv T.] Med Birth Registry Norway, Norwegian Inst Publ Hlth, Bergen, Norway.
[Romitti, Paul A.] Univ Iowa, Dept Epidemiol, Coll Publ Hlth, Iowa City, IA USA.
[Pedersen, Dorthe Almind] Univ Southern Denmark, Inst Publ Hlth, Epidemiol Biostat & Biodemog, Odense, Denmark.
[Munger, Ronald G.] Utah State Univ, Dept Nutr Dietet & Food Sci, Logan, UT 84322 USA.
[Uribe, Lina M. Moreno] Univ Iowa, Dept Orthodont, Coll Dent & Dent Clin, Iowa City, IA USA.
[Wehby, George L.] Univ Iowa, Dept Hlth Management & Policy, 105 River St, Iowa City, IA 52242 USA.
RP Deroo, LA (reprint author), Univ Bergen, Dept Global Publ Hlth & Primary Care, Postboks 7804, N-5020 Bergen, Norway.; Deroo, LA (reprint author), NIEHS, Epidemiol Branch, NIH, Durham, NC 27711 USA.; Wehby, GL (reprint author), Univ Iowa, Dept Hlth Management & Policy, 105 River St, Iowa City, IA 52242 USA.
EM Lisa.De.Roo@igs.uib.no; george-wehby@uiowa.edu
OI Wilcox, Allen/0000-0002-3376-1311
FU National Institutes of Health (NIH), National Institute of Dental and
Craniofacial Research (NIDCR) [1 R01 DE020895]; Intramural Research
Program of the National Institute of Environmental Health Sciences
(NIEHS) [ZIA-ES-49027]; NIH [R01 HD39061]; U.S. Centers for Disease
Control and Prevention (CDC) [U01-DD000492, U01-D000698, U01-DD001035];
Norwegian Ministry of Health; Ministry of Education and Research
FX The main funding for this study was provided by Grant 1 R01 DE020895
from the National Institutes of Health (NIH), National Institute of
Dental and Craniofacial Research (NIDCR). This research was also
supported in part by the Intramural Research Program of the National
Institute of Environmental Health Sciences (NIEHS) (ZIA-ES-49027).
Additional partial funding was from NIH grant R01 HD39061, U.S. Centers
for Disease Control and Prevention (CDC) grants U01-DD000492,
U01-D000698, and U01-DD001035, and the Norwegian Ministry of Health and
the Ministry of Education and Research. We thank Drs. Abee L. Boyles,
Lorenzo D. Botto, Sonja A. Rasmussen and Donna D. Baird and for helpful
comments on an earlier draft of this manuscript.
NR 35
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U1 4
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0393-2990
EI 1573-7284
J9 EUR J EPIDEMIOL
JI Eur. J. Epidemiol.
PD OCT
PY 2016
VL 31
IS 10
BP 1021
EP 1034
DI 10.1007/s10654-016-0171-5
PG 14
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA EA1SP
UT WOS:000386372500006
PM 27350158
ER
PT J
AU Chiang, YJ
Hodes, RJ
AF Chiang, Y. Jeffrey
Hodes, Richard J.
TI T-cell development is regulated by the coordinated function of proximal
and distal Lck promoters active at different developmental stages
SO EUROPEAN JOURNAL OF IMMUNOLOGY
LA English
DT Article
DE Development; T cell; Thymus; Lck; Promoter
ID MAMMALIAN GENOMES; EXPRESSION; P56(LCK); THYMOCYTES; DISSECTION;
ACTIVATION; GENE
AB Expression of Lck, a T-cell lineage-specific tyrosine kinase critical for T-cell development and activation, can be mediated by either proximal or distal lck promoter. We generated BAC transgenic mice in which BAC lck promoter was deleted and bred these transgenes to an Lck knockout background. Lck-PROX mice, in which only the proximal promoter is functional, have maximal Lck protein and normal thymic development through CD4(-)CD8(-) double negative (DN) and CD4(+)CD8(+) double positive (DP) stages, but undetectable Lck later in development and reduced mature single positive thymocytes. In contrast, Lck-DIST mice, in which only distal promoter was functional, are deficient in Lck protein in DN and DP thymocytes and severely defective in early T-cell development, with a block at the DN3-DN4 beta checkpoint equivalent to complete Lck knockouts. The ability of the proximal lck promoter to support thymic development is independent of Fyn; while, in contrast, the distal lck promoter alone is completely unable to support development in the absence of Fyn. Notably, normal thymocyte development is restored by presence of both proximal and distal promoters, even when independently expressed on different lck genes. These results define distinct and complementary requirements for proximal and distal lck promoters during T-cell development.
C1 [Chiang, Y. Jeffrey; Hodes, Richard J.] NCI, Expt Immunol Branch, Bldg 10, Bethesda, MD 20892 USA.
[Hodes, Richard J.] NIA, NIH, Bethesda, MD 20892 USA.
RP Hodes, RJ (reprint author), NCI, Expt Immunol Branch, Bldg 10, Bethesda, MD 20892 USA.; Hodes, RJ (reprint author), NIA, NIH, Bethesda, MD 20892 USA.
EM hodesr@31.nia.nih.gov
FU 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.
NR 20
TC 1
Z9 1
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0014-2980
EI 1521-4141
J9 EUR J IMMUNOL
JI Eur. J. Immunol.
PD OCT
PY 2016
VL 46
IS 10
BP 2401
EP 2408
DI 10.1002/eji.201646440
PG 8
WC Immunology
SC Immunology
GA DZ9VV
UT WOS:000386229600013
PM 27469439
ER
PT J
AU Tikkanen, R
Saukkonen, T
Fex, M
Bennet, H
Rautiainen, MR
Paunio, T
Koskinen, M
Panarsky, R
Bevilacqua, L
Sjoberg, RL
Tiihonen, J
Virkkunen, M
AF Tikkanen, R.
Saukkonen, T.
Fex, M.
Bennet, H.
Rautiainen, M. -R.
Paunio, T.
Koskinen, M.
Panarsky, R.
Bevilacqua, L.
Sjoberg, R. L.
Tiihonen, J.
Virkkunen, M.
TI Influence of a HTR2B Stop Codon on Glucagon Homeostasis and Glucose
Excursion in Non-Diabetic Men
SO EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES
LA English
DT Article
DE glucose; glucagon; serotonin 2B receptor; oral glucose tolerance test;
insulin resistance; BMI
ID INSULIN-SECRETION; GLYCOGEN-SYNTHESIS; SEROTONIN; PHOSPHORYLASE;
DYSREGULATION; HYPERGLYCEMIA; METABOLISM; ACTIVATION; MECHANISMS; RATS
AB Limited data are available about the role of the serotonin 2B (5-HT2B) receptor in the function of human islets. This study aimed to test whether the 5-HT2B receptor contributes to glucose, insulin, and glucagon homeostasis in humans, utilizing a hereditary loss-of-function gene mutation in the receptor, which causes a 50% reduction in the production of the receptor protein in heterozygotes. This clinical study enrolled participants recruited by newspaper advertisements and from mental status examinations. A cohort of participants from a young Finnish founder population composed of 68 non-diabetic males with a mean age of 30 was divided into groups for comparison based on being a 5-HT2B receptor loss-of-function gene mutation (HTR2B Q20*) heterozygote carrier (n=11) or not (n=57). Serum levels of glucose, insulin, and glucagon were measured in a 5h oral glucose tolerance test using a 75g glucose challenge. Insulin resistance, insulin sensitivity, and beta cell activity were calculated using the homeostasis model assessment (HOMA2) and whole body insulin sensitivity index (WBISI), as well as the ratio of glucagon to insulin was noted. The areas under the curves (AUCs) were also determined. Concentrations of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) were measured in cerebrospinal fluid (CSF). Covariate adjusted mean score comparisons were applied. Lower glucagon secretion and decreased glucose excursion were observed among HTR2B Q20* carriers as compared with individuals who were homozygotes for the wild-type Q20 allele (controls). No differences in insulin secretion, beta cell activity, insulin resistance, or insulin sensitivity were observed. The glucagon to insulin ratio differed between the HTR2B Q20* carriers and controls. CSF levels of 5-HIAA were similar between groups. Our findings indicate that the 5-HT2B receptor may contribute to the regulation of human glucagon and glucose homeostasis and the interplay between glucagon and insulin secretion.
C1 [Tikkanen, R.; Paunio, T.; Virkkunen, M.] Univ Helsinki, Dept Psychiat, Cent Hosp, Helsinki, Finland.
[Tikkanen, R.] Rinnekoti Fdn, Res & Dev, Espoo, Finland.
[Saukkonen, T.] Univ Helsinki, Cent Hosp, Childrens Hosp, Helsinki, Finland.
[Saukkonen, T.] Univ Helsinki, Helsinki, Finland.
[Saukkonen, T.] Novo Nordisk Farma Oy, Espoo, Finland.
[Fex, M.; Bennet, H.] Lund Univ, Ctr Diabet, Scania Univ Hosp, Dept Clin Sci, Malmo, Sweden.
[Rautiainen, M. -R.; Paunio, T.; Tiihonen, J.] Natl Inst Hlth & Welf, Helsinki, Finland.
[Koskinen, M.] Oy Aava Dev Ltd, Helsinki, Finland.
[Panarsky, R.] NIAAA, Neurogenet Lab, Bethesda, MD USA.
[Bevilacqua, L.] NYU, Sch Med, Dept Psychiat, New York, NY USA.
[Sjoberg, R. L.; Tiihonen, J.] Umea Univ, Dept Pharmacol & Clin Neurosci, Umea, Sweden.
[Tiihonen, J.] Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.
[Tiihonen, J.] Univ Eastern Finland, Niuvanniemi Hosp, Dept Forens Psychiat, Kuopio, Finland.
RP Tikkanen, R (reprint author), Univ Helsinki, Dept Psychiat, Valskarinkatu 12,POB 22, Helsinki 00260, Finland.
EM roope.tikkanen@gmail.com
FU Orion Research Foundation; Swedish Research Council [2012-1552];
Waldemar von Frenckell Foundation
FX We thank for receiving the following grants: the Orion Research
Foundation (R.T), Swedish Research Council (project number: 2012-1552 to
M.F), and Waldemar von Frenckell Foundation (MR.R). Excellence in
diabetes research (EXODIAB), Krapperup foundation, Ake Wiberg
foundation, Royal Physiographic Society, Albert Pahlsson foundation,
Crafoord foundation, Childhood Diabetes Foundation, and the Foundation
of Sigurd and Elsa Golijes Minne.
NR 30
TC 0
Z9 0
U1 0
U2 0
PU JOHANN AMBROSIUS BARTH VERLAG MEDIZINVERLAGE HEIDELBERG GMBH
PI STUTTGART
PA RUEDIGERSTR 14, D-70469 STUTTGART, GERMANY
SN 0947-7349
EI 1439-3646
J9 EXP CLIN ENDOCR DIAB
JI Exp. Clin. Endocrinol. Diabet.
PD OCT
PY 2016
VL 124
IS 9
BP 529
EP 534
DI 10.1055/s-0042-109263
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA EA0XR
UT WOS:000386313300002
PM 27437919
ER
PT J
AU Mookherjee, S
Banerjee, D
Chakraborty, S
Mukhopadhyay, I
Sen, A
Ray, K
AF Mookherjee, Suddhasil
Banerjee, Deblina
Chakraborty, Subhadip
Mukhopadhyay, Indranil
Sen, Abhijit
Ray, Kunal
TI Evaluation of the IL1 Gene Cluster Single Nucleotide Polymorphisms in
Primary Open-Angle Glaucoma Pathogenesis
SO GENETIC TESTING AND MOLECULAR BIOMARKERS
LA English
DT Article
DE genetics; glaucoma; POAG; interleukins; association study
ID HEAT-SHOCK PROTEINS; AQUEOUS-HUMOR; IL-1F7 GENE; ASSOCIATION;
IDENTIFICATION; POPULATION; IMMUNITY; DISEASE
AB Aims: Dysregulation of the immune system has previously been implicated in glaucoma pathogenesis. In this study, we investigated the potential association of SNPs in the IL1 gene cluster, consisting of nine genes, with primary open-angle glaucoma (POAG) cases. These cases presented with low to normal intraocular pressures (<20mmHg), and are referred to as non-high tension glaucoma (non-HTG) cases. Materials and Methods: In this biphasic study, the discovery phase was conducted with 198 non-HTG cases and 112 controls from eastern India. A total of 68 single nucleotide polymorphisms (SNPs) spanning the IL1 nine-gene cluster region were genotyped using the MALDI-TOF based Sequenom platform. SNPs, which were found to be significantly associated with non-HTG cases in the first phase of the study, were further genotyped by Sanger sequencing in a replication cohort consisting of 194 non-HTG cases and 242 controls. Results: In the discovery phase, two nonsynonymous SNPs (rs3811046 and rs3811047), located in the IL1F7 gene and in an intergenic region, respectively were found to be weakly associated with non-HTG cases. However, the association was not sustained in the replication cohort. Conclusion: Our study did not reveal any reproducible association of SNPs in the IL1 gene cluster with POAG.
C1 [Mookherjee, Suddhasil; Banerjee, Deblina; Chakraborty, Subhadip; Ray, Kunal] CSIR Indian Inst Chem Biol, Mol & Human Genet Div, Kolkata, India.
[Mukhopadhyay, Indranil] Indian Stat Inst, Human Genet Unit, Kolkata, India.
[Sen, Abhijit] Dristi Pradip, Kolkata, India.
[Mookherjee, Suddhasil] NEI, NIH, 6 Ctr Dr, Bethesda, MD 20892 USA.
[Banerjee, Deblina] NCI, NIH, Bethesda, MD 20892 USA.
[Chakraborty, Subhadip] Univ Calcutta, SN Pradhan Ctr Neurosci, Kolkata, India.
[Ray, Kunal] CSIR Cent Rd Res Inst, Acad Sci & Innovat Res, CRRI PO Delhi,Mathura Rd, New Delhi 110025, India.
RP Mookherjee, S (reprint author), NEI, NIH, 6 Ctr Dr, Bethesda, MD 20892 USA.; Ray, K (reprint author), CSIR Cent Rd Res Inst, Acad Sci & Innovat Res, CRRI PO Delhi,Mathura Rd, New Delhi 110025, India.
EM suddhasil.mookherjee@nih.gov; kunalray@acsir.res.in
FU Council of Scientific and Industrial Research, Govt. of India [SIP-007,
MLP-0016, NWP 004]
FX The authors are grateful to the donors who participated in this study
and to Dr. Keya Sen for helping with clinical evaluation of patients. We
thank Ananya Ray-Soni for critically proofreading the article for
improving the language and grammar of the article. The Council of
Scientific and Industrial Research, Govt. of India supported the study
through funding grants (SIP-007, MLP-0016, and NWP 004) and predoctoral
fellowships to S.M., D.B., and S.C.
NR 33
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1945-0265
EI 1945-0257
J9 GENET TEST MOL BIOMA
JI Genet. Test. Mol. Biomark.
PD OCT
PY 2016
VL 20
IS 10
BP 633
EP 636
DI 10.1089/gtmb.2015.0344
PG 4
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA EA3AV
UT WOS:000386470900012
PM 27533638
ER
PT J
AU Qian, F
Feng, Y
Zheng, YL
Ogundiran, TO
Ojengbede, O
Zheng, W
Blot, W
Ambrosone, CB
John, EM
Bernstein, L
Hu, JJ
Ziegler, RG
Nyante, S
Bandera, EV
Ingles, SA
Press, MF
Nathanson, KL
Hennis, A
Nemesure, B
Ambs, S
Kolonel, LN
Olopade, OI
Haiman, CA
Huo, DZ
AF Qian, Frank
Feng, Ye
Zheng, Yonglan
Ogundiran, Temidayo O.
Ojengbede, Oladosu
Zheng, Wei
Blot, William
Ambrosone, Christine B.
John, Esther M.
Bernstein, Leslie
Hu, Jennifer J.
Ziegler, Regina G.
Nyante, Sarah
Bandera, Elisa V.
Ingles, Sue A.
Press, Michael F.
Nathanson, Katherine L.
Hennis, Anselm
Nemesure, Barbara
Ambs, Stefan
Kolonel, Laurence N.
Olopade, Olufunmilayo I.
Haiman, Christopher A.
Huo, Dezheng
TI Genetic variants in microRNA and microRNA biogenesis pathway genes and
breast cancer risk among women of African ancestry
SO HUMAN GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; ESTROGEN-RECEPTOR; SUSCEPTIBILITY LOCI;
INDIGENOUS AFRICANS; AMERICAN WOMEN; HUMAN-DISEASE; POPULATION;
POLYMORPHISMS; EXPRESSION; BRCA1
AB MicroRNAs (miRNA) regulate breast biology by binding to specific RNA sequences, leading to RNA degradation and inhibition of translation of their target genes. While germline genetic variations may disrupt some of these interactions between miRNAs and their targets, studies assessing the relationship between genetic variations in the miRNA network and breast cancer risk are still limited, particularly among women of African ancestry. We systematically put together a list of 822 and 10,468 genetic variants among primary miRNA sequences and 38 genes in the miRNA biogenesis pathway, respectively; and examined their association with breast cancer risk in the ROOT consortium which includes women of African ancestry. Findings were replicated in an independent consortium. Logistic regression was used to estimate the odds ratio (OR) and 95 % confidence intervals (CI). For overall breast cancer risk, three single-nucleotide polymorphisms (SNPs) in miRNA biogenesis genes DROSHA rs78393591 (OR = 0.69, 95 % CI: 0.55-0.88, P = 0.003), ESR1 rs523736 (OR = 0.88, 95 % CI: 0.82-0.95, P = 3.99 x 10(-4)), and ZCCHC11 rs114101502 (OR = 1.33, 95 % CI: 1.11-1.59, P = 0.002), and one SNP in primary miRNA sequence (rs116159732 in miR-6826, OR = 0.74, 95 % CI: 0.63-0.89, P = 0.001) were found to have significant associations in both discovery and validation phases. In a subgroup analysis, two SNPs were associated with risk of estrogen receptor (ER)-negative breast cancer, and three SNPs were associated with risk of ER-positive breast cancer. Several variants in miRNA and miRNA biogenesis pathway genes were associated with breast cancer risk. Risk associations varied by ER status, suggesting potential new mechanisms in etiology.
C1 [Qian, Frank; Zheng, Yonglan; Olopade, Olufunmilayo I.] Univ Chicago, Dept Med, 5841 S Maryland Ave, Chicago, IL 60637 USA.
[Feng, Ye; Ingles, Sue A.; Haiman, Christopher A.] Univ Southern Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA USA.
[Feng, Ye; Ingles, Sue A.; Press, Michael F.; Haiman, Christopher A.] Univ Southern Calif, Norris Comprehens Canc Ctr, Los Angeles, CA USA.
[Ogundiran, Temidayo O.] Univ Ibadan, Dept Surg, Coll Med, Ibadan, Nigeria.
[Ojengbede, Oladosu] Univ Ibadan, Coll Med, Ctr Populat & Reprod Hlth, Ibadan, Nigeria.
[Zheng, Wei; Blot, William] Vanderbilt Univ, Vanderbilt Ingram Canc Ctr, Vanderbilt Epidemiol Ctr, Div Epidemiol,Dept Med, Nashville, TN USA.
[Ambrosone, Christine B.] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
[John, Esther M.] Canc Prevent Inst Calif, Fremont, CA USA.
[John, Esther M.] Stanford Univ, Sch Med Stanford, Dept Hlth Res & Policy Epidemiol, Stanford, CA 94305 USA.
[John, Esther M.] Stanford Univ, Sch Med Stanford, Stanford Canc Inst, Stanford, CA 94305 USA.
[Bernstein, Leslie] City Hope Natl Med Ctr, Beckman Res Inst, Dept Populat Sci, Div Canc Etiol, Duarte, CA USA.
[Hu, Jennifer J.] Univ Miami, Miller Sch Med, Sylvester Comprehens Canc Ctr, Miami, FL 33136 USA.
[Hu, Jennifer J.] Univ Miami, Miller Sch Med, Dept Epidemiol & Publ Hlth, Miami, FL 33136 USA.
[Ziegler, Regina G.] NCI, Epidemiol & Biostat Program, Div Canc Epidemiol & Genet, Bethesda, DC USA.
[Nyante, Sarah] Univ N Carolina, Gillings Sch Global Publ Hlth, Dept Epidemiol, Chapel Hill, NC USA.
[Nyante, Sarah] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC USA.
[Bandera, Elisa V.] Rutgers Canc Inst New Jersey, New Brunswick, NJ USA.
[Press, Michael F.] Univ Southern Calif, Keck Sch Med, Dept Pathol, Los Angeles, CA USA.
[Nathanson, Katherine L.] Univ Penn, Dept Med, Philadelphia, PA 19104 USA.
[Hennis, Anselm] Univ West Indies, Chron Dis Res Ctr, Bridgetown, Barbados.
[Hennis, Anselm] Univ West Indies, Res Inst Trop Med, Bridgetown, Barbados.
[Nemesure, Barbara] SUNY Stony Brook, Dept Prevent Med, Stony Brook, NY 11794 USA.
[Ambs, Stefan] NCI, Human Carcinogenesis Lab, Bldg 37, Bethesda, MD 20892 USA.
[Kolonel, Laurence N.] Univ Hawaii, Ctr Canc, Program Epidemiol, Honolulu, HI 96822 USA.
[Huo, Dezheng] Univ Chicago, Dept Publ Hlth Sci, 5841 S Maryland Ave,MC 2007, Chicago, IL 60637 USA.
RP Huo, DZ (reprint author), Univ Chicago, Dept Publ Hlth Sci, 5841 S Maryland Ave,MC 2007, Chicago, IL 60637 USA.
EM dhuo@health.bsd.uchicago.edu
FU National Cancer Institute [R01-CA142996, P50-CA125183, R01-CA89085]
FX This work was supported by National Cancer Institute Grants
R01-CA142996, P50-CA125183, and R01-CA89085.
NR 75
TC 0
Z9 0
U1 1
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-6717
EI 1432-1203
J9 HUM GENET
JI Hum. Genet.
PD OCT
PY 2016
VL 135
IS 10
BP 1145
EP 1159
DI 10.1007/s00439-016-1707-1
PG 15
WC Genetics & Heredity
SC Genetics & Heredity
GA DX2UC
UT WOS:000384225700004
PM 27380242
ER
PT J
AU Santoro, N
Eisenberg, E
Trussell, JC
Craig, LB
Gracia, C
Huang, H
Alvero, R
Casson, P
Christman, G
Coutifaris, C
Diamond, M
Jin, SS
Legro, RS
Robinson, RD
Schlaff, WD
Zhang, HP
AF Santoro, Nanette
Eisenberg, Esther
Trussell, J. C.
Craig, LaTasha B.
Gracia, Clarisa
Huang, Hao
Alvero, Ruben
Casson, Peter
Christman, Gregory
Coutifaris, Christos
Diamond, Michael
Jin, Susan
Legro, Richard S.
Robinson, Randal D.
Schlaff, William D.
Zhang, Heping
CA Reprod Med Network Investigators
TI Fertility-related quality of life from two RCT cohorts with infertility:
unexplained infertility and polycystic ovary syndrome
SO HUMAN REPRODUCTION
LA English
DT Article
DE quality of life; polycystic ovary syndrome; unexplained infertility;
FertiQOL; infertility
ID IN-VITRO FERTILIZATION; MULTIPLE INTRAUTERINE GESTATIONS; STIMULATION
AMIGOS TRIAL; PSYCHOLOGICAL DISTRESS; EMOTIONAL DISTRESS; PSYCHOMETRIC
PROPERTIES; PROBLEM STRESS; SOCIAL IMPACT; WOMEN; COUPLES
AB Does fertility-related quality of life (FertiQOL) differ by infertility diagnosis between women with polycystic ovary syndrome (PCOS) and their partners, compared with couples with unexplained infertility (UI)?
Women with PCOS report lower QOL than those with UI, whereas males with UI report lower QOL than males with PCOS partners.
The fertility-specific QOL survey, FertiQOL, has been used to examine fertility-related QOL in a number of worldwide cohorts. Few data have addressed fertility-related QOL as a function of infertility diagnosis. Overall, men report better QOL than women with infertility, and there is variation in FertiQOL scores across different samples from different countries.
This was a prospective, cohort study derived from two concurrent, randomized clinical trials, and designed to examine QOL in infertile females with PCOS and UI at the time of enrollment compared with each other and their male partners; to compare concordance FertiQOL scores in this study across other worldwide cohorts; and to determine if baseline FertiQOL was associated with pregnancy outcome.
Women with PCOS and their partners (n = 733 and n = 641, respectively), and couples with UI (n = 865 women and 849 men) completed a validated fertility-specific QOL survey (FertiQOL) at the time of the study screening visit. PCOS women were randomized to either clomiphene citrate or letrozole treatment; couples with UI were randomized to clomiphene citrate, letrozole or gonadotrophin plus IUI. FertiQOL results were compiled by diagnosis (PCOS or UI) and compared by diagnosis and sex using Wilcoxon Rank-Sum testing. Relationships between baseline FertiQOL and pregnancy outcomes were examined using logistic regression. Multivariable models were performed to assess the association between FertiQOL scores and key participant characteristics.
Women with PCOS had lower total FertiQOL scores (72.3 +/- 14.8) than those with UI (77.1 +/- 12.8; P < 0.001); this was true for each domain (except Relational). These differences were largely explained by variation in BMI, hirsutism, household income and age. Women had lower overall FertiQOL scores than their male partners. Males with PCOS partners had higher scores than males with UI (84.9 +/- 10.2 versus 83.3 +/- 10.8; P = 0.003). Scores were not consistently associated with conception or pregnancy outcome.
The use of multiple tests of association may have resulted in spurious statistically significant findings. Inherent sociodemographic differences between women with PCOS and those with UI largely account for the lower QOL in women with PCOS. Our study was unable to assess if changes in QOL affected pregnancy outcome as FertiQOL data were collected prior to treatment. Finally, the participants for both studies represent their local communities, but are not a population-based sample and thus firm conclusions about how representative these couples are to the general population must be made with caution.
Women with PCOS with elevated BMI and hirsutism scores and with lower socioeconomic status may require more, targeted psychosocial support than those with other diagnoses. Possible attribution of infertility to the male partner appears to result in a lower QOL. There appears to be substantial national variation in FertiQOL scores, with US-based cohorts reporting overall higher QOL.
This work was supported by National Institutes of Health (NIH)/Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) Grants U10 HD39005 (to M.D.), U10 HD38992 (to R.S.L.), (to C.C.), U10 HD38998 (to R.A.), U10 HD055942 (to R.D.R.), HD055944 (to P.C.), U10 HD055936 (to G.C.), U10HD055925 (to H.Z.); and U10 U54-HD29834 (to the University of Virginia Center for Research in Reproduction Ligand Assay and Analysis Core of the Specialized Cooperative Centers Program in Reproduction and Infertility Research). Most importantly, this research was made possible by the funding by American Recovery and Reinvestment Act. N.S., E.E., J.C.T., C.G., H.H., R.A., P.C., G.C., C.C., M.D., S.J., W.D.S. and H.Z. report no conflicts of interests/disclosures. L.B.C. reports research support from Ferring Pharmaceuticals and Roche Diagnostics; R.S.L. reports receipt of consulting fees from AstraZeneca, Euroscreen, Sprout Pharmaceuticals, Taken, Kindex, Clarus and Bayer, Inc., and research support from AstraZeneca and Ferring Pharmaceuticals. R.D.R. reports research support from AbbVie.
Pregnancy in Polycystic Ovary Syndrome II (PPCOS II), NCT00719186; Assessment of Multiple Intrauterine Gestations in Ovulation Stimulation (AMIGOS) NCT01044862, clinicaltrials.gov.
PPCOS II 17 July 2008; AMIGOS 7 January 2010.
PPCOS II 19 February 2009; AMIGOS 2 August 2010.
C1 [Santoro, Nanette; Alvero, Ruben] Univ Colorado, Dept Obstet & Gynecol, Sch Med, 12631 E 17th Ave AO,Room 4010, Aurora, CO 80045 USA.
[Eisenberg, Esther] NICHD, Fertil & Infertil Branch, NIH, Bethesda, MD 20892 USA.
[Trussell, J. C.] SUNY Upstate Med Univ, Dept Urol, 750 E Adams St, Syracuse, NY 13210 USA.
[Craig, LaTasha B.] Univ Oklahoma, Hlth Sci Ctr, Dept Obstet & Gynecol, POB 26901,WP 2410, Oklahoma City, OK 73126 USA.
[Gracia, Clarisa; Coutifaris, Christos] Univ Penn, Dept Obstet & Gynecol, Penn Fertil Ctr, 3701 Market St, Philadelphia, PA 19104 USA.
[Huang, Hao; Jin, Susan; Zhang, Heping] Yale Sch Publ Hlth, Collaborat Ctr Stat Sci, 60 Coll St, New Haven, CT 06520 USA.
[Legro, Richard S.] Penn State Coll Med, 500 Univ Dr, Hershey, PA 17033 USA.
[Robinson, Randal D.] Univ Texas San Antonio, Hlth Sci Ctr, 8300 Floyd Curl Dr, San Antonio, TX 78229 USA.
[Casson, Peter] Northeastern Reprod Med, 105 West View Rd Suite 305, Colchester, VT 05446 USA.
[Christman, Gregory] Univ Florida, Coll Med, Dept Obstet & Gynecol, 1600 SW Archer Rd, Gainesville, FL 32611 USA.
[Diamond, Michael] Georgia Regents Univ, Med Coll Georgia, 1120 15th St,BA-7300, Augusta, GA 30912 USA.
[Schlaff, William D.] Thomas Jefferson Univ, Dept Obstet & Gynecol, 834 Chestnut St,Suite 400, Philadelphia, PA 19107 USA.
[Alvero, Ruben] Brown Univ, Warren Alpert Med Sch, Dept Obstet & Gynecol, Providence, RI 02903 USA.
RP Santoro, N (reprint author), Univ Colorado, Dept Obstet & Gynecol, Sch Med, 12631 E 17th Ave AO,Room 4010, Aurora, CO 80045 USA.
EM nanette.santoro@ucdenver.edu
FU National Institutes of Health (NIH)/Eunice Kennedy Shriver National
Institute of Child Health and Human Development (NICHD) [U10 HD39005,
U10 HD38992, U10 HD38998, U10 HD055942, HD055944, U10 HD055936,
U10HD055925, U10 U54-HD29834]; American Recovery and Reinvestment Act
FX This work was supported by National Institutes of Health (NIH)/Eunice
Kennedy Shriver National Institute of Child Health and Human Development
(NICHD) Grants U10 HD39005 (to M.D.), U10 HD38992 (to R.S.L., to C.C.),
U10 HD38998 (to R.A.), U10 HD055942 (to R.D.R.), HD055944 (to P.C.), U10
HD055936 (to G.C.), U10HD055925 (to H.Z.); and U10 U54-HD29834 (to the
University of Virginia Center for Research in Reproduction Ligand Assay
and AnalysisCore of the Specialized Cooperative Centers Program in
Reproduction and Infertility Research). Most importantly, this research
was made possible by the funding by American Recovery and Reinvestment
Act.
NR 62
TC 0
Z9 0
U1 9
U2 9
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 2016
VL 31
IS 10
BP 2268
EP 2279
DI 10.1093/humrep/dew175
PG 12
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA DZ7ZH
UT WOS:000386087000014
PM 27402910
ER
PT J
AU Eisenberg, ML
Sundaram, R
Maisog, J
Louis, GMB
AF Eisenberg, Michael L.
Sundaram, Rajeshwari
Maisog, Jose
Louis, Germaine M. Buck
TI Diabetes, medical comorbidities and couple fecundity
SO HUMAN REPRODUCTION
LA English
DT Article
DE diabetes; hypertension; hyperlipidemia; hyperthyroidism; hypothyroidism;
fertility
ID SEMEN QUALITY DATA; TIME-TO-PREGNANCY; BODY-MASS INDEX;
MALE-INFERTILITY; UNITED-STATES; LIPID CONCENTRATIONS; METABOLIC
SYNDROME; LIFE; MELLITUS; INSULIN
AB What is the relationship between couple's health and fecundity in a preconception cohort?
Somatic health may impact fecundity in men and women as couples whose male partner had diabetes or whose female partner had two or more medical conditions had a longer time-to-pregnancy (TTP).
The impact of somatic health on human fecundity is hypothesized given the reported declines in spermatogenesis and ovulation among individuals with certain medical comorbidities.
A population-based prospective cohort study recruiting couples from 16 counties in Michigan and Texas (2005-2009) using sampling frameworks allowing for identification of couples planning pregnancy in the near future. Five hundred and one couples desiring pregnancy and discontinuing contraception were followed-up for 12 months or until a human chorionic gonadotropin pregnancy was detected.
In all, 33 (21.4%) female and 41 (26.6%) male partners had medical conditions at baseline.
Couples' medical comorbidity was associated with pregnancy status. Diabetes in either partner was associated with diminished fecundity, as measured by a longer TTP. Specifically, fecundability odds ratios (FORs) were below 1, indicating a longer TTP, for male partners with diabetes (0.35, 95% confidence interval (CI): 0.14-0.86) even in adjusted models (0.35, 95% CI: 0.13-0.88). Female partners with diabetes had comparable reductions in FORs; however, the analyses did not reach statistical significance (0.26, 95% CI: 0.03-1.98). Female partners with two or more medical conditions had a significantly longer TTP compared with women with no health problems (0.36, 95% CI: 0.14-0.92). Importantly, the presence of medical conditions was not associated with sexual frequency. We cannot rule out residual confounding, Type 2 errors for less prevalent medical conditions, or chance findings in light of the multiple comparisons made in the analysis.
The findings require cautious interpretation given that medical diagnoses are subject to possible reporting errors, although we are unaware of any potential biases that may have been introduced, as participants were unaware of how long it would take to become pregnant upon enrollment.
The current report suggests a relationship between male and female diabetes and fecundity, and possibly somatic health more globally. Moreover, while the mechanism is uncertain, if corroborated, our data suggest that early evaluation and treatment may be warranted for diabetics prior to attempting to conceive.
Intramural research of the Eunice Kennedy Shriver National Institute of Child Health and Human Development (Contract nos. #N01-HD-3-3355, N01-HD-3-3356 and N01-HD-3-3358). The authors have no conflicts of interest to declare.
C1 [Eisenberg, Michael L.] Stanford Univ, Dept Urol, 300 Pasteur Dr, Stanford, CA 94305 USA.
[Eisenberg, Michael L.] Stanford Univ, Dept Obstet & Gynecol, 300 Pasteur Dr, Stanford, CA 94305 USA.
[Sundaram, Rajeshwari] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Biostat & Bioinformat Branch, Div Intramural Populat Hlth Res, 6100 Execut Blvd,Room 7B03, Rockville, MD 20852 USA.
[Maisog, Jose] Glotech Inc, 1801 Res Blvd,Suite 605, Rockville, MD 20852 USA.
[Louis, Germaine M. Buck] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, 6100 Execut Blvd,Room 7B03, Rockville, MD 20852 USA.
RP Eisenberg, ML (reprint author), Stanford Univ, Sch Med, Dept Urol, Male Reprod Med & Surg, 300 Pasteur Dr, Stanford, CA 94305 USA.
EM eisenberg@stanford.edu
OI Sundaram, Rajeshwari/0000-0002-6918-5002; Buck Louis,
Germaine/0000-0002-1774-4490
FU Intramural research of the Eunice Kennedy Shriver National Institute of
Child Health and Human Development [N01-HD-3-3355, N01-HD-3-3356,
N01-HD-3-3358]
FX Intramural research of the Eunice Kennedy Shriver National Institute of
Child Health and Human Development (Contract nos. # N01-HD-3-3355,
N01-HD-3-3356 and N01-HD-3-3358).
NR 41
TC 0
Z9 0
U1 2
U2 2
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 2016
VL 31
IS 10
BP 2369
EP 2376
DI 10.1093/humrep/dew200
PG 8
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA DZ7ZH
UT WOS:000386087000025
PM 27591240
ER
PT J
AU Fleg, JL
Evans, GW
Margolis, KL
Barzilay, J
Basile, JN
Bigger, JT
Cutler, JA
Grimm, R
Pedley, C
Peterson, K
Pop-Busui, R
Sperl-Hillen, J
Cushman, WC
AF Fleg, Jerome L.
Evans, Gregory W.
Margolis, Karen L.
Barzilay, Joshua
Basile, Jan N.
Bigger, J. Thomas
Cutler, Jeffrey A.
Grimm, Richard
Pedley, Carolyn
Peterson, Kevin
Pop-Busui, Rodica
Sperl-Hillen, JoAnn
Cushman, William C.
TI Orthostatic Hypotension in the ACCORD (Action to Control Cardiovascular
Risk in Diabetes) Blood Pressure Trial: Prevalence, Incidence, and
Prognostic Significance
SO HYPERTENSION
LA English
DT Article
DE cardiovascular diseases; clinical trials; randomized; diabetes mellitus;
type 2; hypertension; hypotension; orthostatic
ID POSTURAL HYPOTENSION; ATHEROSCLEROSIS RISK; HEART-FAILURE; PROGRAM;
INSULIN; VASODILATION; HYPERTENSION; COMMUNITIES; MORTALITY
AB Orthostatic hypotension (OH) is associated with hypertension and diabetes mellitus. However, in populations with both hypertension and diabetes mellitus, its prevalence, the effect of intensive versus standard systolic blood pressure (BP) targets on incident OH, and its prognostic significance are unclear. In 4266 participants in the ACCORD (Action to Control Cardiovascular Risk in Diabetes) BP trial, seated BP was measured 3x, followed by readings every minute for 3 minutes after standing. Orthostatic BP change, calculated as the minimum standing minus the mean seated systolic BP and diastolic BP, was assessed at baseline, 12 months, and 48 months. The relationship between OH and clinical outcomes (total and cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, heart failure hospitalization or death and the primary composite outcome of nonfatal myocardial infarction, nonfatal stroke, and cardiovascular death) was assessed using proportional hazards analysis. Consensus OH, defined by orthostatic decline in systolic BP 20 mmHg or diastolic BP 10 mmHg, occurred at 1 time point in 20% of participants. Neither age nor systolic BP treatment target (intensive, <120 mmHg versus standard, <140 mmHg) was related to OH incidence. Over a median follow-up of 46.9 months, OH was associated with increased risk of total death (hazard ratio, 1.61; 95% confidence interval, 1.11-2.36) and heart failure death/hospitalization (hazard ratio, 1.85, 95% confidence interval, 1.17-2.93), but not with the primary outcome or other prespecified outcomes. In patients with type 2 diabetes mellitus and hypertension, OH was common, not associated with intensive versus standard BP treatment goals, and predicted increased mortality and heart failure events.
C1 [Fleg, Jerome L.; Cutler, Jeffrey A.] NHLBI, Bldg 10, Bethesda, MD 20892 USA.
[Evans, Gregory W.; Pedley, Carolyn] Wake Forest Univ, Bowman Gray Sch Med, Winston Salem, NC USA.
[Margolis, Karen L.; Sperl-Hillen, JoAnn] Hlth Partners Inst Educ & Res, Minneapolis, MN USA.
[Barzilay, Joshua] Kaiser Permanente Georgia, Atlanta, GA USA.
[Basile, Jan N.] Med Univ South Carolina, Charleston, SC USA.
[Bigger, J. Thomas] Columbia Univ, Sch Med, New York, NY USA.
[Grimm, Richard] Berman Ctr Outcomes & Clin Res, Minneapolis, MN USA.
[Peterson, Kevin] Univ Minnesota, Sch Med, Minneapolis, MN 55455 USA.
[Pop-Busui, Rodica] Univ Michigan, Sch Med, Ann Arbor, MI USA.
[Cushman, William C.] Vet Affairs Med Ctr, Memphis, TN USA.
RP Fleg, JL (reprint author), NHLBI, Div Cardiovasc Sci, 6701 Rockledge Dr,Room 8154, Bethesda, MD 20892 USA.
EM flegj@nhlbi.nih.gov
FU National Heart, Lung, and Blood Institute
FX The ACCORD (Action to Control Cardiovascular Risk in Diabetes) Blood
Pressure trial was funded by a contract from the National Heart, Lung,
and Blood Institute.
NR 24
TC 3
Z9 3
U1 3
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0194-911X
EI 1524-4563
J9 HYPERTENSION
JI Hypertension
PD OCT
PY 2016
VL 68
IS 4
BP 888
EP 895
DI 10.1161/HYPERTENSIONAHA.116.07474
PG 8
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA DX1LB
UT WOS:000384127800015
PM 27504006
ER
PT J
AU Sung, VW
Borello-France, D
Dunivan, G
Gantz, M
Lukacz, ES
Moalli, P
Newman, DK
Richter, HE
Ridgeway, B
Smith, AL
Weidner, AC
Meikle, S
AF Sung, Vivian W.
Borello-France, Diane
Dunivan, Gena
Gantz, Marie
Lukacz, Emily S.
Moalli, Pamela
Newman, Diane K.
Richter, Holly E.
Ridgeway, Beri
Smith, Ariana L.
Weidner, Alison C.
Meikle, Susan
CA Pelvic Floor Disorders Network
TI Methods for a multicenter randomized trial for mixed urinary
incontinence: rationale and patient-centeredness of the ESTEEM trial
SO INTERNATIONAL UROGYNECOLOGY JOURNAL
LA English
DT Article
DE Female; Mixed urinary incontinence; Clinical trials; Sling; Behavioral
therapy
ID QUALITY-OF-LIFE; PELVIC FLOOR DISORDERS; STRESS-INCONTINENCE;
BEHAVIORAL-THERAPY; US WOMEN; OVERACTIVE BLADDER; URGE INCONTINENCE;
TRACT SYMPTOMS; ORGAN PROLAPSE; PREVALENCE
AB Introduction and hypothesis Mixed urinary incontinence (MUI) can be a challenging condition to manage. We describe the protocol design and rationale for the Effects of Surgical Treatment Enhanced with Exercise for Mixed Urinary Incontinence (ESTEEM) trial, designed to compare a combined conservative and surgical treatment approach versus surgery alone for improving patient-centered MUI outcomes at 12 months.
Methods ESTEEM is a multisite, prospective, randomized trial of female participants with MUI randomized to a standardized perioperative behavioral/pelvic floor exercise intervention phis midurethral sling versus midurethral sling alone. We describe our methods and four challenges encountered during the design phase: defusing the study population, selecting relevant patient-centered outcomes, determining sample size estimates using a patient-reported outcome measure, and designing an analysis plan that accommodates MUI failure rates. A central theme in the design was patient centeredness, which guided many key decisions. Our primary outcome is patient reported MUI symptoms measured using the Urogenital Distress Inventory (UDI) score at 12 months. Secondary outcomes include quality of life, sexual function, cost-effectiveness, time to failure, and need for additional treatment.
Results The final study design was implemented in November 2013 across eight clinical sites in the Pelvic Floor Disorders Network. As of 27 February 2016, 433 total/472 targeted participants had been randomized.
Conclusions We describe the ESTEEM protocol and our methods for reaching consensus for methodological challenges in designing a trial for MUI by maintaining the patient perspective at the core of key decisions. This trial will provide information that can directly impact patient care and clinical decision making.
C1 [Sung, Vivian W.] Brown Univ, Dept Obstet & Gynecol, Alpert Med Sch, Div Urogynecol & Reconstruct Pelv Surg, 101 Plain St 5th Floor, Providence, RI 02903 USA.
[Sung, Vivian W.] Brown Univ, Warren Alpert Med Sch, Women & Infants Hosp Rhode Isl, Div Urogynecol & Reconstruct Pelv Surg, 101 Plain St 5th Floor, Providence, RI 02903 USA.
[Borello-France, Diane] Duquesne Univ, Dept Phys Therapy, Rangos Sch Hlth Sci, Pittsburgh, PA 15219 USA.
[Dunivan, Gena] Univ New Mexico, Dept Obstet & Gynecol, Div Urogynecol, Albuquerque, NM 87131 USA.
[Gantz, Marie] RTI Int, Social Stat & Environm Sci, Res Triangle Pk, NC USA.
[Lukacz, Emily S.] UC San Diego Hlth Syst, Dept Reprod Med, Div Female Pelv Med & Reconstruct Surg, San Diego, CA USA.
[Moalli, Pamela] Univ Pittsburgh, Med Ctr, Dept Obstet Gynecol & Reprod Sci, Womens Ctr Bladder & Pelv Hlth,Div Urogynecol & R, Pittsburgh, PA USA.
[Newman, Diane K.; Smith, Ariana L.] Univ Penn Hlth Syst, Dept Surg, Div Urol, Philadelphia, PA USA.
[Richter, Holly E.] Univ Alabama Birmingham, Dept Obstet & Gynecol, Div Urogynecol & Pelv Reconstruct Surg, Birmingham, AL 35294 USA.
[Ridgeway, Beri] Cleveland Clin, Ctr Urogynecol & Reconstruct Pelv Surg, Obstet Gynecol & Womens Hlth Inst, Cleveland, OH 44106 USA.
[Weidner, Alison C.] Duke Univ, Med Ctr, Dept Obstet & Gynecol, Div Urogynecol, Durham, NC 27710 USA.
[Meikle, Susan] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
RP Sung, VW (reprint author), Brown Univ, Dept Obstet & Gynecol, Alpert Med Sch, Div Urogynecol & Reconstruct Pelv Surg, 101 Plain St 5th Floor, Providence, RI 02903 USA.; Sung, VW (reprint author), Brown Univ, Warren Alpert Med Sch, Women & Infants Hosp Rhode Isl, Div Urogynecol & Reconstruct Pelv Surg, 101 Plain St 5th Floor, Providence, RI 02903 USA.
EM vsung@wihri.org
OI Markland, Alayne/0000-0002-6567-6744
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development [U10 HD041261, U10 HD069013, U10 HD054214, U10 HD054215, U10
HD041267, U10 HD069025, U10 HD069010, U10 HD069006, U01 HD069031];
National Institutes of Health Office of Research on Women's Health
FX Supported by grants from the Eunice Kennedy Shriver National Institute
of Child Health and Human Development (U10 HD041261, U10 HD069013, U10
HD054214, U10 HD054215, U10 HD041267, U10 HD069025, U10 HD069010, U10
HD069006, U01 HD069031) and the National Institutes of Health Office of
Research on Women's Health.
NR 60
TC 0
Z9 0
U1 2
U2 2
PU SPRINGER LONDON LTD
PI LONDON
PA 236 GRAYS INN RD, 6TH FLOOR, LONDON WC1X 8HL, ENGLAND
SN 0937-3462
EI 1433-3023
J9 INT UROGYNECOL J
JI Int. Urogynecol. J.
PD OCT
PY 2016
VL 27
IS 10
BP 1479
EP 1490
DI 10.1007/s00192-016-3031-7
PG 12
WC Obstetrics & Gynecology; Urology & Nephrology
SC Obstetrics & Gynecology; Urology & Nephrology
GA EA1LR
UT WOS:000386354200004
PM 27287818
ER
PT J
AU Meyer, BJ
Byrne, M
Parletta, N
Gow, R
Hibbeln, JR
AF Meyer, Barbara J.
Byrne, Mitchell
Parletta, Natalie
Gow, Rachel
Hibbeln, Joseph R.
TI Fish Oil and Impulsive Aggressive Behavior
SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY
LA English
DT Letter
ID YOUNG-ADULT PRISONERS; DISORDER; CHILDREN; TRIAL
C1 [Meyer, Barbara J.] Univ Wollongong, Sch Med, Northfields Ave, Wollongong, NSW 2522, Australia.
[Byrne, Mitchell] Univ Wollongong, Sch Psychol, Wollongong, NSW 2522, Australia.
[Parletta, Natalie] Univ S Australia, Sansom Inst Hlth Res, Sch Populat Hlth, Adelaide, SA, Australia.
[Gow, Rachel; Hibbeln, Joseph R.] NIAAA, Sect Nutr Neurosci, Lab Membrane Biol & Biophys, NIH, Bethesda, MD USA.
RP Meyer, BJ (reprint author), Univ Wollongong, Sch Med, Northfields Ave, Wollongong, NSW 2522, Australia.
EM bmeyer@uow.edu.au
OI Byrne, Mitchell/0000-0003-0823-2917
NR 5
TC 0
Z9 0
U1 4
U2 4
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1044-5463
EI 1557-8992
J9 J CHILD ADOL PSYCHOP
JI J. Child Adolesc. Psychopharmacol.
PD OCT
PY 2016
VL 26
IS 8
BP 766
EP 766
DI 10.1089/cap.2015.0065
PG 1
WC Pediatrics; Pharmacology & Pharmacy; Psychiatry
SC Pediatrics; Pharmacology & Pharmacy; Psychiatry
GA DZ8QN
UT WOS:000386136000017
PM 26217883
ER
PT J
AU da Cunha, MG
Franchin, M
de Paula-Eduardo, LF
Freires, IA
Beutler, JA
de Alencar, SM
Ikegaki, M
Tabchoury, CPM
Cunha, TM
Rosalen, PL
AF da Cunha, Marcos Guilherme
Franchin, Marcelo
de Paula-Eduardo, Laila Facin
Freires, Irlan Almeida
Beutler, John A.
de Alencar, Severino Matias
Ikegaki, Masaharu
Machado Tabchoury, Cinthia Pereira
Cunha, Thiago Mattar
Rosalen, Pedro Luiz
TI Anti-inflammatory and anti-biofilm properties of ent-nemorosone from
Brazilian geopropolis
SO JOURNAL OF FUNCTIONAL FOODS
LA English
DT Article
DE Geopropolis; ent-Nemorosone; Anti-inflammatory; Anti-biofilm
ID NF-KAPPA-B; MECHANICAL INFLAMMATORY HYPERNOCICEPTION; ACTIVATED
PROTEIN-KINASES; STREPTOCOCCUS-MUTANS; RED PROPOLIS;
MELIPONA-SCUTELLARIS; TNF-ALPHA; 7-EPICLUSIANONE; BENZOPHENONE;
RECRUITMENT
AB ent-Nemorosone is a benzophenone isolated from geopropolis from Melipona scutellaris whose biological properties remain unexplored. Herein, we evaluated the anti-inflammatory activity of ent-nemorosone by in vivo neutrophil migration and TNF-alpha quantification, as well as by in vitro TNF-alpha quantification, ERK 1/2 phosphorylation, NF-kB activation and nuclear translocation of p65 in stimulated macrophages. ent-Nemorosone was also tested for its antimicrobial effects against Streptococcus mutans biofilm adhesion, polysaccharide production, and viability ent-Nemorosone reduced the influx of neutrophils and TNF-alpha release into the peritoneal cavity of mice, as well as the in vitro TNF-alpha levels, ERK 1/2 phosphorylation, NF-kB activation and nuclear p65 translocation. Furthermore, this compound inhibited biofilm adhesion and reduced the amount of extra- and intracellular polysaccharides synthesized by S. mutans. Thus, ent-nemorosone showed promising anti-inflammatory activity by acting on TNF-alpha release in macrophages, as well as anti-biofilm properties by reducing S. mutans polysaccharide production. (C) 2016 Elsevier Ltd. All rights reserved.
C1 [da Cunha, Marcos Guilherme; Franchin, Marcelo; de Paula-Eduardo, Laila Facin; Freires, Irlan Almeida; Machado Tabchoury, Cinthia Pereira; Rosalen, Pedro Luiz] Univ Estadual Campinas, UNICAMP, Piracicaba Dent Sch, Dept Physiol Sci, Campinas, SP, Brazil.
[da Cunha, Marcos Guilherme; Beutler, John A.] NCI, Mol Targets Lab, NIH, Frederick, MD 21701 USA.
[de Alencar, Severino Matias] Univ Sao Paulo, Luiz de Queiroz Coll Agr, Dept Agrifood Ind Food & Nutr, Piracicaba, SP, Brazil.
[Ikegaki, Masaharu] Univ Fed Alfenas, Coll Pharmaceut Sci, Alfenas, MG, Brazil.
[Cunha, Thiago Mattar] Univ Sao Paulo, Ribeirao Preto Med Sch, Ribeirao Preto, SP, Brazil.
RP Rosalen, PL (reprint author), Univ Estadual Campinas, UNICAMP, Piracicaba Dent Sch, Dept Physiol Sci, Campinas, SP, Brazil.
EM rosalen@fop.unicamp.br
RI Alencar, Severino/B-7743-2012; CEPID, CRID/J-2644-2015; Cunha,
Thiago/B-7729-2012;
OI Alencar, Severino/0000-0002-6637-7973; Cunha,
Thiago/0000-0003-1084-0065; Freires, Irlan/0000-0002-1079-6941
FU FAPESP [2011/16501-3, 2011/23635-6, 2012/22378-2, 2012/22002-2];
Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research [1ZIABC011469-04]
FX This research was supported by FAPESP (No. 2011/16501-3, 2011/23635-6,
2012/22378-2 and 2012/22002-2) and by the Intramural Research Program of
the NIH, National Cancer Institute, Center for Cancer Research (No.
1ZIABC011469-04). The authors would like to thank Mr. Jose Emidio Borges
de Souza for providing the geopropolis samples. We thank Sergey Tarasov
and Marzena Dyba (Biophysics Resource Core, Structural Biophysics
Laboratory, CCR) for assistance with mass spectrometry.
NR 33
TC 0
Z9 0
U1 7
U2 7
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1756-4646
J9 J FUNCT FOODS
JI J. Funct. Food.
PD OCT
PY 2016
VL 26
BP 27
EP 35
DI 10.1016/j.jff.2016.07.009
PG 9
WC Food Science & Technology
SC Food Science & Technology
GA DZ9KG
UT WOS:000386193400003
ER
PT J
AU Mudd, JC
Brenchley, JM
AF Mudd, Joseph C.
Brenchley, Jason M.
TI Gut Mucosal Barrier Dysfunction, Microbial Dysbiosis, and Their Role in
HIV-1 Disease Progression
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
DE HIV-1 pathognesis; gastrointestinal tract; microbiome; Th17; cART;
residual inflammation; probiotics
ID HUMAN-IMMUNODEFICIENCY-VIRUS; SYSTEMIC IMMUNE ACTIVATION;
T-CELL-ACTIVATION; INFLAMMATORY-BOWEL-DISEASE; INFECTED RHESUS MACAQUES;
INNATE LYMPHOID-CELLS; ANTIRETROVIRAL THERAPY; SIV INFECTION; INTESTINAL
INFLAMMATION; VIRAL SUPPRESSION
AB Distinct pathological events occur within the gastrointestinal (GI) tract of Asian macaques with progressive simian immunodeficiency virus (SIV) infection and humans with human immunodeficiency virus type 1 (HIV-1) infection that are critical in shaping disease course. These events include depletion and functional alteration of GI-resident CD4(+) T cells, loss of antigen-presenting cells, loss of innate lymphocytes, and possible alterations to the composition of the gut microbiota. These contribute to structural damage to the GI tract and systemic translocation of GI tract microbial products. These translocated microbial products directly stimulate the immune system, and there is now overwhelming evidence that this drives chronic immune activation in HIV-1 and SIV infection. While combined antiretroviral therapy (cART) in HIV-1-infected subjects generally allows for immune reconstitution in peripheral blood, reconstitution of the GI tract occurs at a much slower pace, and both immunological and structural abnormalities persist in the GI tract. Importantly, studies of large cohorts of individuals have linked suboptimal GI reconstitution to residual inflammation and heightened morbidities in HIV-1-infected cART recipients. As a result, current era treatments aimed at augmenting restoration of the GI tract hold promise in returning cART recipients to full health.
C1 [Mudd, Joseph C.; Brenchley, Jason M.] NIAID, Parasit Dis Lab, NIH, 4 Mem Dr, Bethesda, MD 20814 USA.
RP Brenchley, JM (reprint author), NIAID, Parasit Dis Lab, NIH, 4 Mem Dr, Bethesda, MD 20814 USA.
EM jbrenchl@niaid.nih.gov
FU Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, National Institutes of Health
FX This work was supported by the Division of Intramural Research, National
Institute of Allergy and Infectious Diseases, National Institutes of
Health.
NR 98
TC 2
Z9 2
U1 6
U2 6
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 2016
VL 214
SU 2
BP S58
EP S66
DI 10.1093/infdis/jiw258
PG 9
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA DZ8UP
UT WOS:000386147600004
PM 27625432
ER
PT J
AU Du Toit, J
Millum, J
AF Du Toit, Jessica
Millum, Joseph
TI Are Indirect Benefits Relevant to Health Care Allocation Decisions?
SO JOURNAL OF MEDICINE AND PHILOSOPHY
LA English
DT Article
DE direct benefits; indirect benefits; resource allocation
ID INFLUENZA; HEADACHES; COUNT; LIVES
AB When allocating scarce healthcare resources, the expected benefits of alternative allocations matter. But, there are different kinds of benefits. Some are direct benefits to the recipient of the resource such as the health improvements of receiving treatment. Others are indirect benefits to third parties such as the economic gains from having a healthier workforce. This article considers whether only the direct benefits of alternative healthcare resource allocations are relevant to allocation decisions, or whether indirect benefits are relevant too. First, we distinguish different conceptions of direct and indirect benefits and argue that only a recipient conception could be morally relevant. We analyze four arguments for thinking that indirect benefits should not count and argue that none is successful in showing that the indirectness of a benefit is a good reason not to count it. We conclude that direct and indirect benefits should be evaluated in the same way.
C1 [Du Toit, Jessica; Millum, Joseph] NIH, Bldg 10, Bethesda, MD 20892 USA.
RP Du Toit, J (reprint author), NIH, Dept Bioeth, 10 Ctr Dr,Bldg 10,Room 1C118, Bethesda, MD 20892 USA.
EM jess.dutoit@gmail.com
FU National Institutes of Health Clinical Center; Fogarty International
Center
FX The authors would like to thank audiences at the NIH Clinical Center
Department of Bioethics and the New Scholars in Bioethics 4th Annual
Symposium for helpful comments on earlier drafts of this article. This
work was supported, in part, by intramural funds from the National
Institutes of Health Clinical Center and Fogarty International Center.
The views expressed are the authors' own. They do not represent the
position or policy of the National Institutes of Health, US Public
Health Service, or the Department of Health and Human Services.
NR 29
TC 2
Z9 2
U1 1
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0360-5310
EI 1744-5019
J9 J MED PHILOS
JI J. Med. Philos.
PD OCT
PY 2016
VL 41
IS 5
BP 540
EP 557
DI 10.1093/jmp/jhw018
PG 18
WC Ethics; Social Sciences, Biomedical
SC Social Sciences - Other Topics; Biomedical Social Sciences
GA DZ8WB
UT WOS:000386152000007
PM 27465773
ER
PT J
AU Moaddel, R
Fabbri, E
Khadeer, MA
Carlson, OD
Gonzalez-Freire, M
Zhang, PB
Semba, RD
Ferrucci, L
AF Moaddel, Ruin
Fabbri, Elisa
Khadeer, Mohammed A.
Carlson, Olga D.
Gonzalez-Freire, Marta
Zhang, Pingbo
Semba, Richard D.
Ferrucci, Luigi
TI Plasma Biomarkers of Poor Muscle Quality in Older Men and Women from the
Baltimore Longitudinal Study of Aging
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Sarcopenia; Muscles; Metabolomics
ID SKELETAL-MUSCLE; INDOLEAMINE 2,3-DIOXYGENASE; BODY-COMPOSITION;
HEALTHY-MEN; STRENGTH; MASS; MORTALITY; POLYAMINES; ADULTS; AGE
AB Aging is characterized by progressive decline in muscle mass, strength, and quality all of which contribute to functional impairment, falls, mobility disability, and frailty. Circulating factors may provide clues on the mechanisms for decline in muscle quality with aging. Characterizing the metabolic profile associated with reduced muscle quality in older persons could have important translational implications for the early identification of subjects at high risk of developing sarcopenia and the identification of targets for new preventive strategies and treatments. In a pilot cross-sectional, case-control study nested in the Baltimore Longitudinal Study on Aging, we compared circulating metabolites between 79 participants with low muscle quality ratio and 79 controls with high muscle quality, matched by age, sex, and height. The concentrations of 180 metabolites were determined by LC MS/MS, using the Biocrates p180 system, a targeted metabolomics approach. Participants with low muscle quality had significantly higher levels of leucine, isoleucine, tryptophan, serotonin, and methionine, while those with high muscle quality had significantly lower levels of putrescine and the selected phophatidylcholine (PCs) and lysoPCs. The results of this study open a new road for future investigations aimed at identifying new metabolic pathways involved in the decline of muscle quality with aging.
C1 [Moaddel, Ruin; Fabbri, Elisa; Khadeer, Mohammed A.; Carlson, Olga D.; Gonzalez-Freire, Marta; Ferrucci, Luigi] NIA, Intramural Res Programs, NIH, Baltimore, MD 21224 USA.
[Zhang, Pingbo; Semba, Richard D.] Johns Hopkins Univ, Sch Med, Wilmer Eye Inst, Baltimore, MD 21205 USA.
RP Moaddel, R (reprint author), 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM moaddelru@mail.nih.gov
FU Intramural Research Program of the National Institutes of Health;
National Institute on Aging
FX Intramural Research Program of the National Institutes of Health;
National Institute on Aging.
NR 46
TC 1
Z9 1
U1 2
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
EI 1758-535X
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD OCT
PY 2016
VL 71
IS 10
BP 1266
EP 1272
DI 10.1093/gerona/glw046
PG 7
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA DZ7WI
UT WOS:000386078800003
PM 27029859
ER
PT J
AU Shea, MK
Loeser, RF
Hsu, FC
Booth, SL
Nevitt, M
Simonsick, EM
Strotmeyer, ES
Vermeer, C
Kritchevsky, SB
AF Shea, M. Kyla
Loeser, Richard F.
Hsu, Fang-Chi
Booth, Sarah L.
Nevitt, Michael
Simonsick, Eleanor M.
Strotmeyer, Elsa S.
Vermeer, Cees
Kritchevsky, Stephen B.
CA Hlth ABC Study
TI Vitamin K Status and Lower Extremity Function in Older Adults: The
Health Aging and Body Composition Study
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Physical performance; Nutrition; Physical function; Vitamin K
ID MATRIX GLA PROTEIN; PHYSICAL PERFORMANCE; KNEE OSTEOARTHRITIS; MOBILITY
DISABILITY; MEANINGFUL CHANGE; CLINICAL-TRIAL; ASSOCIATION;
CALCIFICATION; WOMEN; INFLAMMATION
AB While low vitamin K status has been associated with several chronic diseases that can lead to lower extremity disability, it is not known if low vitamin K status is associated with worse lower extremity function.
Vitamin K status was measured according to plasma phylloquinone (vitamin K1) and dephosphorylated-uncarboxylated MGP (dp-ucMGP) in 1,089 community-dwelling older adults (mean +/- SD age =74 +/- 3 years; 67% female). Lower extremity function was assessed using the short physical performance battery (SPPB), gait speed, and isokinetic leg strength. Linear regression and mixed models were used to determine the cross-sectional and longitudinal associations between vitamin K status and functional outcome measures.
Cross-sectionally, higher plasma phylloquinone was associated with better SPPB scores and 20-m gait speed (p a parts per thousand currency sign .05). After 4-5 years, those with a parts per thousand yen1.0nM plasma phylloquinone (the concentration achieved when recommended intakes are met) had better SPPB scores (p = .03) and 20-m gait speed (p < .05). Lower plasma dp-ucMGP (reflective of better vitamin K status) was associated with better SPPB scores and leg strength cross-sectionally (p a parts per thousand currency sign .04), but not longitudinally. Neither measure of vitamin K status was associated with walking endurance or with the rate of decline in function.
Older adults with higher vitamin K status had better physical performance scores at baseline, but data are less consistent longitudinally. Since lower extremity disability is a common consequence of multiple chronic diseases for which a role of vitamin K has been suggested, future studies are needed to determine if vitamin K supplementation could improve function in those with vitamin K insufficiency and clarify underlying mechanism(s).
C1 [Shea, M. Kyla; Booth, Sarah L.] Tufts Univ, USDA, Human Nutr Res Ctr Aging, 711 Washington St, Boston, MA 02111 USA.
[Loeser, Richard F.] Univ N Carolina, Div Rheumatol Allergy & Immunol, Chapel Hill, NC USA.
[Hsu, Fang-Chi] Wake Forest Sch Med, Div Publ Hlth Sci, Winston Salem, NC USA.
[Nevitt, Michael] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Simonsick, Eleanor M.] NIA, NIH, Baltimore, MD 21224 USA.
[Strotmeyer, Elsa S.] Univ Pittsburgh, Grad Sch Publ Hlth, Pittsburgh, PA 15260 USA.
[Vermeer, Cees] Maastricht Univ, VitaK, NL-6200 MD Maastricht, Netherlands.
[Kritchevsky, Stephen B.] Wake Forest Sch Med, Sticht Ctr Aging, Winston Salem, NC USA.
RP Shea, MK (reprint author), Tufts Univ, USDA, Human Nutr Res Ctr Aging, 711 Washington St, Boston, MA 02111 USA.
EM kyla.shea@tufts.edu
FU NIH Intramural Research Program; NIA; NINR [R01-NR012459]; NIAMS
[R21AR062284, K01AR063167]; Arthritis Foundation New Investigator Grant;
USDA, Agricultural Research Service Cooperative Agreement
[58-1950-7-707]; [N01-AG-6-2101]; [N01-AG-6-2103]; [N01-AG-6-2106];
[R01-AG028050]
FX This study was supported by the NIH Intramural Research Program, the NIA
and contracts (N01-AG-6-2101, N01-AG-6-2103, and N01-AG-6-2106;
R01-AG028050); the NINR (R01-NR012459); the NIAMS (R21AR062284,
K01AR063167); an Arthritis Foundation New Investigator Grant and the
USDA, Agricultural Research Service Cooperative Agreement
(58-1950-7-707).
NR 30
TC 1
Z9 1
U1 1
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
EI 1758-535X
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD OCT
PY 2016
VL 71
IS 10
BP 1348
EP 1355
DI 10.1093/gerona/glv209
PG 8
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA DZ7WI
UT WOS:000386078800014
PM 26576842
ER
PT J
AU McNeil, SE
AF McNeil, Scott E.
TI Evaluation of nanomedicines: stick to the basics
SO NATURE REVIEWS MATERIALS
LA English
DT Letter
ID DELIVERY; TUMORS
C1 [McNeil, Scott E.] NCI, Nanotechnol Characterizat Lab, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
RP McNeil, SE (reprint author), NCI, Nanotechnol Characterizat Lab, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
EM ncl@mail.nih.gov
NR 9
TC 0
Z9 0
U1 7
U2 7
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2058-8437
J9 NAT REV MATER
JI Nat. Rev. Mater.
PD OCT
PY 2016
VL 1
IS 10
PG 2
WC Materials Science, Multidisciplinary
SC Materials Science
GA EA0ET
UT WOS:000386259300005
ER
PT J
AU Liao, Y
Berghoff, AS
Osswald, M
Ilhan-Mutlu, A
Gil, B
Thome, C
Ratliff, M
Steeg, P
Wick, W
Winkler, F
AF Liao, Y.
Berghoff, A. S.
Osswald, M.
Ilhan-Mutlu, A.
Gil, B.
Thome, C.
Ratliff, M.
Steeg, P.
Wick, W.
Winkler, F.
TI IDENTIFICATION AND CHARACTERIZATION OF BRAIN METASTASIS INITIATING CELLS
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 12th Meeting of the European-Association-of-Neuro-Oncology
CY OCT 12-16, 2016
CL GERMANY
SP European Assoc Neuro Oncol
C1 [Liao, Y.; Berghoff, A. S.; Osswald, M.; Thome, C.; Ratliff, M.; Wick, W.; Winkler, F.] German Canc Res Ctr, Clin Cooperat Unit Neurooncol, German Canc Consortium DKTK, Heidelberg, Germany.
[Liao, Y.; Osswald, M.; Wick, W.; Winkler, F.] Univ Heidelberg Hosp, Neurol Clin, Heidelberg, Germany.
[Liao, Y.; Osswald, M.; Wick, W.; Winkler, F.] Univ Heidelberg Hosp, Natl Ctr Tumor Dis, Heidelberg, Germany.
[Berghoff, A. S.; Ilhan-Mutlu, A.] Med Univ Vienna, Dept Med 1, Clin Div Oncol, Vienna, Austria.
[Berghoff, A. S.; Ilhan-Mutlu, A.] Med Univ Vienna, Vienna, Austria.
[Gil, B.; Steeg, P.] NCI, Womens Malignancies Branch, NIH, Bethesda, MD 20892 USA.
[Gil, B.; Steeg, P.] NCI, Pathol Lab, Ctr Canc Res, NIH, Bldg 10, Bethesda, MD 20892 USA.
[Gil, B.; Steeg, P.] NCI, Biostat & Data Management Sect, NIH, Bethesda, MD 20892 USA.
[Gil, B.; Steeg, P.] NCI, Lab Anim Sci Program, SAIC Frederick, NIH, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
EI 1523-5866
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2016
VL 18
SU 4
MA OS7.1
BP 15
EP 16
PG 2
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA DZ9MT
UT WOS:000386200200053
ER
PT J
AU Mankodi, A
Bishop, CA
Auh, S
Newbould, RD
Fischbeck, KH
Janiczek, RL
AF Mankodi, Ami
Bishop, Courtney A.
Auh, Sungyoung
Newbould, Rexford D.
Fischbeck, Kenneth H.
Janiczek, Robert L.
TI Quantifying disease activity in fatty-infiltrated skeletal muscle by
IDEAL-CPMG in Duchenne muscular dystrophy
SO NEUROMUSCULAR DISORDERS
LA English
DT Article
DE Duchenne muscular dystrophy; Magnetic resonance imaging; IDEAL-CPMG;
Skeletal muscle; Apparent fat fraction; Fatty degeneration; T-2
relaxation times; Water T-2
ID STIMULATED ECHO COMPENSATION; TRANSVERSE RELAXOMETRY; QUANTIFICATION
METHODS; NATURAL-HISTORY; WATER; MRI; PROGRESSION; BOYS; MULTICENTER;
ACCURACY
AB The purpose of this study was to explore the use of iterative decomposition of water and fat with echo asymmetry and least-squares estimation Carr-Purcell-Meiboom-Gill (IDEAL-CPMG) to simultaneously measure skeletal muscle apparent fat fraction and water T-2 (T-2,T-w) in patients with Duchenne muscular dystrophy (DMD). In twenty healthy volunteer boys and thirteen subjects with DMD, thigh muscle apparent fat fraction was measured by Dixon and IDEAL-CPMG, with the IDEAL-CPMG also providing T-2,T-w as a measure of muscle inflammatory activity. A subset of subjects with DMD was followed up during a 48-week clinical study. The study was in compliance with the Patient Privacy Act and approved by the Institutional Review Board. Apparent fat fraction in the thigh muscles of subjects with DMD was significantly increased compared to healthy volunteer boys (p < 0.001). There was a strong correlation between Dixon and IDEAL-CPMG apparent fat fraction. Muscle T-2,T-w measured by IDEAL-CPMG was independent of changes in apparent fat fraction. Muscle T-2,T-w was higher in the biceps femoris and vastus lateralis muscles of subjects with DMD (p < 0.05). There was a strong correlation (p < 0.004) between apparent fat fraction in all thigh muscles and six-minute walk distance (6MWD) in subjects with DMD. IDEAL-CPMG allowed independent and simultaneous quantification of skeletal muscle fatty degeneration and disease activity in DMD. IDEAL-CPMG apparent fat fraction and T-2,T-w may be useful as biomarkers in clinical trials of DMD as the technique disentangles two competing biological processes. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
C1 [Mankodi, Ami; Auh, Sungyoung; Fischbeck, Kenneth H.] NINDS, Neurogenet Branch, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
[Bishop, Courtney A.; Newbould, Rexford D.] Hammersmith Hosp, Imanova Ctr Imaging Sci, London W12 0NN, England.
[Janiczek, Robert L.] GlaxoSmithKline, Expt Med Imaging, Expt Med Unit, Middlesex UB11 1BT, England.
RP Mankodi, A (reprint author), NINDS, Hereditary Muscle Dis Unit, Neurogenet Branch, NIH, 35 Convent Dr,Bldg 35,Room 2A-1002, Bethesda, MD 20892 USA.
EM Ami.Mankodi@nih.gov
FU Intramural NIH HHS [Z99 NS999999]
NR 31
TC 1
Z9 1
U1 2
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2016
VL 26
IS 10
BP 650
EP 658
DI 10.1016/j.nmd.2016.07.013
PG 9
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA EA2FL
UT WOS:000386408100003
PM 27593185
ER
PT J
AU Goldstein, DS
Holmes, C
Sullivan, P
Jinsmaa, Y
Kopin, IJ
Sharabi, Y
AF Goldstein, David S.
Holmes, Courtney
Sullivan, Patricia
Jinsmaa, Yunden
Kopin, Irwin J.
Sharabi, Yehonatan
TI Elevated cerebrospinal fluid ratios of
cysteinyl-dopamine/3,4-dihydroxyphenylacetic acid in parkinsonian
synucleinopathies
SO PARKINSONISM & RELATED DISORDERS
LA English
DT Article
DE Parkinson disease; Multiple system atrophy; Aldehyde dehydrogenase
ID MULTIPLE SYSTEM ATROPHY; DOPAMINE METABOLITE
3,4-DIHYDROXYPHENYLACETALDEHYDE; NEUROGENIC ORTHOSTATIC HYPOTENSION;
ALDEHYDE DEHYDROGENASE-ACTIVITY; PURE AUTONOMIC FAILURE;
ALPHA-SYNUCLEIN; MONOAMINE-OXIDASE; PC12 CELLS; MITOCHONDRIAL
DYSFUNCTION; REACTIVE INTERMEDIATE
AB Introduction: There is intense interest in identifying cerebrospinal fluid (CSF) biomarkers of Parkinson's disease (PD), both for early diagnosis and to track effects of putative treatments. Nigrostriatal dopamine depletion characterizes PD. Predictably, CSF levels of 3,4-dihydroxyphenylacetic acid (DOPAC), the main neuronal metabolite of dopamine, are decreased in PD, even in patients with recent onset of the movement disorder. Whether low CSF DOPAC is associated specifically with parkinsonism has been unclear. In the neuronal cytoplasm dopamine undergoes not only enzymatic oxidation to form DOPAC but also spontaneous oxidation to form 5-S-cysteinyl-dopamine (Cys-DA). Theoretically, oxidative stress or decreased activity of aldehyde dehydrogenase (ALDH) in the residual nigrostriatal dopaminergic neurons would increase CSF Cys-DA levels with respect to DOPAC levels. PD, parkinsonian multiple system atrophy (MSA-P), and pure autonomic failure (PAF) are synucleinopathies; however, PAF does not entail parkinsonism. We examined whether an elevated Cys-DA/DOPAC ratio provides a specific biomarker of parkinsonism in synucleinopathy patients.
Methods: CSF catechols were assayed in PD (n = 24), MSA-P (n = 32), PAF (n = 18), and control subjects (n = 32).
Results: Compared to controls, CSF DOPAC was decreased in PD and MSA-P (p < 0.0001 each). In both diseases Cys-DA/DOPAC ratios averaged more than twice control (0.14 +/- 0.02 and 0.13 +/- 0.02 vs. 0.05 +/- 0.01, p < 0.0001 each), whereas in PAF the mean Cys-DA/DOPAC ratio was normal (0.05 +/- 0.01).
Conclusions: CSF Cys-DA/DOPAC ratios are substantially increased in PD and MSA-P and are normal in PAF. Thus, in synucleinopathies an elevated CSF Cys-DA/DOPAC ratio seems to provide a specific biomarker of parkinsonism. Published by Elsevier Ltd.
C1 [Goldstein, David S.; Holmes, Courtney; Sullivan, Patricia; Jinsmaa, Yunden; Kopin, Irwin J.; Sharabi, Yehonatan] NINDS, Clin Neurocardiol Sect, NIH, 10 Ctr Dr MSC 1620,Bldg 10 Room 5N220, Bethesda, MD 20892 USA.
[Sharabi, Yehonatan] Tel Aviv Univ, Tel Hashomer Affiliated Sackler Fac Med, Sheba Med Ctr, Hypertens Unit, IL-69978 Tel Aviv, Israel.
RP Goldstein, DS (reprint author), NINDS, Clin Neurocardiol Sect, NIH, 10 Ctr Dr MSC 1620,Bldg 10 Room 5N220, Bethesda, MD 20892 USA.
EM goldsteind@ninds.nih.gov
FU Intramural Research Program of the NIH, NINDS
FX This research was supported by the Intramural Research Program of the
NIH, NINDS.
NR 53
TC 1
Z9 1
U1 1
U2 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1353-8020
EI 1873-5126
J9 PARKINSONISM RELAT D
JI Parkinsonism Relat. Disord.
PD OCT
PY 2016
VL 31
BP 79
EP 86
DI 10.1016/j.parkreldis.2016.07.009
PG 8
WC Clinical Neurology
SC Neurosciences & Neurology
GA EA1AG
UT WOS:000386320100013
PM 27474472
ER
PT J
AU Lin, YH
Brown, JA
DiMartino, C
Dahms, I
Salem, N
Hibbeln, JR
AF Lin, Yu-Hong
Brown, James A.
DiMartino, Carmine
Dahms, Irina
Salem, Norman, Jr.
Hibbeln, Joseph R.
TI Differences in long chain polyunsaturates composition and metabolism in
male and female rats
SO PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS
LA English
DT Article
DE Essential fatty acid; Alpha-linolenic acid; Linoleic acid; DHA; DPA;
Omega-3; Omega-6; Gender; Stable isotope; GC/MS
ID ALPHA-LINOLENIC ACID; DOCOSAHEXAENOIC ACID; FATTY-ACIDS;
GONADAL-HORMONES; SEX-DIFFERENCES; GENDER-DIFFERENCES; ARACHIDONIC-ACID;
LIVER MICROSOMES; METHYL-ESTERS; FISH-OIL
AB Human studies and some animal work have shown more docosahexaenoic acid (DHA) and arachidonic acid (ARA) was accumulated or converted from precursors in females compared to males. This study explored in-depth the effect of gender on fatty acid composition and polyunsaturated fatty acid metabolism in rats fed one of two well-defined diets containing 10% total fat. One diet contained 15% of linoleic acid (LA) and 3% of alpha-linolenic acid (ALA) of the total fatty acids (LA+ALA diet), while the other diet contained 15% LA and 0.05% ALA (LA diet). At the age of 20 weeks, all animals were orally administered a single dose of a mixture of deuterium-labeled LA and ALA. Caudal venous blood was then drawn at 0, 2, 4, 8, 12, 24, 48, 96 and 168 h. The concentrations of the deuterated precursors and their metabolites in plasma total lipids were quantified by GC/MS negative chemical ionization. Endogenous fatty acids were quantified by GC/FID analysis. When expressed as the percentage of oral dosage, female rats accumulated more precursors and more products, deuterated DHA and deuterated n-6 docosapentaenoic acid (H-2(5)-DPAn-6), in plasma than did male rats in both the LA+ALA diet and the LA diet. For the endogenous non-labeled PUFA, greater concentrations of DHA and DPAn-6 were similarly observed in female rats compared to males within each diet. A lower concentration of non-labeled ARA was observed only in female rats fed the LA+ALA diet. In summary, greater endogenous and exogenous DHA and DPAn-6 was observed in female rat plasma and this was independent of dietary ALA status. Published by Elsevier Ltd.
C1 [Lin, Yu-Hong; Brown, James A.; DiMartino, Carmine; Hibbeln, Joseph R.] NIAAA, Sect Nutr Neurosci, LMBB, NIH, Bethesda, MD 20892 USA.
[Dahms, Irina; Salem, Norman, Jr.] DSM Nutr Prod LLC, Nutr Lipids, Columbia, MD USA.
RP Lin, YH (reprint author), NIAAA, Sect Nutr Neurosci, LMBB, NIH, Bethesda, MD 20892 USA.
EM yuhong.lin@nih.gov
FU Intramural Research Program of the National Institute on Alcohol Abuse
and Alcoholism, NIH, United States [Z99 AA999999]
FX The authors wish to acknowledge Dr. Lee Chedester and Dr. Raouf Kechrid
for their expert assistance with the animal work. This project was
funded by the Intramural Research Program of the National Institute on
Alcohol Abuse and Alcoholism, NIH, United States (Grant no. Z99
AA999999).
NR 46
TC 0
Z9 0
U1 3
U2 3
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0952-3278
EI 1532-2823
J9 PROSTAG LEUKOTR ESS
JI Prostaglandins Leukot. Essent. Fatty Acids
PD OCT
PY 2016
VL 113
BP 19
EP 27
DI 10.1016/j.plefa.2016.08.008
PG 9
WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology &
Metabolism
SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology &
Metabolism
GA EA2ER
UT WOS:000386406100003
PM 27720036
ER
PT J
AU Quinn, G
Vadaparampil, S
Kanetsky, P
Simmons, V
Hudson, J
Sutton, S
Wheldon, C
Sanchez, J
Schabath, M
AF Quinn, Gwendolyn
Vadaparampil, Susan
Kanetsky, Peter
Simmons, Vani
Hudson, Janella
Sutton, Steven
Wheldon, Christopher
Sanchez, Julian
Schabath, Matthew
TI Sexual and Gender Minorities Cancer Screening and Health Behaviours
SO PSYCHO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Quinn, Gwendolyn; Vadaparampil, Susan; Kanetsky, Peter; Simmons, Vani; Hudson, Janella; Sutton, Steven; Sanchez, Julian; Schabath, Matthew] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
[Wheldon, Christopher] NCI, 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 1057-9249
EI 1099-1611
J9 PSYCHO-ONCOLOGY
JI Psycho-Oncol.
PD OCT
PY 2016
VL 25
IS SP. S3
MA 141
BP 47
EP 47
PG 1
WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences,
Biomedical
SC Oncology; Psychology; Biomedical Social Sciences
GA DZ6AA
UT WOS:000385942700100
ER
PT J
AU Bell, C
Weaver, M
Dickens, D
Diver, J
Smythe, E
Iacoboni, A
Hinds, P
AF Bell, Cynthia
Weaver, Meaghann
Dickens, David
Diver, Jessica
Smythe, Elizabeth
Iacoboni, Alyssa
Hinds, Pamela
TI Assessing Adolescent and Young Adult Acceptability of a Preliminary
Instrument Measuring Readiness to Engage in End-of-Life Discussions
within Clinical Settings
SO PSYCHO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Bell, Cynthia] Wayne State Univ, Detroit, MI USA.
[Diver, Jessica] NIH, Washington, DC USA.
[Dickens, David; Iacoboni, Alyssa] Helen DeVos Childrens Hosp, Grand Rapids, MI USA.
[Smythe, Elizabeth] Childrens Hosp Michigan, Detroit, MI 48201 USA.
[Hinds, Pamela] Childrens Natl Hlth Syst, Washington, DC USA.
[Weaver, Meaghann] Childrens Hosp & Med Ctr, Pediat Palliat Care Program, Omaha, NE 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 1057-9249
EI 1099-1611
J9 PSYCHO-ONCOLOGY
JI Psycho-Oncol.
PD OCT
PY 2016
VL 25
IS SP. S3
MA 514
BP 171
EP 171
PG 1
WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences,
Biomedical
SC Oncology; Psychology; Biomedical Social Sciences
GA DZ6AA
UT WOS:000385942700387
ER
PT J
AU Aziz, N
Rahman, A
AF Aziz, Noreen
Rahman, A.
TI Lifestyle Health Behavior Interventions among Long Term Cancer Survivors
SO PSYCHO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Aziz, Noreen] NIH, Bldg 10, Bethesda, MD 20892 USA.
[Rahman, A.] Univ Maryland, College Pk, MD 20742 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1057-9249
EI 1099-1611
J9 PSYCHO-ONCOLOGY
JI Psycho-Oncol.
PD OCT
PY 2016
VL 25
IS SP. S3
MA 594
BP 189
EP 189
PG 1
WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences,
Biomedical
SC Oncology; Psychology; Biomedical Social Sciences
GA DZ6AA
UT WOS:000385942700432
ER
PT J
AU Louis, GMB
Sapra, KJ
Barr, DB
Lu, ZH
Sundaram, R
AF Louis, Germaine M. Buck
Sapra, Katherine J.
Barr, Dana Boyd
Lu, Zhaohui
Sundaram, Rajeshwari
TI Preconception perfluoroalkyl and polyfluoroalkyl substances and incident
pregnancy loss, LIFE Study
SO REPRODUCTIVE TOXICOLOGY
LA English
DT Article
DE Cohort; Epidemiology; Miscarriage; Perfluoroalkyl; Perfluoroalkyl acids;
Polyfluoroalkyl; Pregnancy loss; Reproductive toxicity
ID PERFLUOROOCTANOIC ACID EXPOSURE; HUMAN SEMEN QUALITY; PERFLUORINATED
CHEMICALS; SERUM-LEVELS; TIME; WOMEN; PERFLUOROCHEMICALS; FERTILITY;
SULFONATE; TOXICITY
AB Equivocal findings are reported for perfluoroalkyl and polyfluoroalkyl substances (PFASs) and self-reported pregnancy loss. We prospectively assessed PFASs and pregnancy loss in a cohort comprising 501 couples recruited preconception and followed daily through 7 post-conception weeks. Seven PFAS5 were quantified: 2-N-ethyl-perfluorooctane sulfonamide acetate (Et-PFOSA-AcOH); 2-N-methyl-perfluorooctane sulfonamido acetate (Me-PFOSA-AcOH); perfluorodecanoate (PFDeA); perfluorononanoate (PFNA); perfluorooctane sulfonamide (PFOSA); perfluorooctane sulfonate (PFOS); and perfluorooctanoate (PFOA). Women used home pregnancy test kits. Loss denoted conversion from a positive to a negative pregnancy test, onset of menses or clinical confirmation (n = 98; 28%). Chemicals were log transformed and rescaled by their standard deviations to estimate adjusted hazard ratios (HRs) and 95% confidence intervals. No significantly elevated HRs were observed for any PFASs suggesting no association with loss: Et-PFOSA-AcOH (1.04; 0.87, 1.23), Me-PFOSA-AcOH (0.79; 0.61, 1.00; p < 0.05), PFDeA (0.83; 0.66, 1.04), PFNA (0.86; 0.70, 1.06), PFOSA (0.74; 0.50, 1.09), PFOS (0.81; 0.65, 1.00), and PFOA (0.93; 0.75, 1.16). Published by Elsevier Inc.
C1 [Louis, Germaine M. Buck; Sapra, Katherine J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Off Director, Div Intramural Populat Hlth Res, Rockville, MD USA.
[Barr, Dana Boyd] Emory Univ, Rollins Sch Publ Hlth, Dept Environm Hlth, Atlanta, GA 30322 USA.
[Lu, Zhaohui] Glotech Inc, Rockville, MD USA.
[Sundaram, Rajeshwari] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, Biostat & Bioinformat Branch, Rockville, MD USA.
RP Louis, GMB (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Off Director, Div Intramural Populat Hlth Res, Rockville, MD USA.
EM louisg@mail.nih.gov
OI Buck Louis, Germaine/0000-0002-1774-4490; Sundaram,
Rajeshwari/0000-0002-6918-5002
FU Intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development [N01-HD-3-3355,
N01-HD-3-3356, NOH-HD-3-3358]
FX Supported by the Intramural Research Program of the Eunice Kennedy
Shriver National Institute of Child Health and Human Development
(#N01-HD-3-3355; N01-HD-3-3356; NOH-HD-3-3358). We acknowledge the
technical assistance of Antonia Calafat, Division of Laboratory
Sciences, Centers for Disease Control and Prevention who performed the
analytic chemistry work under a Memo of Understanding with the NICHD.
NR 46
TC 0
Z9 0
U1 5
U2 5
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0890-6238
J9 REPROD TOXICOL
JI Reprod. Toxicol.
PD OCT
PY 2016
VL 65
BP 11
EP 17
DI 10.1016/j.reprotox.2016.06.011
PG 7
WC Reproductive Biology; Toxicology
SC Reproductive Biology; Toxicology
GA DZ6RZ
UT WOS:000385990900002
PM 27319395
ER
PT J
AU Hessel, EVS
Ezendam, J
van Broekhuizen, FA
Hakkert, B
DeWitt, J
Granum, B
Guzylack, L
Lawrence, BP
Penninks, A
Rooney, AA
Piersma, AH
van Loveren, H
AF Hessel, Ellen V. S.
Ezendam, Janine
van Broekhuizen, Fleur A.
Hakkert, Betty
DeWitt, Jamie
Granum, Berit
Guzylack, Laurence
Lawrence, B. Paige
Penninks, Andre
Rooney, Andrew A.
Piersma, Aldert H.
van Loveren, Henk
TI Assessment of recent developmental immunotoxicity studies with bisphenol
A in the context of the 2015 EFSA t-TDI
SO REPRODUCTIVE TOXICOLOGY
LA English
DT Article
ID INNER-CITY CHILDREN; PRENATAL EXPOSURE; ASTHMA; INFLAMMATION; ADULTHOOD;
ALLERGY; RISK; MICE
AB Humans are exposed to bisphenol A (BPA) mainly through the diet, air, dust, skin contact and water. There are concerns about adverse health effects in humans due to exposure to bisphenol A (BPA). The European Food Safety Authority (EFSA) has extensively reviewed the available literature to establish a temporary Tolerable Daily Intake (t-TDI). This exposure level was based on all available literature published before the end of 2012. Since then, new experimental animal studies have emerged, including those that identified effects of BPA on the immune system after developmental exposure. These studies indicate that developmental immunotoxicity might occur at lower dose levels than previously observed and on which the current EFSA t-TDI is based. The Dutch National Institute for Public Health and the Environment (RIVM) organized an expert workshop in September 2015 to consider recently published studies on the developmental immunotoxicity of bisphenol A (BPA). Key studies were discussed in the context of other experimental studies. The workshop concluded that these new experimental studies provide credible evidence for adverse immune effects after developmental exposure to BPA at 5 mu g/kg BW/day from gestation day 15 to postnatal day 21. Supportive evidence for adverse immune effects in similar dose ranges was obtained from other publications that were discussed during the workshop. The dose level associated with adverse immune effects is considerably lower than the dose used by EFSA for deriving the t-TDI. The workshop unanimously concluded that the current EFSA t-TDI warrants reconsideration in the context of all currently available data. (C) 2016 Elsevier Inc. All rights reserved.
C1 [Hessel, Ellen V. S.; Ezendam, Janine; Piersma, Aldert H.; van Loveren, Henk] Natl Inst Publ Hlth & Environm RIVM, Ctr Hlth Protect, Bilthoven, Netherlands.
[van Broekhuizen, Fleur A.; Hakkert, Betty] Natl Inst Publ Hlth & Environm RIVM, Ctr Safety Subst & Prod, Bilthoven, Netherlands.
[DeWitt, Jamie] East Carolina Univ, Dept Pharmacol & Toxicol, Greenville, NC USA.
[Granum, Berit] Norwegian Inst Publ Hlth, Dept Toxicol & Risk Assessment, Oslo, Norway.
[Guzylack, Laurence] Univ Toulouse, Dept Intestinal Dev Xenobiot & Immunotoxicol, INRA, Res Ctr Food Toxicol Toxalim, Toulouse, France.
[Lawrence, B. Paige] Univ Rochester, Sch Med & Dent, Dept Environm Med, Rochester, NY USA.
[Lawrence, B. Paige] Univ Rochester, Sch Med & Dent, Dept Microbiol & Immunol, Rochester, NY 14642 USA.
[Penninks, Andre] TNO Triskel BV, Dept Toxicol & Risk Assessment, Zeist, Netherlands.
[Rooney, Andrew A.] NIEHS, Natl Toxicol Program, Off Hlth Assessment & Translat, POB 12233, Res Triangle Pk, NC 27709 USA.
[Piersma, Aldert H.] Univ Utrecht, Inst Risk Assessment Sci, Fac Vet, Utrecht, Netherlands.
[van Loveren, Henk] Maastricht Univ, Dept Toxicogen, Maastricht, Netherlands.
RP Piersma, AH (reprint author), Natl Inst Publ Hlth & Environm RIVM, Ctr Hlth Protect, Bilthoven, Netherlands.
EM aldert.piersma@rivm.nl
OI DeWitt, Jamie/0000-0002-0440-4059
NR 21
TC 0
Z9 0
U1 6
U2 6
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0890-6238
J9 REPROD TOXICOL
JI Reprod. Toxicol.
PD OCT
PY 2016
VL 65
BP 448
EP 456
DI 10.1016/j.reprotox.2016.06.020
PG 9
WC Reproductive Biology; Toxicology
SC Reproductive Biology; Toxicology
GA DZ6RZ
UT WOS:000385990900045
PM 27352639
ER
PT J
AU McFadden, WC
Jaffe, AE
Ye, TZ
Paltan-Ortiz, JD
Hyde, TM
Kleinman, JE
AF McFadden, Whitney C.
Jaffe, Andrew E.
Ye, Tianzhang
Paltan-Ortiz, Jose D.
Hyde, Thomas M.
Kleinman, Joel E.
TI Assessment of genetic risk for distribution of total interstitial white
matter neurons in dorsolateral prefrontal cortex: role in schizophrenia
SO SCHIZOPHRENIA RESEARCH
LA English
DT Article
DE Interstitial white matter neurons; Schizophrenia; Dorsolateral
prefrontal cortex; Postmortem brain
ID DENSITY; EXPRESSION; BRAINS
C1 [McFadden, Whitney C.; Paltan-Ortiz, Jose D.; Kleinman, Joel E.] NIMH, Clin Brain Disorders Branch, Genes Cognit & Psychosis, Div Intramural Res Programs,NIH, Bethesda, MD 20892 USA.
[Jaffe, Andrew E.; Ye, Tianzhang; Hyde, Thomas M.; Kleinman, Joel E.] Lieber Inst Brain Dev, Rangos Bldg,Johns Hopkins Med Campus, Baltimore, MD 21205 USA.
RP McFadden, WC (reprint author), Mt Sinai Hosp, Dept Psychiat, One Gustave L Levy Pl, New York, NY 10029 USA.
FU NIH; Intramural Research Program of the NIH, NIMH
FX This research was made possible through the National Institutes of
Health (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. This research was supported in part by the
Intramural Research Program of the NIH, NIMH.
NR 17
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0920-9964
EI 1573-2509
J9 SCHIZOPHR RES
JI Schizophr. Res.
PD OCT
PY 2016
VL 176
IS 2-3
BP 141
EP 143
DI 10.1016/j.schres.2016.04.007
PG 3
WC Psychiatry
SC Psychiatry
GA DX1LZ
UT WOS:000384130200009
PM 27237599
ER
PT J
AU Luo, Z
Dauter, Z
AF Luo, Zhipu
Dauter, Zbigniew
TI Detection of twinning in macromolecular crystallography
SO ZEITSCHRIFT FUR KRISTALLOGRAPHIE-CRYSTALLINE MATERIALS
LA English
DT Article
DE macromolecular crystallography; merohedral twinning; pseudo-merohedral
twinning; twinning fraction; twinning tests
ID INTENSITY STATISTICS; STRUCTURE REFINEMENT; CRYSTAL-STRUCTURE; PROTEIN
CRYSTALS; TWINS; MEROHEDRY
AB The merohedrally or pseudo-merohedrally twinned crystals cannot be identified during diffraction pattern inspection at the stage of data collection. Several methods for identifying twinning and estimating the twin fraction are suitable for macromolecular crystals, and all are based on the statistical properties of the measured diffraction intensities. They can be based on either the overall statistical properties of the measured reflection intensities or on the comparison of reflection intensities related by the twinning operation. The application of various tests for identification of twinning and estimation of twinning fraction is discussed, with examples of diffraction data from the Protein Data Bank. Twinning makes the solution of crystal structures more difficult, but once initially solved, the atomic models can be properly refined by the existing programs.
C1 [Luo, Zhipu; Dauter, Zbigniew] NCI, Argonne Natl Lab, Synchrotron Radiat Res Sect, Argonne, IL 60439 USA.
RP Dauter, Z (reprint author), NCI, Argonne Natl Lab, Synchrotron Radiat Res Sect, Argonne, IL 60439 USA.
EM dauter@anl.gov
FU Intramural Research Program of the National Cancer Institute
FX This work was supported by the Intramural Research Program of the
National Cancer Institute.
NR 35
TC 0
Z9 0
U1 1
U2 1
PU WALTER DE GRUYTER GMBH
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 2194-4946
EI 2196-7105
J9 Z KRIST-CRYST MATER
JI Z. Krist.-Cryst. Mater.
PD OCT
PY 2016
VL 231
IS 10
SI SI
BP 561
EP 571
DI 10.1515/zkri-2016-1946
PG 11
WC Crystallography
SC Crystallography
GA DZ7NB
UT WOS:000386051600004
ER
PT J
AU Lin, J
Chen, XY
Huang, P
AF Lin, Jing
Chen, Xiaoyuan
Huang, Peng
TI Graphene-based nanomaterials for bioimaging
SO ADVANCED DRUG DELIVERY REVIEWS
LA English
DT Review
DE Graphene; Graphene oxide; Reduced graphene oxide; Graphene quantum dots;
Photoacoustic imaging; PET/SPECT; MRI; Bioimaging
ID ENHANCED RAMAN-SCATTERING; NEAR-INFRARED WINDOW; MESOPOROUS SILICA
NANOPARTICLES; GUIDED PHOTOTHERMAL THERAPY; RAY-COMPUTED-TOMOGRAPHY; MRI
CONTRAST AGENTS; DRUG-DELIVERY; IN-VIVO; NANO-GRAPHENE; QUANTUM DOTS
AB Graphene-based nanomaterials, due to their unique physicochemical properties, versatile surface functionalization, ultra-high surface area, and good biocompatibility, have attracted considerable interest in biomedical applications such as biosensors, drug delivery, bioimaging, theranostics, and so on. In this review, we will summarize the current advances in bioimaging of graphene-based nanomaterials, including graphene, graphene oxide (GO), reduced graphene oxide (rGO), graphene quantum dots (GQDs), and their derivatives. There are two methods to synthesize graphene-based nanomaterials: in situ synthesis and binding method. We will highlight the molecular imaging modalities including optical imaging (fluorescence (FL), two-photon FL, and Raman imaging), PET/SPECT (positron emission tomography/single photon emission computed tomography), MM (magnetic resonance imaging), PAI (photoacoustic imaging), CT (computed tomography), and multimodal imaging. In the end, we will elaborate on the prospects and challenges of their future bioimaging applications. Published by Elsevier B.V.
C1 [Lin, Jing; Huang, Peng] Shenzhen Univ, Sch Med, Dept Biomed Engn, Guangdong Key Lab Biomed Measurements & Ultrasoun, Shenzhen 518060, Peoples R China.
[Chen, Xiaoyuan] NIBIB, Lab Mol Imaging & Nanomed LOMIN, NIH, Bethesda, MD 20892 USA.
RP Huang, P (reprint author), Shenzhen Univ, Sch Med, Dept Biomed Engn, Guangdong Key Lab Biomed Measurements & Ultrasoun, Shenzhen 518060, Peoples R China.; Chen, XY (reprint author), NIBIB, Lab Mol Imaging & Nanomed LOMIN, NIH, Bethesda, MD 20892 USA.
EM shawn.chen@nih.gov; peng.huang@szu.edu.cn
RI Huang, Peng/R-2480-2016
OI Huang, Peng/0000-0003-3651-7813
FU National Science Foundation of China [51573096, 81401465]; Intramural
Research Program (IRP) of the NIBIB; NIH
FX This work was supported by the National Science Foundation of China
(51573096, 81401465), and the Intramural Research Program (IRP) of the
NIBIB, NIH.
NR 128
TC 6
Z9 6
U1 108
U2 108
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0169-409X
EI 1872-8294
J9 ADV DRUG DELIVER REV
JI Adv. Drug Deliv. Rev.
PD OCT 1
PY 2016
VL 105
BP 242
EP 254
DI 10.1016/j.addr.2016.05.013
PN B
PG 13
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA DZ1LW
UT WOS:000385600900009
PM 27233213
ER
PT J
AU Xuan, ZM
Naimi, TS
Kaplan, MS
Bagge, CL
Few, LR
Maisto, S
Saitz, R
Freeman, R
AF Xuan, Ziming
Naimi, Timothy S.
Kaplan, Mark S.
Bagge, Courtney L.
Few, Lauren R.
Maisto, Stephen
Saitz, Richard
Freeman, Robert
TI Alcohol Policies and Suicide: A Review of the Literature
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Review
DE Alcohol Policies; Suicide; Blood Alcohol Content; Critical Review
ID LEGAL DRINKING AGE; DEATH REPORTING SYSTEM; TIME-SERIES ANALYSIS;
UNITED-STATES; PSYCHIATRIC-DISORDERS; YOUTH SUICIDE; RISK-FACTORS;
MORTALITY; TAX; US
AB Both intoxication and chronic heavy alcohol use are associated with suicide. There is extensive population-level evidence linking per capita alcohol consumption with suicide. While alcohol policies can reduce excessive alcohol consumption, the relationship between alcohol policies and suicide warrants a critical review of the literature. This review summarizes the associations between various types of alcohol policies and suicide, both in the United States and internationally, as presented in English-language literature published between 1999 and 2014. Study designs, methodological challenges, and limitations in ascertaining the associations are discussed. Because of the substantial between-states variation in alcohol policies, U.S.-based studies contributed substantially to the literature. Repeated cross-sectional designs at both the ecological level and decedent level were common among U.S.-based studies. Non-U.S. studies often used time series data to evaluate pre-post comparisons of a hybrid set of policy changes. Although inconsistency remained, the published literature in general supported the protective effect of restrictive alcohol policies on reducing suicide as well as the decreased level of alcohol involvement among suicide decedents. Common limitations included measurement and selection bias and a focus on effects of a limited number of alcohol policies without accounting for other alcohol policies. This review summarizes a number of studies that suggest restrictive alcohol policies may contribute to suicide prevention on a general population level and to a reduction of alcohol involvement among suicide deaths.
C1 [Xuan, Ziming; Saitz, Richard] Boston Univ, Dept Community Hlth Sci, Sch Publ Hlth, 801 Massachusetts Ave,Crosstown 443, Boston, MA 02118 USA.
[Naimi, Timothy S.] Boston Med Ctr, Sect Gen Internal Med, Boston, MA USA.
[Kaplan, Mark S.] Univ Calif Los Angeles, Sch Publ Affairs, Dept Social Welf, Los Angeles, CA USA.
[Bagge, Courtney L.] Univ Mississippi, Med Ctr, Dept Psychiat & Human Behav, Jackson, MS 39216 USA.
[Few, Lauren R.] Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA.
[Maisto, Stephen] Syracuse Univ, Dept Psychol, Syracuse, NY USA.
[Freeman, Robert] NIAAA, NIH, Bethesda, MD USA.
RP Xuan, ZM (reprint author), Boston Univ, Dept Community Hlth Sci, Sch Publ Hlth, 801 Massachusetts Ave,Crosstown 443, Boston, MA 02118 USA.
EM zxuan@bu.edu
FU NIAAA NIH HHS [F32 AA023693, K05 AA016928, R01 AA020063, R01 AA021335,
R01 AA021791, R01 AA023376, U01 AA020784]
NR 71
TC 0
Z9 0
U1 3
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0145-6008
EI 1530-0277
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD OCT
PY 2016
VL 40
IS 10
BP 2043
EP 2055
DI 10.1111/acer.13203
PG 13
WC Substance Abuse
SC Substance Abuse
GA DZ0PT
UT WOS:000385542900002
PM 27618526
ER
PT J
AU Williams, EC
Hahn, JA
Saitz, R
Bryant, K
Lira, MC
Samet, JH
AF Williams, Emily C.
Hahn, Judith A.
Saitz, Richard
Bryant, Kendall
Lira, Marlene C.
Samet, Jeffrey H.
TI Alcohol Use and Human Immunodeficiency Virus (HIV) Infection: Current
Knowledge, Implications, and Future Directions
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Review
DE Alcohol; Alcohol Use; Substance Use; HIV; HIV-Related Comorbidities
ID RANDOMIZED CONTROLLED-TRIAL; ACTIVE ANTIRETROVIRAL THERAPY; INTERACTIVE
TOXICITY BELIEFS; NUTRITION EXAMINATION SURVEY; SYSTEMIC IMMUNE
ACTIVATION; MULTICENTER AIDS COHORT; HEALTH-CARE-UTILIZATION; ALL-CAUSE
MORTALITY; SUB-SAHARAN AFRICA; ILLICIT DRUG-USE
AB Alcohol use is common among people living with human immunodeficiency virus (HIV). In this narrative review, we describe literature regarding alcohol's impact on transmission, care, coinfections, and comorbidities that are common among people living with HIV (PLWH), as well as literature regarding interventions to address alcohol use and its influences among PLWH. This narrative review identifies alcohol use as a risk factor for HIV transmission, as well as a factor impacting the clinical manifestations and management of HIV. Alcohol use appears to have additive and potentially synergistic effects on common HIV-related comorbidities. We find that interventions to modify drinking and improve HIV-related risks and outcomes have had limited success to date, and we recommend research in several areas. Consistent with Office of AIDS Research/National Institutes of Health priorities, we suggest research to better understand how and at what levels alcohol influences comorbid conditions among PLWH, to elucidate the mechanisms by which alcohol use is impacting comorbidities, and to understand whether decreases in alcohol use improve HIV-relevant outcomes. This should include studies regarding whether state-of-the-art medications used to treat common coinfections are safe for PLWH who drink alcohol. We recommend that future research among PLWH include validated self-report measures of alcohol use and/or biological measurements, ideally both. Additionally, subgroup variation in associations should be identified to ensure that the risks of particularly vulnerable populations are understood. This body of research should serve as a foundation for a next generation of intervention studies to address alcohol use from transmission to treatment of HIV. Intervention studies should inform implementation efforts to improve provision of alcohol-related interventions and treatments for PLWH in healthcare settings. By making further progress on understanding how alcohol use affects PLWH in the era of HIV as a chronic condition, this research should inform how we can mitigate transmission, achieve viral suppression, and avoid exacerbating common comorbidities of HIV and alcohol use and make progress toward the 90-90-90 goals for engagement in the HIV treatment cascade.
C1 [Williams, Emily C.] Ctr Innovat Vet Ctr & Value Driven Care, Vet Hlth Adm VA Hlth Serv Res & Dev, Seattle, WA USA.
[Williams, Emily C.] Univ Washington, Dept Hlth Serv, Seattle, WA 98195 USA.
[Hahn, Judith A.] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Hahn, Judith A.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Saitz, Richard; Samet, Jeffrey H.] Boston Univ, Sch Publ Hlth, Dept Community Hlth Sci, Boston, MA USA.
[Saitz, Richard; Lira, Marlene C.; Samet, Jeffrey H.] Boston Univ, Sch Med, Dept Med, CARE Unit,Sect Gen Internal Med,Boston Med Ctr, Boston, MA 02118 USA.
[Bryant, Kendall] NIAAA, CHAART, NIH, Bethesda, MD USA.
RP Samet, JH (reprint author), Boston Univ, Boston Med Ctr, Sch Med, 801 Massachusetts Ave,2nd Floor, Boston, MA 02118 USA.; Samet, JH (reprint author), Boston Univ, Boston Med Ctr, Sch Publ Hlth, 801 Massachusetts Ave,2nd Floor, Boston, MA 02118 USA.
EM jsamet@bu.edu
FU HSRD VA [IK2 HX001161]; NIAAA NIH HHS [U24 AA020778, K24 AA022586, U01
AA020776, U01 AA020780, U01 AA020784]
NR 285
TC 0
Z9 0
U1 7
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0145-6008
EI 1530-0277
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD OCT
PY 2016
VL 40
IS 10
BP 2056
EP 2072
DI 10.1111/acer.13204
PG 17
WC Substance Abuse
SC Substance Abuse
GA DZ0PT
UT WOS:000385542900003
PM 27696523
ER
PT J
AU Vatsalya, V
Song, M
Schwandt, ML
Cave, MC
Barve, SS
George, DT
Ramchandani, VA
McClain, CJ
AF Vatsalya, Vatsalya
Song, Ming
Schwandt, Melanie L.
Cave, Matthew C.
Barve, Shirish S.
George, David T.
Ramchandani, Vijay A.
McClain, Craig J.
TI Effects of Sex, Drinking History, and Omega-3 and Omega-6 Fatty Acids
Dysregulation on the Onset of Liver Injury in Very Heavy Drinking
Alcohol-Dependent Patients
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Alcohol; Sex; Heavy Drinking Markers; Fatty Acids; Liver Injury
ID DISEASE; INFLAMMATION; SUSCEPTIBILITY; STEATOSIS; MEDIATORS
AB BackgroundHeavy alcohol consumption frequently causes liver inflammation/injury, and certain fatty acids (FAs) may be involved in this liver pathology. In this study, we evaluated the association of heavy drinking and the changes in the FA levels involved in the -6 (pro-inflammatory) and -3 (anti-inflammatory) state in alcohol-dependent (AD) patients who had no clinical manifestations of liver injury. We aimed to identify sex-based differences in patients with mild or no biochemical evidence of liver injury induced by heavy drinking.
MethodsA total of 114 heavy drinking AD female and male patients aged 21 to 65years without clinical manifestations of liver injury, who were admitted to an alcohol dependence treatment program, were grouped by the alanine aminotransferase (ALT) levels: 40 IU/l, as no liver injury (GR.1), and >40 IU/l, as mild liver injury (GR.2). Patients were actively drinking until the day of admission. Comprehensive metabolic panel, comprehensive FA panel, and drinking history data were evaluated.
ResultsElevated ALT and aspartate aminotransferase (AST) showed close association with markers of heavy alcohol intake. In the patients with mild biochemical liver injury (GR.2), females showed significantly higher AST level than males. Significant association of AST and total drinks in past 90 days (TD90) in females, and AST and heavy drinking days in past 90 days (HDD90) in males was observed. The -6:-3 ratio showed a significant pro-inflammatory response only in females with mild liver injury (GR.2) when adjusted by drinking history marker, TD90. Docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) were increased in males with liver injury, while females did not show any comparable rise in EPA; and DHA levels were lower.
ConclusionsMeasures of heavy drinking, TD90 and HDD90, predicted changes in liver injury. Changes in the -3 and -6 FA levels and the -6:-3 ratio showed a pro-inflammatory shift in patients with biochemical liver injury with a significant effect in females. Changes in FAs involved in the inflammatory state may represent one mechanism for liver inflammation/injury in response to heavy alcohol drinking.
C1 [Vatsalya, Vatsalya; Song, Ming; Cave, Matthew C.; Barve, Shirish S.; McClain, Craig J.] Univ Louisville, Dept Med, Sch Med, 505 S Hancock St CTR Room 521A, Louisville, KY 40202 USA.
[Vatsalya, Vatsalya; Cave, Matthew C.; McClain, Craig J.] Robley Rex Vet Affairs Med Ctr, Louisville, KY USA.
[Vatsalya, Vatsalya; Schwandt, Melanie L.; George, David T.; Ramchandani, Vijay A.] NIAAA, Lab Clin & Translat Studies, Bethesda, MD USA.
[Cave, Matthew C.; Barve, Shirish S.; McClain, Craig J.] Univ Louisville, Sch Med, Dept Pharmacol & Toxicol, Louisville, KY 40292 USA.
RP Vatsalya, V (reprint author), Univ Louisville, Dept Med, Sch Med, 505 S Hancock St CTR Room 521A, Louisville, KY 40202 USA.
EM vatsalya.vatsalya@louisville.edu
OI Vatsalya, Vatsalya/0000-0001-6764-6891
FU Intramural NIH HHS [Z99 AA999999]; NIAAA NIH HHS [P50 AA024337, U01
AA021901, ZIA AA000213, ZIA AA000466]; NIGMS NIH HHS [P20 GM113226]
NR 26
TC 0
Z9 0
U1 3
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0145-6008
EI 1530-0277
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD OCT
PY 2016
VL 40
IS 10
BP 2085
EP 2093
DI 10.1111/acer.13197
PG 9
WC Substance Abuse
SC Substance Abuse
GA DZ0PT
UT WOS:000385542900006
PM 27589090
ER
PT J
AU Wardell, JD
Ramchandani, VA
Hendershot, CS
AF Wardell, Jeffrey D.
Ramchandani, Vijay A.
Hendershot, Christian S.
TI Drinking Motives Predict Subjective Effects of Alcohol and Alcohol
Wanting and Liking During Laboratory Alcohol Administration: A Mediated
Pathway Analysis
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Subjective Response; Craving; Liking; Coping; Alcohol Challenge
ID COLLEGE-STUDENTS; PSYCHOMETRIC SUPPORT; MOTIVATED DRINKERS; ACUTE
TOLERANCE; FAMILY-HISTORY; BINGE DRINKING; EFFECTS SCALE; YOUNG-PEOPLE;
MODEL; RESPONSES
AB BackgroundMotivational models of alcohol use suggest that individual differences in sensitivity to the acute subjective effects of alcohol play an important role in motivational pathways to alcohol use. However, few studies have examined the link between drinking motives and subjective responses to alcohol. This study investigated the associations of coping and enhancement drinking motives with subjective stimulant and sedative effects during a laboratory alcohol administration session. We also examined whether stimulation and sedation following alcohol administration mediated the relationships between drinking motives and postalcohol ratings of alcohol wanting and liking.
MethodsHeavy episodic drinkers (n=147, ages 19 to 25) at 2 sites participated in an intravenous alcohol administration session in which blood alcohol concentration was raised to a target of 80mg% over 20minutes. Participants completed measures of stimulation and sedation at baseline and 20minutes and also rated alcohol liking and wanting at 20minutes. Drinking motives and alcohol use were assessed during a previous laboratory visit.
ResultsA path analysis controlling for baseline stimulation and sedation showed that enhancement motives were positively associated with postalcohol stimulation and negatively associated with postalcohol sedation. In contrast, coping motives were positively associated with postalcohol sedation. In turn, postalcohol stimulation, but not sedation, was associated with alcohol wanting and liking. Further, indirect pathways from enhancement motives to postalcohol wanting and liking mediated through postalcohol stimulation were statistically significant. Coping motives, on the other hand, were directly associated with increased postalcohol wanting and liking.
ConclusionsThe results demonstrate that drinking motives are linked with individual differences in sensitivity to the effects of alcohol, which may serve as a mechanism underlying alcohol reinforcement and the motivation to consume more alcohol during a drinking episode.
C1 [Wardell, Jeffrey D.; Hendershot, Christian S.] Ctr Addict & Mental Hlth, Campbell Family Mental Hlth Res Inst, Toronto, ON, Canada.
[Ramchandani, Vijay A.] NIAAA, Sect Human Psychopharmacol, Div Intramural Clin & Biol Res, NIH, Bethesda, MD USA.
[Hendershot, Christian S.] Ctr Addict & Mental Hlth, Inst Mental Hlth Policy Res, Toronto, ON, Canada.
[Hendershot, Christian S.] Univ Toronto, Dept Psychiat, Toronto, ON, Canada.
[Hendershot, Christian S.] Univ Toronto, Dept Psychol, Toronto, ON, Canada.
RP Hendershot, CS (reprint author), Ctr Addict & Mental Hlth, 100 Stokes St, Toronto, ON M6J 1H4, Canada.
EM christian.hendershot@utoronto.ca
FU NIAAA NIH HHS [R21 AA020304, P60 AA007611]
NR 49
TC 0
Z9 0
U1 5
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0145-6008
EI 1530-0277
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD OCT
PY 2016
VL 40
IS 10
BP 2190
EP 2198
DI 10.1111/acer.13174
PG 9
WC Substance Abuse
SC Substance Abuse
GA DZ0PT
UT WOS:000385542900016
PM 27527738
ER
PT J
AU Karlsson, C
Aziz, AMA
Rehman, F
Pitcairn, C
Barchiesi, R
Barbier, E
Wendel Hansen, M
Gehlert, D
Steensland, P
Heilig, M
Thorsell, A
AF Karlsson, Camilla
Aziz, Abdul Maruf Asif
Rehman, Faazal
Pitcairn, Caleb
Barchiesi, Riccardo
Barbier, Estelle
Wendel Hansen, Mikaela
Gehlert, Don
Steensland, Pia
Heilig, Markus
Thorsell, Annika
TI Melanin-Concentrating Hormone and Its MCH-1 Receptor: Relationship
Between Effects on Alcohol and Caloric Intake
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Alcohol Escalation; Reward; Motivation; Calorie Intake;
Melanin-Concentrating Hormone Receptor-1
ID VOLUNTARY ETHANOL-CONSUMPTION; APPETITE REGULATION; NUCLEUS-ACCUMBENS;
DRUG-ADDICTION; RAT-BRAIN; DOPAMINE; SYSTEM; REWARD; FOOD; OBESITY
AB BackgroundReward and energy homeostasis are both regulated by a network of hypothalamic neuropeptide systems. The melanin-concentrating hormone (MCH) and its MCH-1 receptor (MCH1-R) modulate alcohol intake, but it remains unknown to what extent this reflects actions on energy balance or reward. Here, we evaluated the MCH1-R in regulation of caloric intake and motivation to consume alcohol in states of escalated consumption.
MethodsRats had intermittent access (IA) to alcohol and were divided into high- and low-drinking groups. Food and alcohol consumption was assessed after administration of an MCH1-R antagonist, GW803430. Next, GW803430 was evaluated on alcohol self-administration in protracted abstinence induced by IA in high-drinking rats. Finally, the effect of GW803430 was assessed on alcohol self-administration in acute withdrawal in rats exposed to alcohol vapor. Gene expression of MCH and MCH1-R was measured in the hypothalamus and nucleus accumbens (NAc) in both acute and protracted abstinence.
ResultsHigh-drinking IA rats consumed more calories from alcohol than chow and GW803430 decreased both chow and alcohol intake. In low-drinking rats, only food intake was affected. In protracted abstinence from IA, alcohol self-administration was significantly reduced by pretreatment with GW803430 and gene expression of both MCH and the MCH1-R were dysregulated in hypothalamus and NAc. In contrast, during acute withdrawal from vapor exposure, treatment with GW803430 did not affect alcohol self-administration, and no changes in MCH or MCH1-R gene expression were observed.
ConclusionsOur data suggest a dual role of MCH and the MCH1-R in regulation of alcohol intake, possibly through mechanisms involving caloric intake and reward motivation. A selective suppression of alcohol self-administration during protracted abstinence by GW803430 was observed and accompanied by adaptations in gene expression of MCH and MCH1-R. Selective suppression of escalated consumption renders the MCH1-R an attractive target for treatment of alcohol use disorders.
C1 [Karlsson, Camilla; Aziz, Abdul Maruf Asif; Barchiesi, Riccardo; Barbier, Estelle; Wendel Hansen, Mikaela; Heilig, Markus; Thorsell, Annika] Linkoping Univ, Dept Clin & Expt Med, Linkoping, Sweden.
[Rehman, Faazal; Pitcairn, Caleb] NIAAA, Lab Clin & Translat Studies, NIH, Bethesda, MD USA.
[Gehlert, Don] Eli Lilly & Co, Lilly Res Labs, CNS Res, Indianapolis, IN 46285 USA.
[Steensland, Pia] Karolinska Inst, Clin Neurosci, Stockholm, Sweden.
RP Karlsson, C (reprint author), Linkoping Univ, Dept Clin & Expt Med, Linkoping, Sweden.
EM camilla.s.karlsson@liu.se
NR 37
TC 1
Z9 1
U1 5
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0145-6008
EI 1530-0277
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD OCT
PY 2016
VL 40
IS 10
BP 2199
EP 2207
DI 10.1111/acer.13181
PG 9
WC Substance Abuse
SC Substance Abuse
GA DZ0PT
UT WOS:000385542900017
PM 27579857
ER
PT J
AU Patel, VS
Sampat, V
Espey, MG
Sitapara, R
Wang, HC
Yang, XJ
Ashby, CR
Thomas, DD
Mantell, LL
AF Patel, Vivek S.
Sampat, Vaishali
Espey, Michael Graham
Sitapara, Ravikumar
Wang, Haichao
Yang, Xiaojing
Ashby, Charles R., Jr.
Thomas, Douglas D.
Mantell, Lin L.
TI Ascorbic Acid Attenuates Hyperoxia-Compromised Host Defense against
Pulmonary Bacterial Infection
SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
LA English
DT Article
DE hyperoxia; ascorbic acid; pneumonia; high-mobility group box 1
ID NF-KAPPA-B; VENTILATOR-ASSOCIATED PNEUMONIA; OXYGEN RADICAL PRODUCTION;
CHROMATIN PROTEIN HMGB1; MOBILITY GROUP BOX-1; INDUCED LUNG INJURY;
VITAMIN-C; OXIDATIVE STRESS; PSEUDOMONAS-AERUGINOSA; IN-VITRO
AB Supraphysiological concentrations of oxygen (hyperoxia) can compromise host defense and increase susceptibility to bacterial infections, causing ventilator-associated pneumonia. The phagocytic activity of macrophages is impaired by hyperoxia-induced increases in the levels of reactive oxygen species (ROS) and extracellular high-mobility group box protein B1 (HMGB1). Ascorbic acid (AA), an essential nutrient and antioxidant, has been shown to be beneficial in various animal models of ROS-mediated diseases. The aim of this study was to determine whether AA could attenuate hyperoxia-compromised host defense and improve macrophage functions against bacterial infections. C57BL/6 male mice were exposed to hyperoxia (>= 98% O-2, 48 h), followed by intratracheal inoculation with Pseudomonas aeruginosa, and simultaneous intraperitoneal administration of AA. AA(50mg/kg) significantly improved bacterial clearance in the lungs and airways, and significantly reduced HMGB1 accumulation in the airways. The incubation of RAW 264.7 cells (a macrophage-like cell line) with AA (0-1,000 mu M) before hyperoxic exposure (95% O-2) stabilized the phagocytic activity of macrophages in a concentration-dependent manner. The AA-enhanced macrophage function was associated with significantly decreased production of intracellular ROS and accumulation of extracellular HMGB1. These data suggest that AA supplementation can prevent or attenuate the development of ventilator-associated pneumonia in patients receiving oxygen support.
C1 [Patel, Vivek S.; Sampat, Vaishali; Sitapara, Ravikumar; Yang, Xiaojing; Ashby, Charles R., Jr.; Mantell, Lin L.] St Johns Univ, Coll Pharm & Hlth Sci, Dept Pharmaceut Sci, 128 St Albert Hall,8000 Utopia Pkwy, Queens, NY 11439 USA.
[Espey, Michael Graham] NCI, Bethesda, MD 20892 USA.
[Wang, Haichao; Mantell, Lin L.] North Shore Long Isl Jewish Hlth Syst, Feinstein Inst Med Res, Manhasset, NY USA.
[Thomas, Douglas D.] Univ Illinois, Coll Pharm, Dept Med Chem & Pharmacognosy, Chicago, IL USA.
RP Mantell, LL (reprint author), St Johns Univ, Coll Pharm & Hlth Sci, Dept Pharmaceut Sci, 128 St Albert Hall,8000 Utopia Pkwy, Queens, NY 11439 USA.
EM lmantell@nshs.edu
OI Wang, Haichao/0000-0002-0211-9000
FU National Heart, Lung, and Blood Institute [HL093708]; St. John's
University
FX This work was supported by National Heart, Lung, and Blood Institute
grant HL093708 (L.L.M.) and a grant from St. John's University.
NR 72
TC 0
Z9 0
U1 3
U2 3
PU AMER THORACIC SOC
PI NEW YORK
PA 25 BROADWAY, 18 FL, NEW YORK, NY 10004 USA
SN 1044-1549
EI 1535-4989
J9 AM J RESP CELL MOL
JI Am. J. Respir. Cell Mol. Biol.
PD OCT 1
PY 2016
VL 55
IS 4
BP 511
EP 520
DI 10.1165/rcmb.2015-0310OC
PG 10
WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
GA DZ2DY
UT WOS:000385653700007
PM 27120084
ER
PT J
AU Hunter, CM
AF Hunter, Christine M.
TI Understanding Diabetes and the Role of Psychology in Its Prevention and
Treatment
SO AMERICAN PSYCHOLOGIST
LA English
DT Article
DE diabetes; treatment; prevention; biopsychosocial model; health
psychology
ID LIFE-STYLE INTERVENTION; EXCHANGE CLINIC REGISTRY; HEALTH
BEHAVIOR-CHANGE; FUTURE-DIRECTIONS; YOUNG-CHILDREN; MENTAL-HEALTH; OBESE
ADULTS; TYPE-1; PREVALENCE; MELLITUS
AB Diabetes is a common, chronic, and costly condition that currently affects millions of individuals in the United States and worldwide with even greater numbers at high risk for developing the disease. Dramatic increases in diagnosed diabetes are projected for the decades to come meaning that most people will be affected by diabetes; either personally or through a family member. This article introduces the special issue of the American Psychologist focused on diabetes by providing an overview of the scope of diabetes and the importance of psychologists for improving disease management and quality of life. This includes an overview of the contributions of the behavioral and social sciences toward improved diabetes prevention and treatment. Finally, the article will point to opportunities for psychologists to close the gaps in the research, develop practice competencies, and increase training opportunities to meet the challenges of diabetes today and in the future.
C1 [Hunter, Christine M.] NIDDK, Bethesda, MD 20892 USA.
RP Hunter, CM (reprint author), NIDDK, Div Diabet Endocrinol & Metab Dis, NIH, 6707 Democracy Blvd,Room 6071, Bethesda, MD 20892 USA.
EM hunterchristine@niddk.nih.gov
NR 79
TC 5
Z9 5
U1 16
U2 16
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0003-066X
EI 1935-990X
J9 AM PSYCHOL
JI Am. Psychol.
PD OCT
PY 2016
VL 71
IS 7
SI SI
BP 515
EP 525
DI 10.1037/a0040344
PG 11
WC Psychology, Multidisciplinary
SC Psychology
GA DZ0YV
UT WOS:000385566500001
PM 27690481
ER
PT J
AU Lenis, YY
Wang, XQ
Tang, WJ
Wu, GY
Bazer, FW
AF Lenis, Yasser Y.
Wang, Xiaoqiu
Tang, Wanjin
Wu, Guoyao
Bazer, Fuller W.
TI Effects of agmatine on secretion of interferon tau and catecholamines
and expression of genes related to production of polyamines by ovine
trophectoderm cells
SO AMINO ACIDS
LA English
DT Article
DE Arginine; Agmatine; Polyamines; Trophectoderm cells; Interferon tau
ID NITRIC-OXIDE SYNTHASE; SELECT NUTRIENTS; AMINO-ACIDS; ARGININE
SUPPLEMENTATION; PERIIMPLANTATION PERIOD; MAMMALIAN CONCEPTUSES;
DEVELOPMENTAL-CHANGES; SIGNALING PATHWAYS; EARLY-PREGNANCY; TUMOR-CELLS
AB Embryonic survival requires histotrophic nutrition, including molecules secreted or transported into the uterine lumen by uterine epithelia. l-Arginine (Arg) is a common substrate for synthesis of nitric oxide, ornithine, proline, glutamate, creatinine, urea, polyamines and agmatine. Agmatine (Agm) is a product of arginine decarboxylation and it is a substrate for agmatinase for synthesis of putrescine and other polyamines in the ovine conceptus. Polyamines are essential for conceptus development. Therefore, this study compared effects of Arg and Agm on the behavior of ovine trophectoderm (oTr1) cells cultured in vitro. Arg, but not Agm, increased proliferation and migration of oTr1 cells, but neither Arg nor Agm affected cell adhesion. The total amount of IFNT in culture medium of oTr1 cells was increased by Arg, but Agm increased the IFNT production per oTr1 cell. Arg and Agm plus Arg decreased secretion of dopamine and norepinephrine by oTr1 cells. Agm upregulates expression of mRNAs SLC7A1, agmatinase and OAZ2 while the combination of Arg and Agm decreased expression of mRNAs for ODC1, SLC7A1, OAZ1 and OAZ3 by oTr1 cells. Although Agm does not stimulate proliferation, migration or adhesion of oTr1 cells or their secretion of catecholamines, Agm did increase transcription of SLC7A1, agmatinase and OAZ2 genes which would increase the capacity of oTr1 cells to produce polyamines. Collectively, our findings suggest a role for Arg and Agm in the regulation of transport of basic amino acids (including Arg), polyamine synthesis, and secretion of catecholamines by oTr1 cells.
C1 [Lenis, Yasser Y.; Wang, Xiaoqiu; Tang, Wanjin; Wu, Guoyao; Bazer, Fuller W.] Texas A&M Univ, Dept Anim Sci, College Stn, TX 77843 USA.
[Lenis, Yasser Y.; Wang, Xiaoqiu; Tang, Wanjin; Wu, Guoyao; Bazer, Fuller W.] Texas A&M Univ, Ctr Anim Biotechnol & Genom, College Stn, TX 77843 USA.
[Lenis, Yasser Y.] Univ Antioquia, Sch Vet Med, Fac Agr Sci, Centauro Res Grp, Calle 70 52-21, Medellin, Colombia.
[Wang, Xiaoqiu] NIEHS, Res Triangle Pk, NC 27709 USA.
RP Bazer, FW (reprint author), Texas A&M Univ, Dept Anim Sci, College Stn, TX 77843 USA.; Bazer, FW (reprint author), Texas A&M Univ, Ctr Anim Biotechnol & Genom, College Stn, TX 77843 USA.
EM fbazer@cvm.tamu.edu
FU CODI University of Antioquia (UdeA); Medellin; Colombia Scholarship
"Becas Doctorado UdeA; Agriculture and Food Research Initiative
Competitive Grants from the USDA National Institute of Food and
Agriculture [2011-67015-20028, 2015-67015-23276]
FX This work was supported by Sustainability Strategy 2013-2014, from CODI
University of Antioquia (UdeA), Medellin, Colombia Scholarship "Becas
Doctorado UdeA 2014" (to YYL; PhD student in Veterinary Science, Faculty
of Agrarian Science, Antioquia University) and by Agriculture and Food
Research Initiative Competitive Grants (2011-67015-20028 and
2015-67015-23276) from the USDA National Institute of Food and
Agriculture (to FWB and GW). Yasser Lenis is also a Research Fellow in
the Department of Animal Science, Texas A&M University.
NR 52
TC 0
Z9 0
U1 1
U2 1
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 0939-4451
EI 1438-2199
J9 AMINO ACIDS
JI Amino Acids
PD OCT
PY 2016
VL 48
IS 10
BP 2389
EP 2399
DI 10.1007/s00726-016-2216-1
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA DY8XC
UT WOS:000385414500011
PM 27074718
ER
PT J
AU Charlifue, S
Tate, D
Biering-Sorensen, F
Burns, S
Chen, YY
Chun, S
Jakeman, LB
Kowalski, RG
Noonan, VK
Ullrich, P
AF Charlifue, Susan
Tate, Denise
Biering-Sorensen, Fin
Burns, Stephen
Chen, Yuying
Chun, Sophia
Jakeman, Lyn B.
Kowalski, Robert G.
Noonan, Vanessa K.
Ullrich, Philip
TI Harmonization of Databases: A Step for Advancing the Knowledge About
Spinal Cord Injury
SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION
LA English
DT Article
DE Dataset; Database; Rehabilitation; Spinal cord injuries
ID POPULATION HEALTH SURVEY; QUALITY-OF-LIFE; DEVELOPING-COUNTRIES;
NEUROLOGICAL DISORDERS; NATIONAL INSTITUTE; DATA SET; CLASSIFICATION;
EPIDEMIOLOGY; INDIVIDUALS; INSTRUMENTS
AB The objectives of this article are to (1) provide an overview of existing spinal cord injury (SCI) clinical research databases-their purposes, characteristics, and accessibility to users; and (2) present a vision for future collaborations required for cross-cutting research in SCI. This vision highlights the need for validated and relevant data for longitudinal clinical trials and observational and epidemiologic SCI-related studies. Three existing SCI clinical research databases/registries are reviewed and summarized with regard to current formats, collection methods, and uses, including major strengths and weaknesses. Efforts to provide a uniform approach to data collection are also reviewed. The databases reviewed offer different approaches to capture important clinical information on SCI. They vary on size, purpose, data points, inclusion of standard outcomes, and technical requirements. Each presents with a set of limitations including lack of population data and lack of a common platform for data comparisons and exchanges. It is clear that numerous issues need to be considered when planning to establish common ways of collecting data through data sets or patient registries, ranging from a carefully crafted implementation plan that lists purposes, cost, resources required, and policies to guide such development to establishing a framework for dissemination of data and findings. For the present, taking advantage of the vast but different data already collected over many decades may require a variety of statistical skills and epidemiologic techniques. Ultimately, our ability to speak the same language with regard to variables and assessment tools will facilitate international collaborations and enhance comparability, data pooling, and the ability to generalize findings to a broader population. (C) 2016 by the American Congress of Rehabilitation Medicine
C1 [Charlifue, Susan; Kowalski, Robert G.] Craig Hosp, Rocky Mt Reg Spinal Injury Syst, Englewood, CO USA.
[Tate, Denise] Univ Michigan Spinal Cord Injury Model Syst, Dept Phys Med & Rehabil, Ann Arbor, MI USA.
[Biering-Sorensen, Fin] Univ Copenhagen, Clin Spinal Cord Injuries, Rigshosp, Copenhagen, Denmark.
[Burns, Stephen; Ullrich, Philip] Puget Sound Vet Adm Med Ctr, Vet Adm Spinal Cord Injury & Disorder Serv, Seattle, WA USA.
[Burns, Stephen; Ullrich, Philip] Univ Washington, Dept Rehabil Med, Seattle, WA 98195 USA.
[Chen, Yuying] Univ Alabama Birmingham, Dept Phys Med & Rehabil, Birmingham, AL USA.
[Chun, Sophia] Vet Adm Long Beach Healthcare Syst, Spinal Cord Injury Ctr, Long Beach, CA USA.
[Jakeman, Lyn B.] NINDS, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
[Noonan, Vanessa K.] Rick Hansen Inst, Vancouver, BC, Canada.
RP Charlifue, S (reprint author), Craig Hosp, 3425 S Clarkson St, Englewood, CO 80110 USA.
EM susie@craighospital.org
FU National Institute on Disability, Independent Living, and Rehabilitation
Research (NIDILRR) [90S15003, 90DP0011, 90SI5000]; Health Canada;
Western Economic Diversification Canada; Government of Alberta;
Government of British Columbia; Government of Manitoba; Government of
Ontario
FX Supported by the National Institute on Disability, Independent Living,
and Rehabilitation Research (NIDILRR grant nos. 90S15003, 90DP0011,
90SI5000). NIDILRR is a Center within the Administration for Community
Living (ACL), Department of Health and Human Services (HHS). The Rick
Hansen Spinal Cord Injury Registry is supported by funding from Health
Canada, Western Economic Diversification Canada, and the Governments of
Alberta, British Columbia, Manitoba, and Ontario. The contents of this
manuscript do not represent the opinions or policy of NIDILRR, ACL,
National Institutes of Health, National Institute of Neurological
Disorders and Stroke, or HHS, and do not imply endorsement by the
respective institutes, agencies, or the U.S. Federal Government.
NR 45
TC 1
Z9 1
U1 2
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 2016
VL 97
IS 10
BP 1805
EP 1818
DI 10.1016/j.apmr.2016.03.030
PG 14
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA DY7TX
UT WOS:000385333300027
PM 27137095
ER
PT J
AU Hourigan, CS
Aplan, PD
AF Hourigan, Christopher S.
Aplan, Peter D.
TI Accurate Medicine: Indirect Targeting of NPM1-Mutated AML
SO CANCER DISCOVERY
LA English
DT Editorial Material
ID ACUTE MYELOID-LEUKEMIA; CLASSIFICATION; HOXA9
AB Acute myeloid leukemia (AML) is now recognized to be an imprecise term that refers to a range of myeloid malignancies that have different genetical etiologies, clinical characteristics, and therapeutic sensitivities. Targeting the MLL1 and DOT1L histone modification complexes, both alone and in combination, showed activity against AML driven by a mutant NPM1 protein in several preclinical models and may represent a new treatment direction for this devastating disease. (C) 2016 AACR.
C1 [Hourigan, Christopher S.] NHLBI, Myeloid Malignancies Sect, Hematol Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
[Aplan, Peter D.] NCI, Leukemia Biol Sect, Genet Branch, NIH, Bethesda, MD 20892 USA.
RP Hourigan, CS; Aplan, PD (reprint author), NCI, NIH, 37 Convent Dr,Bldg 37 Room 6002, Bethesda, MD 20892 USA.
EM christopher.hourigan@nih.gov; aplanp@mail.nih.gov
RI Hourigan, Christopher/S-2476-2016
OI Hourigan, Christopher/0000-0002-6189-8067
FU Intramural Research Program of the NCI [ZIA SC 010378, ZIA BC 010982];
National Heart, Lung and Blood Institute of the NIH [ZIA HL 006163]
FX This work was supported by the Intramural Research Program of the NCI
(Grants ZIA SC 010378 and ZIA BC 010982 to P.D. Aplan) and the National
Heart, Lung and Blood Institute of the NIH (Grant ZIA HL 006163 to C.S.
Hourigan).
NR 10
TC 0
Z9 0
U1 2
U2 2
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 2016
VL 6
IS 10
BP 1087
EP 1089
DI 10.1158/2159-8290.CD-16-0917
PG 3
WC Oncology
SC Oncology
GA DZ1ZW
UT WOS:000385642200019
PM 27698101
ER
PT J
AU Trabert, B
AF Trabert, Britton
TI Body Powder and Ovarian Cancer Risk-What Is the Role of Recall Bias?
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Editorial Material
ID RANDOMIZED CONTROLLED-TRIAL; TALC USE; INFLAMMATION; MORTALITY; EXPOSURE
C1 [Trabert, Britton] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
RP Trabert, B (reprint author), NCI, 9609 Med Ctr Dr, Bethesda, MD 20892 USA.
EM britton.trabert@nih.gov
RI Trabert, Britton/F-8051-2015
FU Intramural NIH HHS [ZIA CP010126-21]
NR 17
TC 0
Z9 0
U1 4
U2 4
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 2016
VL 25
IS 10
BP 1369
EP 1370
DI 10.1158/1055-9965.EPI-16-0476
PG 2
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA DZ2AA
UT WOS:000385642800001
PM 27697794
ER
PT J
AU Kennedy, AE
Khoury, MJ
Ioannidis, JPA
Brotzman, M
Miller, A
Lane, C
Lai, GY
Rogers, SD
Harvey, C
Elena, JW
Seminara, D
AF Kennedy, Amy E.
Khoury, Muin J.
Ioannidis, John P. A.
Brotzman, Michelle
Miller, Amy
Lane, Crystal
Lai, Gabriel Y.
Rogers, Scott D.
Harvey, Chinonye
Elena, Joanne W.
Seminara, Daniela
TI The Cancer Epidemiology Descriptive Cohort Database: A Tool to Support
Population-Based Interdisciplinary Research
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; PROSTATE-CANCER; PRECISION MEDICINE;
PANCREATIC-CANCER; CLINICAL-TRIALS; PUBLIC-HEALTH; CONSORTIUM; RISK;
TRANSFORMATION; BREAST
AB Background: We report on the establishment of a web-based Cancer Epidemiology Descriptive Cohort Database (CEDCD). The CEDCD's goals are to enhance awareness of resources, facilitate interdisciplinary research collaborations, and support existing cohorts for the study of cancer-related outcomes.
Methods: Comprehensive descriptive data were collected from large cohorts established to study cancer as primary outcome using a newly developed questionnaire. These included an inventory of baseline and follow-up data, biospecimens, genomics, policies, and protocols. Additional descriptive data extracted from publicly available sources were also collected. This information was entered in a searchable and publicly accessible database. We summarized the descriptive data across cohorts and reported the characteristics of this resource.
Results: As of December 2015, the CEDCD includes data from 46 cohorts representing more than 6.5 million individuals (29% ethnic/racial minorities). Overall, 78% of the cohorts have collected blood at least once, 57% at multiple time points, and 46% collected tissue samples. Genotyping has been performed by 67% of the cohorts, while 46% have performed whole-genome or exome sequencing in subsets of enrolled individuals. Information on medical conditions other than cancer has been collected in more than 50% of the cohorts. More than 600,000 incident cancer cases and more than 40,000 prevalent cases are reported, with 24 cancer sites represented.
Conclusions: The CEDCD assembles detailed descriptive information on a large number of cancer cohorts in a searchable database.
Impact: Information from the CEDCD may assist the interdisciplinary research community by facilitating identification of well-established population resources and large-scale collaborative and integrative research. (C) 2016 AACR.
C1 [Kennedy, Amy E.; Lai, Gabriel Y.; Rogers, Scott D.; Harvey, Chinonye; Elena, Joanne W.] NCI, Epidemiol & Genom Res Program, Div Canc Control & Populat Sci, NIH, Rockville, MD USA.
[Khoury, Muin J.] Ctr Dis Control & Prevent, Off Publ Hlth Genom, Atlanta, GA USA.
[Ioannidis, John P. A.] Stanford Univ, Dept Med, Stanford, CA 94305 USA.
[Ioannidis, John P. A.] Stanford Univ, Dept Hlth Res & Policy, Stanford, CA 94305 USA.
[Ioannidis, John P. A.] Stanford Univ, Dept Stat, Stanford, CA 94305 USA.
[Ioannidis, John P. A.] Stanford Univ, Meta Res Innovat Ctr Stanford METRICS, Stanford, CA 94305 USA.
[Brotzman, Michelle; Miller, Amy] Westat Corp, Rockville, MD USA.
[Lane, Crystal] US Hlth Resources & Serv Adm, Off Epidemiol & Res, Maternal & Child Hlth Bur, Rockville, MD 20857 USA.
[Seminara, Daniela] NCI, Div Canc Control & Populat Sci, NIH, Rockville, MD USA.
RP Seminara, D (reprint author), NCI, 9609 Med Ctr Dr,Room 3E336,MSC 9763, Bethesda, MD 20850 USA.
EM seminard@mail.nih.gov
OI Kennedy, Amy/0000-0001-9589-5510
NR 34
TC 0
Z9 0
U1 2
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD OCT
PY 2016
VL 25
IS 10
BP 1392
EP 1401
DI 10.1158/1055-9965.EPI-16-0412
PG 10
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA DZ2AA
UT WOS:000385642800004
PM 27439404
ER
PT J
AU Long, AH
Highfill, SL
Cui, YZ
Smith, JP
Walker, AJ
Ramakrishna, S
El-Etriby, R
Galli, S
Tsokos, MG
Orentas, RJ
Mackall, CL
AF Long, Adrienne H.
Highfill, Steven L.
Cui, Yongzhi
Smith, Jillian P.
Walker, Alec J.
Ramakrishna, Sneha
El-Etriby, Rana
Galli, Susana
Tsokos, Maria G.
Orentas, Rimas J.
Mackall, Crystal L.
TI Reduction of MDSCs with All-trans Retinoic Acid Improves CAR Therapy
Efficacy for Sarcomas
SO CANCER IMMUNOLOGY RESEARCH
LA English
DT Article
ID MODIFIED T-CELLS; CHIMERIC ANTIGEN RECEPTORS; SUPPRESSOR-CELLS; MYELOID
CELLS; IMMUNE-RESPONSE; CANCER; NEUROBLASTOMA; EXPANSION; CYTOKINE;
ANTIBODY
AB Genetically engineered T cells expressing CD19-specific chimeric antigen receptors (CAR) have shown impressive activity against B-cell malignancies, and preliminary results suggest that T cells expressing a first-generation disialoganglioside (GD2)-specific CAR can also provide clinical benefit in patients with neuroblastoma. We sought to assess the potential of GD2-CAR therapies to treat pediatric sarcomas. We observed that 18 of 18 (100%) of osteosarcomas, 2 of 15 (13%) of rhabdomyosarcomas, and 7 of 35 (20%) of Ewing sarcomas expressed GD2. T cells engineered to express a third-generation GD2-CAR incorporating the 14g2a-scFv with the CD28, OX40, and CD3 zeta signaling domains (14g2a.CD28.OX40.zeta) mediated efficient and comparable lysis of both GD2(+) sarcoma and neuroblastoma cell lines in vitro. However, in xenograft models, GD2-CAR T cells had no antitumor effect against GD2(+) sarcoma, despite effectively controlling GD2(+) neuroblastoma. We observed that pediatric sarcoma xenografts, but not neuroblastoma xenografts, induced large populations of monocytic and granulocytic murine myeloid-derived suppressor cells (MDSC) that inhibited human CAR T-cell responses in vitro. Treatment of sarcoma-bearing mice with all-trans retinoic acid (ATRA) largely eradicated monocytic MDSCs and diminished the suppressive capacity of granulocytic MDSCs. Combined therapy using GD2-CAR T cells plus ATRA significantly improved antitumor efficacy against sarcoma xenografts. We conclude that retinoids provide a clinically accessible class of agents capable of diminishing the suppressive effects of MDSCs, and that co-administration of retinoids may enhance the efficacy of CAR therapies targeting solid tumors. (C) 2016 AACR.
C1 [Long, Adrienne H.; Highfill, Steven L.; Cui, Yongzhi; Smith, Jillian P.; Walker, Alec J.; Ramakrishna, Sneha; Orentas, Rimas J.; Mackall, Crystal L.] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Long, Adrienne H.] Northwestern Univ, Feinberg Sch Med, Dept Microbiol & Immunol, Chicago, IL 60611 USA.
[El-Etriby, Rana; Galli, Susana; Tsokos, Maria G.] NCI, Pathol Lab, CCR, NIH, Bldg 10, Bethesda, MD 20892 USA.
[Mackall, Crystal L.] Stanford Univ, Sch Med, Dept Pediat, 265 Campus Dr G3141A, Stanford, CA 94305 USA.
[Galli, Susana] Georgetown Univ, Med Ctr, Dept Biochem & Mol & Cellular Biol, Washington, DC 20007 USA.
[Tsokos, Maria G.] Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02215 USA.
[Orentas, Rimas J.] Lentigen Technol Inc, Gaithersburg, MD USA.
RP Mackall, CL (reprint author), Stanford Univ, 265 Campus Dr G3141A,MC5456, Stanford, CA 94305 USA.
EM cmackall@stanford.edu
FU Intramural NIH HHS [ZIA BC011073-03]; NIGMS NIH HHS [T32 GM008152]
NR 50
TC 1
Z9 1
U1 6
U2 6
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2326-6066
EI 2326-6074
J9 CANCER IMMUNOL RES
JI Cancer Immunol. Res.
PD OCT
PY 2016
VL 4
IS 10
BP 869
EP 880
DI 10.1158/2326-6066.CIR-15-0230
PG 12
WC Oncology; Immunology
SC Oncology; Immunology
GA DZ1WR
UT WOS:000385632900007
PM 27549124
ER
PT J
AU Cook, KL
Soto-Pantoja, DR
Clarke, PAG
Cruz, MI
Zwart, A
Warri, A
Hilakivi-Clarke, L
Roberts, DD
Clarke, R
AF Cook, Katherine L.
Soto-Pantoja, David R.
Clarke, Pamela A. G.
Cruz, M. Idalia
Zwart, Alan
Warri, Anni
Hilakivi-Clarke, Leena
Roberts, David D.
Clarke, Robert
TI Endoplasmic Reticulum Stress Protein GRP78 Modulates Lipid Metabolism to
Control Drug Sensitivity and Antitumor Immunity in Breast Cancer
SO CANCER RESEARCH
LA English
DT Article
ID FATTY-ACID OXIDATION; ANTIESTROGEN RESPONSIVENESS; THERAPEUTIC TARGET;
HEPATIC STEATOSIS; GENE-EXPRESSION; CELL FATE; RESISTANCE; TAMOXIFEN;
AUTOPHAGY; CHOLESTEROL
AB The unfolded protein response is an endoplasmic reticulum stress pathway mediated by the protein chaperone glucose regulated-protein 78 (GRP78). Metabolic analysis of breast cancer cells shows that GRP78 silencing increases the intracellular concentrations of essential polyunsaturated fats, including linoleic acid. Accumulation of fatty acids is due to an inhibition of mitochondrial fatty acid transport, resulting in a reduction of fatty acid oxidation. These data suggest a novel role of GRP78-mediating cellular metabolism. We validated the effect of GRP78-regulated metabolite changes by treating tumor-bearing mice with tamoxifen and/or linoleic acid. Tumors treated with linoleic acid plus tamoxifen exhibited reduced tumor area and tumor weight. Inhibition of either GRP78 or linoleic acid treatment increased MCP-1 serum levels, decreased CD47 expression, and increased macrophage infiltration, suggesting a novel role for GRP78 in regulating innate immunity. GRP78 control of fatty acid oxidation may represent a new homeostatic function for GRP78. (C) 2016 AACR.
C1 [Cook, Katherine L.; Soto-Pantoja, David R.] Wake Forest Univ, Bowman Gray Sch Med, Dept Surg, Winston Salem, NC 27103 USA.
[Cook, Katherine L.; Soto-Pantoja, David R.] Wake Forest Univ, Bowman Gray Sch Med, Hypertens & Vasc Res Ctr, Winston Salem, NC USA.
[Cook, Katherine L.; Clarke, Pamela A. G.; Cruz, M. Idalia; Zwart, Alan; Warri, Anni; Hilakivi-Clarke, Leena; Clarke, Robert] Georgetown Univ, Med Ctr, Dept Oncol, Washington, DC 20007 USA.
[Cook, Katherine L.; Clarke, Pamela A. G.; Cruz, M. Idalia; Zwart, Alan; Warri, Anni; Hilakivi-Clarke, Leena; Clarke, Robert] Georgetown Univ, Med Ctr, Lombardi Comprehens Canc Ctr, Washington, DC 20007 USA.
[Roberts, David D.] NCI, Pathol Lab, NIH, Bldg 10, Bethesda, MD 20892 USA.
RP Cook, KL (reprint author), Wake Forest Univ, Med Ctr Blvd, Winston Salem, NC 27157 USA.
EM klcook@wakehealth.edu
RI Clarke, Robert/A-6485-2008; Roberts, David/A-9699-2008
OI Clarke, Robert/0000-0002-9278-0854; Roberts, David/0000-0002-2481-2981
FU NCATS NIH HHS [KL2 TR001421]; NCI NIH HHS [U54 CA149147, U01 CA184902,
K22 CA181274, R01 CA131465]
NR 45
TC 1
Z9 1
U1 7
U2 7
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD OCT
PY 2016
VL 76
IS 19
BP 5657
EP 5670
DI 10.1158/0008-5472.CAN-15-2616
PG 14
WC Oncology
SC Oncology
GA DZ1UD
UT WOS:000385625500012
PM 27698188
ER
PT J
AU He, XZ
Yan, B
Liu, S
Jia, JT
Lai, WW
Xin, X
Tang, CE
Luo, DX
Tan, T
Jiang, YQ
Shi, Y
Liu, YT
Xiao, DS
Chen, L
Liu, S
Mao, C
Yin, G
Cheng, Y
Fan, J
Cao, Y
Muegge, K
Tao, YG
AF He, Xiaozhen
Yan, Bin
Liu, Shuang
Jia, Jiantao
Lai, Weiwei
Xin, Xing
Tang, Can-e
Luo, Dixian
Tan, Tan
Jiang, Yiqun
Shi, Ying
Liu, Yating
Xiao, Desheng
Chen, Ling
Liu, Shao
Mao, Chao
Yin, Gang
Cheng, Yan
Fan, Jia
Cao, Ya
Muegge, Kathrin
Tao, Yongguang
TI Chromatin Remodeling Factor LSH Drives Cancer Progression by Suppressing
the Activity of Fumarate Hydratase
SO CANCER RESEARCH
LA English
DT Article
ID EPITHELIAL-MESENCHYMAL TRANSITION; NF-KAPPA-B; DNA METHYLATION;
GENE-EXPRESSION; NASOPHARYNGEAL CARCINOMA; STEM-CELLS; IKK-ALPHA;
EPIGENETICS; METABOLISM; PHOSPHORYLATION
AB Chromatin modification is pivotal to the epithelial-mesenchymal transition (EMT), which confers potent metastatic potential to cancer cells. Here, we report a role for the chromatin remodeling factor lymphoid-specific helicase (LSH) in nasopharyngeal carcinoma (NPC), a prevalent cancer in China. LSH expression was increased in NPC, where it was controlled by the Epstein-Barr virus-encoded protein LMP1. In NPC cells in vitro and in vivo, LSH promoted cancer progression in part by regulating expression of fumarate hydratase (FH), a core component of the tricarboxylic acid cycle. LSH bound to the FH promoter, recruiting the epigenetic silencer factor G9a to repress FH transcription. Clinically, we found that the concentration of TCA intermediates in NPC-patient sera was deregulated in the presence of LSH. RNAi-mediated silencing of FH mimicked LSH overexpression, establishing FH as downstream mediator of LSH effects. The TCA intermediates a-KG and citrate potentiated the malignant character of NPC cells, in part by altering IKK alpha-dependent EMT gene expression. In this manner, LSH furthered malignant progression of NPC by modifying cancer cell metabolism to support EMT. (C) 2016 AACR.
C1 [He, Xiaozhen; Yan, Bin; Liu, Shuang; Jia, Jiantao; Lai, Weiwei; Xin, Xing; Tang, Can-e; Jiang, Yiqun; Shi, Ying; Liu, Yating; Chen, Ling; Mao, Chao; Cao, Ya; Tao, Yongguang] Cent S Univ, Xiangya Hosp, Ctr Med Res, Changsha, Hunan, Peoples R China.
[He, Xiaozhen; Yan, Bin; Jia, Jiantao; Lai, Weiwei; Xin, Xing; Jiang, Yiqun; Shi, Ying; Liu, Yating; Chen, Ling; Mao, Chao; Cao, Ya; Tao, Yongguang] Cent S Univ, Sch Basic Med, Canc Res Inst, Changsha, Hunan, Peoples R China.
[He, Xiaozhen; Yan, Bin; Jia, Jiantao; Lai, Weiwei; Xin, Xing; Jiang, Yiqun; Shi, Ying; Liu, Yating; Chen, Ling; Mao, Chao; Cao, Ya; Tao, Yongguang] Cent S Univ, Minist Educ, Key Lab Carcinogenesis & Canc Invas, Changsha, Hunan, Peoples R China.
[He, Xiaozhen; Yan, Bin; Xin, Xing; Shi, Ying; Liu, Yating; Chen, Ling; Cao, Ya; Tao, Yongguang] Cent S Univ, Minist Hlth, Key Lab Carcinogenesis, Changsha, Hunan, Peoples R China.
[Luo, Dixian; Tan, Tan] Univ South China, Peoples Hosp Chenzhou 1, Natl & Local Joint Engn Lab High Throughput Mol D, Translat Med Inst, Chenzhou, Hunan, Peoples R China.
[Xiao, Desheng] Cent S Univ, Xiangya Hosp, Dept Pathol, Changsha, Hunan, Peoples R China.
[Liu, Shao] Cent S Univ, Xiangya Hosp, Dept Pharm, Changsha, Hunan, Peoples R China.
[Yin, Gang] Cent S Univ, Sch Basic Med, Dept Pathol, Changsha, Hunan, Peoples R China.
[Cheng, Yan] Cent S Univ, Sch Pharmaceut Sci, Dept Pharmacol, Changsha, Hunan, Peoples R China.
[Fan, Jia] Fudan Univ, Key Lab Carcinogenesis & Canc Invas, Liver Canc Inst, Liver Surg Dept,Zhongshan Hosp,Minist Educ, Shanghai, Peoples R China.
[Fan, Jia] Fudan Univ, Inst Biomed Sci, Shanghai, Peoples R China.
[Muegge, Kathrin] NCI, Mouse Canc Genet Program, Basic Sci Program, Leidos Biomed Res Inc,Frederick Natl Lab Canc Res, Frederick, MD 21701 USA.
RP Tao, YG (reprint author), Cent S Univ, Xiangya Hosp, 110 Xiangya Rd, Changsha 410078, Hunan, Peoples R China.
EM taoyong@csu.edu.cn
RI Shi, Ying-Hong/B-7063-2017
NR 56
TC 1
Z9 1
U1 5
U2 5
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD OCT
PY 2016
VL 76
IS 19
BP 5743
EP 5755
DI 10.1158/0008-5472.CAN-16-0268
PG 13
WC Oncology
SC Oncology
GA DZ1UD
UT WOS:000385625500019
PM 27302170
ER
PT J
AU Patel, YM
Park, SL
Han, YH
Wilkens, LR
Bickeboller, H
Rosenberger, A
Caporaso, N
Landi, MT
Bruske, I
Risch, A
Wei, YY
Christiani, DC
Brennan, P
Houlston, R
McKay, J
McLaughlin, J
Hung, R
Murphy, S
Stram, DO
Amos, C
Le Marchand, L
AF Patel, Yesha M.
Park, Sunghim L.
Han, Younghun
Wilkens, Lynne R.
Bickeboeller, Heike
Rosenberger, Albert
Caporaso, Neil
Landi, Maria Teresa
Brueske, Irene
Risch, Angela
Wei, Yongyue
Christiani, David C.
Brennan, Paul
Houlston, Richard
McKay, James
McLaughlin, John
Hung, Rayjean
Murphy, Sharon
Stram, Daniel O.
Amos, Christopher
Le Marchand, Loic
TI Novel Association of Genetic Markers Affecting CYP2A6 Activity and Lung
Cancer Risk
SO CANCER RESEARCH
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; NICOTINE METABOLISM; SUSCEPTIBILITY LOCUS;
ETHNIC/RACIAL GROUPS; SMOKING-BEHAVIOR; COMPLEX TRAITS; METAANALYSIS;
VARIANTS; GENOTYPE; GLUCURONIDATION
AB Metabolism of nicotine by cytochrome P450 2A6 (CYP2A6) is a suspected determinant of smoking dose and, consequently, lung cancer risk. We conducted a genome-wide association study (GWAS) of CYP2A6 activity, as measured by the urinary ratio of trans-3'-hydroxycotinine and its glucuronide conjugate over cotinine (total 3HCOT/COT), among 2,239 smokers in the Multiethnic Cohort (MEC) study. We identified 248 CYP2A6 variants associated with CYP2A6 activity (P < 5 x 10(-8)). CYP2A6 activity was correlated (r = 0.32; P < 0.0001) with total nicotine equivalents (a measure of nicotine uptake). When we examined the effect of these variants on lung cancer risk in the Transdisciplinary Research in Cancer of the Lung (TRICL) consortium GWAS dataset (13,479 cases and 43,218 controls), we found that the vast majority of these individual effects were directionally consistent and associated with an increased lung cancer risk. Two hundred and twenty-six of the 248 variants associated with CYP2A6 activity in the MEC were available in TRICL. Of them, 81% had directionally consistent risk estimates, and six were globally significantly associated with lung cancer. When conditioning on nine known functional variants and two deletions, the top two SNPs (rs56113850 in MEC and rs35755165 in TRICL) remained significantly associated with CYP2A6 activity in MEC and lung cancer in TRICL. The present data support the hypothesis that a greater CYP2A6 activity causes smokers to smoke more extensively and be exposed to higher levels of carcinogens, resulting in an increased risk for lung cancer. Although the variants identified in these studies may be used as risk prediction markers, the exact causal variants remain to be identified. (C) 2016 AACR.
C1 [Patel, Yesha M.; Park, Sunghim L.; Stram, Daniel O.] Univ Southern Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA USA.
[Patel, Yesha M.; Park, Sunghim L.; Stram, Daniel O.] Univ Southern Calif, Keck Sch Med, Norris Comprehens Canc Ctr, Los Angeles, CA USA.
[Han, Younghun; Amos, Christopher] Dartmouth Coll, Dept Biomed Data Sci, Hanover, NH 03755 USA.
[Wilkens, Lynne R.; Le Marchand, Loic] Univ Hawaii, Ctr Canc, Program Epidemiol, Honolulu, HI 96822 USA.
[Bickeboeller, Heike; Rosenberger, Albert] Univ Gottingen, Univ Med Ctr, Dept Genet Epidemiol, Gottingen, Germany.
[Caporaso, Neil; Landi, Maria Teresa] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Brueske, Irene] German Res Ctr Environm Hlth, Helmholtz Ctr Munich, Inst Epidemiol 1, Neuherberg, Germany.
[Risch, Angela] Salzburg Univ, Dept Mol Biol, Salzburg, Austria.
[Wei, Yongyue] Nanjing Med Univ, Sch Publ Hlth, Nanjing, Jiangsu, Peoples R China.
[Christiani, David C.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Christiani, David C.] Harvard Sch Publ Hlth, Dept Environm Hlth, Boston, MA USA.
[Brennan, Paul; McKay, James] Int Agcy Res Canc, Genet Epidemiol Grp, Lyon, France.
[Houlston, Richard] Inst Canc Res, Div Genet & Epidemiol, London, England.
[McLaughlin, John] Publ Hlth Ontario, Toronto, ON, Canada.
[Hung, Rayjean] Mt Sinai Hosp, Lunenfeld Tanenbaum Res Inst, Toronto, ON, Canada.
[Murphy, Sharon] Univ Minnesota, Dept Biochem Mol Biol & Biophys, Minneapolis, MN USA.
[Murphy, Sharon] Univ Minnesota, Masonic Canc Ctr, Minneapolis, MN USA.
RP Le Marchand, L (reprint author), Univ Hawaii, Ctr Canc, 701 Ilalo St,Room 530, Honolulu, HI 96813 USA.
EM loic@cc.hawaii.edu
RI Risch, Angela/H-2669-2013
OI Risch, Angela/0000-0002-8026-5505
FU CCR NIH HHS [N01RC37004]; NCI NIH HHS [K07 CA160753, N01 CN045165, N01
CN25404, N01 CN25476, N01 CN25511, N01 CN25512, N01 CN25513, N01
CN25514, N01 CN25515, N01 CN25516, N01 CN25518, N01 CN25522, N01
CN25524, N01 CN75022, P01 CA138338, P20 CA090578, P30 CA023108, P50
CA070907, P50 CA090578, R01 CA055769, R01 CA074386, R01 CA092039, R01
CA092824, R01 CA111703, R01 CA121197, R01 CA127219, R01 CA133996, U01
CA063673, U01 CA164973, U19 CA148127, UM1 CA167462]; NHGRI NIH HHS
[HHSN268200782096C, U01 HG004438, U01 HG004446]
NR 50
TC 2
Z9 2
U1 5
U2 5
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD OCT
PY 2016
VL 76
IS 19
BP 5768
EP 5776
DI 10.1158/0008-5472.CAN-16-0446
PG 9
WC Oncology
SC Oncology
GA DZ1UD
UT WOS:000385625500021
PM 27488534
ER
PT J
AU Murphy, B
Yin, H
Maris, JM
Kolb, EA
Gorlick, R
Reynolds, CP
Kang, MH
Keir, ST
Kurmasheva, RT
Dvorchik, I
Wu, JR
Billups, CA
Boateng, N
Smith, MA
Lock, RB
Houghton, PJ
AF Murphy, Brendan
Yin, Han
Maris, John M.
Kolb, E. Anders
Gorlick, Richard
Reynolds, C. Patrick
Kang, Min H.
Keir, Stephen T.
Kurmasheva, Raushan T.
Dvorchik, Igor
Wu, Jianrong
Billups, Catherine A.
Boateng, Nana
Smith, Malcolm A.
Lock, Richard B.
Houghton, Peter J.
TI Evaluation of Alternative In Vivo Drug Screening Methodology: A Single
Mouse Analysis
SO CANCER RESEARCH
LA English
DT Article
ID PRECLINICAL TESTING PROGRAM; ACUTE LYMPHOBLASTIC-LEUKEMIA; HUMAN
COLORECTAL TUMORS; IMMUNE-DEPRIVED MICE; CELL LUNG-CANCER;
MONOCLONAL-ANTIBODY; XENOGRAFT MODELS; STAGE 1; BMN 673;
RHABDOMYOSARCOMA
AB Traditional approaches to evaluating antitumor agents using human tumor xenograft models have generally used cohorts of 8 to 10 mice against a limited panel of tumor models. An alternative approach is to use fewer animals per tumor line, allowing a greater number of models that capture greater molecular/genetic heterogeneity of the cancer type. We retrospectively analyzed 67 agents evaluated by the Pediatric Preclinical Testing Program to determine whether a single mouse, chosen randomly from each group of a study, predicted the median response for groups of mice using 83 xenograft models. The individual tumor response from a randomly chosen mouse was compared with the group median response using established response criteria. A total of 2,134 comparisons were made. The single tumor response accurately predicted the group median response in 1,604 comparisons (75.16%). The mean tumor response correct prediction rate for 1,000 single mouse random samples was 78.09%. Models had a range for correct prediction (60%-87.5%). Allowing for misprediction of +/- one response category, the overall mean correct single mouse prediction rate was 95.28%, and predicted overall objective response rates for group data in 66 of 67 drug studies. For molecularly targeted agents, occasional exceptional responder models were identified and the activity of that agent confirmed in additional models with the same genotype. Assuming that large treatment effects are targeted, this alternate experimental design has similar predictive value as traditional approaches, allowing for far greater numbers of models to be used that more fully encompass the heterogeneity of disease types. (C) 2016 AACR.
C1 [Murphy, Brendan; Yin, Han; Houghton, Peter J.] Nationwide Childrens Hosp, Res Inst, Ctr Childhood Canc & Blood Dis, Columbus, OH USA.
[Maris, John M.] Univ Penn, Childrens Hosp Philadelphia, Sch Med, Dept Pediat, Philadelphia, PA 19104 USA.
[Maris, John M.] Abramson Family Canc Res Inst, Philadelphia, PA USA.
[Kolb, E. Anders] Alfred I DuPont Hosp Children, Dept Pediat, Wilmington, DE USA.
[Gorlick, Richard] Childrens Hosp Montefiore, Dept Pediat, Bronx, NY USA.
[Reynolds, C. Patrick] Texas Tech Univ, Hlth Sci Ctr, Dept Internal Med & Pediat, Lubbock, TX 79430 USA.
[Kang, Min H.] Texas Tech Univ, Hlth Sci Ctr, Dept Cell Biol & Biochem, Lubbock, TX 79430 USA.
[Keir, Stephen T.] Duke Univ, Med Ctr, Dept Surg, Durham, NC 27710 USA.
[Kurmasheva, Raushan T.; Houghton, Peter J.] Univ Texas Hlth Sci Ctr San Antonio, Greehey Childrens Canc Res Inst, Dept Mol Med, San Antonio, TX 78229 USA.
[Dvorchik, Igor] Nationwide Childrens Hosp, Res Inst, Biostat, Columbus, OH USA.
[Wu, Jianrong; Billups, Catherine A.; Boateng, Nana] St Jude Childrens Res Hosp, Dept Biostat, 332 N Lauderdale St, Memphis, TN 38105 USA.
[Smith, Malcolm A.] NCI, Clin Invest Branch, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Lock, Richard B.] Childrens Canc Inst Australia Med Res, Randwick, NSW, Australia.
RP Houghton, PJ (reprint author), Univ Texas Hlth Sci Ctr San Antonio, 8403 Floyd Curl Dr,Mail Code 7794, San Antonio, TX 78229 USA.
EM houghtonp@uthscsa.edu
RI Lock, Richard/G-4253-2013
FU NCI NIH HHS [N01 CM042216, N01CM42216, P01 CA165995, U01 CA199297]
NR 48
TC 1
Z9 1
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD OCT
PY 2016
VL 76
IS 19
BP 5798
EP 5809
DI 10.1158/0008-5472.CAN-16-0122
PG 12
WC Oncology
SC Oncology
GA DZ1UD
UT WOS:000385625500024
PM 27496711
ER
PT J
AU Xu, R
Shimizu, F
Hoyinga, K
Beal, K
Karimi, S
Droms, L
Peck, KK
Gutin, P
Iorgulescu, JB
Kaley, T
DeAngelis, L
Pentsova, E
Nolan, C
Grommes, C
Chan, T
Bobrow, D
Hormigo, A
Cross, JR
Wu, N
Takebe, N
Panageas, K
Ivy, P
Supko, JG
Tabar, V
Omuro, A
AF Xu, Ran
Shimizu, Fumiko
Hoyinga, Koos
Beal, Kathryn
Karimi, Sasan
Droms, Leif
Peck, Kyung K.
Gutin, Philip
Iorgulescu, J. Bryan
Kaley, Thomas
DeAngelis, Lisa
Pentsova, Elena
Nolan, Craig
Grommes, Christian
Chan, Timothy
Bobrow, Dylan
Hormigo, Adilia
Cross, Justin R.
Wu, Nian
Takebe, Naoko
Panageas, Katherine
Ivy, Percy
Supko, Jeffrey G.
Tabar, Viviane
Omuro, Antonio
TI Molecular and Clinical Effects of Notch Inhibition in Glioma Patients: A
Phase O/I Trial
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID GAMMA-SECRETASE INHIBITOR; ADVANCED SOLID TUMORS; NEWLY-DIAGNOSED
GLIOBLASTOMA; CANCER STEM-CELLS; SIGNALING PATHWAY; INITIATING CELLS;
RO4929097; ANGIOGENESIS; COMBINATION; GROWTH
AB Purpose: High-grade gliomas are associated with a dismal prognosis. Notch inhibition via the gamma-secretase inhibitor RO4929097 has emerged as a potential therapeutic option based on modulation of the cancer-initiating cell (CIS) population and a presumed antiangiogenic role.
Experimental Design: In this phase O/I trial, 21 patients with newly diagnosed glioblastoma or anaplastic as trocytoma received RO4929097 combined with temozolomide and radiotherapy. In addition to establishing the MTD, the study design enabled exploratory studies evaluating tumor and brain drug penetration and neuroimaging parameters. We also determined functional effects on the Notch pathway and targeting of CISs through analysis of tumor tissue sampled from areas with and without blood-brain barrier disruption. Finally, recurrent tumors were also sampled and assessed for Notch pathway responses while on treatment.
Results: Treatment was well tolerated and no dose-limiting toxicities were observed. 1FIC of treated tumors showed a significant decrease in proliferation and in the expression of the Notch intracellular domain (NICD) by tumor cells and blood vessels. Patient-specific organotypic tumor explants cultures revealed a specific decrease in the CD133(+) CIS population upon treatment. Perfusion MRI demonstrated a significant decrease in relative plasma volume after drug exposure. Gene expression data in recurrent tumors suggested low Notch signaling activity, the upregulation of key mesenchymal genes, and an increase in VEGF-dependent angiogenic factors.
Conclusions: The addition of RO4929097 to temozolomide and radiotherapy was well tolerated; the drug has a variable blood-brain barrier penetration. Evidence of target modulation was observed, but recurrence occurred, associated with alterations in angiogenesis signaling pathways. (C) 2016 AACR.
C1 [Xu, Ran; Shimizu, Fumiko; Hoyinga, Koos; Droms, Leif; Gutin, Philip; Iorgulescu, J. Bryan; Tabar, Viviane] Mem Sloan Kettering Canc Ctr, Dept Neurosurg, 1275 York Ave, New York, NY 10065 USA.
[Xu, Ran; Shimizu, Fumiko; Hoyinga, Koos; Droms, Leif; Gutin, Philip; Iorgulescu, J. Bryan; Tabar, Viviane] Mem Sloan Kettering Canc Ctr, Ctr Stem Cell Biol, 1275 York Ave, New York, NY 10021 USA.
[Xu, Ran] Charite, Dept Neurosurg, Berlin, Germany.
[Beal, Kathryn; Chan, Timothy] Mem Sloan Kettering Canc Ctr, Dept Radiat Oncol, 1275 York Ave, New York, NY 10021 USA.
[Karimi, Sasan; Peck, Kyung K.] Mem Sloan Kettering Canc Ctr, Dept Radiol, 1275 York Ave, New York, NY 10021 USA.
[Kaley, Thomas; DeAngelis, Lisa; Pentsova, Elena; Nolan, Craig; Grommes, Christian; Bobrow, Dylan; Hormigo, Adilia; Omuro, Antonio] Mem Sloan Kettering Canc Ctr, Dept Neurol, 1275 York Ave, New York, NY 10021 USA.
[Hormigo, Adilia] Icahn Sch Med Mt Sinai, Dept Neurol, New York, NY 10029 USA.
[Hormigo, Adilia] Icahn Sch Med Mt Sinai, Dept Med, New York, NY 10029 USA.
[Hormigo, Adilia] Icahn Sch Med Mt Sinai, Dept Neurosurg, New York, NY 10029 USA.
[Hormigo, Adilia] Icahn Sch Med Mt Sinai, Tisch Canc Inst, New York, NY 10029 USA.
[Cross, Justin R.] Mem Sloan Kettering Canc Ctr, Donald B & Catherine C Marron Canc Metab Ctr, 1275 York Ave, New York, NY 10021 USA.
[Wu, Nian] Mem Sloan Kettering Canc Ctr, Analyt Pharmacol Core, 1275 York Ave, New York, NY 10021 USA.
[Wu, Nian] LipoSeuticals Inc, Princeton, NJ USA.
[Takebe, Naoko] NCI, Canc Therapy Evaluat Program, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
[Panageas, Katherine] Mem Sloan Kettering Canc Ctr, Epidemiol & Stat, 1275 York Ave, New York, NY 10021 USA.
[Ivy, Percy] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Supko, Jeffrey G.] Harvard Med Sch, Massachusetts Gen Hosp, Boston, MA USA.
[Iorgulescu, J. Bryan] Harvard Med Sch, Brigham & Womens Hosp, Dept Pathol, Boston, MA USA.
RP Tabar, V (reprint author), Mem Sloan Kettering Canc Ctr, Dept Neurosurg, 1275 York Ave, New York, NY 10065 USA.
EM tabarv@mskcc.org
FU NIH/NCI (NCI Cancer Clinical Investigator Team Leadership Award)
[3P30CA008748-47S2, U01CA069856]; B*Cured Foundation; Philadelphia
Foundation; Have a Chance Foundation
FX The study was partially funded by NIH/NCI through grants
3P30CA008748-47S2 (NCI Cancer Clinical Investigator Team Leadership
Award; to A.M.P. Omuro) and U01CA069856. Additional funding was provided
by B*Cured Foundation, Philadelphia Foundation, and Have a Chance
Foundation.
NR 36
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Z9 6
U1 4
U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD OCT 1
PY 2016
VL 22
IS 19
BP 4786
EP 4796
DI 10.1158/1078-0432.CCR-16-0048
PG 11
WC Oncology
SC Oncology
GA DZ1VV
UT WOS:000385630500006
PM 27154916
ER
PT J
AU Muller, F
Cunningham, T
Liu, XF
Wayne, AS
Pastan, I
AF Mueller, Fabian
Cunningham, Tyler
Liu, Xiu Fen
Wayne, Alan S.
Pastan, Ira
TI Wide Variability in the Time Required for Immunotoxins to Kill B Lineage
Acute Lymphoblastic Leukemia Cells: Implications for Trial Design
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID PHASE-II TRIAL; RECOMBINANT IMMUNOTOXIN; ANTI-CD22 IMMUNOTOXIN;
RFB4(DSFV)-PE38 BL22; MOXETUMOMAB PASUDOTOX; IN-VITRO; THERAPY;
BLINATUMOMAB; MALIGNANCIES; CONJUGATE
AB Purpose: Recombinant immunotoxins (rITs) targeting CD22 are highly active in hairy cell leukemia, but less so in acute lymphoblastic leukemia (ALL). This study aims to understand the variable activity of an rIT against ALL toward improving responses in clinical application.
Experimental Design: We determined in vitro activity of rITs by WST-8 assays and the time needed to kill ALL cell lines and patient-derived ALL blasts by flow cytometry. The findings were translated into two systemic ALL xenograft models. Differences in time needed to kill KOPN-8 cells for distinct rITs were addressed biochemically.
Results: In vitro activity (IC50) of anti-CD22 rIT varied 210-fold from 0.02 to 4.6 ng/mL. Activity also varied greatly depending on the time ALL cells were exposed to immunotoxin from < 30 minutes to > 4 days. For KOPN-8, the difference in exposure time was related to intracellular rIT processing. We showed in newly developed ALL xenograft models, where immunotoxins have a short half-life, that the needed exposure time in vitro predicted the responses in vivo. By replacing bolus dose with small doses at frequent intervals or with continuous infusion, responses were substantially improved. We confirmed exposure time variability on patient-derived ALL samples and showed a correlation between exposure time needed to reach maximal cytotoxicity in vitro and their clinical response.
Conclusions: The exposure time needed for rITs targeting CD22 to kill ALL cells varies widely. Our results suggest that ALL patients would have a better response rate to anti-CD22 immunotoxins if treated by continuous infusion rather than by bolus injections. (C) 2016 AACR.
C1 [Mueller, Fabian; Cunningham, Tyler; Liu, Xiu Fen; Pastan, Ira] NCI, Mol Biol Lab, NIH, Bldg 37, Bethesda, MD 20892 USA.
[Wayne, Alan S.] Univ Southern Calif, Keck Sch Med, Norris Comprehens Canc Ctr,Childrens Ctr Canc & B, Childrens Hosp Los Angeles,Div Hematol Oncol & Bl, Los Angeles, CA USA.
RP Pastan, I (reprint author), NCI, NIH, 37 Convent Dr,Rm 5106, Bethesda, MD 20892 USA.
EM pastani@mail.nih.gov
FU NCI [P30CA014089]; Intramural Research Program of the NIH, National
Cancer Institute, Center for Cancer Research; Medimmune, LLC; German
Research Foundation [MU 3619/1 1]; Cooperative Research and Development
Agreement
FX The work was supported in part by award number P30CA014089 from the NCI,
the Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research, and with a Cooperative Research and
Development Agreement (#1975) with Medimmune, LLC. F. Muller was
supported in part by the German Research Foundation (award number MU
3619/1 1).
NR 42
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U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD OCT 1
PY 2016
VL 22
IS 19
BP 4913
EP 4922
DI 10.1158/1078-0432.CCR-15-2500
PG 10
WC Oncology
SC Oncology
GA DZ1VV
UT WOS:000385630500018
PM 27114443
ER
PT J
AU Lozier, JN
Kloos, MT
Merricks, EP
Lemoine, N
Whitford, MH
Raymer, RA
Bellinger, DA
Nichols, TC
AF Lozier, Jay N.
Kloos, Mark T.
Merricks, Elizabeth P.
Lemoine, Nathaly
Whitford, Margaret H.
Raymer, Robin A.
Bellinger, Dwight A.
Nichols, Timothy C.
TI Severe Hemophilia A in a Male Old English Sheep Dog with a C -> T
Transition that Created a Premature Stop Codon in Factor VIII
SO COMPARATIVE MEDICINE
LA English
DT Article
ID DEFICIENT MOUSE MODEL; MOLECULAR CHARACTERIZATION; INHIBITOR
DEVELOPMENT; BLEEDING DISORDERS; ANIMAL-MODELS; GENE; MUTATION;
SPECTRUM; DISEASE; IDENTIFICATION
AB Animals with hemophilia are models for gene therapy, factor replacement, and inhibitor development in humans. We have actively sought dogs with severe hemophilia A that have novel factor VIII mutations unlike the previously described factor VIII intron 22 inversion. A male Old English Sheepdog with recurrent soft-tissue hemorrhage and hemarthrosis was diagnosed with severe hemophilia A (factor VIII activity less than 1% of normal). We purified genomic DNA from this dog and ruled out the common intron 22 inversion; we then sequenced all 26 exons. Comparing the results with the normal canine factor VIII sequence revealed a C -> T transition in exon 12 of the factor VIII gene that created a premature stop codon at amino acid 577 in the A2 domain of the protein. In addition, 2 previously described polymorphisms that do not cause hemophilia were present at amino acids 909 and 1184. The hemophilia mutation creates a new TaqI site that facilitates rapid genotyping of affected offspring by PCR and restriction endonuclease analyses. This mutation is analogous to the previously described human factor VIII mutation at Arg583, which likewise is a CpG dinucleotide transition causing a premature stop codon in exon 12. Thus far, despite extensive treatment with factor VIII, this dog has not developed neutralizing antibodies ('inhibitors') to the protein. This novel mutation in a dog gives rise to severe hemophilia A analogous to a mutation seen in humans. This model will be useful for studies of the treatment of hemophilia.
C1 [Lozier, Jay N.] NIH, Dept Lab Med, Ctr Clin, Bldg 10, Bethesda, MD 20892 USA.
[Kloos, Mark T.; Merricks, Elizabeth P.; Lemoine, Nathaly; Whitford, Margaret H.; Raymer, Robin A.; Bellinger, Dwight A.; Nichols, Timothy C.] Univ North Carolina Chapel Hill, Dept Pathol & Lab Med, Chapel Hill, NC 27599 USA.
RP Nichols, TC (reprint author), Univ North Carolina Chapel Hill, Dept Pathol & Lab Med, Chapel Hill, NC 27599 USA.
EM tnichols@med.unc.edu
FU NIH Intramural Research Program; NHLBI [HL63098]
FX Funded by the NIH Intramural Research Program and NHLBI grant no.
HL63098.
NR 50
TC 0
Z9 0
U1 2
U2 2
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI MEMPHIS
PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA
SN 1532-0820
J9 COMPARATIVE MED
JI Comparative Med.
PD OCT
PY 2016
VL 66
IS 5
BP 405
EP 411
PG 7
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA DZ1OP
UT WOS:000385608000007
PM 27780008
ER
PT J
AU Cadena, AM
Klein, EC
White, AG
Tomko, JA
Chedrick, CL
Reed, DS
Via, LE
Lin, PL
Flynn, JL
AF Cadena, Anthony M.
Klein, Edwin C.
White, Alexander G.
Tomko, Jaime A.
Chedrick, Chelsea L.
Reed, Douglas S.
Via, Laura E.
Lin, Philana Ling
Flynn, JoAnne L.
TI Very Low Doses of Mycobacterium tuberculosis Yield Diverse Host Outcomes
in Common Marmosets (Callithrix jacchus)
SO COMPARATIVE MEDICINE
LA English
DT Article
ID CYNOMOLGUS MACAQUES; BIOMEDICAL-RESEARCH; INFECTION; MODEL; VIRULENCE;
DISEASE
AB Identifying and refining small-animal models of tuberculosis that recapitulate aspects of human Mycobacterium tuberculosis infection can contribute to advancing our understanding of critical facets of the disease. To study the effects of very low-dose infections with 2 strains of M. tuberculosis on disease progression and survival in common marmosets, animals were challenged with strains Erdman and CDC1551 at doses ranging from 1 to 12 cfu. These data revealed that the susceptibility of marmosets to M. tuberculosis infection is influenced by strain virulence and initial dose. Marmoset infection with the Erdman strain, even at very low doses, resulted in rapid disease progression associated with severe weight loss, extensive pathology, and poor survival. By contrast, challenge with the less virulent CDC1551 strain resulted in slower disease progression, delayed weight loss, and prolonged survival. One marmoset infected with CDC1551 at a very low dose (approximately 1 cfu) was able to contain and control M. tuberculosis infection in a subclinical state that persisted as long as 300 d. These findings underscore the critical importance of understanding the heterogeneity in host outcome that can arise in association with different infectious doses and strains in the marmoset model of tuberculosis.
C1 [Cadena, Anthony M.; White, Alexander G.; Tomko, Jaime A.; Chedrick, Chelsea L.; Flynn, JoAnne L.] Univ Pittsburgh, Sch Med, Dept Microbiol & Mol Genet, Pittsburgh, PA 15260 USA.
[Klein, Edwin C.] Univ Pittsburgh, Sch Med, Dept Immunol, Ctr Vaccine Res, Pittsburgh, PA USA.
[Reed, Douglas S.] Univ Pittsburgh, Div Lab Anim Res, Pittsburgh, PA USA.
[Via, Laura E.] NIAID, TB Res Sect, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Via, Laura E.] Univ Cape Town, Dept Pathol, Inst Infect Dis & Mol Med, Cape Town, South Africa.
[Lin, Philana Ling] Univ Pittsburgh, Childrens Hosp Pittsburgh UPMC, Sch Med, Div Infect Dis,Dept Pediat, Pittsburgh, PA USA.
RP Flynn, JL (reprint author), Univ Pittsburgh, Sch Med, Dept Microbiol & Mol Genet, Pittsburgh, PA 15260 USA.
EM joanne@pitt.edu
FU NIH training grant [T32 AI089443]; Bill and Melinda Gates Foundation
[OPP1034408]; intramural research program of NIAID, NIH
FX We thank Mark Rodgers, Carolyn Bigbee, Catherine Cochran, and Charles
Scanga for technical assistance. We also thank Daniel Filmore for
veterinary and animal assistance. We gratefully acknowledge Pauline
Maiello and Teresa Coleman for imaging support and Danielle Weiner,
Daniel Schimel, and Manny Dayao for veterinary assistance at NIAID.
These studies were funded in part by a NIH training grant (T32 AI089443
[to AMC]), the Bill and Melinda Gates Foundation (grant no. OPP1034408
[to JLF]), and the intramural research program of NIAID, NIH (to LEV).
NR 23
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Z9 0
U1 2
U2 2
PU AMER ASSOC LABORATORY ANIMAL SCIENCE
PI MEMPHIS
PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA
SN 1532-0820
J9 COMPARATIVE MED
JI Comparative Med.
PD OCT
PY 2016
VL 66
IS 5
BP 412
EP 419
PG 8
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA DZ1OP
UT WOS:000385608000008
PM 27780009
ER
PT J
AU Wang, XW
Wang, HR
Guo, B
Zhang, Y
Gong, Y
Zhang, C
Xu, H
Wu, XH
AF Wang, Xiaowen
Wang, Herui
Guo, Bin
Zhang, Ya
Gong, Yinv
Zhang, Chi
Xu, Hong
Wu, Xiaohui
TI Gen1 and Eme1 Play Redundant Roles in DNA Repair and Meiotic
Recombination in Mice
SO DNA AND CELL BIOLOGY
LA English
DT Article
DE Gen1; Eme1; DNA repair; meiotic recombination
ID HOLLIDAY JUNCTION RESOLVASE; STRUCTURE-SPECIFIC NUCLEASES;
MAMMALIAN-CELLS; RESOLUTION; MUS81-EME1; SLX1-SLX4; YEN1; PATHWAYS;
MEIOSIS; YEAST
AB Resolution of the Holliday junction (HJ) is essential for homologous recombination and DNA repair. In Saccharomyces cerevisiae, HJ resolvase Yen1 and the Mus81-Mms4 complex are redundant in DNA damage repair. In cultured mammalian cells, such redundancy also exists between Yen1 ortholog GEN1 and the Mus81-Mms1 ortholog MUS81-EME1. In this report, we further tested if GEN1 and EME1 redundantly affect HJ-related physiological processes in mice. We found that combined homozygous mutations of Gen1 and Eme1 led to synthetic lethality during early embryonic stages. Homozygous Gen1 mutations did not cause DNA repair deficiency in mouse embryonic fibroblast (MEF) cells, but made heterozygous Eme1 mutant MEFs more sensitive to various DNA-damaging reagents. Gen1 mutations also reduced the meiotic recombination efficiency in Eme1 mutant mice. These results suggest that Gen1 and Eme1 play redundant roles in DNA repair and meiotic recombination in vivo.
C1 [Wang, Xiaowen; Zhang, Ya; Gong, Yinv; Xu, Hong; Wu, Xiaohui] Fudan Univ, Childrens Hosp, Shanghai Kidney Dev & Pediat Kidney Dis Res Ctr, Shanghai, Peoples R China.
[Wang, Xiaowen] Wuhan Med & Healthcare Ctr Women & Children, Dept Nephrol, Wuhan, Peoples R China.
[Wang, Herui; Guo, Bin; Zhang, Chi; Wu, Xiaohui] Fudan Univ, Collaborat Innovat Ctr Genet & Dev, Inst Dev Biol & Mol Med, State Key Lab Genet Engn,Sch Life Sci, Shanghai, Peoples R China.
[Wang, Herui; Guo, Bin; Zhang, Chi; Wu, Xiaohui] Fudan Univ, Collaborat Innovat Ctr Genet & Dev, Inst Dev Biol & Mol Med, Natl Ctr Int Res Dev & Dis,Sch Life Sci, Shanghai, Peoples R China.
[Wang, Herui] Natl Inst Neurol Disorders & Stroke, Surg Neurol Branch, NIH, Bethesda, MD USA.
[Zhang, Chi] Univ Colorado, Dept Mol Cellular & Dev Biol, Boulder, CO 80309 USA.
RP Wu, XH (reprint author), Fudan Univ, Inst Dev Biol & Mol Med, Shanghai 200433, Peoples R China.; Xu, H (reprint author), Fudan Univ, Childrens Hosp, Dept Nephrol & Rheumatol, Shanghai 201102, Peoples R China.
EM hxu@shmu.edu.cn; xiaohui_wu@fudan.edu.cn
FU National Natural Science Foundation of China [81270763]; Chinese Hi-Tech
Research and Development Project [2014AA021104]; Chinese Key Projects
for Basic Research [2011CB944001]; Shanghai Municipal Government
[15XD1500500, 12431900100]; State Key Laboratory of Genetic Engineering,
Fudan University
FX The authors thank Dr. Kai Lei, Zhisheng Ye, and Xiaoqiang Zhu for
helpful discussion, and Guicheng Wang, Yanyan Nie, Xiaorong Huang, and
Zhiyan Xia for technical assistance. This study was supported by grants
from the National Natural Science Foundation of China (81270763),
Chinese Hi-Tech Research and Development Project (2014AA021104), Chinese
Key Projects for Basic Research (2011CB944001), Shanghai Municipal
Government (15XD1500500 and 12431900100), and the Research Fund of the
State Key Laboratory of Genetic Engineering, Fudan University.
NR 31
TC 0
Z9 0
U1 3
U2 3
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1044-5498
EI 1557-7430
J9 DNA CELL BIOL
JI DNA Cell Biol.
PD OCT
PY 2016
VL 35
IS 10
BP 585
EP 590
DI 10.1089/dna.2015.3022
PG 6
WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity
GA DZ2DV
UT WOS:000385653400004
PM 27383418
ER
PT J
AU Woloshchuk, CJ
Nelson, KH
Rice, KC
Riley, AL
AF Woloshchuk, Claudia J.
Nelson, Katharine H.
Rice, Kenner C.
Riley, Anthony L.
TI Effects of 3,4-methylenedioxypyrovalerone (MDPV) pre-exposure on the
aversive effects of MDPV, cocaine and lithium chloride: Implications for
abuse vulnerability
SO DRUG AND ALCOHOL DEPENDENCE
LA English
DT Article
DE MDPV; Cocaine; LiCl; Conditioned taste avoidance; Drug pre-exposure
ID INTRACRANIAL SELF-STIMULATION; CONDITIONED PLACE PREFERENCE;
TASTE-AVERSION; BATH SALTS; CONSTITUENT 3,4-METHYLENEDIOXYPYROVALERONE;
DESIGNER CATHINONES; LOCOMOTOR-ACTIVITY; RAT STRAINS; MEPHEDRONE; MICE
AB Background: Drug use is thought to be a balance of the rewarding and aversive effects of drugs. Understanding how various factors impact these properties and their relative balance may provide insight into their abuse potential. In this context, the present study attempted to evaluate the effects of drug history on the aversive effects of 3,4-methylenedioxypyrovalerone (MDPV), one of a variety of synthetic cathinones (collectively known as "bath salts").
Methods: Different groups of male Sprague-Dawley rats were exposed to either vehicle or MDPV (1.8 mg/kg) once every fourth day for five total injections prior to taste avoidance conditioning in which a novel saccharin solution was repeatedly paired with either vehicle, MDPV (1.8 mg/kg), the related psychostimulant cocaine (18 mg/kg) or the emetic lithium chloride (LiCl) (13.65 mg/kg).
Results: In animals pre-exposed to vehicle, all three drugs induced significant and comparable taste avoidance relative to animals injected with vehicle during conditioning. MDPV pre-exposure attenuated the avoidance induced by both MDPV and cocaine (greater attenuation for MDPV than cocaine), but had no effect on that induced by LiCl.
Conclusions: These findings suggest that a history of MDPV use may reduce or attenuate MDPV and cocaine's (but not Lid 's) aversive effects. The implications for such changes in MDPV's aversive effects to its potential use and abuse were discussed. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
C1 [Woloshchuk, Claudia J.; Nelson, Katharine H.; Riley, Anthony L.] Amer Univ, Ctr Behav Neurosci, Psychopharmacol Lab, 4400 Massachusetts Ave NW, Washington, DC 20016 USA.
[Rice, Kenner C.] NIDA, Mol Targets & Medicat Discovery Branch, NIAAA, Bethesda, MD 20892 USA.
RP Woloshchuk, CJ (reprint author), Amer Univ, Ctr Behav Neurosci, Psychopharmacol Lab, 4400 Massachusetts Ave NW, Washington, DC 20016 USA.
EM cw2606a@student.american.edu; alriley@american.edu
FU Mellon Foundation
FX This research was supported in part by a grant from the Mellon
Foundation to ALR. The Mellon Foundation had no further role in the
study design, data collection, analysis and interpretation, the writing
of the report or the decision to submit the manuscript for publication.
NR 65
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U1 1
U2 1
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 2016
VL 167
BP 121
EP 127
DI 10.1016/j.drugalcdep.2016.08.008
PG 7
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA DY7QT
UT WOS:000385325100017
PM 27520883
ER
PT J
AU Heinssen, R
McGorry, P
Nordentoft, M
AF Heinssen, Robert
McGorry, Patrick
Nordentoft, Merete
TI RAISE 2.0-Establishing a National Early Psychosis Intervention Network
in the US
SO EARLY INTERVENTION IN PSYCHIATRY
LA English
DT Meeting Abstract
C1 [Heinssen, Robert] NIMH, Div Serv & Intervent Res, Bethesda, MD 20892 USA.
[McGorry, Patrick] Univ Melbourne, Ctr Youth Mental Hlth, Orygen, Parkville, Vic, Australia.
[Nordentoft, Merete] Univ Copenhagen, Mental Hlth Serv Capital Reg Denmark, DK-1168 Copenhagen, Denmark.
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 1751-7885
EI 1751-7893
J9 EARLY INTERV PSYCHIA
JI Early Interv. Psychiatry
PD OCT
PY 2016
VL 10
SU 1
BP 4
EP 4
PG 1
WC Psychiatry
SC Psychiatry
GA DZ1EX
UT WOS:000385582800004
ER
PT J
AU Adelsheim, S
Harrison, V
Heinssen, R
Lowe, JI
Blau, GM
AF Adelsheim, Steven
Harrison, Vicki
Heinssen, Robert
Lowe, Jane Isaacs
Blau, Gary M.
TI Implementation of a National Early Psychosis Clinical Support Program in
the United States: The Prodrome and Early Psychosis Program Network
(PEPPNET)
SO EARLY INTERVENTION IN PSYCHIATRY
LA English
DT Meeting Abstract
C1 [Adelsheim, Steven; Harrison, Vicki] Stanford Univ, Palo Alto, CA 94304 USA.
[Heinssen, Robert] NIMH, Div Serv & Intervent Res, Bethesda, MD 20892 USA.
[Lowe, Jane Isaacs] Robert Wood Johnson Fdn, Princeton, NJ 08540 USA.
[Blau, Gary M.] Subst Abuse & Mental Hlth Serv Adm, Ctr Mental Hlth Serv, 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 1751-7885
EI 1751-7893
J9 EARLY INTERV PSYCHIA
JI Early Interv. Psychiatry
PD OCT
PY 2016
VL 10
SU 1
BP 23
EP 23
PG 1
WC Psychiatry
SC Psychiatry
GA DZ1EX
UT WOS:000385582800062
ER
PT J
AU Addington, J
Cadenhead, KS
Cannon, TD
Cornblatt, BA
McGlashan, TH
Perkins, DO
Seidman, LJ
Walker, EF
Woods, S
Bearden, CE
Mathalon, D
Buchy, L
AF Addington, Jean
Cadenhead, Kristin S.
Cannon, Tyrone D.
Cornblatt, Barbara A.
McGlashan, Thomas H.
Perkins, Diana O.
Seidman, Larry J.
Walker, Elaine F.
Woods, Scott
Bearden, Carrie E.
Mathalon, Daniel
Buchy, Lisa
TI Cannabis Use in Individuals at Clinical High Risk of Psychosis
SO EARLY INTERVENTION IN PSYCHIATRY
LA English
DT Meeting Abstract
C1 [Addington, Jean; Buchy, Lisa] Univ Calgary, Calgary, AB T2N 1N4, Canada.
[Cadenhead, Kristin S.] Univ Calif San Diego, San Diego, CA 92103 USA.
[Cannon, Tyrone D.; McGlashan, Thomas H.; Woods, Scott] Yale Univ, New Haven, CT USA.
[Cornblatt, Barbara A.] Zucker Hillside Hosp, New York, NY USA.
[Perkins, Diana O.] Univ N Carolina, Chapel Hill, NC 27515 USA.
[Seidman, Larry J.] Harvard Med Sch, Beth Israel Deaconess Med Ctr, Boston, MA USA.
[Seidman, Larry J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Walker, Elaine F.] Emory Univ, Atlanta, GA 30322 USA.
NIMH, Bethesda, MD 20892 USA.
[Bearden, Carrie E.] Univ Calif Los Angeles, Los Angeles, CA USA.
[Mathalon, Daniel] Univ Calif San Francisco, San Francisco, CA 94143 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1751-7885
EI 1751-7893
J9 EARLY INTERV PSYCHIA
JI Early Interv. Psychiatry
PD OCT
PY 2016
VL 10
SU 1
BP 30
EP 30
PG 1
WC Psychiatry
SC Psychiatry
GA DZ1EX
UT WOS:000385582800084
ER
PT J
AU Adelsheim, S
Harrison, V
Heinssen, R
Lowe, JI
Blau, GM
AF Adelsheim, Steven
Harrison, Vicki
Heinssen, Robert
Lowe, Jane Isaacs
Blau, Gary M.
TI Creating a National Early Psychosis Clinical Support Program in the
United States: The Development of the Prodrome and Early Psychosis
Program Network (PEPPNET)
SO EARLY INTERVENTION IN PSYCHIATRY
LA English
DT Meeting Abstract
C1 [Adelsheim, Steven; Harrison, Vicki] Stanford Univ, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA.
[Heinssen, Robert] NIMH, Div Serv & Intervent Res, Bethesda, MD 20892 USA.
[Lowe, Jane Isaacs] Robert Wood Johnson Fdn, Program Dev, Princeton, NJ 08540 USA.
[Blau, Gary M.] Subst Abuse & Mental Hlth Serv Adm, Ctr Mental Hlth Serv, 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 1751-7885
EI 1751-7893
J9 EARLY INTERV PSYCHIA
JI Early Interv. Psychiatry
PD OCT
PY 2016
VL 10
SU 1
BP 99
EP 99
PG 1
WC Psychiatry
SC Psychiatry
GA DZ1EX
UT WOS:000385582800295
ER
PT J
AU Schooler, N
Mueser, K
Estroff, S
Correll, C
Robinson, D
Marcy, P
Severe, J
Azrin, S
Goldstein, A
Heinssen, R
Kane, J
AF Schooler, Nina
Mueser, Kim
Estroff, Sue
Correll, Christoph
Robinson, Delbert
Marcy, Patricia
Severe, Joanne
Azrin, Susan
Goldstein, Amy
Heinssen, Robert
Kane, John
TI Elements of Recovery in First Episode Psychosis: Developing Measurable
Criteria
SO EARLY INTERVENTION IN PSYCHIATRY
LA English
DT Meeting Abstract
C1 [Schooler, Nina; Kane, John] Suny Downstate Med Ctr, Brooklyn, NY 11203 USA.
[Mueser, Kim] Boston Univ, Boston, MA 02215 USA.
[Estroff, Sue] Univ N Carolina, Chapel Hill, NC USA.
[Correll, Christoph; Robinson, Delbert] Zucker Hillside Hosp, New York, NY USA.
[Correll, Christoph; Robinson, Delbert; Marcy, Patricia] Northwell Hlth Syst NY, Great Neck, NY USA.
[Severe, Joanne; Azrin, Susan; Goldstein, Amy; Heinssen, Robert] NIMH, 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 1751-7885
EI 1751-7893
J9 EARLY INTERV PSYCHIA
JI Early Interv. Psychiatry
PD OCT
PY 2016
VL 10
SU 1
MA A106
BP 149
EP 149
PG 1
WC Psychiatry
SC Psychiatry
GA DZ1EX
UT WOS:000385582800445
ER
PT J
AU Vyas, NS
Lehrer, DS
Merrill, B
DeCastro, A
Doninger, NA
Christian, BT
Buchsbaum, MS
AF Vyas, Nora S.
Lehrer, Douglas S.
Merrill, Brian
DeCastro, Alex
Doninger, Nicholas A.
Christian, Bradley T.
Buchsbaum, Monte S.
TI D2/D3 Dopamine Receptor Binding with [F-18] fallypride correlates of
executive function in medication-naive patients with schizophrenia
SO EARLY INTERVENTION IN PSYCHIATRY
LA English
DT Meeting Abstract
C1 [Vyas, Nora S.] Kingston Univ London, Kingston Upon Thames, Surrey, England.
[Vyas, Nora S.] NIH, Bldg 10, Bethesda, MD 20892 USA.
[Vyas, Nora S.] Imperial Coll Healthcare NHS Trust, London, England.
[Lehrer, Douglas S.; Merrill, Brian] Wright State Univ, Dayton, OH 45435 USA.
[DeCastro, Alex; Buchsbaum, Monte S.] Univ Calif San Diego, La Jolla, CA 92093 USA.
[Doninger, Nicholas A.] Wright State Univ, SOM, Dayton, OH 45435 USA.
[Christian, Bradley T.] Univ Wisconsin, Madison, WI 53706 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1751-7885
EI 1751-7893
J9 EARLY INTERV PSYCHIA
JI Early Interv. Psychiatry
PD OCT
PY 2016
VL 10
SU 1
BP 246
EP 246
PG 1
WC Psychiatry
SC Psychiatry
GA DZ1EX
UT WOS:000385582800758
ER
PT J
AU Hoffmann, GR
Shelby, MD
Zeiger, E
AF Hoffmann, George R.
Shelby, Michael D.
Zeiger, Errol
TI Remembering Heinrich Malling In Memoriam
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Biographical-Item
C1 [Hoffmann, George R.] Coll Holy Cross, Dept Biol, One Coll St, Worcester, MA 01610 USA.
[Shelby, Michael D.] NIEHS, POB 12233, Res Triangle Pk, NC 27709 USA.
[Zeiger, Errol] Errol Zeiger Consulting, Chapel Hill, NC 27514 USA.
RP Hoffmann, GR (reprint author), Coll Holy Cross, Dept Biol, One Coll St, Worcester, MA 01610 USA.
EM ghoffmann@holycross.edu
NR 1
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0893-6692
EI 1098-2280
J9 ENVIRON MOL MUTAGEN
JI Environ. Mol. Mutagen.
PD OCT
PY 2016
VL 57
IS 8
BP 575
EP 578
DI 10.1002/em.22056
PG 4
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA DZ4OA
UT WOS:000385836800001
PM 27696552
ER
PT J
AU Dai, YF
Niu, Y
Duan, HW
Bassig, BA
Ye, M
Zhang, X
Meng, T
Bin, P
Jia, XW
Shen, ML
Zhang, R
Hu, W
Yang, XF
Vermeulen, R
Silverman, D
Rothman, N
Lan, Q
Yu, SF
Zheng, YX
AF Dai, Yufei
Niu, Yong
Duan, Huawei
Bassig, Bryan A.
Ye, Meng
Zhang, Xiao
Meng, Tao
Bin, Ping
Jia, Xiaowei
Shen, Meili
Zhang, Rong
Hu, Wei
Yang, Xiaofa
Vermeulen, Roel
Silverman, Debra
Rothman, Nathaniel
Lan, Qing
Yu, Shanfa
Zheng, Yuxin
TI Effects of occupational exposure to carbon black on peripheral white
blood cell counts and lymphocyte subsets
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Article
DE carbon black; occupational exposure; inflammation; immunotoxicity
ID LUNG-CANCER; PARTICULATE MATTER; INHALED PARTICLES; COHORT MORTALITY;
DIESEL EXHAUST; AIR-POLLUTION; INFLAMMATION; WORKERS; HEALTH; DISEASE
AB The International Agency for Research on Cancer has classified carbon black (CB) as a possible (Group 2B) human carcinogen. Given that most CB manufacturing processes result in the emission of various types of chemicals, it is uncertain if the adverse health effects that have been observed in CB-exposed workers are related to CB specifically or are due to other exposures. To address this issue, we conducted a cross-sectional molecular epidemiology study in China of 106 male factory workers who were occupationally exposed to pure CB and 112 unexposed male workers frequency-matched by age and smoking status from the same geographic region. Repeated personal exposure measurements were taken in workers before biological sample collection. Peripheral blood from all workers was used for the complete blood cell count and lymphocyte subsets analysis. Compared to unexposed workers, eosinophil counts in workers exposed to CB were increased by 30.8% (P=0.07) after adjusting for potential confounders. When stratified by smoking status, statistically significant differences in eosinophils between CB exposed and unexposed workers were only present among never smokers (P=0.040). Smoking is associated with alterations in various cell counts; however, no significant interaction between CB exposure and smoking status for any cell counts was observed. Given that inflammation, characterized in part by elevated eosinophils in peripheral blood, may be associated with increased cancer risk, our findings provide new biologic insights into the potential relationship between CB exposure and lung carcinogenesis. Environ. Mol. Mutagen. 57:589-604, 2016. (c) 2016 Wiley Periodicals, Inc.
C1 [Dai, Yufei; Niu, Yong; Duan, Huawei; Ye, Meng; Zhang, Xiao; Meng, Tao; Bin, Ping; Jia, Xiaowei; Shen, Meili; Zhang, Rong; Zheng, Yuxin] Chinese Ctr Dis Control & Prevent, Natl Inst Occupat Hlth & Poison Control, Key Lab, Beijing 100050, Peoples R China.
[Dai, Yufei; Bassig, Bryan A.; Hu, Wei; Silverman, Debra; Rothman, Nathaniel; Lan, Qing] NCI, Occupat & Environm Epidemiol Branch, Rockville, MD 20850 USA.
[Zhang, Rong] Hebei Med Univ, Dept Toxicol, Sch Publ Hlth, Shijiazhuang, Peoples R China.
[Yang, Xiaofa] Jiao Zuo Ctr Dis Control & Prevent, Jiaozuo, Peoples R China.
[Vermeulen, Roel] Univ Utrecht, Inst Risk Assessment Sci, Div Environm Epidemiol, Utrecht, Netherlands.
[Yu, Shanfa] Henan Prov Inst Occupat Hlth, Zhengzhou, Peoples R China.
RP Lan, Q (reprint author), NCI, Occupat & Environm Epidemiol Branch, Rockville, MD 20850 USA.; Yu, SF (reprint author), Henan Prov Inst Occupat Hlth, Zhengzhou, Peoples R China.; Zheng, YX (reprint author), Chinese Ctr Dis Control & Prevent, Natl Inst Occupat Hlth & Poison Control, Beijing 100050, Peoples R China.
EM qingl@mail.nih.gov; yu-shanfa@163.com; zhengyx@chinacdc.cn
RI Vermeulen, Roel/F-8037-2011
OI Vermeulen, Roel/0000-0003-4082-8163
NR 42
TC 0
Z9 0
U1 6
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0893-6692
EI 1098-2280
J9 ENVIRON MOL MUTAGEN
JI Environ. Mol. Mutagen.
PD OCT
PY 2016
VL 57
IS 8
BP 615
EP 622
DI 10.1002/em.22036
PG 8
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA DZ4OA
UT WOS:000385836800005
PM 27671983
ER
PT J
AU Dal-Re, R
Rid, A
Emanuel, E
Wendler, D
AF Dal-Re, Rafael
Rid, Annette
Emanuel, Ezekiel
Wendler, David
TI Addressing exploitation of poor clinical trial participants in North
America and the European Union
SO EUROPEAN JOURNAL OF INTERNAL MEDICINE
LA English
DT Letter
DE Clinical research; Clinical trial regulations; Fair benefits; Poor
participants; Uninsured patients
C1 [Dal-Re, Rafael] Univ Autonoma Madrid, BUC Biosci UAM CSIC Program, Clin Res, Int Campus Excellence, Madrid, Spain.
[Rid, Annette] Kings Coll London, Dept Social Sci Hlth & Med, London, England.
[Emanuel, Ezekiel] Univ Penn, Dept Med Eth & Hlth Policy, Philadelphia, PA 19104 USA.
[Wendler, David] NIH, Dept Bioeth, Ctr Clin, Bethesda, MD 20892 USA.
RP Dal-Re, R (reprint author), Univ Autonoma Madrid, Invest Clin, Programa BUC Biociencias UAM CSIC, Campus Excelencia Int,Ciudad Univ Cantoblanco, E-28049 Madrid, Spain.
EM Rafael.dalre@fuam.uam.es
NR 10
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0953-6205
EI 1879-0828
J9 EUR J INTERN MED
JI Eur. J. Intern. Med.
PD OCT
PY 2016
VL 34
BP E37
EP E38
DI 10.1016/j.ejim.2016.06.026
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA DY9XG
UT WOS:000385488500018
PM 27425655
ER
PT J
AU Mead, B
Tomarev, S
AF Mead, Ben
Tomarev, Stanislav
TI Evaluating retinal ganglion cell loss and dysfunction
SO EXPERIMENTAL EYE RESEARCH
LA English
DT Review
DE Retina; Retinal ganglion cells; Electroretinography; Visual evoked
potential; Quantification; Dysfunction
ID OPTIC-NERVE CRUSH; PHOTOPIC NEGATIVE RESPONSE; RETROGRADE
AXONAL-TRANSPORT; OCULAR HYPERTENSION MODEL; RNA-BINDING PROTEIN;
OPEN-ANGLE GLAUCOMA; MOUSE MODEL; IN-VIVO; ADULT-RATS;
ELECTROPHYSIOLOGICAL ASSESSMENT
AB Retinal ganglion cells (RGC) bear the sole responsibility of propagating visual stimuli to the brain. Their axons, which make up the optic nerve, project from the retina to the brain through the lamina cribrosa and in rodents, decussate almost entirely at the optic chiasm before synapsing at the superior colliculus. For many traumatic and degenerative ocular conditions, the dysfunction and/or loss of RGC is the primary determinant of visual loss and are the measurable endpoints in current research into experimental therapies. To actually measure these endpoints in rodent models, techniques must ascertain both the quantity of surviving RGC and their functional capacity. Quantification techniques include phenotypic markers of RGC, retrogradely transported fluorophores and morphological measurements of retinal thickness whereas functional assessments include electroretinography (flash and pattern) and visual evoked potential. The importance of the accuracy and reliability of these techniques cannot be understated, nor can the relationship between RGC death and dysfunction. The existence of up to 30 types of RGC complicates the measuring process, particularly as these may respond differently to disease and treatment. Since the above techniques may selectively identify and ignore particular subpopulations, their appropriateness as measures of RGC survival and function may be further limited. This review discusses the above techniques in the context of their subtype specificity. (C) 2016 Elsevier Ltd. All rights reserved.
C1 [Mead, Ben; Tomarev, Stanislav] NEI, Sect Retinal Gangl Cell Biol, Lab Retinal Cell & Mol Biol, NIH, 6 Ctr Dr,Bldg 6,Room 213B, Bethesda, MD 20892 USA.
RP Mead, B (reprint author), NEI, Sect Retinal Gangl Cell Biol, Lab Retinal Cell & Mol Biol, NIH, 6 Ctr Dr,Bldg 6,Room 213B, Bethesda, MD 20892 USA.
EM ben.mead@nih.gov
FU National Eye Institute Intramural Research Program
FX This work was funded by a grant from the National Eye Institute
Intramural Research Program.
NR 113
TC 1
Z9 1
U1 12
U2 12
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0014-4835
EI 1096-0007
J9 EXP EYE RES
JI Exp. Eye Res.
PD OCT
PY 2016
VL 151
BP 96
EP 106
DI 10.1016/j.exer.2016.08.006
PG 11
WC Ophthalmology
SC Ophthalmology
GA DZ1OI
UT WOS:000385607300014
PM 27523467
ER
PT J
AU Dreger, DL
Davis, BW
Cocco, R
Sechi, S
Di Cerbo, A
Parker, HG
Polli, M
Marelli, SP
Crepaldi, P
Ostrander, EA
AF Dreger, Dayna L.
Davis, Brian W.
Cocco, Raffaella
Sechi, Sara
Di Cerbo, Alessandro
Parker, Heidi G.
Polli, Michele
Marelli, Stefano P.
Crepaldi, Paola
Ostrander, Elaine A.
TI Commonalities in Development of Pure Breeds and Population Isolates
Revealed in the Genome of the Sardinian Fonni's Dog
SO GENETICS
LA English
DT Article
DE dog; whole-genome sequence; demography; population structure
ID BARDET-BIEDL-SYNDROME; HEREDITARY PROSTATE-CANCER; OLD ORDER AMISH;
DOMESTIC DOG; LINKAGE DISEQUILIBRIUM; GENETIC-STRUCTURE; SEQUENCING
DATA; WIDE SEARCH; SNP DATA; DISEASE
AB The island inhabitants of Sardinia have long been a focus for studies of complex human traits due to their unique ancestral background and population isolation reflecting geographic and cultural restriction. Population isolates share decreased genomic diversity, increased linkage disequilibrium, and increased inbreeding coefficients. In many regions, dogs and humans have been exposed to the same natural and artificial forces of environment, growth, and migration. Distinct dog breeds have arisen through human-driven selection of characteristics to meet an ideal standard of appearance and function. The Fonni's Dog, an endemic dog population on Sardinia, has not been subjected to an intensive system of artificial selection, but rather has developed alongside the human population of Sardinia, influenced by geographic isolation and unregulated selection based on its environmental adaptation and aptitude for owner-desired behaviors. Through analysis of 28 dog breeds, represented with whole-genome sequences from 13 dogs and similar to 170,000 genome-wide single nucleotide variants from 155 dogs, we have produced a genomic illustration of the Fonni's Dog. Genomic patterns confirm within-breed similarity, while population and demographic analyses provide spatial identity of Fonni's Dog to other Mediterranean breeds. Investigation of admixture and fixation indices reveals insights into the involvement of Fonni's Dogs in breed development throughout the Mediterranean. We describe how characteristics of population isolates are reflected in dog breeds that have undergone artificial selection, and are mirrored in the Fonni's Dog through traditional isolating factors that affect human populations. Lastly, we show that the genetic history of Fonni's Dog parallels demographic events in local human populations.
C1 [Dreger, Dayna L.; Davis, Brian W.; Parker, Heidi G.; Ostrander, Elaine A.] NHGRI, Canc Genet & Comparat Genom Branch, NIH, Bethesda, MD 20892 USA.
[Cocco, Raffaella; Sechi, Sara] Univ Sassari, Dipartimento Med Vet, Sez Clin Med, I-07100 Sassari, Italy.
[Di Cerbo, Alessandro] Univ G dAnnunzio, Specializzaz Biochim Clin, Dipartimento Sci Med Orali & Biotecnol, I-66100 Chieti, Italy.
[Polli, Michele; Marelli, Stefano P.; Crepaldi, Paola] Univ Milan, Dipartimento Med Vet, I-20133 Milan, Italy.
RP Ostrander, EA (reprint author), NHGRI, NIH, Bldg 50,Room 5351,50 South Dr, Bethesda, MD 20892 USA.
EM eostrand@mail.nih.gov
OI Ostrander, Elaine/0000-0001-6075-9738
FU Intramural Program of the International Human Genome Research Institute;
misura 3.13 del Programma Operativo Regione (P.O.R.) Sardegna (Fondi
Europep di Sviluppo Regionale (FESR))
FX The authors thank all the dog owners and their dogs for providing DNA
samples. Special thanks to Sir Terence Clark, Mauricio Lima, and Robert
Gennari for obtaining DNA samples from regional dog breeds from Italy,
North Africa, and the Middle East. D.L.D., E.A.O, B.W.D, and H.G.P.
acknowledge support from the Intramural Program of the International
Human Genome Research Institute. This study is part of an Italian study
"Detection of morphological, genetic, and behavioral characteristics of
Fonni's Dog, aimed at selection and official recognition of this breed
by ENCI", funded in part by misura 3.13 del Programma Operativo Regione
(P.O.R.) Sardegna 2006-2008 (Fondi Europep di Sviluppo Regionale
(FESR)).
NR 76
TC 0
Z9 0
U1 14
U2 14
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 2016
VL 204
IS 2
BP 737
EP 755
DI 10.1534/genetics.116.192427
PG 19
WC Genetics & Heredity
SC Genetics & Heredity
GA DZ4ZP
UT WOS:000385871400028
PM 27519604
ER
PT J
AU Rehman, AU
Bird, JE
Faridi, R
Shahzad, M
Shah, S
Lee, K
Khan, SN
Imtiaz, A
Ahmed, ZM
Riazuddin, S
Santos-Cortez, RLP
Ahmad, W
Leal, SM
Riazuddin, S
Friedman, TB
AF Rehman, Atteeq U.
Bird, Jonathan E.
Faridi, Rabia
Shahzad, Mohsin
Shah, Sujay
Lee, Kwanghyuk
Khan, Shaheen N.
Imtiaz, Ayesha
Ahmed, Zubair M.
Riazuddin, Saima
Santos-Cortez, Regie Lyn P.
Ahmad, Wasim
Leal, Suzanne M.
Riazuddin, Sheikh
Friedman, Thomas B.
TI Mutational Spectrum of MYO15A and the Molecular Mechanisms of DFNB3
Human Deafness
SO HUMAN MUTATION
LA English
DT Article
DE DFNB3; deafness; myosin 15; MYO15A; shaker 2; giant exon; micro exon
ID NONSYNDROMIC HEARING-LOSS; HAIR-CELL STEREOCILIA; MYOSIN-VIIA GENE;
TARGETED GENOMIC CAPTURE; NON-SYNDROMIC DEAFNESS; RECESSIVE DEAFNESS;
UNCONVENTIONAL MYOSIN; PROFOUND DEAFNESS; USHER-SYNDROME; STEM-CELLS
AB Deafness in humans is a common neurosensory disorder and is genetically heterogeneous. Across diverse ethnic groups, mutations of MYO15A at the DFNB3 locus appear to be the third or fourth most common cause of autosomal-recessive, nonsyndromic deafness. In 49 of the 67 exons of MYO15A, there are currently 192 recessive mutations identified, including 14 novel mutations reported here. These mutations are distributed uniformly across MYO15A with one enigmatic exception; the alternatively spliced giant exon 2, encoding 1,233 residues, has 17 truncating mutations but no convincing deafness-causing missense mutations. MYO15A encodes three distinct isoform classes, one of which is 395 kDa (3,530 residues), the largest member of the myosin superfamily of molecular motors. Studies of Myo15 mouse models that recapitulate DFNB3 revealed two different pathogenic mechanisms of hearing loss. In the inner ear, myosin 15 is necessary both for the development and the long-term maintenance of stereocilia, mechanosensory sound-transducing organelles that extend from the apical surface of hair cells. The goal of this Mutation Update is to provide a comprehensive review of mutations and functions of MYO15A. (C) 2016 Wiley Periodicals, Inc.
C1 [Rehman, Atteeq U.; Bird, Jonathan E.; Faridi, Rabia; Shah, Sujay; Imtiaz, Ayesha; Friedman, Thomas B.] Natl Inst Deafness & Other Commun Disorders, Lab Mol Genet, NIH, Bethesda, MD 20892 USA.
[Faridi, Rabia; Khan, Shaheen N.] Univ Punjab, Ctr Excellence Mol Biol, Lahore 54550, Pakistan.
[Shahzad, Mohsin; Ahmed, Zubair M.; Riazuddin, Saima] Univ Maryland, Sch Med, Dept Otorhinolaryngol Head & Neck Surg, Baltimore, MD 21201 USA.
[Lee, Kwanghyuk; Santos-Cortez, Regie Lyn P.; Leal, Suzanne M.] Baylor Coll Med, Dept Mol & Human Genet, Ctr Stat Genet, Houston, TX 77030 USA.
[Ahmad, Wasim] Quaid I Azam Univ, Fac Biol Sci, Dept Biochem, Islamabad 45320, Pakistan.
[Riazuddin, Sheikh] Univ Hlth Sci, Allama Iqbal Med Res Ctr, Jinnah Hosp Complex, Lahore 54550, Pakistan.
[Rehman, Atteeq U.] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
RP Friedman, TB (reprint author), Natl Inst Deafness & Other Commun Disorders, Lab Mol Genet, NIH, Bethesda, MD 20892 USA.
EM friedman@nidcd.nih.gov
OI Bird, Jonathan/0000-0001-5531-8794
FU Intramural Research Program of the NIDCD/NIH [DC000048-19]; Higher
Education Commission of Pakistan (HEC); NIDCD [R01 DC003594, R01
DC011651, R01DC012564, R01DC011803]
FX Contract grant sponsors: Intramural Research Program of the NIDCD/NIH
(DC000048-19); Higher Education Commission of Pakistan (HEC); NIDCD
(grants R01 DC003594, R01 DC011651, R01DC012564, R01DC011803).
NR 106
TC 2
Z9 2
U1 5
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 2016
VL 37
IS 10
BP 991
EP 1003
DI 10.1002/humu.23042
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA DZ4CQ
UT WOS:000385805800013
PM 27375115
ER
PT J
AU Olfson, M
Blanco, C
Marcus, SC
AF Olfson, Mark
Blanco, Carlos
Marcus, Steven C.
TI Treatment of Adult Depression in the United States
SO JAMA INTERNAL MEDICINE
LA English
DT Article
ID COMORBIDITY SURVEY REPLICATION; SERIOUS MENTAL-ILLNESS; HEALTH-CARE;
GENERAL-POPULATION; MAJOR DEPRESSION; NATIONAL TRENDS; METAANALYSIS;
PSYCHOTHERAPY; DISORDER; SETTINGS
AB IMPORTANCE Despite recent increased use of antidepressants in the United States, concerns persist that many adults with depression do not receive treatment, whereas others receive treatments that do not match their level of illness severity.
OBJECTIVE To characterize the treatment of adult depression in the United States.
DESIGN, SETTING, AND PARTICIPANTS Analysis of screen-positive depression, psychological distress, and depression treatment data from 46 417 responses to the Medical Expenditure Panel Surveys taken in US households by participants aged 18 years or older in 2012 and 2013.
MAIN OUTCOME AND MEASURES Percentages of adults with screen-positive depression (Patient Health Questionnaire-2 score of > 3) and adjusted odds ratios (AORs) of the effects of sociodemographic characteristics on odds of screen-positive depression; percentages with treatment for screen-positive depression and AORs; percentages with any treatment of depression and AORs stratified by presence of serious psychological distress (Kessler 6 scale score of >= 13); and percentages with depression treatment by health care professional group (psychiatrists, other health care professionals, and general medical providers); and type of depression treatment (antidepressants, psychotherapy, and both) all stratified by distress level.
RESULTS Approximately 8.4%(95% CI, 7.9-8.8) of adults screened positive for depression, of which 28.7% received any depression treatment. Conversely, among all adults treated for depression, 29.9% had screen-positive depression and 21.8% had serious psychological distress. Adults with serious compared with less serious psychological distress who were treated for depression were more likely to receive care from psychiatrists (33.4% vs 17.3%, P < .001) or other mental health specialists (16.2% vs 9.6%, P < .001), and less likely to receive depression care exclusively from general medical professionals (59.0% vs 74.4%, P < .001). They were also more likely to receive psychotherapy (32.5% vs 20.6%, P < .001), though not antidepressant medications (81.1% vs 88.6%, P < .001).
CONCLUSIONS AND RELEVANCE Most US adults who screen positive for depression did not receive treatment for depression, whereas most who were treated did not screen positive. In light of these findings, it is important to strengthen efforts to align depression care with each patient's clinical needs.
C1 [Olfson, Mark] Columbia Univ Coll Phys & Surg, Dept Psychiat, 722 W 168th St, New York, NY 10032 USA.
[Olfson, Mark] New York State Psychiat Inst & Hosp, New York, NY 10032 USA.
[Blanco, Carlos] NIDA, Bethesda, MD 20892 USA.
[Marcus, Steven C.] Univ Penn, Sch Social Practice & Policy, Philadelphia, PA 19104 USA.
RP Olfson, M (reprint author), Columbia Univ Coll Phys & Surg, New York State Psychiat Inst, Dept Psychiat, 1051 Riverside Dr, New York, NY 10032 USA.
EM mo49@cumc.columbia.edu
FU Agency for Healthcare Quality and Research [U19 HS02112]; National
Institute on Drug Abuse; AHRQ
FX This work was supported by the Agency for Healthcare Quality and
Research U19 HS02112. Work by Dr. Blanco was supported by the National
Institute on Drug Abuse and he had no role in the grant from AHRQ.
NR 50
TC 5
Z9 5
U1 10
U2 10
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2168-6106
EI 2168-6114
J9 JAMA INTERN MED
JI JAMA Intern. Med.
PD OCT
PY 2016
VL 176
IS 10
BP 1482
EP 1491
DI 10.1001/jamainternmed.2016.5057
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA DZ1ZU
UT WOS:000385642000013
PM 27571438
ER
PT J
AU Goedert, JJ
AF Goedert, James J.
TI Intestinal Microbiota and Health of Adults Who Were Born by Cesarean
Delivery
SO JAMA PEDIATRICS
LA English
DT Letter
C1 [Goedert, James J.] NCI, Div Canc Epidemiol & Genet, NIH, 9609 Med Ctr Dr,Room 6E106,MSC 9767, Bethesda, MD 20892 USA.
RP Goedert, JJ (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, 9609 Med Ctr Dr,Room 6E106,MSC 9767, Bethesda, MD 20892 USA.
EM goedertj@mail.nih.gov
NR 5
TC 0
Z9 0
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2168-6203
EI 2168-6211
J9 JAMA PEDIATR
JI JAMA Pediatr.
PD OCT
PY 2016
VL 170
IS 10
BP 1027
EP 1027
DI 10.1001/jamapediatrics.2016.2310
PG 1
WC Pediatrics
SC Pediatrics
GA DZ2AB
UT WOS:000385643000026
PM 27548071
ER
PT J
AU Blanco, C
Compton, WM
Grant, BF
AF Blanco, Carlos
Compton, Wilson M.
Grant, Bridget F.
TI Toward Precision Epidemiology
SO JAMA PSYCHIATRY
LA English
DT Editorial Material
ID COMMON PSYCHIATRIC-DISORDERS; GENERAL-POPULATION; ANXIETY DISORDERS;
MENTAL-DISORDERS; DEPRESSION; ILLNESS; ALCOHOL; SAMPLE
C1 [Blanco, Carlos] NIDA, Div Epidemiol Serv & Prevent Res, 6001 Execut Blvd, Bethesda, MD 20852 USA.
[Compton, Wilson M.] NIDA, Off Director, Bethesda, MD 20892 USA.
[Grant, Bridget F.] NIAAA, Lab Epidemiol & Biometry, Div Intramural Clin & Biol Res, Rockville, MD 20852 USA.
RP Blanco, C (reprint author), NIDA, Div Epidemiol Serv & Prevent Res, 6001 Execut Blvd, Bethesda, MD 20852 USA.
EM carlos.blanco2@nih.gov
NR 16
TC 1
Z9 1
U1 2
U2 2
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2168-622X
EI 2168-6238
J9 JAMA PSYCHIAT
JI JAMA Psychiatry
PD OCT
PY 2016
VL 73
IS 10
BP 1008
EP 1009
DI 10.1001/jamapsychiatry.2016.1869
PG 2
WC Psychiatry
SC Psychiatry
GA DZ5QG
UT WOS:000385916000003
PM 27603943
ER
PT J
AU Paksarian, D
Cui, LH
Angst, J
Ajdacic-Gross, V
Rossler, W
Merikangas, KR
AF Paksarian, Diana
Cui, Lihong
Angst, Jules
Ajdacic-Gross, Vladeta
Rossler, Wulf
Merikangas, Kathleen R.
TI Latent Trajectories of Common Mental Health Disorder Risk Across 3
Decades of Adulthood in a Population-Based Cohort
SO JAMA PSYCHIATRY
LA English
DT Article
ID EPIDEMIOLOGIC CATCHMENT-AREA; NATIONAL-COMORBIDITY-SURVEY; SUBSTANCE USE
DISORDERS; OF-ONSET DISTRIBUTIONS; UNITED-STATES; LIFETIME PREVALENCE;
FOLLOW-UP; PSYCHIATRIC-DISORDERS; DEPRESSIVE DISORDER; ZURICH COHORT
AB IMPORTANCE Epidemiologic evidence indicates that most of the general population will experience a mental health disorder at some point in their lives. However, few prospective population-based studies have estimated trajectories of risk for mental disorders from young through middle adulthood to estimate the proportion of individuals who experience persistent mental disorder across this age period.
OBJECTIVES To describe the proportion of the population who experience persistent mental disorder across adulthood and to estimate latent trajectories of disorder risk across this age period.
DESIGN, SETTING, AND PARTICIPANTS A population-based, prospective cohort study was conducted between 1979 and 2008 in the canton of Zurich, Switzerland. A stratified random sample of 591 Swiss citizens was enrolled in 1978 at ages 19 years (men) and 20 years (women); 7 interviews were performed during a 29-year period. Men were sampled from military enrollment records and women from electoral records. From those initially enrolled, participants with high levels of psychiatric symptoms were oversampled for follow-up. Data analysis was performed from July 28, 2015, to June 8, 2016.
MAIN OUTCOMES AND MEASURES Latent trajectories, estimated using growth mixture modeling, of past-year mood/anxiety disorder (ie, major depressive episode, phobias, panic, generalized anxiety disorder, and obsessive-compulsive disorder), substance use disorder (ie, drug abuse or dependence and alcohol abuse or dependence), and any mental disorder (ie, any of the above) assessed during in-person semistructured interviews at each wave. Diagnoses were based on DSM-III, DSM-III-R, and DSM-IV criteria.
RESULTS Of the 591 participants at baseline, 299 (50.6%) were female. Persistent mental health disorder across multiple study waves was rare. Among 252 individuals (42.6%) who participated in all 7 study waves, only 1.2% met criteria for disorder every time. Growth mixture modeling identified 3 classes of risk for any disorder across adulthood: low (estimated prevalence, 40.0%; 95% CI, -8.7% to 88.9%), increasing-decreasing (estimated prevalence, 15.3%; 95% CI, 1.0% to 29.6%), and increasing (estimated prevalence, 44.7%; 95% CI, -0.9% to 90.1%). Although no classes were characterized by persistently high disorder risk, for those in the increasing-decreasing class, risk was high from the late 20s to early 40s. Sex-specific models indicated 4 trajectory classes for women but only 3 for men.
CONCLUSIONS AND RELEVANCE Persistently high mental health disorder risk across 3 decades of adulthood was rare in this population-based sample. Identifying early determinants of sex-specific risk trajectories would benefit prevention efforts.
C1 [Paksarian, Diana; Cui, Lihong; Merikangas, Kathleen R.] NIMH, Genet Epidemiol Res Branch, Intramural Res Program, Bethesda, MD 20892 USA.
[Angst, Jules; Ajdacic-Gross, Vladeta] Univ Zurich, Hosp Psychiat, Dept Psychiat Psychotherapy & Psychosomat, Zurich, Switzerland.
[Rossler, Wulf] Univ Sao Paulo, Inst Psychiat, Lab Neurosci, Sao Paulo, Brazil.
[Rossler, Wulf] Univ Zurich, Coll Helveticum, Zurich, Switzerland.
[Rossler, Wulf] Swiss Tech Inst, Zurich, Switzerland.
RP Merikangas, KR (reprint author), NIMH, Genet Epidemiol Res Branch, 35A Convent Dr,MSC 3720, Bethesda, MD 20892 USA.
EM kathleen.merikangas@nih.gov
FU Intramural Research Program of the National Institute of Mental Health
[ZIAMH002807]; Swiss National Science Foundation [3200-050881.97/1,
32-50881.97]
FX This study was supported by project ZIAMH002807 from the Intramural
Research Program of the National Institute of Mental Health and grants
3200-050881.97/1 and 32-50881.97 from the Swiss National Science
Foundation.
NR 59
TC 1
Z9 1
U1 14
U2 14
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2168-622X
EI 2168-6238
J9 JAMA PSYCHIAT
JI JAMA Psychiatry
PD OCT
PY 2016
VL 73
IS 10
BP 1023
EP 1031
DI 10.1001/jamapsychiatry.2016.1921
PG 9
WC Psychiatry
SC Psychiatry
GA DZ5QG
UT WOS:000385916000007
PM 27602550
ER
PT J
AU Pongracic, JA
Krouse, RZ
Babineau, DC
Zoratti, EM
Cohen, RT
Wood, RA
Hershey, GKK
Kercsmar, CM
Gruchalla, RS
Kattan, M
Teach, SJ
Johnson, CC
Bacharier, LB
Gern, JE
Sigelman, SM
Gergen, PJ
Togias, A
Visness, CM
Busse, WW
Liu, AH
AF Pongracic, Jacqueline A.
Krouse, Rebecca Z.
Babineau, Denise C.
Zoratti, Edward M.
Cohen, Robyn T.
Wood, Robert A.
Hershey, Gurjit K. Khurana
Kercsmar, Carolyn M.
Gruchalla, Rebecca S.
Kattan, Meyer
Teach, Stephen J.
Johnson, Christine C.
Bacharier, Leonard B.
Gern, James E.
Sigelman, Steven M.
Gergen, Peter J.
Togias, Alkis
Visness, Cynthia M.
Busse, William W.
Liu, Andrew H.
TI Distinguishing characteristics of difficult-to-control asthma in
inner-city children and adolescents
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Article
DE Child; asthma; inner-city asthma; asthma phenotype; asthma morbidity;
asthma severity; asthma exacerbations; pulmonary function; rhinitis;
allergen sensitization; IgE
ID ALLERGIC RHINITIS; BRONCHODILATOR RESPONSIVENESS; PRESCHOOL-CHILDREN;
MODERATE ASTHMA; YOUNG-ADULTS; IMPACT; CHILDHOOD; OBSTRUCTION;
VALIDATION; MANAGEMENT
AB Background: Treatment levels required to control asthma vary greatly across a population with asthma. The factors that contribute to variability in treatment requirements of inner-city children have not been fully elucidated.
Objective: We sought to identify the clinical characteristics that distinguish difficult-to-control asthma from easy-to-control asthma.
Methods: Asthmatic children aged 6 to 17 years underwent baseline assessment and bimonthly guideline-based management visits over 1 year. Difficult-to-control and easy-to-control asthma were defined as daily therapy with 500 mg of fluticasone or greater with or without a long-acting beta-agonist versus 100 mu g or less assigned on at least 4 visits. Forty-four baseline variables were used to compare the 2 groups by using univariate analyses and to identify the most relevant features of difficult-to-control asthma by using a variable selection algorithm. Nonlinear seasonal variation in longitudinal measures (symptoms, pulmonary physiology, and exacerbations) was examined by using generalized additive mixed-effects models.
Results: Among 619 recruited participants, 40.9% had difficult-to-control asthma, 37.5% had easy-to-control asthma, and 21.6% fell into neither group. At baseline, FEV1 bronchodilator responsiveness was the most important characteristic distinguishing difficult-to-control asthma from easy-to-control asthma. Markers of rhinitis severity and atopy were among the other major discriminating features. Over time, difficult-tocontrol asthma was characterized by high exacerbation rates, particularly in spring and fall; greater daytime and nighttime symptoms, especially in fall and winter; and compromised pulmonary physiology despite ongoing high-dose controller therapy.
Conclusions: Despite good adherence, difficult-to-control asthma showed little improvement in symptoms, exacerbations, or pulmonary physiology over the year. In addition to pulmonary physiology measures, rhinitis severity and atopy were associated with high-dose asthma controller therapy requirement.
C1 [Pongracic, Jacqueline A.] Ann & Robert H Lurie Childrens Hosp Chicago, Chicago, IL 60611 USA.
[Krouse, Rebecca Z.; Babineau, Denise C.; Visness, Cynthia M.] Rho Fed Syst Div, Chapel Hill, NC USA.
[Zoratti, Edward M.; Johnson, Christine C.] Henry Ford Hlth Syst, Detroit, MI USA.
[Cohen, Robyn T.] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Wood, Robert A.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Hershey, Gurjit K. Khurana; Kercsmar, Carolyn M.] Cincinnati Childrens Hosp, Cincinnati, OH USA.
[Gruchalla, Rebecca S.] Univ Texas Southwestern Med Ctr Dallas, Dallas, TX 75390 USA.
[Kattan, Meyer] Columbia Univ, Coll Phys & Surg, New York, NY USA.
[Teach, Stephen J.] Childrens Natl Hlth Syst, Washington, DC USA.
[Teach, Stephen J.] George Washington Univ, Sch Med & Hlth Sci, Washington, DC 20052 USA.
[Bacharier, Leonard B.] St Louis Childrens Hosp, St Louis, MO 63178 USA.
[Gern, James E.] Univ Wisconsin, Sch Med & Publ Hlth, Madison, WI USA.
[Sigelman, Steven M.; Gergen, Peter J.; Togias, Alkis] NIAID, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Liu, Andrew H.] Natl Jewish Hlth, Denver, CO USA.
[Liu, Andrew H.] Childrens Hosp Colorado, Aurora, CO USA.
[Liu, Andrew H.] Univ Colorado, Sch Med, Aurora, CO USA.
RP Pongracic, JA (reprint author), 225 E Chicago Av 60, Chicago, IL 60614 USA.
EM jpongracic@luriechildrens.org
OI Cohen, Robyn/0000-0002-6902-3118
FU National Institute of Allergy and Infectious Diseases (NIAID), National
Institutes of Health (NIH), Department of Health and Human Services
[HHSN272200900052C, HHSN272201000052I, 1UM1AI114271-01]; National Center
for Research Resources (NCRR); National Center for Advancing
Translational Sciences (NCATS), NIH [NCRR/NIH UL1TR000451, UL1RR025780,
UL1TR000075 Q1, NCATS/NIH UL1TR000154, UL1TR001082, UL1TR000077-04,
UL1TR000040, UL1TR000150, UL1TR001105]
FX This project has been funded in whole or in part with federal funds from
the National Institute of Allergy and Infectious Diseases (NIAID),
National Institutes of Health (NIH), Department of Health and Human
Services (under contract nos. HHSN272200900052C and HHSN272201000052I,
and 1UM1AI114271-01). Additional support was provided by the National
Center for Research Resources (NCRR), and the National Center for
Advancing Translational Sciences (NCATS), NIH (under grant nos. NCRR/NIH
UL1TR000451, UL1RR025780, UL1TR000075 Q1 and NCATS/NIH UL1TR000154,
UL1TR001082, UL1TR000077-04, UL1TR000040, UL1TR000150, and UL1TR001105).
GlaxoSmithKline (GSK) provided Ventolin, Flovent, Advair, and Flonase
under a clinical trial agreement with NIH NIAID; GSK did not have a role
in the development or approval of the protocol, conduct of the trial,
data analysis, manuscript preparation, or the decision to submit the
manuscript for publication.
NR 38
TC 4
Z9 4
U1 2
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
EI 1097-6825
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD OCT
PY 2016
VL 138
IS 4
BP 1030
EP 1041
DI 10.1016/j.jaci.2016.06.059
PG 12
WC Allergy; Immunology
SC Allergy; Immunology
GA DZ0AP
UT WOS:000385499400008
PM 27720017
ER
PT J
AU Liu, AH
Babineau, DC
Krouse, RZ
Zoratti, EM
Pongracic, JA
O'Connor, GT
Wood, RA
Hershey, GKK
Kercsmar, CM
Gruchalla, RS
Kattan, M
Teach, SJ
Makhija, M
Pillai, D
Lamm, CI
Gern, JE
Sigelman, SM
Gergen, PJ
Togias, A
Visness, CM
Busse, WW
AF Liu, Andrew H.
Babineau, Denise C.
Krouse, Rebecca Z.
Zoratti, Edward M.
Pongracic, Jacqueline A.
O'Connor, George T.
Wood, Robert A.
Hershey, Gurjit K. Khurana
Kercsmar, Carolyn M.
Gruchalla, Rebecca S.
Kattan, Meyer
Teach, Stephen J.
Makhija, Melanie
Pillai, Dinesh
Lamm, Carin I.
Gern, James E.
Sigelman, Steven M.
Gergen, Peter J.
Togias, Alkis
Visness, Cynthia M.
Busse, William W.
TI Pathways through which asthma risk factors contribute to asthma severity
in inner-city children
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Article
DE Asthma; children; inner-city; allergy; sensitization; inflammation; lung
function; pulmonary physiology; rhinitis; environmental tobacco smoke
exposure
ID ALLERGIC RHINITIS; ADOLESCENTS; MORBIDITY; EXACERBATIONS; VALIDATION;
EXPOSURE; VALIDITY; VIOLENCE; STRESS; IMPACT
AB Background: Pathway analyses can be used to determine how host and environmental factors contribute to asthma severity.
Objective: To investigate pathways explaining asthma severity in inner-city children.
Methods: On the basis of medical evidence in the published literature, we developed a conceptual model to describe how 8 risk-factor domains (allergen sensitization, allergic inflammation, pulmonary physiology, stress, obesity, vitamin D, environmental tobacco smoke [ETS] exposure, and rhinitis severity) are linked to asthma severity. To estimate the relative magnitude and significance of hypothesized relationships among these domains and asthma severity, we applied a causal network analysis to test our model in an Inner-City Asthma Consortium study. Participants comprised 6- to 17-year-old children (n = 561) with asthma and rhinitis from 9 US inner cities who were evaluated every 2 months for 1 year. Asthma severity was measured by a longitudinal composite assessment of day and night symptoms, exacerbations, and controller usage.
Results: Our conceptual model explained 53.4% of the variance in asthma severity. An allergy pathway (linking allergen sensitization, allergic inflammation, pulmonary physiology, and rhinitis severity domains to asthma severity) and the ETS exposure pathway (linking ETS exposure and pulmonary physiology domains to asthma severity) exerted significant effects on asthma severity. Among the domains, pulmonary physiology and rhinitis severity had the largest significant standardized total effects on asthma severity (-0.51 and 0.48, respectively), followed by ETS exposure (0.30) and allergic inflammation (0.22). Although vitamin D had modest but significant indirect effects on asthma severity, its total effect was insignificant (0.01).
Conclusions: The standardized effect sizes generated by a causal network analysis quantify the relative contributions of different domains and can be used to prioritize interventions to address asthma severity.
C1 [Liu, Andrew H.] Natl Jewish Hlth, Denver, CO USA.
[Liu, Andrew H.] Childrens Hosp Colorado, 13123 East 16th Ave,Box B395, Aurora, CO 80045 USA.
[Liu, Andrew H.] Univ Colorado, Sch Med, Aurora, CO USA.
[Babineau, Denise C.; Krouse, Rebecca Z.; Visness, Cynthia M.] Rho Fed Syst Div, Chapel Hill, NC USA.
[Zoratti, Edward M.] Henry Ford Hlth Syst, Detroit, MI USA.
[Pongracic, Jacqueline A.; Makhija, Melanie] Ann & Robert H Lurie Childrens Hosp Chicago, Chicago, IL 60611 USA.
[O'Connor, George T.] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Wood, Robert A.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Hershey, Gurjit K. Khurana; Kercsmar, Carolyn M.] Cincinnati Childrens Hosp, Cincinnati, OH USA.
[Gruchalla, Rebecca S.] Univ Texas Southwestern Med Ctr Dallas, Dallas, TX 75390 USA.
[Kattan, Meyer; Lamm, Carin I.] Columbia Univ, Coll Phys & Surg, New York, NY USA.
[Teach, Stephen J.; Pillai, Dinesh] Childrens Natl Hlth Syst, Washington, DC USA.
[Teach, Stephen J.; Pillai, Dinesh] George Washington Univ, Sch Med & Hlth Sci, Washington, DC 20052 USA.
[Gern, James E.; Busse, William W.] Univ Wisconsin, Sch Med & Publ Hlth, Madison, WI USA.
[Sigelman, Steven M.; Gergen, Peter J.; Togias, Alkis] NIAID, 9000 Rockville Pike, Bethesda, MD 20892 USA.
RP Liu, AH (reprint author), Childrens Hosp Colorado, 13123 East 16th Ave,Box B395, Aurora, CO 80045 USA.
EM Andrew.liu@childrenscolorado.org
FU National Institute of Allergy and Infectious Diseases (NIAID), National
Institutes of Health (NIH), Department of Health and Human Services
[HHSN272200900052C, HHSN272201000052I, 1UM1AI114271-01]; National Center
for Research Resources (NCRR); National Center for Advancing
Translational Sciences (NCATS), NIH [NCRR/NIH UL1TR000451, UL1RR025780,
UL1TR000075, NCATS/NIH UL1TR000154, UL1TR001082, UL1TR000077-04,
UL1TR000040, UL1TR000150, UL1TR001105]
FX This project has been funded in whole or in part with federal funds from
the National Institute of Allergy and Infectious Diseases (NIAID),
National Institutes of Health (NIH), Department of Health and Human
Services (under contract nos. HHSN272200900052C and HHSN272201000052I,
and 1UM1AI114271-01). Additional support was provided by the National
Center for Research Resources (NCRR), and the National Center for
Advancing Translational Sciences (NCATS), NIH (under grant nos. NCRR/NIH
UL1TR000451, UL1RR025780, UL1TR000075 and NCATS/NIH UL1TR000154,
UL1TR001082, UL1TR000077-04, UL1TR000040, UL1TR000150, and UL1TR001105).
GlaxoSmithKline (GSK) provided Ventolin, Flovent, Advair, and Flonase
under a clinical trial agreement with NIH NIAID; GSK did not have a role
in the development or approval of the protocol, conduct of the trial,
data analysis, manuscript preparation, or the decision to submit the
manuscript for publication.
NR 34
TC 2
Z9 2
U1 8
U2 8
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
EI 1097-6825
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD OCT
PY 2016
VL 138
IS 4
BP 1042
EP 1050
DI 10.1016/j.jaci.2016.06.060
PG 9
WC Allergy; Immunology
SC Allergy; Immunology
GA DZ0AP
UT WOS:000385499400009
PM 27720018
ER
PT J
AU Feeney, M
Du Toit, G
Roberts, G
Sayre, PH
Lawson, K
Bahnson, HT
Sever, ML
Radulovic, S
Plaut, M
Lack, G
AF Feeney, Mary
Du Toit, George
Roberts, Graham
Sayre, Peter H.
Lawson, Kaitie
Bahnson, Henry T.
Sever, Michelle L.
Radulovic, Suzana
Plaut, Marshall
Lack, Gideon
CA Immune Tolerance Network Leap Stu
TI Impact of peanut consumption in the LEAP Study: Feasibility, growth, and
nutrition
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Article
DE Food allergy; allergy prevention; peanut; infant feeding;
breast-feeding; nutrition; growth; prospective food diary; protein
homeostasis
ID HIGH-RISK INFANTS; CONSENSUS COMMUNICATION; ALLERGY; CHILDREN;
ADOLESCENTS; PREVENTION; PREVALENCE; ACCEPTANCE; CHILDHOOD; FRUIT
AB Background: Early introduction of peanut is an effective strategy to prevent peanut allergy in high-risk infants; however, feasibility and effects on growth and nutritional intake are unknown.
Objective: We sought to evaluate the feasibility of introducing peanut in infancy and explore effects on growth and nutritional intake up to age 60 months.
Methods: In the Learning Early About Peanut Allergy trial, 640 atopic infants aged 4 to 11 months were randomly assigned to consume (6 g peanut protein per week) or avoid peanut until age 60 months. Peanut consumption and early feeding practices were assessed by questionnaire. Dietary intake was evaluated with prospective food diaries. Anthropometric measurements were taken at all study visits.
Results: Peanut was successfully introduced and consumed until 60 months, with median peanut protein intake of 7.5 g/wk (interquartile range, 6.0-9.0 g/wk) in the consumption group compared with 0 g in the avoidance group. Introduction of peanut in breast-feeding infants did not affect the duration of breast-feeding. There were no differences in anthropometric measurements or energy intakes between groups at any visits. Regular peanut consumption led to differences in dietary intakes. Consumers had higher intakes of fat and avoiders had higher carbohydrate intakes; differences were greatest at the upper quartiles of peanut consumption. Protein intakes remained consistent between groups.
Conclusions: Introduction of peanut proved feasible in infants at high risk of peanut allergy and did not affect the duration of breast-feeding nor impact negatively on growth or nutrition. Energy balance was achieved in both groups through variations in intakes from fat and carbohydrate while protein homeostasis was maintained.
C1 [Feeney, Mary; Du Toit, George; Radulovic, Suzana; Lack, Gideon] Kings Coll London, Dept Pediat Allergy, Div Asthma Allergy & Lung Biol, London, England.
[Feeney, Mary; Du Toit, George; Roberts, Graham; Radulovic, Suzana; Lack, Gideon] Guys & St Thomas NHS Fdn Trust, London, England.
[Roberts, Graham] Univ Southampton, Southampton, Hants, England.
[Roberts, Graham] Natl Inst Hlth, Res Resp Biomed Res Unit, Southampton, Hants, England.
[Roberts, Graham] David Hide Ctr, Isle Of Wight, England.
[Sayre, Peter H.] Immune Tolerance Network, San Francisco, CA USA.
[Sayre, Peter H.] Univ Calif San Francisco, Dept Med, Div Hematol Oncol, San Francisco, CA USA.
[Lawson, Kaitie; Bahnson, Henry T.; Sever, Michelle L.] Rho Fed Syst Div, Chapel Hill, NC USA.
[Plaut, Marshall] NIAID, 9000 Rockville Pike, Bethesda, MD 20892 USA.
RP Lack, G (reprint author), Guys & St Thomas NHS Fdn Trust, Childrens Allergy Unit, 2nd Fl,South Wing,Westminster Bridge Rd, London SE1 7EH, England.
EM gideon.lack@kcl.ac.uk
FU National Institute of Allergy and Infectious Diseases [UM1AI109565,
NO1-AI-15416, HHSN272200800029C]; National Institute of Allergy and
Infectious Diseases of the National Institutes of Health; Food Allergy
Research & Education (FARE), McLean, Virginia; Medical Research Council
& Asthma UK Centre; UK Department of Health through the National
Institute for Health Research comprehensive Biomedical Research Centre
award; King's College London; King's College Hospital NHS Foundation
Trust; National Peanut Board, Atlanta, Georgia; UK Food Standards Agency
FX This study was funded by the National Institute of Allergy and
Infectious Diseases (award nos. UM1AI109565, NO1-AI-15416, and
HHSN272200800029C) and others. This research was performed as a project
of the Immune Tolerance Network, an international clinical research
consortium headquartered at the Benaroya Research Institute and
supported by the National Institute of Allergy and Infectious Diseases
of the National Institutes of Health. The content is solely the
responsibility of the authors and does not necessarily represent the
official views of the National Institutes of Health. Additional support
came from Food Allergy Research & Education (FARE), McLean, Virginia;
the Medical Research Council & Asthma UK Centre; the UK Department of
Health through the National Institute for Health Research comprehensive
Biomedical Research Centre award to Guy's & St Thomas' National Health
Service (NHS) Foundation Trust, in partnership with King's College
London and King's College Hospital NHS Foundation Trust. The clinical
trials unit is supported by the National Peanut Board, Atlanta, Georgia.
The UK Food Standards Agency provided additional support for the costs
of phlebotomy.
NR 41
TC 9
Z9 9
U1 5
U2 5
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
EI 1097-6825
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD OCT
PY 2016
VL 138
IS 4
BP 1108
EP 1118
DI 10.1016/j.jaci.2016.04.016
PG 11
WC Allergy; Immunology
SC Allergy; Immunology
GA DZ0AP
UT WOS:000385499400016
PM 27297994
ER
PT J
AU Koplin, JJ
Peters, RL
Dharmage, SC
Gurrin, L
Tang, MLK
Ponsonby, AL
Matheson, M
Togias, A
Lack, G
Allen, KJ
AF Koplin, Jennifer J.
Peters, Rachel L.
Dharmage, Shyamali C.
Gurrin, Lyle
Tang, Mimi L. K.
Ponsonby, Anne-Louise
Matheson, Melanie
Togias, Alkis
Lack, Gideon
Allen, Katrina J.
CA HealthNuts Study Investigators
TI Understanding the feasibility and implications of implementing early
peanut introduction for prevention of peanut allergy
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Article
DE Peanut allergy; infant feeding; guidelines; skin prick test; specific
IgE; prevention
ID FOOD ALLERGY; EARLY CONSUMPTION; PREVALENCE; INFANTS; HEALTHNUTS;
PREDICTORS; DIAGNOSIS; CRITERIA; COHORT; TIME
AB Background: A recent randomized trial (the Learning Early About Peanut Allergy [LEAP] study) provided evidence that earlier dietary peanut introduction reduces peanut allergy prevalence in high-risk infants. However, questions remain as to how to identify and target the "at-risk'' population to facilitate timely introduction of peanut.
Objective: We sought to use population-based infant peanut allergy data to understand feasibility and implications of implementing the LEAP trial intervention.
Methods: Using the HealthNuts study cohort (n = 5276) of 1-year-old infants, we explored the impact of using various criteria to identify infants at high risk of developing peanut allergy, and the implications of skin prick test (SPT) screening before peanut introduction.
Results: Screening all infants with early onset eczema and/or egg allergy could require testing 16% of the population and would still miss 23% of peanut allergy cases; 29% of screened infants would require clinical follow-up because of being SPT-positive. Around 11% of high-risk infants were excluded from the LEAP study because of an SPT wheal size of more than 4 mm to peanut at baseline; data from the HealthNuts study suggest that 80% of these would be peanut allergic on food challenge. There were no life-threatening events among either low-or high-risk infants whose parents chose to introduce peanut at home in the first year of life, or in 150 peanut-allergic infants during hospital-based challenges.
Conclusions: Based on this large epidemiological study, a population program aiming to identify and screen all infants at risk of peanut allergy would pose major cost and logistic challenges that need to be carefully considered. Further research might be required to provide data for low-risk infants.
C1 [Koplin, Jennifer J.; Peters, Rachel L.; Tang, Mimi L. K.; Ponsonby, Anne-Louise; Allen, Katrina J.] Univ Melbourne, Dept Paediat, Murdoch Childrens Res Inst, Parkville, Vic, Australia.
[Koplin, Jennifer J.; Peters, Rachel L.; Tang, Mimi L. K.; Ponsonby, Anne-Louise; Allen, Katrina J.] Royal Childrens Hosp, Dept Allergy & Clin Immunol, Parkville, Vic, Australia.
[Koplin, Jennifer J.; Dharmage, Shyamali C.; Gurrin, Lyle; Matheson, Melanie] Univ Melbourne, Sch Populat & Global Hlth, Parkville, Vic, Australia.
[Togias, Alkis] NIAID, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Lack, Gideon] Kings Coll London, Dept Pediat Allergy, Div Asthma Allergy & Lung Biol, London, England.
[Lack, Gideon] Guys & St Thomas Natl Hlth Serv Fdn Trust, London, England.
[Allen, Katrina J.] Univ Manchester, Sch Inflammat & Repair, Manchester, Lancs, England.
RP Allen, KJ (reprint author), Royal Childrens Hosp, Murdoch Childrens Res Inst, Flemington Rd, Parkville, Vic 3052, Australia.
EM katie.allen@rch.org.au
RI Matheson, Melanie/O-4721-2015;
OI Matheson, Melanie/0000-0002-5822-3499; Peters,
Rachel/0000-0002-2411-6628; Allen, Katrina/0000-0002-1921-4493
FU National Health & Medical Research Council (NHMRC) of Australia;
Australian Food Allergy Foundation; Anaphylaxi-Stop; Victorian
Government's Operational Infrastructure Support Program
FX This work was supported by funding from the National Health & Medical
Research Council (NHMRC) of Australia, Australian Food Allergy
Foundation, Anaphylaxi-Stop, and the Victorian Government's Operational
Infrastructure Support Program. The study sponsors had no involvement in
the study design, collection, analysis, and interpretation of data,
writing of the report, or decision to submit the article for
publication.
NR 19
TC 7
Z9 7
U1 3
U2 3
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
EI 1097-6825
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD OCT
PY 2016
VL 138
IS 4
BP 1131
EP +
DI 10.1016/j.jaci.2016.04.011
PG 13
WC Allergy; Immunology
SC Allergy; Immunology
GA DZ0AP
UT WOS:000385499400019
PM 27260320
ER
PT J
AU Chandrasekaran, P
Zimmerman, O
Paulson, M
Sampaio, EP
Freeman, AF
Sowerwine, KJ
Hurt, D
Alcantara-Montiel, JC
Hsu, AP
Holland, SM
AF Chandrasekaran, Prabha
Zimmerman, Ofer
Paulson, Michelle
Sampaio, Elizabeth P.
Freeman, Alexandra F.
Sowerwine, Kathryn J.
Hurt, Darell
Alcantara-Montiel, Julio C.
Hsu, Amy P.
Holland, Steven M.
TI Distinct mutations at the same positions of STAT3 cause either loss or
gain of function
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Letter
ID GRANULAR LYMPHOCYTIC-LEUKEMIA; HYPER-IGE SYNDROME
C1 [Chandrasekaran, Prabha; Zimmerman, Ofer; Paulson, Michelle; Sampaio, Elizabeth P.; Freeman, Alexandra F.; Sowerwine, Kathryn J.; Hsu, Amy P.; Holland, Steven M.] NIAID, Immunopathogenesis Sect, Lab Clin Infect Dis, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Chandrasekaran, Prabha] Univ Maryland, Dept Cell Biol & Mol Genet, College Pk, MD 20742 USA.
[Hurt, Darell] NIAID, Bioinformat & Computat Biosci Branch, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Alcantara-Montiel, Julio C.] CINVES TAV IPN, Dept Mol Biomed, Mexico City, DF, Mexico.
RP Holland, SM (reprint author), NIAID, Immunopathogenesis Sect, Lab Clin Infect Dis, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM smh@nih.gov
FU CCR NIH HHS [HHSN261200800001C]; Intramural NIH HHS [Z01 AI000646-16];
NCI NIH HHS [HHSN261200800001E]
NR 13
TC 1
Z9 1
U1 1
U2 1
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
EI 1097-6825
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD OCT
PY 2016
VL 138
IS 4
BP 1222
EP 1224
DI 10.1016/j.jaci.2016.05.007
PG 7
WC Allergy; Immunology
SC Allergy; Immunology
GA DZ0AP
UT WOS:000385499400037
PM 27345172
ER
PT J
AU Weeks, J
Briggs, JP
AF Weeks, John
Briggs, Josephine P.
TI The New USA NIH Strategic Plan for Complementary and Integrative Health:
Interview with Josephine Briggs, MD: Director, National Center for
Complementary and Integrative Health (Part 2)
SO JOURNAL OF ALTERNATIVE AND COMPLEMENTARY MEDICINE
LA English
DT Editorial Material
C1 [Briggs, Josephine P.] NIH, NCCIH, USA Natl Inst Hlth NIH, Bldg 10, Bethesda, MD 20892 USA.
[Briggs, Josephine P.] NIH, Precis Med Initiat, Cohort Program, Bldg 10, Bethesda, MD 20892 USA.
[Briggs, Josephine P.] NIH, Common Fund Hlth Care Syst Res Collaboratory, Bldg 10, Bethesda, MD 20892 USA.
[Briggs, Josephine P.] NIH, Steering Comm, Bldg 10, Bethesda, MD 20892 USA.
[Briggs, Josephine P.] NIH, Sci Management Review Board, Bldg 10, Bethesda, MD 20892 USA.
[Briggs, Josephine P.] NIH, Pain Consortium, Bldg 10, Bethesda, MD 20892 USA.
[Briggs, Josephine P.] Univ Munich, Inst Physiol, Munich, Germany.
[Briggs, Josephine P.] Univ Michigan, Internal Med & Physiol, Ann Arbor, MI 48109 USA.
[Briggs, Josephine P.] Univ Michigan, Dept Med, Ann Arbor, MI 48109 USA.
[Briggs, Josephine P.] NIH, Div Kidney Urol & Hematol Dis, Bldg 10, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1075-5535
EI 1557-7708
J9 J ALTERN COMPLEM MED
JI J. Altern. Complement Med.
PD OCT
PY 2016
VL 22
IS 10
BP 765
EP 767
DI 10.1089/acm.2016.29011.jjw
PG 3
WC Integrative & Complementary Medicine
SC Integrative & Complementary Medicine
GA DZ5SU
UT WOS:000385922600002
PM 27653499
ER
PT J
AU Scott, JM
Robinson, SE
Holroyd, T
Coppola, R
Sato, S
Inati, SK
AF Scott, Jonathan M.
Robinson, Stephen E.
Holroyd, Tom
Coppola, Richard
Sato, Susumu
Inati, Sara K.
TI Localization of Interictal Epileptic Spikes With MEG: Optimization of an
Automated Beamformer Screening Method (SAMepi) in a Diverse Epilepsy
Population
SO JOURNAL OF CLINICAL NEUROPHYSIOLOGY
LA English
DT Article
DE Magnetoencephalography; Source localization; Epilepsy; Beamforming;
Kurtosis
ID INTRACRANIAL EEG; MAGNETOENCEPHALOGRAPHY
AB Purpose: To describe and optimize an automated beamforming technique followed by identification of locations with excess kurtosis (g2) for efficient detection and localization of interictal spikes in patients with medically refractory epilepsy.
Methods: Synthetic aperture magnetometry with g2 averaged over a sliding time window (SAMepi) was performed in seven patients with focal epilepsy and five healthy volunteers. The effect of varied window lengths on detection of spiking activity was evaluated.
Results: Sliding window lengths of 0.5 to 10 seconds performed similarly, with 0.5- and 1-second windows detecting spiking activity in 1 of the 3 virtual sensor locations with highest kurtosis. These locations were concordant with the region of eventual surgical resection in these seven patients who remained seizure-free at 1 year. Average g2 values increased with increasing sliding window length in all subjects. In healthy volunteers, kurtosis values stabilized in data sets longer than 2 minutes.
Conclusions: SAMepi using g2 averaged over 1-second sliding time windows in data sets of at least 2 minutes of duration reliably identified interictal spiking and the presumed seizure focus in these seven patients. Screening the five locations with highest kurtosis values for spiking activity is an efficient and accurate technique for localizing interictal activity using magnetoencephalography.
Significance: SAMepi should be applied using the parameter values and procedure described for optimal detection and localization of interictal spikes. Use of this screening procedure could significantly improve the efficiency of magnetoencephalography analysis if clinically validated.
C1 [Scott, Jonathan M.; Sato, Susumu; Inati, Sara K.] NINDS, EEG Sect, NIH, 10 CRC,Room 7-3753,10 Ctr Dr,MSC 1404, Bethesda, MD 20892 USA.
[Robinson, Stephen E.; Holroyd, Tom; Coppola, Richard] NIMH, MEG Core Facil, NIH, Bethesda, MD 20892 USA.
RP Scott, JM (reprint author), NINDS, EEG Sect, NIH, 10 CRC,Room 7-3753,10 Ctr Dr,MSC 1404, Bethesda, MD 20892 USA.
EM jonathan.m.scott2013@gmail.com
FU Intramural Research Program of the National Institutes of Health,
National Institute of Neurological Disorders and Stroke (NINDS)
FX Supported by the Intramural Research Program of the National Institutes
of Health, National Institute of Neurological Disorders and Stroke
(NINDS).
NR 18
TC 0
Z9 0
U1 4
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0736-0258
EI 1537-1603
J9 J CLIN NEUROPHYSIOL
JI J. Clin. Neurophysiol.
PD OCT
PY 2016
VL 33
IS 5
BP 414
EP 420
DI 10.1097/WNP.0000000000000255
PG 7
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA DZ2HP
UT WOS:000385663200007
PM 27760068
ER
PT J
AU Clark, C
Thomas, D
Mejzner, N
Llewellyn, D
Ferrucci, L
Campbell, J
AF Clark, Christopher
Thomas, Daniel
Mejzner, Natasha
Llewellyn, David
Ferrucci, Luigi
Campbell, John
TI Can we predict who should be tested for postural hypotension? Derivation
and validation of a prediction tool
SO JOURNAL OF HUMAN HYPERTENSION
LA English
DT Meeting Abstract
C1 [Clark, Christopher; Thomas, Daniel; Mejzner, Natasha; Llewellyn, David; Campbell, John] Univ Exeter, Sch Med, Exeter EX4 4QJ, Devon, England.
[Ferrucci, Luigi] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9240
EI 1476-5527
J9 J HUM HYPERTENS
JI J. Hum. Hypertens.
PD OCT
PY 2016
VL 30
IS 10
SI SI
MA O-15
BP 640
EP 640
PG 1
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA DZ3ZY
UT WOS:000385797000025
ER
PT J
AU Murphy, J
Mark, H
AF Murphy, Jeanne
Mark, Hayley
TI Self-Sampling as an Intervention to Promote Cervical Cancer Screening
Among Women With HIV
SO JOURNAL OF LOWER GENITAL TRACT DISEASE
LA English
DT Letter
C1 [Murphy, Jeanne] NCI, Canc Prevent Fellowship Program, Canc Prevent Div, Rockville, MD 20850 USA.
[Mark, Hayley] Towson Univ, Dept Nursing, Towson, MD USA.
RP Murphy, J (reprint author), NCI, Canc Prevent Fellowship Program, Canc Prevent Div, Rockville, MD 20850 USA.
EM jeanne.murphy@nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 2
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1089-2591
EI 1526-0976
J9 J LOW GENIT TRACT DI
JI J. Low. Genit. Tract. Dis.
PD OCT
PY 2016
VL 20
IS 4
BP e63
EP e63
DI 10.1097/LGT.0000000000000259
PG 1
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA DY8II
UT WOS:000385372600006
PM 27556424
ER
PT J
AU Kim, H
Sanchez, GAM
Goldbach-Mansky, R
AF Kim, Hanna
Sanchez, Gina A. Montealegre
Goldbach-Mansky, Raphaela
TI Insights from Mendelian Interferonopathies: Comparison of CANDLE, SAVI
with AGS, Monogenic Lupus
SO JOURNAL OF MOLECULAR MEDICINE-JMM
LA English
DT Review
DE Type I IFN; Autoinflammatory; Autoimmune; Candle; SAVI;
Interferonopathies
ID AICARDI-GOUTIERES-SYNDROME; FAMILIAL CHILBLAIN LUPUS; ATYPICAL
NEUTROPHILIC DERMATOSIS; INNATE IMMUNE-RESPONSE; SINGLETON-MERTEN
SYNDROME; NAKAJO-NISHIMURA SYNDROME; OF-FUNCTION MUTATION; MEDIATED
CELL-DEATH; I INTERFERON; EXTRACELLULAR TRAPS
AB Autoinflammatory disorders are sterile inflammatory conditions characterized by episodes of early-onset fever and disease-specific patterns of organ inflammation. Recently, the discoveries of monogenic disorders with strong type I interferon (IFN) signatures caused by mutations in proteasome degradation and cytoplasmic RNA and DNA sensing pathways suggest a pathogenic role of IFNs in causing autoinflammatory phenotypes. The IFN response gene signature (IGS) has been associated with systemic lupus erythematosus (SLE) and other autoimmune diseases. In this review, we compare the clinical presentations and pathogenesis of two IFN-mediated autoinflammatory diseases, CANDLE and SAVI, with Aicardi GoutiSres syndrome (AGS) and monogenic forms of SLE (monoSLE) caused by loss-of-function mutations in complement 1 (C1q) or the DNA nucleases, DNASE1 and DNASE1L3. We outline differences in intracellular signaling pathways that fuel a pathologic type I IFN amplification cycle. While IFN amplification is caused by predominantly innate immune cell dysfunction in SAVI, CANDLE, and AGS, autoantibodies to modified RNA and DNA antigens interact with tissues and immune cells including neutrophils and contribute to IFN upregulation in some SLE patients including monoSLE, thus justifying a grouping of "autoinflammatory" and "autoimmune" interferonopathies. Understanding of the differences in the cellular sources and signaling pathways will guide new drug development and the use of emerging targeted therapies.
C1 [Kim, Hanna] NIAMSD, Translat Res, Pediat Translat Res Branch, NIH, Bethesda, MD 20892 USA.
[Sanchez, Gina A. Montealegre; Goldbach-Mansky, Raphaela] NIAID, Translat Autoinflammatory Dis Studies, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Sanchez, Gina A. Montealegre; Goldbach-Mansky, Raphaela] NIAMS, NIH, Bethesda, MD USA.
RP Kim, H (reprint author), NIAMSD, Translat Res, Pediat Translat Res Branch, NIH, Bethesda, MD 20892 USA.; Goldbach-Mansky, R (reprint author), NIAID, Translat Autoinflammatory Dis Studies, 9000 Rockville Pike, Bethesda, MD 20892 USA.; Goldbach-Mansky, R (reprint author), NIAMS, NIH, Bethesda, MD USA.
EM hanna.kim@nih.gov; gina.montealegre@nih.gov; goldbacr@mail.nih.gov
OI Kim, Hanna/0000-0002-0595-6533
FU Intramural Research Program of the NIH; NIAID; NIAMS
FX This research was supported by the Intramural Research Program of the
NIH, NIAID, and NIAMS. The authors would like to thank Dr. Ann
Marschuk-Rothstein and Dr. Adriana Almeida de Jesus for helpful
discussions.
NR 120
TC 1
Z9 1
U1 4
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0946-2716
EI 1432-1440
J9 J MOL MED
JI J. Mol. Med.
PD OCT
PY 2016
VL 94
IS 10
BP 1111
EP 1127
DI 10.1007/s00109-016-1465-5
PG 17
WC Genetics & Heredity; Medicine, Research & Experimental
SC Genetics & Heredity; Research & Experimental Medicine
GA DY6PP
UT WOS:000385250200005
PM 27678529
ER
PT J
AU Akgul, G
McBain, CJ
AF Akguel, Guelcan
McBain, Chris J.
TI Diverse roles for ionotropic glutamate receptors on inhibitory
interneurons in developing and adult brain
SO JOURNAL OF PHYSIOLOGY-LONDON
LA English
DT Review
ID CA2+-PERMEABLE AMPA RECEPTORS; RAT HIPPOCAMPAL-NEURONS;
PARVALBUMIN-EXPRESSING INTERNEURONS; LACUNOSUM MOLECULARE INTERNEURONS;
DUAL INTRACELLULAR-RECORDINGS; PRESYNAPTIC NMDA RECEPTORS;
CALCIUM-PERMEABLE AMPA; LONG-TERM POTENTIATION; SUBUNIT MESSENGER-RNAS;
KAINATE RECEPTORS
AB Glutamate receptor-mediated recruitment of GABAergic inhibitory interneurons is a critical determinant of network processing. Early studies observed that many, but not all, interneuron glutamatergic synapses contain AMPA receptors that are GluA2-subunit lacking and Ca2+ permeable, making them distinct from AMPA receptors at most principal cell synapses. Subsequent studies demonstrated considerable alignment of synaptic AMPA and NMDA receptor subunit composition within specific subtypes of interneurons, suggesting that both receptor expression profiles are developmentally and functionally linked. Indeed glutamate receptor expression profiles are largely predicted by the embryonic origins of cortical interneurons within the medial and caudal ganglionic eminences of the developing telencephalon. Distinct complements of AMPA and NMDA receptors within different interneuron subpopulations contribute to the differential recruitment of functionally divergent interneuron subtypes by common afferent inputs for appropriate feed-forward and feedback inhibitory drive and network entrainment. In contrast, the lesser-studied kainate receptors, which are often present at both pre- and postsynaptic sites, appear to follow an independent developmental expression profile. Loss of specific ionotropic glutamate receptor (iGluR) subunits during interneuron development has dramatic consequences for both cellular and network function, often precipitating circuit inhibition-excitation imbalances and in some cases lethality. Here we briefly review recent findings highlighting the roles of iGluRs in interneuron development.
C1 [Akguel, Guelcan; McBain, Chris J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Porter Neurosci Res Ctr, Rm3C903,Lincoln Dr, Bethesda, MD 20892 USA.
RP McBain, CJ (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD 20892 USA.
EM mcbainc@mail.nih.gov
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development [Z1A-HD001205-21]
FX This work was funded by an Intramural research award from the Eunice
Kennedy Shriver National Institute of Child Health and Human Development
(Z1A-HD001205-21).
NR 137
TC 2
Z9 2
U1 5
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3751
EI 1469-7793
J9 J PHYSIOL-LONDON
JI J. Physiol.-London
PD OCT 1
PY 2016
VL 594
IS 19
BP 5471
EP 5490
DI 10.1113/JP271764
PG 20
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA DY8DK
UT WOS:000385358500011
PM 26918438
ER
PT J
AU Lawrence, E
Fry, RJ
AF Lawrence, Emily
Fry, Richard J.
TI Content Blocking and the Patron as Situated Knower: What Would It Take
for an Internet Filter to Work?
SO LIBRARY QUARTERLY
LA English
DT Article
ID INTELLECTUAL FREEDOM; LIBRARIES
AB Librarians often object to Internet filters on the grounds that filters are prone to overblocking and underblocking. This argument implies that a significant problem with contemporary filters is that they are insufficiently fine-grained. In this article, we posit that present-day filters will always be conceptually capable of failure, regardless of how granular their content analysis becomes. This is because, we argue, objections to content are best understood as objections to problematic interactions between content and particular knowers. We import the concept of the situated knower from feminist epistemology to capture the heterogeneous, socially embedded nature of patrons, about whom we cannot make blunt generalizations for filtering purposes. A successful filter would need information about these differently situated patrons, the content they seek, and the interactions between the two. We conclude that a genuinely successful Internet filter would therefore need to be both mind reading and fortune-telling.
C1 [Lawrence, Emily] Univ Illinois, Grad Sch Lib & Informat Sci, Champaign, IL 61801 USA.
[Lawrence, Emily] Natl Lib Med, Reference Serv, Bethesda, MD 20894 USA.
[Lawrence, Emily] Natl Lib Med, Web Serv, Bethesda, MD 20894 USA.
[Fry, Richard J.] Southern Illinois Univ, Edwardsville, IL USA.
RP Lawrence, E (reprint author), Univ Illinois, Grad Sch Lib & Informat Sci, Champaign, IL 61801 USA.; Lawrence, E (reprint author), Natl Lib Med, Reference Serv, Bethesda, MD 20894 USA.; Lawrence, E (reprint author), Natl Lib Med, Web Serv, Bethesda, MD 20894 USA.
EM elawrnc2@illinois.edu; rfry@siue.edu
NR 38
TC 0
Z9 0
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA
SN 0024-2519
EI 1549-652X
J9 LIBR QUART
JI Libr. Q.
PD OCT
PY 2016
VL 86
IS 4
BP 403
EP 418
DI 10.1086/688030
PG 16
WC Information Science & Library Science
SC Information Science & Library Science
GA DZ2EU
UT WOS:000385655900003
ER
PT J
AU Park, YMM
Fung, TT
Steck, SE
Zhang, JJ
Hazlett, LJ
Han, K
Lee, SH
Merchant, AT
AF Park, Yong-Moon Mark
Fung, Teresa T.
Steck, Susan E.
Zhang, Jiajia
Hazlett, Linda J.
Han, Kyungdo
Lee, Seung-Hwan
Merchant, Anwar T.
TI Diet Quality and Mortality Risk in Metabolically Obese Normal-Weight
Adults
SO MAYO CLINIC PROCEEDINGS
LA English
DT Article
ID HEALTHY EATING INDEX; NONDIABETIC KOREAN POPULATION;
GUIDELINES-FOR-AMERICANS; HYPERTENSION DASH DIET; MAJOR CHRONIC DISEASE;
C-REACTIVE PROTEIN; BODY-MASS INDEX; CARDIOVASCULAR-DISEASE; WAIST
CIRCUMFERENCE; NATIONAL-HEALTH
AB Objective: To examine the associations among the Dietary Approaches to Stop Hypertension (DASH)-style diet, the Healthy Eating Index (HEI), and mortality risk in metabolically obese normal-weight (MONW) adults.
Patients and Methods: Data were from normal-weight (body mass index of 18.5 to < 25) adults aged 30 to 90 years at baseline in the Third National Health and Nutrition Examination Survey, October 18, 1988, through October 15, 1994, followed up for deaths (all-cause, cardiovascular, and cancer related) until December 31, 2011. A total of 2103 participants without known cardiovascular disease and cancer at baseline were included in this prospective cohort study. Metabolic obesity was defined as having 2 or more of the following: high glucose, blood pressure, triglyceride, C-reactive protein, and insulin resistance values and low high-density lipoprotein cholesterol levels; metabolic healthy status was defined as having 0 or 1 of these metabolic derangements.
Results: During median follow-up of 18.6 years, there were 344 and 296 deaths in the MONW and metabolically healthy normal-weight (MHNW) phenotypes, respectively. In MONW individuals, a 1-SD increment in adherence to a DASH diet (2 points) or HEI (14 points) was significantly associated with reductions (17% [hazard ratio (HR), 0.83; 95% CI, 0.72-0.97] and 22% [HR, 0.78; 95% CI, 0.68-0.90], respectively) in the risk of all-cause mortality, after adjustment for potential confounders. The corresponding HRs for cardiovascular disease mortality were 0.72 (95% CI, 0.55-0.94) and 0.79 (95% CI, 0.65-0.97), respectively. In addition, reduction of cancer mortality was observed with 1-SD increment of HEI (HR, 0.63; 95% CI, 0.46-0.88). However, no association was observed in the MHNW phenotype. Sensitivity analyses suggested relationships robust to different definitions of MONW and also dose responses with the number of metabolic derangements.
Conclusion: Higher diet quality scores were associated with lower risk of mortality in normal-weight individuals with metabolic abnormalities. (C) 2016 Mayo Foundation for Medical Education and Research
C1 [Park, Yong-Moon Mark; Steck, Susan E.; Zhang, Jiajia; Hazlett, Linda J.; Merchant, Anwar T.] Univ South Carolina, Arnold Sch Publ Hlth, Dept Epidemiol & Biostat, 915 Greene St, Columbia, SC 29208 USA.
[Park, Yong-Moon Mark] NIEHS, Epidemiol Branch, NIH, Res Triangle Pk, NC 27709 USA.
[Fung, Teresa T.] Simmons Coll, Dept Nutr, Boston, MA 02115 USA.
[Fung, Teresa T.] Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA.
[Han, Kyungdo] Catholic Univ Korea, Coll Med, Dept Biostat, Seoul, South Korea.
[Lee, Seung-Hwan] Catholic Univ Korea, Coll Med, Dept Internal Med, Div Endocrinol & Metab, Seoul, South Korea.
RP Merchant, AT (reprint author), Univ South Carolina, Arnold Sch Publ Hlth, Dept Epidemiol & Biostat, 915 Greene St, Columbia, SC 29208 USA.
EM merchant@mailbox.sc.edu
OI Lee, Seung-Hwan/0000-0002-3964-3877; PARK, YONG-MOON/0000-0002-5879-6879
NR 50
TC 1
Z9 1
U1 1
U2 1
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 2016
VL 91
IS 10
BP 1372
EP 1383
DI 10.1016/j.mayocp.2016.06.022
PG 12
WC Medicine, General & Internal
SC General & Internal Medicine
GA DZ6AQ
UT WOS:000385944400011
PM 27712636
ER
PT J
AU Maio, N
Rouault, TA
AF Maio, N.
Rouault, T. A.
TI Mammalian Fe-S proteins: definition of a consensus motif recognized by
the co-chaperone HSC20
SO METALLOMICS
LA English
DT Review
ID IRON-SULFUR CLUSTER; MITOCHONDRIAL CYSTEINE DESULFURASE; RESONANCE EPR
SPECTROSCOPY; ASSEMBLY SCAFFOLD PROTEIN; X-RAY-STRUCTURE;
ESCHERICHIA-COLI; COMPLEX-I; SACCHAROMYCES-CEREVISIAE;
ADENOSYLMETHIONINE ENZYMES; AZOTOBACTER-VINELANDII
AB Iron-sulfur (Fe-S) clusters are inorganic cofactors that are fundamental to several biological processes in all three kingdoms of life. In most organisms, Fe-S clusters are initially assembled on a scaffold protein, ISCU, and subsequently transferred to target proteins or to intermediate carriers by a dedicated chaperone/co-chaperone system. The delivery of assembled Fe-S clusters to recipient proteins is a crucial step in the biogenesis of Fe-S proteins, and, in mammals, it relies on the activity of a multiprotein transfer complex that contains the chaperone HSPA9, the co-chaperone HSC20 and the scaffold ISCU. How the transfer complex efficiently engages recipient Fe-S target proteins involves specific protein interactions that are not fully understood. This mini review focuses on recent insights into the molecular mechanism of amino acid motif recognition and discrimination by the co-chaperone HSC20, which guides Fe-S cluster delivery.
C1 [Maio, N.; Rouault, T. A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Mol Med, 9000 Rockville Pike, Bethesda, MD 20892 USA.
RP Rouault, TA (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Mol Med, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM rouault@mail.nih.gov
FU intramural program of the Eunice Kennedy Shriver National Institute of
Child Health and Human Development, Bethesda, MD
FX This work was supported by the intramural program of the Eunice Kennedy
Shriver National Institute of Child Health and Human Development,
Bethesda, MD.
NR 163
TC 0
Z9 0
U1 8
U2 8
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
ENGLAND
SN 1756-5901
EI 1756-591X
J9 METALLOMICS
JI Metallomics
PD OCT 1
PY 2016
VL 8
IS 10
BP 1032
EP 1046
DI 10.1039/c6mt00167j
PG 15
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA DZ1JF
UT WOS:000385594000001
PM 27714045
ER
PT J
AU Yi, MN
Yu, PP
Lu, Q
Geller, HM
Yu, ZH
Chen, HZ
AF Yi, Mengni
Yu, Panpan
Lu, Qin
Geller, Herbert M.
Yu, Zhihua
Chen, Hongzhuan
TI KCa3.1 constitutes a pharmacological target for astrogliosis associated
with Alzheimer's disease
SO MOLECULAR AND CELLULAR NEUROSCIENCE
LA English
DT Article
DE Astrogliosis; Alzheimer's disease; GFAP; Mouse; Culture
ID ACCELERATED MOUSE SAMP8; K+ CHANNEL; REACTIVE ASTROCYTES; THERAPEUTIC
TARGET; UP-REGULATION; IN-VIVO; INHIBITION; CALCIUM; MODEL; MEMORY
AB Alzheimer's disease (AD) is the most common type of dementia and is characterized by a progression from decline of episodic memory to a global impairment of cognitive function. Astrogliosis is a hallmark feature of AD, and reactive gliosis has been considered as an important target for intervention in various neurological disorders. We previously found in astrocyte cultures that the expression of the intermediate conductance calcium-activated potassium channel KCa3.1 was increased in reactive astrocytes induced by TGF-beta, while pharmacological blockade or genetic deletion of KCa3.1 attenuated astrogliosis. In this study, we sought to suppress reactive gliosis in the context of AD by inhibiting KCa3.1 and evaluate its effects on the cognitive impairment using murine animal models such as the senescence-accelerated mouse prone 8 (SAMP8) model that exhibits some AD-like symptoms. We found KCa3.1 expression was increased in reactive astrocytes as well as neurons in the brains of both SAMP8 mice and Alzheimer's disease patients. Blockade of KCa3.1 with the selective inhibitor TRAM-34 in SAMP8 mice resulted in a decrease in astrogliosis as well as microglia activation, and moreover an attenuation of memory deficits. Using KCa3.1 knockout mice, we further confirmed that deletion of KCa3.1 reduced the activation of astrocytes and microglia, and rescued the memory loss induced by intrahippocampal A beta(1-42) peptide injection. We also found in astrocyte cultures that blockade of KCa3.1 or deletion of KCa3.1 suppressed A beta oligomer-induced astrogliosis. Our data suggest that KCa3.1 inhibition might represent a promising therapeutic strategy for AD treatment. (C) 2016 Elsevier Inc. All rights reserved.
C1 [Yi, Mengni; Lu, Qin; Yu, Zhihua; Chen, Hongzhuan] Shanghai Jiao Tong Univ, Sch Med, Inst Med Sci, Dept Pharmacol, 280 South Chongqing Rd, Shanghai 200025, Peoples R China.
[Yu, Panpan] Jinan Univ, Guangdong Hongkong Macau Inst CNS Regenerat, Guangzhou 510632, Guangdong, Peoples R China.
[Yu, Panpan] Jinan Univ, Minist Educ, Joint Int Res Lab CNS Regenerat, Guangzhou 510632, Guangdong, Peoples R China.
[Geller, Herbert M.] NHLBI, Dev Neurobiol Sect, Div Intramural Res, NIH, Bldg 10, Bethesda, MD 20892 USA.
RP Yu, ZH; Chen, HZ (reprint author), Shanghai Jiao Tong Univ, Sch Med, Inst Med Sci, Dept Pharmacol, 280 South Chongqing Rd, Shanghai 200025, Peoples R China.
EM yuzhihua@shsmu.edu.cn; hongzhuan_chen@hotmail.com
FU Science and Technology Commission of Shanghai Municipality
[16ZR1418700]; National Natural Science Foundation of China [81102491];
Natural Science Foundation of Guangdong Province [2016A030313096];
Fundamental Research Funds for the Central Universities [21616340]
FX This work was supported by Science and Technology Commission of Shanghai
Municipality grant 16ZR1418700, National Natural Science Foundation of
China grant 81102491, Natural Science Foundation of Guangdong Province
(2016A030313096), the Fundamental Research Funds for the Central
Universities (21616340). The authors declare no competing financial
interests.
NR 48
TC 1
Z9 1
U1 3
U2 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1044-7431
EI 1095-9327
J9 MOL CELL NEUROSCI
JI Mol. Cell. Neurosci.
PD OCT
PY 2016
VL 76
BP 21
EP 32
DI 10.1016/j.mcn.2016.08.008
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA DY9RA
UT WOS:000385471600003
PM 27567685
ER
PT J
AU Keasey, SL
Natesan, M
Pugh, C
Kamata, T
Wuchty, S
Ulrich, RG
AF Keasey, Sarah L.
Natesan, Mohan
Pugh, Christine
Kamata, Teddy
Wuchty, Stefan
Ulrich, Robert G.
TI Cell-free Determination of Binary Complexes That Comprise Extended
Protein-Protein Interaction Networks of Yersinia pestis
SO MOLECULAR & CELLULAR PROTEOMICS
LA English
DT Article
ID TANDEM AFFINITY PURIFICATION; RNA CHAPERONE HFQ; ESCHERICHIA-COLI;
HELICOBACTER-PYLORI; INTERACTION MAP; III SECRETION; IN-VITRO;
PSEUDOTUBERCULOSIS; INHIBITORS; BIOLOGY
AB Binary protein interactions form the basic building blocks of molecular networks and dynamic assemblies that control all cellular functions of bacteria. Although these protein interactions are a potential source of targets for the development of new antibiotics, few high-confidence data sets are available for the large proteomes of most pathogenic bacteria. We used a library of recombinant proteins from the plague bacterium Yersinia pestis to probe planar microarrays of immobilized proteins that represented similar to 85% (3552 proteins) of the bacterial proteome, resulting in >77,000 experimentally determined binary interactions. Moderate (K-D similar to mu M) to high-affinity (K-D similar to nM) interactions were characterized for >1600 binary complexes by surface plasmon resonance imaging of microarrayed proteins. Core binary interactions that were in common with other gram-negative bacteria were identified from the results of both microarray methods. Clustering of proteins within the interaction network by function revealed statistically enriched complexes and pathways involved in replication, biosynthesis, virulence, metabolism, and other diverse biological processes. The interaction pathways included many proteins with no previously known function. Further, a large assembly of proteins linked to transcription and translation were contained within highly interconnected subregions of the network. The two-tiered microarray approach used here is an innovative method for detecting binary interactions, and the resulting data will serve as a critical resource for the analysis of protein interaction networks that function within an important human pathogen.
C1 [Keasey, Sarah L.; Natesan, Mohan; Pugh, Christine; Kamata, Teddy; Ulrich, Robert G.] US Army Med Res Inst Infect Dis, Mol & Translat Sci Div, Frederick, MD 21702 USA.
[Keasey, Sarah L.] Univ Maryland Baltimore Cty, Dept Biol Sci, Baltimore, MD 21250 USA.
[Wuchty, Stefan] NIH, Natl Ctr Biotechnol Informat, Bldg 10, Bethesda, MD 20892 USA.
[Wuchty, Stefan] Univ Miami, Dept Comp Sci, Coral Gables, FL 33124 USA.
RP Ulrich, RG (reprint author), USAMRIID, Mol & Translat Sci, 1425 Porter St, Frederick, MD 21702 USA.
EM rulrich@bhsai.org
FU Defense Threat Reduction Agency (RGU)
FX This work was supported in part by a grant from the Defense Threat
Reduction Agency (RGU) and by appointment of SLK to the Research
Participation Program for the U.S. Army Medical Research and Materiel
Command, administered through an agreement between the U.S. Department
of Energy and the USAMRMC. Opinions, interpretations, conclusions, and
recommendations are those of the authors and are not necessarily
endorsed by the U.S. Army or the National Institutes of Health.
10.1074/mcp.M116.059337.
NR 51
TC 0
Z9 0
U1 3
U2 3
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 1535-9476
EI 1535-9484
J9 MOL CELL PROTEOMICS
JI Mol. Cell. Proteomics
PD OCT
PY 2016
VL 15
IS 10
BP 3220
EP 3232
DI 10.1074/mcp.M116.059337
PG 13
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA DY8JB
UT WOS:000385374800010
PM 27489291
ER
PT J
AU Norris, EL
Headlam, MJ
Dave, KA
Smith, DD
Bukreyev, A
Singh, T
Jayakody, BA
Chappell, KJ
Collins, PL
Gorman, JJ
AF Norris, Emma L.
Headlam, Madeleine J.
Dave, Keyur A.
Smith, David D.
Bukreyev, Alexander
Singh, Toshna
Jayakody, Buddhika A.
Chappell, Keith J.
Collins, Peter L.
Gorman, Jeffrey J.
TI Proteoform-Specific Insights into Cellular Proteome Regulation
SO MOLECULAR & CELLULAR PROTEOMICS
LA English
DT Article
ID TRANSFER-RNA-SYNTHETASE; SHOTGUN PROTEOMICS; INTERFERON-GAMMA;
MASS-SPECTROMETRY; PEPTIDE IDENTIFICATION; GEL-ELECTROPHORESIS;
EPITHELIAL-CELLS; GENE-EXPRESSION; VIRUS; PROTEINS
AB Knowledge regarding compositions of proteomes at the proteoform level enhances insights into cellular phenotypes. A strategy is described herein for discovery of proteoform-specific information about cellular proteomes. This strategy involved analysis of data obtained by bottom-up mass spectrometry of multiple protein OGE separations on a fraction by fraction basis. The strategy was exemplified using five matched sets of lysates of uninfected and human respiratory syncytial virus-infected A549 cells. Template matching demonstrated that 67.3% of 10475 protein profiles identified focused to narrow pI windows indicative of efficacious focusing. Furthermore, correlation between experimental and theoretical pI gradients indicated reproducible focusing. Based on these observations a proteoform profiling strategy was developed to identify proteoforms, detect proteoform diversity and discover potential proteoform regulation. One component of this strategy involved examination of the focusing profiles for protein groups. A novel concordance analysis facilitated differentiation between proteoforms, including proteoforms generated by alternate splicing and proteolysis. Evaluation of focusing profiles and concordance analysis were applicable to cells from a single and/or multiple biological states. Statistical analyses identified proteoform variation between biological states. Regulation relevant to cellular responses to human respiratory syncytial virus was revealed. Western blotting and Protomap analyses validated the proteoform regulation. Discovery of STAT1, WARS, MX1, and HSPB1 proteoform regulation by human respiratory syncytial virus highlighted the impact of the profiling strategy. Novel truncated proteoforms of MX1 were identified in infected cells and phosphorylation driven regulation of HSPB1 proteoforms was correlated with infection. The proteoform profiling strategy is generally applicable to investigating interactions between viruses and host cells and the analysis of other biological systems.
C1 [Norris, Emma L.; Headlam, Madeleine J.; Dave, Keyur A.; Singh, Toshna; Jayakody, Buddhika A.; Gorman, Jeffrey J.] QIMR Berghofer Med Res Inst, Prot Discovery Ctr, Herston, Qld, Australia.
[Smith, David D.] QIMR Berghofer Med Res Inst, Stat Unit, Herston, Qld, Australia.
[Bukreyev, Alexander; Collins, Peter L.] NIAID, Resp Virus Sect, Infect Dis Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Chappell, Keith J.; Gorman, Jeffrey J.] Univ Queensland, Sch Chem & Mol Biosci, St Lucia, Qld, Australia.
[Bukreyev, Alexander] Univ Texas Med Branch, Galveston Natl Lab, Dept Pathol, Keiller Bldg,Room 3-145,301 Univ Blvd, Galveston, TX 77555 USA.
[Bukreyev, Alexander] Univ Texas Med Branch, Galveston Natl Lab, Dept Microbiol & Immunol, Keiller Bldg,Room 3-145,301 Univ Blvd, Galveston, TX 77555 USA.
RP Gorman, JJ (reprint author), Royal Brisbane Hosp, Prot Discovery Ctr, QIMR Berghofer, Locked Bag 2000, Herston, Qld 4029, Australia.
EM jeff.gorman@qimr.edu.au
OI Smith, David/0000-0001-9644-2353; Headlam, Madeleine/0000-0001-6812-2459
FU Bioplatforms Australia; Queensland State Government through the
Australian Government National Collaborative Infrastructure Strategy
(NCRIS); EIF Fund
FX Access to proteomic infrastructure in the QIMR Berghofer Protein
Discovery Centre was made possible by funding from Bioplatforms
Australia and the Queensland State Government provided through the
Australian Government National Collaborative Infrastructure Strategy
(NCRIS) and EIF Fund.
NR 65
TC 0
Z9 0
U1 2
U2 2
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 1535-9476
EI 1535-9484
J9 MOL CELL PROTEOMICS
JI Mol. Cell. Proteomics
PD OCT
PY 2016
VL 15
IS 10
BP 3297
EP 3320
DI 10.1074/mcp.O116.058438
PG 24
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA DY8JB
UT WOS:000385374800016
PM 27451424
ER
PT J
AU Turkbey, B
Choyke, PL
AF Turkbey, Baris
Choyke, Peter L.
TI Birth of a standard: MET-RADS-P for metastatic prostate cancer
SO NATURE REVIEWS UROLOGY
LA English
DT Editorial Material
C1 [Turkbey, Baris; Choyke, Peter L.] NCI, Mol Imaging Program, US Natl Inst Hlth, 10 Ctr Dr,Room B3B69, Bethesda, MD 20892 USA.
RP Turkbey, B (reprint author), NCI, Mol Imaging Program, US Natl Inst Hlth, 10 Ctr Dr,Room B3B69, Bethesda, MD 20892 USA.
EM turkbeyi@mail.nih.gov
NR 6
TC 0
Z9 0
U1 2
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-4812
EI 1759-4820
J9 NAT REV UROL
JI Nat. Rev. Urol.
PD OCT
PY 2016
VL 13
IS 10
BP 568
EP 570
DI 10.1038/nrurol.2016.163
PG 3
WC Urology & Nephrology
SC Urology & Nephrology
GA DY9TH
UT WOS:000385477500014
PM 27578044
ER
PT J
AU Cardenas, SA
Kassem, L
Brotman, MA
Leibenluft, E
McMahon, FJ
AF Cardenas, Stephanie A.
Kassem, Layla
Brotman, Melissa A.
Leibenluft, Ellen
McMahon, Francis J.
TI Neurocognitive functioning in euthymic patients with bipolar disorder
and unaffected relatives: A review of the literature
SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS
LA English
DT Review
DE Bipolar disorder; Neuropsychology; Cognition; At-risk; Relatives; Review
ID INCREASED INTRASUBJECT VARIABILITY; TRAUMATIC BRAIN-INJURY; 1ST-DEGREE
RELATIVES; I DISORDER; NEUROPSYCHOLOGICAL DEFICITS; COGNITIVE
IMPAIRMENT; MULTIGENERATIONAL FAMILIES; SUSTAINED ATTENTION; EXECUTIVE
FUNCTIONS; GENETIC LIABILITY
AB Background: Neurocognitive deficits are present in bipolar disorder (BD) patients and their unaffected (nonbipolar) relatives, but it is not clear which domains are most often impaired and the extent of the impairment resulting from shared genetic factors. In this literature review, we address these issues and identify specific neurocognitive tasks most sensitive to cognitive deficits in patients and unaffected relatives.
Method: We conducted a systematic review in Web of Science, PubMed/Medline and PsycINFO databases.
Results: Fifty-one articles assessing cognitive functioning in BD patients (23 studies) and unaffected relatives (28 studies) were examined. Patients and, less so, relatives show impairments in attention, processing speed, verbal learning/memory, and verbal fluency.
Conclusion: Studies were more likely to find impairment in patients than relatives, suggesting that some neurocognitive deficits may be a result of the illness itself and/or its treatment. However, small sample sizes, differences among relatives studied (e.g., relatedness, diagnostic status, age), and differences in assessment instruments may contribute to inconsistencies in reported neurocognitive performance among relatives. Additional studies addressing these issues are needed. (C) 2016 Elsevier Ltd. All rights reserved.
C1 [Cardenas, Stephanie A.] NIH, 10 Ctr Dr,RM 3D54,MSC 1264, Bethesda, MD 20814 USA.
[Kassem, Layla] NIH, 35 Convent Dr,RM 1A202,MSC 3719, Bethesda, MD 20892 USA.
[Brotman, Melissa A.] NIH, 15K North Dr,Room 211, Bethesda, MD 20892 USA.
[Leibenluft, Ellen] NIH, 15K North Dr,RM 210,MSC 2670, Bethesda, MD 20892 USA.
[McMahon, Francis J.] NIH, 35 Convent Dr,RM 1A201,MSC 3719, Bethesda, MD 20892 USA.
RP Cardenas, SA (reprint author), NIH, 10 Ctr Dr,RM 3D54,MSC 1264, Bethesda, MD 20814 USA.
EM sac1@williams.edu; kasseml@mail.nih.gov; brotmanm@mail.nih.gov;
leibs@mail.nih.gov; mcmahonf@mail.nih.gov
RI Brotman, Melissa/H-7409-2013
FU NIMH [1Z01MH002810-11]
FX This work was funded by the NIMH Intramural Research Program
(1Z01MH002810-11).
NR 93
TC 3
Z9 3
U1 9
U2 9
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0149-7634
EI 1873-7528
J9 NEUROSCI BIOBEHAV R
JI Neurosci. Biobehav. Rev.
PD OCT
PY 2016
VL 69
BP 193
EP 215
DI 10.1016/j.neubiorev.2016.08.002
PG 23
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA DY7QE
UT WOS:000385323500015
PM 27502749
ER
PT J
AU Luo, J
AF Luo, Ji
TI Ji Luo elucidates the CRISPR gene editing technology, and how it may
affect cancer therapy in the future
SO ONCOLOGY-NEW YORK
LA English
DT Editorial Material
C1 [Luo, Ji] NCI, Lab Canc Biol & Genet, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Luo, J (reprint author), NCI, Lab Canc Biol & Genet, Ctr Canc Res, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU UBM MEDICA
PI NORWALK
PA 535 CONNECTICUT AVE, STE 300, NORWALK, CT 06854 USA
SN 0890-9091
J9 ONCOLOGY-NY
JI Oncology-NY
PD OCT
PY 2016
VL 30
IS 10
BP 879
EP 879
PG 1
WC Oncology
SC Oncology
GA DZ2TF
UT WOS:000385693800001
ER
PT J
AU Wentzensen, N
AF Wentzensen, Nicolas
TI Epidemiology, prevention and early detection of cervical cancer
SO ONKOLOGE
LA German
DT Article
DE Cervical cancer; Human papillomaviruses; Screening; Biomarker;
Risk-based management
ID HPV-POSITIVE WOMEN; HUMAN-PAPILLOMAVIRUS INFECTION; INTRAEPITHELIAL
NEOPLASIA; AMERICAN SOCIETY; FOLLOW-UP; METHYLATION; RISK; COLPOSCOPY;
PATHOLOGY; VACCINE
AB Persisting infections with human papillomaviruses (HPV) are the indisputable cause of cervical cancer. The development of HPV-based preventive procedures, HPV vaccination and HPV testing are currently leading to major changes in cervical cancer prevention programs worldwide. A reduction of HPV infections and cancer precursors has been observed for young women in many countries one decade after the introduction of HPV vaccination. The focus is now on the integration of new testing approaches for screening of populations with increasing vaccination rates.
A successful cervical cancer prevention program consists of various components including primary screening, triage of screening positives and colposcopy with biopsy to identify women with precursor cancer stages who require treatment. The role of primary screening is to identify a small subset of women with an increased risk of a precancerous stage, while the majority of women can be reassured that the risk is very low. Depending on the primary screening test, additional triage testing is required to decide who should be referred for colposcopy. Currently, there are three major approaches to cervical cancer screening: cervical cytology, HPV testing and HPV cytology co-testing. Several triage tests for HPV-positive women are currently being evaluated, including cytology, HPV genotyping, p16/Ki-67 cytology and various methylation tests. The increasing number of options for cervical cancer screening represent a challenge for clinical guidelines to remain up to date and comprehensible. The increasing complexity can lead to confusion among providers and women who participate in screening programs about the best approaches. Precision prevention is a novel approach to cervical cancer screening that integrates comprehensive risk data based on the individual medical history with test results for uniform, risk-based management decisions.
C1 [Wentzensen, Nicolas] NCI, Div Canc Epidemiol & Genet, Med Ctr Dr,Room 7-E114,9609, Bethesda, MD 20892 USA.
RP Wentzensen, N (reprint author), NCI, Div Canc Epidemiol & Genet, Med Ctr Dr,Room 7-E114,9609, Bethesda, MD 20892 USA.
EM wentzenn@mail.nih.gov
NR 46
TC 0
Z9 0
U1 3
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0947-8965
EI 1433-0415
J9 ONKOLOGE
JI Onkologe
PD OCT
PY 2016
VL 22
IS 10
BP 725
EP 736
DI 10.1007/s00761-016-0092-7
PG 12
WC Oncology
SC Oncology
GA DY5TS
UT WOS:000385166900004
PM 28265177
ER
PT J
AU Olivier, KN
AF Olivier, Kenneth N.
TI ANTIMICROBIAL THERAPY: QUESTIONS, CONCERNS AND LOOKING AHEAD
SO PEDIATRIC PULMONOLOGY
LA English
DT Meeting Abstract
C1 [Olivier, Kenneth N.] NHLBI, Cardiovasc & Pulm Branch, Bldg 10, Bethesda, MD 20892 USA.
NR 2
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 8755-6863
EI 1099-0496
J9 PEDIATR PULM
JI Pediatr. Pulmonol.
PD OCT
PY 2016
VL 51
SU S45
MA S04.2
BP 130
EP 131
PG 2
WC Pediatrics; Respiratory System
SC Pediatrics; Respiratory System
GA DY0VW
UT WOS:000384815300014
ER
PT J
AU Goeckeler-Fried, J
Estabrooks, SK
Chiang, A
Chung, W
Ye, Z
Denny, RA
Weissman, AM
Camacho, CJ
Sorscher, EJ
Brodsky, JL
AF Goeckeler-Fried, J.
Estabrooks, S. K.
Chiang, A.
Chung, W.
Ye, Z.
Denny, R. A.
Weissman, A. M.
Camacho, C. J.
Sorscher, E. J.
Brodsky, J. L.
TI IDENTIFICATION OF NOVEL INHIBITORS OF UBIQUITINATION THAT IMPROVE RESCUE
OF F508DEL-CFTR BY VX-809
SO PEDIATRIC PULMONOLOGY
LA English
DT Meeting Abstract
C1 [Goeckeler-Fried, J.; Estabrooks, S. K.; Chiang, A.; Brodsky, J. L.] Univ Pittsburgh, Biol Sci, Pittsburgh, PA USA.
[Chung, W.] Univ Alabama Birmingham, Neurobiol, Birmingham, AL USA.
[Ye, Z.; Camacho, C. J.] Univ Pittsburgh, Computat Biol, Pittsburgh, PA USA.
[Denny, R. A.] Pfizer Worldwide Med Chem, Cambridge, MA USA.
[Weissman, A. M.] NCI, Lab Prot Dynam & Signaling, Frederick, MD 21701 USA.
[Sorscher, E. J.] Emory Univ, Pediat, Atlanta, GA 30322 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 8755-6863
EI 1099-0496
J9 PEDIATR PULM
JI Pediatr. Pulmonol.
PD OCT
PY 2016
VL 51
SU S45
MA 35
BP 206
EP 206
PG 1
WC Pediatrics; Respiratory System
SC Pediatrics; Respiratory System
GA DY0VW
UT WOS:000384815300112
ER
PT J
AU Liou, TG
Adler, FR
Brown, P
Chatfield, BA
Clancy, JP
Cox, DR
Daines, C
Elborn, JS
Emmett, P
Francis, J
Jensen, JL
Heynekamp, TR
Keogh, RH
Lechtzin, N
Li, Y
Lysinger, J
Nakamura, C
Olivier, KN
Packer, KA
Quittner, AL
Radford, P
Szczesniak, RD
Taylor-Cousar, JL
Vroom, J
Sagel, SD
AF Liou, T. G.
Adler, F. R.
Brown, P.
Chatfield, B. A.
Clancy, J. P.
Cox, D. R.
Daines, C.
Elborn, J. S.
Emmett, P.
Francis, J.
Jensen, J. L.
Heynekamp, T. R.
Keogh, R. H.
Lechtzin, N.
Li, Y.
Lysinger, J.
Nakamura, C.
Olivier, K. N.
Packer, K. A.
Quittner, A. L.
Radford, P.
Szczesniak, R. D.
Taylor-Cousar, J. L.
Vroom, J.
Sagel, S. D.
TI MOUNTAIN WEST CF CONSORTIUM SPUTUM BIOMARKER STUDY
SO PEDIATRIC PULMONOLOGY
LA English
DT Meeting Abstract
C1 [Liou, T. G.; Adler, F. R.; Chatfield, B. A.; Francis, J.; Jensen, J. L.; Li, Y.; Packer, K. A.; Vroom, J.] Univ Utah, Salt Lake City, UT USA.
[Nakamura, C.] Las Vegas CF Ctr, Las Vegas, NV USA.
[Brown, P.] CF Ctr Idaho, Boise, ID USA.
[Lysinger, J.] Billings Clin, Billings, MT USA.
[Clancy, J. P.; Szczesniak, R. D.] Univ Cincinnati, Cincinnati, OH USA.
[Daines, C.] Univ Arizona, Tucson, AZ USA.
[Elborn, J. S.] Queens Univ Belfast, Belfast, Antrim, North Ireland.
[Cox, D. R.] Univ Oxford Nuffield Coll, Oxford, England.
[Emmett, P.; Sagel, S. D.] Univ Colorado, Aurora, CO USA.
[Heynekamp, T. R.] Univ New Mexico, Albuquerque, NM 87131 USA.
[Keogh, R. H.] London Sch Hyg & Trop Med, London, England.
[Lechtzin, N.] Johns Hopkins Univ, Baltimore, MD USA.
[Olivier, K. N.] NHLBI, NIH, Bldg 10, Bethesda, MD 20892 USA.
[Quittner, A. L.] Univ Miami, Miami, FL USA.
[Radford, P.] Phoenix Childrens Hosp, Phoenix, AZ USA.
[Taylor-Cousar, J. L.] Natl Jewish Hlth, Denver, CO USA.
[Sagel, S. D.] Childrens Hosp Colorado, Aurora, CO 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 8755-6863
EI 1099-0496
J9 PEDIATR PULM
JI Pediatr. Pulmonol.
PD OCT
PY 2016
VL 51
SU S45
MA 232
BP 279
EP 280
PG 2
WC Pediatrics; Respiratory System
SC Pediatrics; Respiratory System
GA DY0VW
UT WOS:000384815300309
ER
PT J
AU Tsuchiya, M
Kalurupalle, S
Kumar, P
Ghoshal, S
Zhang, Y
Lehrmann, E
Becker, K
Gorospe, M
Biswas, R
AF Tsuchiya, M.
Kalurupalle, S.
Kumar, P.
Ghoshal, S.
Zhang, Y.
Lehrmann, E.
Becker, K.
Gorospe, M.
Biswas, R.
TI RPTOR, A NOVEL TARGET OF MICRORNA-155, REGULATES THE FIBROTIC PHENOTYPE
OF CYSTIC FIBROSIS LUNG EPITHELIUM THROUGH UP-REGULATION OF CTGF
SO PEDIATRIC PULMONOLOGY
LA English
DT Meeting Abstract
C1 [Tsuchiya, M.; Kalurupalle, S.; Kumar, P.; Ghoshal, S.; Biswas, R.] USUHS, Anat Physiol & Genet, Bethesda, MD USA.
[Zhang, Y.; Lehrmann, E.; Becker, K.; Gorospe, M.] NIA, Genet Lab, NIH, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 8755-6863
EI 1099-0496
J9 PEDIATR PULM
JI Pediatr. Pulmonol.
PD OCT
PY 2016
VL 51
SU S45
MA 237
BP 281
EP 281
PG 1
WC Pediatrics; Respiratory System
SC Pediatrics; Respiratory System
GA DY0VW
UT WOS:000384815300314
ER
PT J
AU Davidson, RM
Hasan, NA
Epperson, LE
Vasireddy, S
Smith, T
Elliot, B
Olivier, KN
Holland, SM
Salfinger, ML
Nick, JA
Zelazny, A
Wallace, RJ
Daley, CL
Strong, M
AF Davidson, R. M.
Hasan, N. A.
Epperson, L. E.
Vasireddy, S.
Smith, T.
Elliot, B.
Olivier, K. N.
Holland, S. M.
Salfinger, M. L.
Nick, J. A.
Zelazny, A.
Wallace, R. J.
Daley, C. L.
Strong, M.
TI GENOMIC AND EVOLUTIONARY ANALYSES OF CLINICAL MYCOBACTERIUM ABSCESSUS
SUBSP MASSILIENSE FROM PATIENTS WITH AND WITHOUT CYSTIC FIBROSIS
SO PEDIATRIC PULMONOLOGY
LA English
DT Meeting Abstract
C1 [Davidson, R. M.; Hasan, N. A.; Epperson, L. E.; Strong, M.] Natl Jewish Hlth, Ctr Genes Environm & Hlth, Denver, CO USA.
[Vasireddy, S.; Smith, T.; Elliot, B.; Wallace, R. J.] Univ Texas Hlth Sci Ctr, Dept Microbiol, Tyler, TX USA.
[Salfinger, M. L.; Nick, J. A.; Daley, C. L.] Natl Jewish Hlth, Dept Med, Denver, CO USA.
[Olivier, K. N.] NHLBI, Cardiovasc & Pulm Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
[Holland, S. M.] NIAID, Lab Clin Infect Dis, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Zelazny, A.] NIH, Dept Microbiol Serv, Dept Lab Med, Bldg 10, 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 8755-6863
EI 1099-0496
J9 PEDIATR PULM
JI Pediatr. Pulmonol.
PD OCT
PY 2016
VL 51
SU S45
MA 392
BP 342
EP 342
PG 1
WC Pediatrics; Respiratory System
SC Pediatrics; Respiratory System
GA DY0VW
UT WOS:000384815300468
ER
PT J
AU Shiroma, EJ
Schepps, MA
Harezlak, J
Chen, KY
Matthews, CE
Koster, A
Caserotti, P
Glynn, NW
Harris, TB
AF Shiroma, E. J.
Schepps, M. A.
Harezlak, J.
Chen, K. Y.
Matthews, C. E.
Koster, A.
Caserotti, P.
Glynn, N. W.
Harris, T. B.
TI Daily physical activity patterns from hip- and wrist-worn accelerometers
SO PHYSIOLOGICAL MEASUREMENT
LA English
DT Article
DE physical activity; epidemiology; exercise; accelerometer; patterns;
aging
ID SEDENTARY BEHAVIOR; OLDER-ADULTS; AGE; CALIBRATION; MONITORS; OUTPUT;
WHITE; SITES; WOMEN; MEN
AB Accelerometer wear location may influence physical activity estimates. This study investigates this relationship through the examination of activity patterns throughout the day. Participants from the aging research evaluating accelerometry (AREA) study (n men = 37, n women = 47, mean age (SD) = 78.9 (5.5) years) were asked to wear accelerometers in a free-living environment for 7 d at three different wear locations; one on each wrist and one on the right hip. During waking hours, wrist-worn accelerometers consistently produced higher median activity counts, about 5 x higher, as well as wider variability compared to hip-worn monitors. However, the shape of the accrual pattern curve over the course of the day for the hip and wrist are similar; there is a spike in activity in the morning, with a prolonged tapering of activity level as the day progresses. The similar patterns of hip and wrist activity accrual provide support that each location is capable of estimating total physical activity volume. The examination of activity patterns over time may provide a more detailed way to examine differences in wear location and different subpopulations.
C1 [Shiroma, E. J.; Schepps, M. A.; Harris, T. B.] NIA, Lab Epidemiol & Populat Sci, 7201 Wisconsin Ave,Gateway Bldg,Suite 3C309, Bethesda, MD 20892 USA.
[Harezlak, J.] Indiana Univ, Richard M Fairbanks Sch Publ Hlth, Dept Biostat, Bloomington, IN 47405 USA.
[Harezlak, J.] Indiana Univ, Sch Med, Bloomington, IN 47405 USA.
[Chen, K. Y.] NIDDK, Diabet Endocrinol & Obes Branch, Bethesda, MD 20892 USA.
[Matthews, C. E.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Koster, A.] Maastricht Univ, CAPHRI Sch Publ Hlth & Primary Care, Dept Social Med, Maastricht, Netherlands.
[Caserotti, P.] Univ Southern Denmark, Dept Sports Sci & Clin Biomech, Odense, Denmark.
[Glynn, N. W.] Univ Pittsburgh, Grad Sch Publ Hlth, Ctr Aging & Populat Hlth, Pittsburgh, PA USA.
RP Shiroma, EJ (reprint author), NIA, Lab Epidemiol & Populat Sci, 7201 Wisconsin Ave,Gateway Bldg,Suite 3C309, Bethesda, MD 20892 USA.
EM Eric.shiroma@nih.gov
RI Dey, Kamalesh/E-6568-2017; Koster, Annemarie/E-7438-2010;
OI Chen, Kong/0000-0002-0306-1904
FU Intramural Research Program of the National Institutes of Health,
National Institute on Aging; National Institutes of Health [AG024826,
AG024827, AG036594, AG000181]; European Union Seventh Framework
Programme (FP7-PEOPLE-CIG) [PCIG09-GA-2011-293621]; National Institute
on Aging [HHSN271201 100605P]
FX This study was supported by the Intramural Research Program of the
National Institutes of Health, National Institute on Aging and by the
research grants AG024826, AG024827, AG036594, and AG000181 from the
National Institutes of Health. A Koster has received funding from the
European Union Seventh Framework Programme (FP7-PEOPLE-2011-CIG) under
grant agreement PCIG09-GA-2011-293621. NW Glynn was supported in part by
National Institute on Aging Professional Services Contract HHSN271201
100605P. We are grateful to the staff of the AREA and DECO studies,
particularly B S Lange-Maia, M E Garcia, and J R Treinish.
NR 25
TC 1
Z9 1
U1 6
U2 6
PU IOP PUBLISHING LTD
PI BRISTOL
PA TEMPLE CIRCUS, TEMPLE WAY, BRISTOL BS1 6BE, ENGLAND
SN 0967-3334
EI 1361-6579
J9 PHYSIOL MEAS
JI Physiol. Meas.
PD OCT
PY 2016
VL 37
IS 10
BP 1852
EP 1861
DI 10.1088/0967-3334/37/10/1852
PG 10
WC Biophysics; Engineering, Biomedical; Physiology
SC Biophysics; Engineering; Physiology
GA DY9ZW
UT WOS:000385497200015
PM 27654140
ER
PT J
AU Karlsson, C
Rehman, F
Damadzic, R
Atkins, AL
Schank, JR
Gehlert, DR
Steensland, P
Thorsell, A
Heilig, M
AF Karlsson, Camilla
Rehman, Faazal
Damadzic, Ruslan
Atkins, Alison L.
Schank, Jesse R.
Gehlert, Donald R.
Steensland, Pia
Thorsell, Annika
Heilig, Markus
TI The melanin-concentrating hormone-1 receptor modulates alcohol-induced
reward and DARPP-32 phosphorylation (vol 233, pg 2355, 2016)
SO PSYCHOPHARMACOLOGY
LA English
DT Correction
C1 [Karlsson, Camilla; Atkins, Alison L.; Thorsell, Annika; Heilig, Markus] Linkopings Univ, Dept Clin & Expt Med, Linkoping, Sweden.
[Rehman, Faazal; Damadzic, Ruslan] NIAAA, Lab Clin & Translat Studies, NIH, Bethesda, MD USA.
[Schank, Jesse R.] Univ Georgia, Dept Physiol & Pharmacol, Athens, GA 30602 USA.
[Gehlert, Donald R.] Lilly Res Labs, Neurosci & Endocrine Discovery Res, Indianapolis, IN USA.
[Steensland, Pia] Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.
RP Heilig, M (reprint author), Linkopings Univ, Dept Clin & Expt Med, Linkoping, Sweden.
EM markus.heilig@liu.se
NR 1
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0033-3158
EI 1432-2072
J9 PSYCHOPHARMACOLOGY
JI Psychopharmacology
PD OCT
PY 2016
VL 233
IS 21-22
BP 3825
EP 3825
DI 10.1007/s00213-016-4434-3
PG 1
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA DZ0HM
UT WOS:000385518500015
PM 27650828
ER
PT J
AU Murad, H
Kipnis, V
Freedman, LS
AF Murad, Havi
Kipnis, Victor
Freedman, Laurence S.
TI Estimating and testing interactions when explanatory variables are
subject to non-classical measurement error
SO STATISTICAL METHODS IN MEDICAL RESEARCH
LA English
DT Article
DE measurement error (ME); errors in variables; interaction; regression
calibration (RC); linear regression calibration; efficient regression
calibration; type I error probability; power
ID STRUCTURAL EQUATION MODELS; REGRESSION CALIBRATION; NUTRITIONAL
EPIDEMIOLOGY
AB Assessing interactions in linear regression models when covariates have measurement error (ME) is complex. We previously described regression calibration (RC) methods that yield consistent estimators and standard errors for interaction coefficients of normally distributed covariates having classical ME. Here we extend normal based RC (NBRC) and linear RC (LRC) methods to a non-classical ME model, and describe more efficient versions that combine estimates from the main study and internal sub-study. We apply these methods to data from the Observing Protein and Energy Nutrition (OPEN) study. Using simulations we show that (i) for normally distributed covariates efficient NBRC and LRC were nearly unbiased and performed well with sub-study size 200; (ii) efficient NBRC had lower MSE than efficient LRC; (iii) the naive test for a single interaction had type I error probability close to the nominal significance level, whereas efficient NBRC and LRC were slightly anti-conservative but more powerful; (iv) for markedly non-normal covariates, efficient LRC yielded less biased estimators with smaller variance than efficient NBRC. Our simulations suggest that it is preferable to use: (i) efficient NBRC for estimating and testing interaction effects of normally distributed covariates and (ii) efficient LRC for estimating and testing interactions for markedly non-normal covariates.
C1 [Murad, Havi; Freedman, Laurence S.] Gertner Inst Epidemiol & Hlth Policy Res, Biostat Unit, IL-52621 Tel Hashomer, Israel.
[Kipnis, Victor] NCI, Biometry Res Grp, Canc Prevent Div, Bethesda, MD 20892 USA.
RP Murad, H (reprint author), Gertner Inst Epidemiol & Hlth Policy Res, Biostat Unit, IL-52621 Tel Hashomer, Israel.
EM HaviM@gertner.health.gov.il
FU Marcia and Eugene Applebaum, Detroit, MI, USA; United States-Israel
Educational Foundation (USIEF)
FX The author(s) disclosed receipt of the following financial support for
the research, authorship, and/or publication of this article: This
research was supported by the Doctoral Fellowship of Excellence grant,
awarded to Bar-Ilan University, Israel by Marcia and Eugene Applebaum,
Detroit, MI, USA. Apart of this research was done during a three months
visit to the National Cancer Institute, Biometry Research Division, USA
supported by the Fulbright Grant for Doctoral Dissertation Students,
awarded by the United States-Israel Educational Foundation (USIEF).
NR 19
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0962-2802
EI 1477-0334
J9 STAT METHODS MED RES
JI Stat. Methods Med. Res.
PD OCT
PY 2016
VL 25
IS 5
BP 1991
EP 2013
DI 10.1177/0962280213509720
PG 23
WC Health Care Sciences & Services; Mathematical & Computational Biology;
Medical Informatics; Statistics & Probability
SC Health Care Sciences & Services; Mathematical & Computational Biology;
Medical Informatics; Mathematics
GA DZ0UO
UT WOS:000385555400015
PM 24334284
ER
PT J
AU Mulatya, CM
McLain, AC
Cai, B
Hardin, JW
Albert, PS
AF Mulatya, Caroline M.
McLain, Alexander C.
Cai, Bo
Hardin, James W.
Albert, Paul S.
TI Estimating time to event characteristics via longitudinal threshold
regression models - an application to cervical dilation progression
SO STATISTICS IN MEDICINE
LA English
DT Article
DE first hitting time; threshold regression; Weiner process
ID NULLIPAROUS WOMEN; LABOR CURVE; INTERVAL; OUTCOMES
AB In longitudinal studies, it is sometimes of interest to estimate the distribution of the time a longitudinal process takes to traverse from one threshold to another. For example, the distribution of the time it takes a woman's cervical dilation to progress from 3 to 4cm can aid the decision-making of obstetricians as to whether a stalled labor should be allowed to proceed or stopped in favor of other options. Often researchers treat this type of data structure as interval censored and employ traditional survival analysis methods. However, the traditional interval censoring approaches are inefficient in that they do not use all of the available data. In this paper, we propose utilizing a longitudinal threshold model to estimate the distribution of the elapsed time between two thresholds of the longitudinal process from repeated measurements. We extend this modeling framework to be used with multiple thresholds. A Wiener process under the first hitting time framework is used to represent survival distribution. We demonstrate our model through simulation studies and an analysis of data from the Consortium on Safe Labor study. Published 2016. This article is a U.S. Government work and is in the public domain in the USA.
C1 [Mulatya, Caroline M.; McLain, Alexander C.; Cai, Bo; Hardin, James W.] Univ South Carolina, Dept Epidemiol & Biostat, 915 Greene St, Columbia, SC 29208 USA.
[Albert, Paul S.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, 6100 Execut Blvd, Rockville, MD 20852 USA.
RP McLain, AC (reprint author), Univ South Carolina, Dept Epidemiol & Biostat, 915 Greene St, Columbia, SC 29208 USA.
EM mclaina@mailbox.sc.edu
RI Hardin, James/Q-7617-2016
OI Hardin, James/0000-0003-0506-5500
FU Intramural Research Program of the National Institutes of Health Eunice
Kennedy Shriver National Institute of Child Health and Human
Development; Division of Intramural Population Health Research, Eunice
Kennedy Shriver National Institute of Child Health and Human Development
FX We thank the editor, associate editor, and two anonymous referees for
their helpful comments, which greatly improved this manuscript. We thank
the Intramural Research Program of the National Institutes of Health
Eunice Kennedy Shriver National Institute of Child Health and Human
Development for allowing us to use these data from the CSL study. The
research by Dr. Albert was supported by the Intramural Research Program
of the National Institutes of Health Eunice Kennedy Shriver National
Institute of Child Health and Human Development. The research by Dr.
McLain was supported, in part, by an Interpersonal Agreement with the
Division of Intramural Population Health Research, Eunice Kennedy
Shriver National Institute of Child Health and Human Development.
NR 28
TC 0
Z9 0
U1 4
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0277-6715
EI 1097-0258
J9 STAT MED
JI Stat. Med.
PD OCT
PY 2016
VL 35
IS 24
BP 4368
EP 4379
DI 10.1002/sim.7031
PG 12
WC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Medicine, Research &
Experimental; Statistics & Probability
SC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Research & Experimental
Medicine; Mathematics
GA DY9XQ
UT WOS:000385490200006
PM 27405611
ER
PT J
AU Follmann, D
Huang, CY
Gabriel, E
AF Follmann, Dean
Huang, Chiung-Yu
Gabriel, Erin
TI Who really gets strep sore throat? Confounding and effect modification
of a time-varying exposure on recurrent events
SO STATISTICS IN MEDICINE
LA English
DT Article
DE attributable fraction; case-crossover design; pattern mixture models;
probability of causation; self-controlled case series
ID CASE-CROSSOVER DESIGN; CAUSAL INFERENCE; CASE SERIES; TESTS; RISK; BIAS
AB Unmeasured confounding is the fundamental obstacle to drawing causal conclusions about the impact of an intervention from observational data. Typically, covariates are measured to eliminate or ameliorate confounding, but they may be insufficient or unavailable. In the special setting where a transient intervention or exposure varies over time within each individual and confounding is time constant, a different tack is possible. The key idea is to condition on either the overall outcome or the proportion of time in the intervention. These measures can eliminate the unmeasured confounding either by conditioning or by use of a proxy covariate. We evaluate existing methods and develop new models from which causal conclusions can be drawn from such observational data even if no baseline covariates are measured. Our motivation for this work was to determine the causal effect of Streptococcus bacteria in the throat on pharyngitis (sore throat) in Indian schoolchildren. Using our models, we show that existing methods can be badly biased and that sick children who are rarely colonized have a high probability that the Streptococcus bacteria are causing their disease. Published 2016. This article is a U.S. Government work and is in the public domain in the USA
C1 [Follmann, Dean; Gabriel, Erin] NIAID, Biostat Res Branch, NIH, 5601 Fishers Lane Room 4C11, Rockville, MD 20852 USA.
[Huang, Chiung-Yu] Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21205 USA.
[Huang, Chiung-Yu] Johns Hopkins Univ, Dept Biostat, Baltimore, MD 21205 USA.
RP Follmann, D (reprint author), NIAID, Biostat Res Branch, NIH, 5601 Fishers Lane Room 4C11, Rockville, MD 20852 USA.
EM dean.follmann@nih.gov
OI Gabriel, Erin/0000-0002-0504-8404
FU National Institutes of Health [1R01CA193888]
FX Huang's work was sponsored by the National Institutes of Health grant
1R01CA193888.
NR 26
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0277-6715
EI 1097-0258
J9 STAT MED
JI Stat. Med.
PD OCT
PY 2016
VL 35
IS 24
BP 4398
EP 4412
DI 10.1002/sim.7000
PG 15
WC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Medicine, Research &
Experimental; Statistics & Probability
SC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Research & Experimental
Medicine; Mathematics
GA DY9XQ
UT WOS:000385490200008
PM 27313096
ER
PT J
AU Asdaghi, N
Romano, JG
Wang, KF
Ciliberti-Vargas, MA
Koch, S
Gardener, H
Dong, CH
Rose, DZ
Waddy, SP
Robichaux, M
Garcia, EJ
Gonzalez-Sanchez, JA
Burgin, WS
Sacco, RL
Rundek, T
AF Asdaghi, Negar
Romano, Jose G.
Wang, Kefeng
Ciliberti-Vargas, Maria A.
Koch, Sebastian
Gardener, Hannah
Dong, Chuanhui
Rose, David Z.
Waddy, Salina P.
Robichaux, Mary
Garcia, Enid J.
Gonzalez-Sanchez, Juan A.
Burgin, W. Scott
Sacco, Ralph L.
Rundek, Tatjana
TI Sex Disparities in Ischemic Stroke Care FL-PR CReSD Study
(Florida-Puerto Rico Collaboration to Reduce Stroke Disparities)
SO STROKE
LA English
DT Article
DE Get With The Guidelines; National Institute of Neurological Disorders
and Stroke; sex characteristics; stroke
ID AMERICAN-HEART-ASSOCIATION; IN-HOSPITAL MORTALITY; EMERGENCY-DEPARTMENT;
GENDER-DIFFERENCES; WOMEN; IMPROVEMENT; OUTCOMES; REGISTRY; PROGRAM;
FUTURE
AB Background and Purpose-Sex-specific disparities in stroke care including thrombolytic therapy and early hospital admission are reported. In a large registry of Florida and Puerto Rico hospitals participating in the Get With The GuidelinesStroke program, we sought to determine sex-specific differences in ischemic stroke performance metrics and overall thrombolytic treatment.
Methods-Around 51317 (49% women) patients were included from 73 sites from 2010 to 2014. Multivariable logistic regression with generalized estimating equations evaluated sex-specific differences in the prespecified Get With The GuidelinesStroke metrics for defect-free care in ischemic stroke, adjusting for age, race-ethnicity, insurance status, hospital characteristics, individual risk factors, and the presenting stroke severity.
Results-As compared with men, women were older (7315 versus 69 +/- 14 years; P<0.0001), more hypertensive (67% versus 63%, P<0.0001), and had more atrial fibrillation (19% versus 16%; P<0.0001). Defect-free care was slightly lower in women than in men (odds ratio, 0.96; 95% confidence interval, 0.93-1.00). Temporal trends in defect-free care improved substantially and similarly for men and women, with a 29% absolute improvement in women (P<0.0001) and 28% in men (P<0.0001), with P value of 0.13 for time-by-sex interaction. Women were less likely to receive thrombolysis (odds ratio, 0.92; 95% confidence interval, 0.86-0.99; P=0.02) and less likely to have a door-to-needle time <1 hour (odds ratio, 0.83; 95% confidence interval, 0.71-0.97; P=0.02) as compared with men.
Conclusions-Women received comparable stroke care to men in this registry as measured by prespecified Get With The Guidelines metrics. However, women less likely received thrombolysis and had door-to-needle time <1 hour, an observation that calls for the implementation of interventions to reduce sex disparity in these measures.
C1 [Asdaghi, Negar; Romano, Jose G.; Wang, Kefeng; Ciliberti-Vargas, Maria A.; Koch, Sebastian; Gardener, Hannah; Dong, Chuanhui; Sacco, Ralph L.; Rundek, Tatjana] Univ Miami, Miller Sch Med, Dept Neurol, Coral Gables, FL 33124 USA.
[Rose, David Z.; Burgin, W. Scott] Univ S Florida, Sch Med, Dept Neurol, Tampa, FL USA.
[Waddy, Salina P.] NINDS, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
[Robichaux, Mary] Amer Heart Assoc, Greater Southeast Affiliate, Marietta, GA USA.
[Garcia, Enid J.] Univ Puerto Rico, Sch Med, Endowed Hlth Serv Res Ctr, San Juan, PR 00936 USA.
[Gonzalez-Sanchez, Juan A.] Univ Puerto Rico, Sch Med, Dept Emergency Med, San Juan, PR 00936 USA.
RP Asdaghi, N (reprint author), 1120 NW 14th St,Clin Res Bldg,13th Floor, Miami, FL 33136 USA.
EM nasdaghi@med.miami.edu
FU National Institute of Health (NIH)/National Institute of Neurological
Disorders (NINDs) and Stroke Prevention and Intervention Research
Program (SPIRP) cooperative grant [U54NS081763]; Office of Research on
Women's Health [3U54NS081763-01S1]
FX The Florida Puerto Rico Collaboration to Reduce Stroke Disparities Study
is supported by the National Institute of Health (NIH)/National
Institute of Neurological Disorders (NINDs) and Stroke Prevention and
Intervention Research Program (SPIRP) cooperative grant (grant number:
U54NS081763). The women's supplement is awarded from the Office of
Research on Women's Health (Grant Number: 3U54NS081763-01S1).
NR 29
TC 1
Z9 1
U1 3
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0039-2499
EI 1524-4628
J9 STROKE
JI Stroke
PD OCT
PY 2016
VL 47
IS 10
BP 2618
EP 2626
DI 10.1161/STROKEAHA.116.013059
PG 9
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA DY8VV
UT WOS:000385410700037
PM 27553032
ER
PT J
AU Allen, ES
Klein, HG
AF Allen, Elizabeth S.
Klein, Harvey G.
TI In a digital age, a relic of manual transfusion records
SO TRANSFUSION
LA English
DT Editorial Material
C1 [Allen, Elizabeth S.; Klein, Harvey G.] NIH, Dept Transfus Med, Ctr Clin, 10 Ctr Dr,MSC 1184,Bldg 10,Room 1C-711, Bethesda, MD 20892 USA.
RP Allen, ES (reprint author), NIH, Dept Transfus Med, Ctr Clin, 10 Ctr Dr,MSC 1184,Bldg 10,Room 1C-711, Bethesda, MD 20892 USA.
EM elizabeth.allen@nih.gov
OI Allen, Elizabeth/0000-0002-1004-3851
NR 1
TC 0
Z9 0
U1 0
U2 0
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 2016
VL 56
IS 10
BP 2405
EP 2405
DI 10.1111/trf.13665
PG 1
WC Hematology
SC Hematology
GA DZ4NG
UT WOS:000385834800003
PM 27739156
ER
PT J
AU Srivastava, K
Polin, H
Sheldon, SL
Wagner, FF
Grabmer, C
Gabriel, C
Denomme, GA
Flegel, WA
AF Srivastava, Kshitij
Polin, Helene
Sheldon, Sherry Lynne
Wagner, Franz Friedrich
Grabmer, Christoph
Gabriel, Christian
Denomme, Gregory Andrew
Flegel, Willy Albert
TI The DAU cluster: a comparative analysis of 18 RHD alleles, some forming
partial D antigens
SO TRANSFUSION
LA English
DT Article
ID SICKLE-CELL-DISEASE; AMINO-ACID SUBSTITUTIONS; PROTEIN-STRUCTURE;
TRANSFUSION THERAPY; CLINICALLY RELEVANT; MOLECULAR-GENETICS;
RHESUS-BOX; D VARIANTS; PHENOTYPE; ENCODES
AB BACKGROUNDThe Rh system is the most complex and polymorphic blood group system in humans with more than 460 alleles known for the RHD gene. The DAU cluster of RHD alleles is characterized by the single-nucleotide change producing the p.Thr379Met amino acid substitution. It is called the DAU-0 allele and has been postulated to be the primordial allele, from which all other alleles of the DAU cluster have eventually evolved.
STUDY DESIGN AND METHODSFor two novel DAU alleles, the nucleotide sequences of all 10 exons as well as adjacent intronic regions, including the 5 and 3 untranslated regions (UTR), were determined for the RHD and RHCE genes. A phylogenetic tree for all DAU alleles was established using the neighbor-joining method with Pan troglodytes as root. Standard hemagglutination and flow cytometry tests were performed.
RESULTSWe characterized two DAU alleles, DAU-11 and DAU-5.1, closely related to DAU-3 and DAU-5, respectively. A phylogenetic analysis of the 18 known DAU alleles indicated point mutations and interallelic recombination contributing to diversification of the DAU cluster.
CONCLUSIONSThe DAU alleles encode a group of RhD protein variants, some forming partial D antigens known to permit anti-D in carriers; all are expected to cause anti-D alloimmunization in recipients of red blood cell transfusions. The DAU alleles evolved through genomic point mutations and recombination. These results suggest that the cluster of DAU alleles represent a clade, which is concordant with our previous postulate that they derived from the primordial DAU-0 allele.
C1 [Srivastava, Kshitij; Sheldon, Sherry Lynne; Flegel, Willy Albert] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
[Polin, Helene; Gabriel, Christian] Red Cross Transfus Serv Upper Austria, Linz, Austria.
[Wagner, Franz Friedrich] Inst Springe, Red Cross Blood Serv NSTOB, Springe, Germany.
[Grabmer, Christoph] SALK Paracelsus Med Univ, Dept Blood Grp Serol & Transfus Med, Salzburg, Austria.
[Gabriel, Christian] Med Univ Graz, Dept Blood Grp Serol & Transfus Med, Graz, Austria.
[Denomme, Gregory Andrew] BloodCtr Wisconsin, Diagnost Labs, Milwaukee, WI USA.
RP Flegel, WA (reprint author), NIH, Lab Serv Sect, Dept Transfus Med, Ctr Clin, Bldg 10, Bethesda, MD 20892 USA.
EM waf@nih.gov
OI Denomme, Gregory/0000-0001-8727-1679
NR 67
TC 0
Z9 0
U1 0
U2 0
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 2016
VL 56
IS 10
BP 2520
EP 2531
DI 10.1111/trf.13739
PG 12
WC Hematology
SC Hematology
GA DZ4NG
UT WOS:000385834800018
PM 27480171
ER
PT J
AU Rooney, MR
Pankow, JS
Sibley, SD
Selvin, E
Reis, JP
Michos, ED
Lutsey, PL
AF Rooney, Mary R.
Pankow, James S.
Sibley, Shalamar D.
Selvin, Elizabeth
Reis, Jared P.
Michos, Erin D.
Lutsey, Pamela L.
TI Serum calcium and incident type 2 diabetes: the Atherosclerosis Risk in
Communities (ARIC) study
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
DE calcium-sensing receptor polymorphism; cohort study; diabetes mellitus;
race; serum calcium
ID GENOME-WIDE ASSOCIATION; CYTOSOLIC-FREE CALCIUM; PARATHYROID-HORMONE;
INSULIN-RESISTANCE; RACIAL-DIFFERENCES; VITAMIN-D; CARDIOVASCULAR RISK;
25-HYDROXYVITAMIN D; BLACK-WOMEN; GLUCOSE
AB Background: Elevated serum calcium has been associated with a variety of metabolic abnormalities and may be associated with a greater risk of diabetes.
Objective: The purpose of this study was to test the hypothesis that serum calcium concentration is positively and independently associated with the incidence of diabetes and to evaluate the association of calcium-sensing receptor (CaSR) gene single nucleotide polymorphism (SNP) rs1801725 with incident diabetes.
Design: Atherosclerosis Risk in Communities study participants free of diabetes at baseline (n = 12,800; mean age: 53.9 y; 22.6% black) were studied for incident diabetes. Serum calcium was measured at baseline and corrected for serum albumin. Diabetes was defined by use of glucose concentrations, self-report, or medication use. Cox proportional hazards regression was used.
Results: During a mean 8.8 y of follow-up, 1516 cases of diabetes were reported. Participants in the highest compared with lowest calcium quintile were at greater risk of incident diabetes after adjustment for demographic and lifestyle factors [BR (95% CI): 1.34 (1.14, 1.57); P-trend across quintiles <0.0001] and with further adjustment for waist circumference and body mass index [1.26 (1.07, 1.48); P-trend = 0.004]. Additional adjustment for biomarkers on the metabolic pathway (e.g., 25-hydroxyvitamin D, parathyroid hormone, phosphorus) had little impact. The calcium-diabetes association was statistically significant in blacks [1.48 (1.11, 1.98); P-trend = 0.002] but not whites [1.17 (0.96, 1.43); P-trend = 0.17] after adjustment for adiposity. In whites, CaSR gene SNP rs1801725 was associated with serum calcium but not with risk of diabetes.
Conclusions: Consistent with 3 previous cohort studies, elevated serum calcium was found to be associated with a greater risk of type 2 diabetes. Further research is needed to understand the role, if any, that calcium plays in the pathogenesis of diabetes.
C1 [Rooney, Mary R.; Pankow, James S.; Lutsey, Pamela L.] Univ Minnesota, Div Epidemiol & Community Hlth, Minneapolis, MN 55455 USA.
[Sibley, Shalamar D.] Univ Minnesota, Div Endocrinol & Diabet, Minneapolis, MN 55455 USA.
[Selvin, Elizabeth; Michos, Erin D.] Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD 21205 USA.
[Selvin, Elizabeth; Michos, Erin D.] Johns Hopkins Univ, Welch Ctr Prevent Epidemiol & Clin Res, Baltimore, MD 21205 USA.
[Michos, Erin D.] Johns Hopkins Univ, Div Cardiol, Baltimore, MD 21205 USA.
[Reis, Jared P.] NHLBI, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
RP Rooney, MR (reprint author), Univ Minnesota, Div Epidemiol & Community Hlth, Minneapolis, MN 55455 USA.
EM roone166@umn.edu
FU NIH National Heart, Lung, and Blood Institute [R01 HL103706]; NIH Office
of Dietary Supplements [R01 HL103706-S1]; National Institute of Diabetes
and Digestive and Kidney Diseases [R01 DK089174]; National Heart, Lung,
and Blood Institute [HHSN268201100005C, HHSN268201100006C,
HHSN268201100007C, HHSN268201100008C, HHSN268201100009C,
HHSN268201100010C, HHSN268201100011C, HHSN268201100012C]; NHLBI
Candidate Gene Resource grant [N01-HC-65226]
FX The research was supported by grants from the NIH National Heart, Lung,
and Blood Institute (R01 HL103706 to PLL), the NIH Office of Dietary
Supplements (R01 HL103706-S1 to PLL), and the National Institute of
Diabetes and Digestive and Kidney Diseases (R01 DK089174 to ES). The
Atherosclerosis Risk in Communities study is a collaborative study
supported by National Heart, Lung, and Blood Institute contracts
HHSN268201100005C, HHSN268201100006C, HHSN268201100007C,
HHSN268201100008C, HHSN268201100009C, HHSN268201100010C,
HHSN268201100011C, and HHSN268201100012C. Reagents for the serum albumin
assays were donated by the manufacturers. Genotyping was supported
through NHLBI Candidate Gene Resource grant no. N01-HC-65226.
NR 42
TC 1
Z9 1
U1 5
U2 5
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
EI 1938-3207
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD OCT
PY 2016
VL 104
IS 4
BP 1023
EP 1029
DI 10.3945/ajcn.115.130021
PG 7
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA DY1SO
UT WOS:000384874900013
PM 27510541
ER
PT J
AU Ahluwalia, N
Herrick, KA
Rossen, LM
Rhodes, D
Kit, B
Moshfegh, A
Dodd, KW
AF Ahluwalia, Namanjeet
Herrick, Kirsten A.
Rossen, Lauren M.
Rhodes, Donna
Kit, Brian
Moshfegh, Alanna
Dodd, Kevin W.
TI Usual nutrient intakes of US infants and toddlers generally meet or
exceed Dietary Reference Intakes: findings from NHANES 2009-2012
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
DE infants and toddlers; nationally representative sample; nutrient
adequacy; recommended intakes; usual nutrient intake
ID NATIONAL-HEALTH; PRESCHOOL-CHILDREN; FEEDING INFANTS; TOTAL-ENERGY;
NUTRITION; COLLECTION; AMERICA; BIRTH; FOODS; B-24
AB Background: To our knowledge, few studies have described the usual nutrient intakes of US children aged <2 y or assessed the nutrient adequacy of their diets relative to the recommended Dietary Reference Intakes (DRIs).
Objective: We estimated the usual nutrient intake of US children aged 6-23 mo examined in NHANES 2009-2012 and compared them to age-specific DRIs as applicable.
Design: Dietary intake was assessed with two 24-h recalls for infants aged 6-11 mo (n = 381) and toddlers aged 12-23 mo (n = 516) with the use of the USDA's Automated Multiple-Pass Method. Estimates of usual nutrient intakes from food and beverages were obtained with the use of the National Cancer Institute method. The proportions of children with intakes below and above the DRI were also estimated.
Results: The estimated usual intakes of infants were adequate for most nutrients; however, 10% had an iron intake below the Estimated Average Requirement (EAR), and only 21% had a vitamin D intake that met or exceeded the recommended Adequate Intake (AI). More nutrient inadequacies were noted among toddlers; 1 in 4 had a lower-than-recommended fat intake (percentage of energy), and most had intakes that were below the EAR for vitamins E (82%) and D (74%). Few toddlers (<1%) met or exceeded the AI for fiber and potassium. In contrast, 1 in 2 had sodium intakes that exceeded the Tolerable Upper Intake Level (UL); >= 16% and 41% of the children had excessive intakes (greater than the ULs) of vitamin A and zinc, respectively.
Conclusions: The estimated usual intakes of infants were adequate for most nutrients. Most toddlers were at risk for inadequate intakes of vitamins D and E and had diets low in fiber and potassium. The sources contributing to excessive intakes of vitamin A and zinc among infants and toddlers may need further evaluation.
C1 [Ahluwalia, Namanjeet; Herrick, Kirsten A.; Kit, Brian] CDC, Div Hlth & Nutr Examinat Survey, Natl Ctr Hlth Stat, Hyattsville, MD 20782 USA.
[Rossen, Lauren M.] CDC, Off Anal & Epidemiol, Natl Ctr Hlth Stat, Hyattsville, MD USA.
[Rhodes, Donna; Moshfegh, Alanna] USDA, Food Surveys Res Grp, Beltsville, MD 20705 USA.
[Dodd, Kevin W.] NCI, NIH, Rockville, MD USA.
RP Ahluwalia, N (reprint author), CDC, Div Hlth & Nutr Examinat Survey, Natl Ctr Hlth Stat, Hyattsville, MD 20782 USA.
EM n.ahluwalia@cdc.gov
NR 40
TC 2
Z9 2
U1 8
U2 8
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
EI 1938-3207
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD OCT
PY 2016
VL 104
IS 4
BP 1167
EP 1174
DI 10.3945/ajcn.116.137752
PG 8
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA DY1SO
UT WOS:000384874900029
PM 27629049
ER
PT J
AU Yanik, EL
Nogueira, LM
Koch, L
Copeland, G
Lynch, CF
Pawlish, KS
Finch, JL
Kahn, AR
Hernandez, BY
Segev, DL
Pfeiffer, RM
Snyder, JJ
Kasiske, BL
Engels, EA
AF Yanik, E. L.
Nogueira, L. M.
Koch, L.
Copeland, G.
Lynch, C. F.
Pawlish, K. S.
Finch, J. L.
Kahn, A. R.
Hernandez, B. Y.
Segev, D. L.
Pfeiffer, R. M.
Snyder, J. J.
Kasiske, B. L.
Engels, E. A.
TI Comparison of Cancer Diagnoses Between the US Solid Organ Transplant
Registry and Linked Central Cancer Registries
SO AMERICAN JOURNAL OF TRANSPLANTATION
LA English
DT Article
ID RECIPIENTS; RISK; MALIGNANCIES
AB US transplant centers are required to report cancers in transplant recipients to the transplant network. The accuracy and completeness of these data, collected in the Scientific Registry of Transplant Recipients (SRTR), are unknown. We compared diagnoses in the SRTR and 15 linked cancer registries for colorectal, liver, lung, breast, prostate and kidney cancers; melanoma; and non-Hodgkin lymphoma (NHL). Among 187 384 transplants, 9323 cancers were documented in the SRTR or cancer registries. Only 36.8% of cancers were in both, with 47.5% and 15.7% of cases additionally documented solely in cancer registries or the SRTR, respectively. Agreement between the SRTR and cancer registries varied (kappa = 0.28 for liver cancer and kappa = 0.52-0.66 for lung, prostate, kidney, colorectum, and breast cancers). Upon evaluation, some NHLs documented only in cancer registries were identified in the SRTR as another type of posttransplant lymphoproliferative disorder. Some SRTR-only cases were explained by miscoding (colorectal cancer instead of anal cancer, metastases as lung or liver cancers) or missed matches with cancer registries, partly due to recipients' outmigration from catchment areas. Estimated sensitivity for identifying cancer was 52.5% for the SRTR and 84.3% for cancer registries. In conclusion, SRTR cancer data are substantially incomplete, limiting their usefulness for surveillance and research.
C1 [Yanik, E. L.; Pfeiffer, R. M.; Engels, E. A.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Nogueira, L. M.] Texas Dept State Hlth Serv, Texas Canc Registry, Austin, TX USA.
[Koch, L.] Illinois Dept Publ Hlth, Illinois State Canc Registry, Springfield, IL 62761 USA.
[Copeland, G.] Michigan Dept Hlth & Human Serv, Michigan Canc Surveillance Program, Lansing, MI USA.
[Lynch, C. F.] Univ Iowa, Coll Publ Hlth, Dept Epidemiol, Iowa City, IA USA.
[Pawlish, K. S.] New Jersey Dept Hlth, Canc Epidemiol Serv, New Jersey State Canc Registry, Trenton, NJ USA.
[Finch, J. L.] Colorado Dept Publ Hlth & Environm, Colorado Cent Canc Registry, Denver, CO USA.
[Kahn, A. R.] New York State Dept Hlth, New York State Canc Registry, Albany, NY USA.
[Hernandez, B. Y.] Univ Hawaii, Ctr Canc, Honolulu, HI USA.
[Segev, D. L.] Johns Hopkins Med Inst, Dept Surg, Baltimore, MD 21205 USA.
[Snyder, J. J.; Kasiske, B. L.] Minneapolis Med Res Fdn Inc, Sci Registry Transplant Recipients, Minneapolis, MN USA.
RP Engels, EA (reprint author), NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
EM engelse@exchange.nih.gov
OI Yanik, Elizabeth/0000-0002-5835-0201
FU Intramural Research Program of the National Cancer Institute;
Minneapolis Medical Research Foundation, Minneapolis, MN
[HHSH250201500009C]; Surveillance, Epidemiology, and End Results Program
of the National Cancer Institute: California [HHSN261201000036C,
HHSN261201000035C, HHSN261201000034C]; Surveillance, Epidemiology, and
End Results Program of the National Cancer Institute: Connecticut [HHSN
261201000024C]; Surveillance, Epidemiology, and End Results Program of
the National Cancer Institute: Hawaii [HHSN261201000037C, N01-PC-35137,
N01-PC-35139]; Surveillance, Epidemiology, and End Results Program of
the National Cancer Institute: Iowa [HSN261201000032C, N01-PC-35143];
Surveillance, Epidemiology, and End Results Program of the National
Cancer Institute: New Jersey [HHSN261201300021I, N01-PC-2013-00021];
Surveillance, Epidemiology, and End Results Program of the National
Cancer Institute: Seattle-Puget Sound [N01-PC-35142]; Surveillance,
Epidemiology, and End Results Program of the National Cancer Institute:
Utah [HHSN2612013000171]; National Program of Cancer Registries of the
Centers for Disease Control and Prevention: California [1U58
DP000807-01]; National Program of Cancer Registries of the Centers for
Disease Control and Prevention: Colorado [U58 DP000848-04]; National
Program of Cancer Registries of the Centers for Disease Control and
Prevention: Georgia [5U58DP003875-01]; National Program of Cancer
Registries of the Centers for Disease Control and Prevention: Illinois
[5U58DP003883-03]; National Program of Cancer Registries of the Centers
for Disease Control and Prevention: Maryland [U58DP12-1205 3919-03];
National Program of Cancer Registries of the Centers for Disease Control
and Prevention: Michigan [5U58DP003921-03]; National Program of Cancer
Registries of the Centers for Disease Control and Prevention: New Jersey
[5U58/DP003931-02]; National Program of Cancer Registries of the Centers
for Disease Control and Prevention: New York [U58DP003879]; National
Program of Cancer Registries of the Centers for Disease Control and
Prevention: North Carolina [U58DP00 0832]; National Program of Cancer
Registries of the Centers for Disease Control and Prevention: Texas
[5U58DP000824-04]; state of California; state of Colorado; state of
Connecticut; state of Illinois; state of Iowa; state of Massachusetts
[5458DP003920]
FX This research was supported in part by the Intramural Research Program
of the National Cancer Institute. The authors gratefully acknowledge the
support and assistance provided by individuals at the Health Resources
and Services Administration (Monica Lin), the SRTR (Ajay Israni and Paul
Newkirk) and the following cancer registries: the states of California
(Tina Clarke), Colorado, Connecticut (Lou Gonsalves), Georgia, Hawaii
(Brenda Hernandez), Iowa, Illinois, Michigan, New Jersey (Xiaoling Niu),
New York, North Carolina (Chandrika Rao), Texas, Utah (Janna Harrell),
and the Seattle-Puget Sound area of Washington (Margaret Madeleine). We
also thank analysts at Information Management Services for programming
support (David Castenson, Matthew Chaloux, Michael Curry, and Ruth
Parsons). The SRTR is currently operated under contract number
HHSH250201500009C (Health Resources and Services Administration) by the
Minneapolis Medical Research Foundation, Minneapolis, MN. Previously,
the SRTR was managed under contracts HHSH250201000018C and
HHSH234200537009C. The following cancer registries were supported by the
Surveillance, Epidemiology, and End Results Program of the National
Cancer Institute: California (contracts HHSN261201000036C,
HHSN261201000035C and HHSN261201000034C); Connecticut (HHSN
261201000024C); Hawaii (HHSN261201000037C, N01-PC-35137 and
N01-PC-35139); Iowa (HSN261201000032C and N01-PC-35143); New Jersey
(HHSN261201300021I and N01-PC-2013-00021); Seattle-Puget Sound
(N01-PC-35142); and Utah (HHSN2612013000171). The following cancer
registries were supported by the National Program of Cancer Registries
of the Centers for Disease Control and Prevention: California (agreement
1U58 DP000807-01), Colorado (U58 DP000848-04), Georgia
(5U58DP003875-01), Illinois (5U58DP003883-03), Maryland (U58DP12-1205
3919-03), Michigan (5U58DP003921-03), New Jersey (5U58/DP003931-02), New
York (U58DP003879), North Carolina (U58DP00 0832), and Texas
(5U58DP000824-04). Additional support was provided by the states of
California, Colorado, Connecticut, Illinois, Iowa, Massachusetts
(Massachusetts Cancer Prevention and Control Cooperative Agreement
5458DP003920), New Jersey, New York (including the Cancer Surveillance
Improvement Initiative), Texas, Utah, and Washington, as well as the
University of Utah and the Fred Hutchinson Cancer Research Center in
Seattle, WA.
NR 12
TC 1
Z9 1
U1 2
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1600-6135
EI 1600-6143
J9 AM J TRANSPLANT
JI Am. J. Transplant.
PD OCT
PY 2016
VL 16
IS 10
BP 2986
EP 2993
DI 10.1111/ajt.13818
PG 8
WC Surgery; Transplantation
SC Surgery; Transplantation
GA DY0UA
UT WOS:000384810500025
ER
PT J
AU Ferrer, RA
Klein, WMP
Persoskie, A
Avishai-Yitshak, A
Sheeran, P
AF Ferrer, Rebecca A.
Klein, William M. P.
Persoskie, Alexander
Avishai-Yitshak, Aya
Sheeran, Paschal
TI The Tripartite Model of Risk Perception (TRIRISK): Distinguishing
Deliberative, Affective, and Experiential Components of Perceived Risk
SO ANNALS OF BEHAVIORAL MEDICINE
LA English
DT Article
DE Risk perception; Vulnerability; Susceptibility; Behavior; Cancer
ID HEALTH BELIEF MODEL; BREAST-CANCER; DECISION-MAKING; MECHANICAL TURK;
BEHAVIOR; METAANALYSIS; INTENTIONS; JUDGMENT; WORRY; VACCINATION
AB Although risk perception is a key predictor in health behavior theories, current conceptions of risk comprise only one (deliberative) or two (deliberative vs. affective/experiential) dimensions.
This research tested a tripartite model that distinguishes among deliberative, affective, and experiential components of risk perception.
In two studies, and in relation to three common diseases (cancer, heart disease, diabetes), we used confirmatory factor analyses to examine the factor structure of the tripartite risk perception (TRIRISK) model and compared the fit of the TRIRISK model to dual-factor and single-factor models. In a third study, we assessed concurrent validity by examining the impact of cancer diagnosis on (a) levels of deliberative, affective, and experiential risk perception, and (b) the strength of relations among risk components, and tested predictive validity by assessing relations with behavioral intentions to prevent cancer.
The tripartite factor structure was supported, producing better model fit across diseases (studies 1 and 2). Inter-correlations among the components were significantly smaller among participants who had been diagnosed with cancer, suggesting that affected populations make finer-grained distinctions among risk perceptions (study 3). Moreover, all three risk perception components predicted unique variance in intentions to engage in preventive behavior (study 3).
The TRIRISK model offers both a novel conceptualization of health-related risk perceptions, and new measures that enhance predictive validity beyond that engendered by unidimensional and bidimensional models. The present findings have implications for the ways in which risk perceptions are targeted in health behavior change interventions, health communications, and decision aids.
C1 [Ferrer, Rebecca A.; Klein, William M. P.] NCI, Behav Res Program, Div Canc Control & Populat Sci, Rockville, MD 20850 USA.
[Persoskie, Alexander] NCI, Behav Res Program, Div Canc Control & Populat Sci, Silver Spring, MD USA.
[Avishai-Yitshak, Aya; Sheeran, Paschal] Univ North Carolina Chapel Hill, Chapel Hill, NC USA.
RP Ferrer, RA (reprint author), NCI, Behav Res Program, Div Canc Control & Populat Sci, Rockville, MD 20850 USA.
EM ferrerra@mail.nih.gov
NR 61
TC 0
Z9 0
U1 11
U2 11
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0883-6612
EI 1532-4796
J9 ANN BEHAV MED
JI Ann. Behav. Med.
PD OCT
PY 2016
VL 50
IS 5
BP 653
EP 663
DI 10.1007/s12160-016-9790-z
PG 11
WC Psychology, Multidisciplinary
SC Psychology
GA DY5ZI
UT WOS:000385184000003
PM 26961206
ER
PT J
AU Shomaker, LB
Kelly, NR
Pickworth, CK
Cassidy, OL
Radin, RM
Shank, LM
Vannucci, A
Thompson, KA
Armaiz-Flores, SA
Brady, SM
Demidowich, AP
Galescu, OA
Courville, AB
Olsen, C
Chen, KY
Stice, E
Tanofsky-Kraff, M
Yanovski, JA
AF Shomaker, Lauren B.
Kelly, Nichole R.
Pickworth, Courtney K.
Cassidy, Omni L.
Radin, Rachel M.
Shank, Lisa M.
Vannucci, Anna
Thompson, Katherine A.
Armaiz-Flores, Sara A.
Brady, Sheila M.
Demidowich, Andrew P.
Galescu, Ovidiu A.
Courville, Amber B.
Olsen, Cara
Chen, Kong Y.
Stice, Eric
Tanofsky-Kraff, Marian
Yanovski, Jack A.
TI A Randomized Controlled Trial to Prevent Depression and Ameliorate
Insulin Resistance in Adolescent Girls at Risk for Type 2 Diabetes
SO ANNALS OF BEHAVIORAL MEDICINE
LA English
DT Article
DE Adolescence; Depression; Insulin resistance; Type 2 diabetes; Randomized
controlled trial
ID EXCESS WEIGHT-GAIN; BETA-CELL FUNCTION; CARDIORESPIRATORY FITNESS;
RECIPROCAL RELATIONS; SENSITIVITY INDEXES; FEMALE ADOLESCENTS; OBESE
ADOLESCENTS; HISPANIC CHILDREN; PLASMA-GLUCOSE; EFFICACY TRIAL
AB Prospective data suggest depressive symptoms worsen insulin resistance and accelerate type 2 diabetes (T2D) onset.
We sought to determine whether reducing depressive symptoms in overweight/obese adolescents at risk for T2D would increase insulin sensitivity and mitigate T2D risk.
We conducted a parallel-group, randomized controlled trial comparing a 6-week cognitive-behavioral (CB) depression prevention group with a 6-week health education (HE) control group in 119 overweight/obese adolescent girls with mild-to-moderate depressive symptoms (Center for Epidemiological Studies-Depression Scale [CES-D] aeyen16) and T2D family history. Primary outcomes were baseline to post-intervention changes in CES-D and whole body insulin sensitivity index (WBISI), derived from 2-h oral glucose tolerance tests. Outcome changes were compared between groups using ANCOVA, adjusting for respective baseline outcome, puberty, race, facilitator, T2D family history degree, baseline age, adiposity, and adiposity change. Multiple imputation was used for missing data.
Depressive symptoms decreased (p < 0.001) in CB and HE from baseline to posttreatment, but did not differ between groups (Delta CESD = -12 vs. -11, 95 % CI difference = -4 to +1, p = 0.31). Insulin sensitivity was stable (p > 0.29) in CB and HE (Delta WBISI = 0.1 vs. 0.2, 95 % CI difference = -0.6 to +0.4, p = 0.63). Among all participants, reductions in depressive symptoms were associated with improvements in insulin sensitivity (p = 0.02).
Girls at risk for T2D displayed reduced depressive symptoms following 6 weeks of CB or HE. Decreases in depressive symptoms related to improvements in insulin sensitivity. Longer-term follow-up is needed to determine whether either program causes sustained decreases in depressive symptoms and improvements in insulin sensitivity.
The trial was registered with clinicaltrials.gov (NCT01425905).
C1 [Shomaker, Lauren B.; Kelly, Nichole R.; Pickworth, Courtney K.; Cassidy, Omni L.; Radin, Rachel M.; Shank, Lisa M.; Vannucci, Anna; Thompson, Katherine A.; Armaiz-Flores, Sara A.; Brady, Sheila M.; Demidowich, Andrew P.; Galescu, Ovidiu A.; Courville, Amber B.; Olsen, Cara; Tanofsky-Kraff, Marian; Yanovski, Jack A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Growth & Obes, NIH, Hatfield Clin Res Ctr, 10 Ctr Dr,Bldg 10,Room 1-3330,MSC 1103, Bethesda, MD 20892 USA.
[Shomaker, Lauren B.; Kelly, Nichole R.; Cassidy, Omni L.; Radin, Rachel M.; Shank, Lisa M.; Vannucci, Anna; Tanofsky-Kraff, Marian] Uniformed Serv Univ Hlth Sci, Dept Med & Clin Psychol, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
[Shomaker, Lauren B.; Kelly, Nichole R.] Colorado State Univ, Dept Human Dev & Family Studies, 303A Behav Sci Bldg,410 Pitkin St, Ft Collins, CO 80523 USA.
[Courville, Amber B.] NIH, Dept Nutr, Mark O Hatfield Clin Ctr, Bldg 10, Bethesda, MD 20892 USA.
[Olsen, Cara] Uniformed Serv Univ Hlth Sci, Dept Prevent Med, Biostat, Bethesda, MD 20814 USA.
[Chen, Kong Y.] NIDDK, Diabet Endocrinol & Obes Branch, NIH, Bethesda, MD 20892 USA.
[Stice, Eric] Oregon Res Inst, Eugene, OR 97403 USA.
RP Shomaker, LB; Tanofsky-Kraff, M; Yanovski, JA (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Growth & Obes, NIH, Hatfield Clin Res Ctr, 10 Ctr Dr,Bldg 10,Room 1-3330,MSC 1103, Bethesda, MD 20892 USA.; Shomaker, LB; Tanofsky-Kraff, M (reprint author), Uniformed Serv Univ Hlth Sci, Dept Med & Clin Psychol, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA.; Shomaker, LB (reprint author), Colorado State Univ, Dept Human Dev & Family Studies, 303A Behav Sci Bldg,410 Pitkin St, Ft Collins, CO 80523 USA.
EM lauren.shomaker@colostate.edu; marian.tanofsky-kraff@usuhs.edu;
jy15i@nih.gov
OI Chen, Kong/0000-0002-0306-1904; Shank, Lisa/0000-0002-6922-7946
FU Intramural NIH HHS [Z01 HD000641-12, Z01 HD000641-13, Z99 HD999999, ZIA
HD000641-21]; NICHD NIH HHS [R00 HD069516, K99 HD069516, ZIA HD000641]
NR 48
TC 0
Z9 0
U1 11
U2 11
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0883-6612
EI 1532-4796
J9 ANN BEHAV MED
JI Ann. Behav. Med.
PD OCT
PY 2016
VL 50
IS 5
BP 762
EP 774
DI 10.1007/s12160-016-9801-0
PG 13
WC Psychology, Multidisciplinary
SC Psychology
GA DY5ZI
UT WOS:000385184000013
PM 27333897
ER
PT J
AU Deligiannidis, KM
Kroll-Desrosiers, AR
Svenson, A
Jaitly, N
Barton, BA
Hall, JE
Rothschild, AJ
AF Deligiannidis, Kristina M.
Kroll-Desrosiers, Aimee R.
Svenson, Abby
Jaitly, Nina
Barton, Bruce A.
Hall, Janet E.
Rothschild, Anthony J.
TI Cortisol response to the Trier Social Stress Test in pregnant women at
risk for postpartum depression
SO ARCHIVES OF WOMENS MENTAL HEALTH
LA English
DT Article
DE Postpartum; Cortisol; Depression; Anxiety
ID CORTICOTROPIN-RELEASING HORMONE; PITUITARY-ADRENAL AXIS; POSTNATAL
DEPRESSION; SALIVARY CORTISOL; PSYCHOSOCIAL STRESS; AWAKENING RESPONSE;
MATERNAL CORTISOL; PHYSICAL ABUSE; REACTIVITY; SYMPTOMS
AB Antepartum depression and anxiety are risk factors for postpartum depression (PPD). Postpartum abnormalities in hypothalamic-pituitary-adrenal (HPA) reactivity are associated with PPD. It is not known if antepartum HPA abnormalities exist in women at risk for PPD (AR-PPD). We measured salivary cortisol response to the Trier Social Stress Test (TSST) in 44 (24 AR-PPD, 20 healthy comparison) pregnant women. Depression and anxiety were measured using the Edinburgh Postnatal Depression Scale (EPDS) and Spielberger State-Trait Anxiety Inventory-State (STAI-S). We analyzed longitudinal changes in cortisol using generalized estimating equation methods to control for the correlation within subjects at the six TSST time points. Group differences in area under the curve (AUC) were examined. A majority (70.8 %) of the AR-PPD had prior depression. EPDS total score was higher in AR-PPD vs. comparison women (mean EPDS = 9.8 +/- 4.9 vs. mean EPDS = 2.4 +/- 2.0 respectively, p < 0.001). Mean STAI-S total score was higher in AR-PPD vs. comparison women at all TSST time points and over time (z = 2.71, df = 1, p = 0.007). There was no significant difference in cortisol concentration over time between groups. We observed no detectable difference in cortisol response to psychosocial stress induced by the TSST despite clinically significant between-group differences in current/past depression and current symptomatology.
C1 [Deligiannidis, Kristina M.; Svenson, Abby; Jaitly, Nina; Rothschild, Anthony J.] Univ Massachusetts, Sch Med, Ctr Psychopharmacol Res & Treatment, Dept Psychiat, Worcester, MA 01605 USA.
[Deligiannidis, Kristina M.] Univ Massachusetts, Dept Psychiat, Womens Mental Hlth Program, Med Sch,UMass Mem Med Ctr, 55 Lake Ave North, Worcester, MA 01605 USA.
[Deligiannidis, Kristina M.] Univ Massachusetts, Dept Obstet & Gynecol, Womens Mental Hlth Program, Med Sch,UMass Mem Med Ctr, 55 Lake Ave North, Worcester, MA 01605 USA.
[Kroll-Desrosiers, Aimee R.; Barton, Bruce A.] Univ Massachusetts, Dept Quantitat Hlth Sci, Sch Med, Worcester, MA 01605 USA.
[Jaitly, Nina; Hall, Janet E.] NIEHS, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
[Hall, Janet E.] Harvard Med Sch, Reprod Endocrine Unit, Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Deligiannidis, KM (reprint author), Univ Massachusetts, Sch Med, Ctr Psychopharmacol Res & Treatment, Dept Psychiat, Worcester, MA 01605 USA.; Deligiannidis, KM (reprint author), Univ Massachusetts, Dept Psychiat, Womens Mental Hlth Program, Med Sch,UMass Mem Med Ctr, 55 Lake Ave North, Worcester, MA 01605 USA.; Deligiannidis, KM (reprint author), Univ Massachusetts, Dept Obstet & Gynecol, Womens Mental Hlth Program, Med Sch,UMass Mem Med Ctr, 55 Lake Ave North, Worcester, MA 01605 USA.
EM Kristina.Deligiannidis@umassmemorial.org; aimee.kroll@umassmed.edu;
abbysve@gmail.com; nina.jaitly@nih.gov; bruce.barton@umassmed.edu;
janet.hall@nih.gov; anthony.rothschild@umassmemorial.org
OI Deligiannidis, Kristina/0000-0001-7439-2236; Barton,
Bruce/0000-0001-7878-8895; Hall, Janet/0000-0003-4644-3061
FU National Center for Advancing Translational Sciences, National
Institutes of Health [UL1 TR000161]; National Institutes of Health
[5K23MH097794]
FX This study was supported by the National Center for Advancing
Translational Sciences, National Institutes of Health Grant (UL1
TR000161), and National Institutes of Health Grant (5K23MH097794)
awarded to Dr. Deligiannidis. The sponsoring agency had no further role
in the study design and analysis, the writing of the report, or the
decision to submit the paper for publication. The authors had full
access to all of the data in the study and take responsibility for the
integrity of the data and the accuracy of the data analysis. The views
expressed in this article are those of the authors and do not
necessarily reflect the position of the NIH.
NR 58
TC 0
Z9 0
U1 5
U2 5
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 1434-1816
EI 1435-1102
J9 ARCH WOMEN MENT HLTH
JI Arch. Womens Ment. Health
PD OCT
PY 2016
VL 19
IS 5
BP 789
EP 797
DI 10.1007/s00737-016-0615-7
PG 9
WC Psychiatry
SC Psychiatry
GA DW4JW
UT WOS:000383610000008
PM 26951216
ER
PT J
AU Musset, L
Allenbach, Y
Benveniste, O
Boyer, O
Bossuyt, X
Bentow, C
Phillips, J
Mammen, A
Van Damme, P
Westhovens, R
Ghirardello, A
Doria, A
Choi, MY
Fritzler, MJ
Schmeling, H
Muro, Y
Garcia-De la Torre, I
Ortiz-Villalvazo, MA
Bizzaro, N
Infantino, M
Imbastaro, T
Peng, QL
Wang, GC
Vencovsky, J
Klein, M
Krystufkova, O
Franceschini, F
Fredi, M
Hue, S
Belmondo, T
Danko, K
Mahler, M
AF Musset, Lucile
Allenbach, Yves
Benveniste, Olivier
Boyer, Olivier
Bossuyt, Xavier
Bentow, Chelsea
Phillips, Joe
Mammen, Andrew
Van Damme, Philip
Westhovens, Rene
Ghirardello, Anna
Doria, Andrea
Choi, May Y.
Fritzler, Marvin J.
Schmeling, Heinrike
Muro, Yoshinao
Garcia-De la Torre, Ignacio
Ortiz-Villalvazo, Miguel A.
Bizzaro, Nicola
Infantino, Maria
Imbastaro, Tiziana
Peng, Qinglin
Wang, Guochun
Vencovsky, Jiri
Klein, Martin
Krystufkova, Olga
Franceschini, Franco
Fredi, Micaela
Hue, Sophie
Belmondo, Thibaut
Danko, Katalin
Mahler, Michael
TI Anti-HMGCR antibodies as a biomarker for immune-mediated necrotizing
myopathies: A history of statins and experience from a large
international multi-center study
SO AUTOIMMUNITY REVIEWS
LA English
DT Review
DE Autoimmune myositis; Autoantibodies; Immune-mediated necrotizing
myopathy; HMGCR; Statins
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; IDIOPATHIC INFLAMMATORY MYOPATHIES;
CLASSIFICATION CRITERIA; AUTOIMMUNE MYOPATHY; AMERICAN-COLLEGE;
RHEUMATOLOGY/EUROPEAN LEAGUE; REDUCTASE AUTOANTIBODIES; RISK-ASSESSMENT;
MYOSITIS; DIAGNOSIS
AB In an effort to find naturally occurring substances that reduce cholesterol by inhibiting 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), statins were first discovered by Endo in 1972. With the widespread prescription and use of statins to decrease morbidity from myocardial infarction and stroke, it was noted that approximately 5% of all statin users experienced muscle pain and weakness during treatment In a smaller proportion of patients, the myopathy progressed to severe morbidity marked by proximal weakness and severe muscle wasting. Remarkably, Mammen and colleagues were the first to discover that the molecular target of statins, 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR), is an autoantibody target in patients that develop an immune-mediated necrotizing myopathy (IMNM). These observations have been confirmed in a number of studies but, until today, a multi-center, international study of IMNM, related idiopathic inflammatory myopathies (IIM), other auto-inflammatory conditions and controls has not been published. Accordingly, an international, multi-center study investigated the utility of anti-HMGCR antibodies in the diagnosis of statin-associated IMNM in comparison to different forms of IIM and controls. This study included samples from patients with different forms of IIM (n = 1250) and patients with other diseases (n = 656) that were collected from twelve sites and tested for anti-HMGCR antibodies by ELISA. This study confirmed that anti-HMGCR autoantibodies, when found in conjunction with statin use, characterize a subset of IIM who are older and have necrosis on muscle biopsy. Taken together, the data to date indicates that testing for anti-HMGCR antibodies is important in the differential diagnosis of IIM and might be considered for future classification criteria. (C) 2016 Published by Elsevier B.V.
C1 [Musset, Lucile] Pitie Salpetriere Univ Hosp Paris, AP HP, Dept Immunol, Immunochem & Autoimmun Lab, Paris, France.
[Allenbach, Yves; Benveniste, Olivier] Pitie Salpetriere Univ Hosp, AP HP, Dept Internal Med & Clin Immunol, Hosp Univ Dept Inflammat Immunopathol & Biotherap, Paris, France.
[Allenbach, Yves; Benveniste, Olivier] Univ Paris 06, Sorbonne Univ, INSERM, U974, Paris, France.
[Boyer, Olivier] Rouen Univ Hosp, Dept Immunol, Rouen, France.
[Boyer, Olivier] INSERM, U905, Rouen, France.
[Boyer, Olivier] Normandie Univ, IRIB, Rouen, France.
[Bossuyt, Xavier] Univ Hosp Leuven, Dept Lab Med, Leuven, Belgium.
[Bossuyt, Xavier] Katholieke Univ Leuven, Dept Microbiol & Immunol, Leuven, Belgium.
[Bentow, Chelsea; Phillips, Joe; Mahler, Michael] Inova Diagnost, Dept Res, San Diego, CA USA.
[Mammen, Andrew] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Van Damme, Philip] Univ Leuven, KU Leuven, Dept Neurosci, VIB Vesalius Res Ctr,Expt Neurol Lab Neurobiol, Leuven, Belgium.
[Van Damme, Philip] Univ Hosp Leuven, Dept Neurol, Leuven, Belgium.
[Westhovens, Rene] Katholieke Univ Leuven, Skeletal Biol & Engn Res Ctr, Dept Dev & Regenerat, Leuven, Belgium.
[Westhovens, Rene] Univ Hosp Leuven, Rheumatol, Leuven, Belgium.
[Ghirardello, Anna; Doria, Andrea] Univ Padua, Dept Med, Div Rheumatol, Padua, Italy.
[Choi, May Y.; Fritzler, Marvin J.] Univ Calgary, Dept Med, Calgary, AB, Canada.
[Schmeling, Heinrike] Univ Calgary, Dept Pediat, Alberta Childrens Hosp, Calgary, AB, Canada.
[Muro, Yoshinao] Nagoya Univ, Div Connect Tissue Dis & Autoimmun, Dept Dermatol, Grad Sch Med, Nagoya, Aichi, Japan.
[Garcia-De la Torre, Ignacio] Hosp Gen Occidente Seguro Social, Dept Immunol & Rheumatol, Zapopan, Jalisco, Mexico.
[Garcia-De la Torre, Ignacio] Univ Guadalajara, Zapopan, Jalisco, Mexico.
[Ortiz-Villalvazo, Miguel A.] Hosp Civil Dr Juan I Menchaca, Dept Internal Med, Guadalajara, Jalisco, Mexico.
[Bizzaro, Nicola] San Antonio Hosp, Clin Pathol Lab, Tolmezzo, Italy.
[Infantino, Maria] S Giovanni di Dio Hosp, Lab Immunol & Allergol, Florence, Italy.
[Imbastaro, Tiziana] Lab Autoimmune Dis Diagnost, PO Spirit Santo, Pescara, Italy.
[Peng, Qinglin; Wang, Guochun] China Japan Friendship Hosp, Dept Rheumatol, Beijing, Peoples R China.
[Vencovsky, Jiri; Klein, Martin; Krystufkova, Olga] Charles Univ Prague, Inst Rheumatol, Prague, Czech Republic.
[Vencovsky, Jiri; Klein, Martin; Krystufkova, Olga] Charles Univ Prague, Dept Rheumatol, Prague, Czech Republic.
[Franceschini, Franco; Fredi, Micaela] Univ Brescia, Rheumatol & Clin Immunol, Spedali Civili Brescia, I-25121 Brescia, Italy.
[Franceschini, Franco; Fredi, Micaela] Univ Pavia, I-27100 Pavia, Italy.
[Hue, Sophie; Belmondo, Thibaut] Henri Mondor Univ Hosp, Dept Immunohematol, Creteil, France.
[Danko, Katalin] Univ Debrecen, Div Immunol, Dept Internal Med 3, Med & Hlth Sci Ctr, Debrecen, Hungary.
RP Mahler, M (reprint author), Inova Diagnost, 9900 Old Grove Rd, San Diego, CA 92131 USA.
EM mmahler@inovadx.com
RI Van Damme, Philip/A-6464-2009
OI Van Damme, Philip/0000-0001-6384-0611
FU Ministry of Health [00023728]
FX The work of Jiri Vencovsky in myositis is supported by project from
Ministry of Health No. 00023728. We acknowledge Laurent Drouot and
Fabienne Jouen (Rouen University Hospital, Department of Immunology,
Rouen, France) as well as Jean-Luc Charuel and Laurent Dufat
(Pitie-Salpetriere Hospital University, Paris, France) for their help
during the study. We acknowledge Lisa Christopher-Stine for proofreading
the draft manuscript and providing valuable suggestions. The local
ethics committees who approved the study for the various centers
involved included the local ethics committee of the University Hospital
Leuven (ML9544, Leuven, Belgium), the local ethics committee of
CPP-Ile-de-France VI GH Pitie-Salpetriere/Ch Foix (President: Dr Laurent
Capelle, Paris, France), the Italian Local Ethics Committee (Comitato
Etico per la Sperimentazione dell'Azienda Ospedaliera di Padova, Prot.
N. 2542P), the Conjoint Health Research Ethics Board (CHREB) of the
University of Calgary (Calgary, Canada), the local ethics committees of
the Nagoya University Graduate School of Medicine (Nagoya, Japan), the
Human Ethics Board of China-Japan Friendship Hospital (Beijing, China),
and the local ethics committee at the Institute of Rheumatology (Prague,
Czech Republic). Where no ethics committee was required per institution
guidelines, informed consent was obtained from the patients involved in
the study.
NR 72
TC 1
Z9 2
U1 9
U2 9
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-9972
EI 1873-0183
J9 AUTOIMMUN REV
JI Autoimmun. Rev.
PD OCT
PY 2016
VL 15
IS 10
BP 983
EP 993
DI 10.1016/j.autrev.2016.07.023
PG 11
WC Immunology
SC Immunology
GA DY1RM
UT WOS:000384872100009
PM 27491568
ER
PT J
AU Alousi, AM
Anasetti, C
Antin, JH
Appelbaum, FR
Bashey, A
Confer, DL
Devine, SM
DiFronzo, N
Giralt, SA
Grupp, SN
Hari, PN
Heslop, HE
Horowitz, MM
Jones, RJ
Kurtzberg, J
Lazarus, HM
Lowsky, R
Mendizabal, AM
Merritt, W
Nakamura, R
Pulsipher, MA
Ratanatharathorn, V
Stadtmauer, EA
Stiff, PJ
Vose, JM
Weisdorf, DJ
Westervelt, P
Wingard, JR
Yanik, GA
AF Alousi, Amin M.
Anasetti, Claudio
Antin, Joseph H.
Appelbaum, Frederick R.
Bashey, Asad
Confer, Dennis L.
Devine, Steven M.
DiFronzo, Nancy
Giralt, Sergio A.
Grupp, Stephan N.
Hari, Parameswaran N.
Heslop, Helen E.
Horowitz, Mary M.
Jones, Richard J.
Kurtzberg, Joanne
Lazarus, Hillard M.
Lowsky, Robert
Mendizabal, Adam M.
Merritt, William
Nakamura, Ryotaro
Pulsipher, Michael A.
Ratanatharathorn, Voravit
Stadtmauer, Edward A.
Stiff, Patrick J.
Vose, Julie M.
Weisdorf, Daniel J.
Westervelt, Peter
Wingard, John R.
Yanik, Gregory A.
CA Blood Marrow Transplant Clinical
TI The Blood and Marrow Transplant Clinical Trials Network: An Effective
Infrastructure for Addressing Important Issues in Hematopoietic Cell
Transplantation
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Review
DE Hematopoietic cell transplantation; Blood and Marrow Transplant;
Clinical Trials Network; Infrastructure; Review
ID VERSUS-HOST-DISEASE; UMBILICAL-CORD BLOOD; COST-EFFECTIVENESS ANALYSIS;
COOPERATIVE-ONCOLOGY-GROUP; INVASIVE FUNGAL-INFECTION; ACUTE
MYELOID-LEUKEMIA; SCIENCE SYMPOSIUM 2007; BMT CTN 0902; BONE-MARROW;
MULTIPLE-MYELOMA
AB Hematopoietic cell transplantation (HCT) is a rapidly evolving field with active preclinical and clinical development of new strategies for patient assessment, graft selection and manipulation, and pre- and post transplantation drug and cell therapy. New strategies require evaluation in definitive clinical trials; however, HCT trials face unique challenges, including the relatively small number of transplantations performed at any single center, the diverse indications for HCT requiring dissimilar approaches, the complex nature of the intervention itself, the risk of multiple complications in the immediate post-transplantation period, and the risk of important, though infrequent, late effects. The Blood and Marrow Transplant Clinical Trials Network (BMT CTN) was established by the US National Heart Lung and Blood Institute and the National Cancer Institute to meet these challenges. In its 15 years as a network, the BMT CTN has proven to be a successful infrastructure for planning, implementing, and completing such trials and for providing definitive answers to questions leading to improvements in the understanding and practice of HCT. It has opened 37 trials, about one-half phase 2 and one-half phase 3, enrolled more than 8000 patients, and published 57 papers addressing important issues in the treatment of patients with life-threatening malignant and nonmalignant blood disorders. This review describes the network's accomplishments, key components of its success, lessons learned over the past 15 years, and challenges for the future. (C) 2016 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc.
C1 [Blood Marrow Transplant Clinical] Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
[Alousi, Amin M.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Anasetti, Claudio] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
[Antin, Joseph H.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Appelbaum, Frederick R.] Fred Hutchinson Canc Res Ctr, 1124 Columbia St, Seattle, WA 98104 USA.
[Bashey, Asad] Northside Hosp, Blood & Marrow Transplant Program, Atlanta, GA USA.
[Confer, Dennis L.] Natl Marrow Donor Program, Minneapolis, MN USA.
[Devine, Steven M.] Ohio State Univ, Med Ctr, Columbus, OH 43210 USA.
[DiFronzo, Nancy] NHLBI, NIH, Bldg 10, Bethesda, MD 20892 USA.
[Giralt, Sergio A.] Mem Sloan Kettering Canc Ctr, 1275 York Ave, New York, NY 10021 USA.
[Grupp, Stephan N.; Horowitz, Mary M.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Hari, Parameswaran N.; Horowitz, Mary M.] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Heslop, Helen E.] Baylor Coll Med, Houston, TX 77030 USA.
[Jones, Richard J.] Johns Hopkins, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
[Kurtzberg, Joanne] Duke Univ, Med Ctr, Durham, NC 27706 USA.
[Lazarus, Hillard M.] Case Western Reserve Univ, Cleveland, OH 44106 USA.
[Lowsky, Robert] Stanford Hosp & Clin, Palo Alto, CA USA.
[Mendizabal, Adam M.] Emmes Corp, Rockville, MD USA.
[Merritt, William] NCI, NIH, Bethesda, MD 20892 USA.
[Nakamura, Ryotaro] City Hope Natl Med Ctr, 1500 E Duarte Rd, Duarte, CA 91010 USA.
[Pulsipher, Michael A.] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Ratanatharathorn, Voravit] Karmanos Canc Inst, Detroit, MI USA.
[Stadtmauer, Edward A.] Univ Penn, Philadelphia, PA 19104 USA.
[Stiff, Patrick J.] Loyola Univ, Med Ctr, 2160 S 1st Ave, Maywood, IL 60153 USA.
[Vose, Julie M.] Univ Nebraska Med Ctr, Omaha, NE USA.
[Weisdorf, Daniel J.] Univ Minnesota, Med Ctr, Minneapolis, MN 55455 USA.
[Westervelt, Peter] Washington Univ, St Louis, MO USA.
[Wingard, John R.] Univ Florida, Gainesville, FL USA.
[Yanik, Gregory A.] Univ Michigan, Ann Arbor, MI 48109 USA.
RP Horowitz, MM (reprint author), Med Coll Wisconsin, Milwaukee, WI 53226 USA.
FU National Institutes of Health; Health Resources and Services
Administration
FX This work was supported by the National Institutes of Health and the
Health Resources and Services Administration. The views expressed do not
necessarily represent the views of the National Institutes of Health,
the Health Resources and Services Administration, or the United States
government.
NR 68
TC 0
Z9 0
U1 4
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
EI 1523-6536
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD OCT
PY 2016
VL 22
IS 10
BP 1747
EP 1757
DI 10.1016/j.bbmt.2016.07.003
PG 11
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA DY3BG
UT WOS:000384965200004
ER
PT J
AU Khan, NE
Rosenberg, PS
Alter, BP
AF Khan, Nicholas E.
Rosenberg, Philip S.
Alter, Blanche P.
TI Preemptive Bone Marrow Transplantation and Event-Free Survival in
Fanconi Anemia
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Article
DE Preemptive transplantation; Fanconi anemia; Markov model; Decision
analysis
ID STEM-CELL TRANSPLANTATION; DIAMOND-BLACKFAN ANEMIA; DECISION-MAKING;
FAILURE SYNDROMES; CANCER; REGISTRY
AB Fanconi anemia (FA) is a rare inherited bone marrow failure syndrome associated with high risks of severe bone marrow failure (BMF), acute myeloid leukemia (AML), and solid tumors (ST). Bone marrow transplantation (BMT) provides a theoretical cure for hematologic risks (BMF, AML), but it introduces uncertain risks of transplantation-related mortality (TRM) and carcinogenicity. We developed a mathematical (Markov) decision model to estimate event-free survival (EFS) conditional on age based on per-year cause-specific hazard rates. We assumed that preemptive (PE) BMT eliminates the risks of BMF and AML, but it may introduce independent risks of TRM or influence the trajectory to ST. Our model suggested that the expected mean EFS in FA is higher for PE-BMT at young ages, with minimal risk of TRM and with little carcinogenicity. PE-BMT in adults decreased expected EFS because of the greater competing risk of ST in adulthood. Estimates of EFS conditioned on attained age may be used in shared decision-making when clinicians must counsel patients using limited data. Our methods may be used to model early transplantation in other blood disorders for which hematopoietic stem cell transplantation mitigates some but not all of the risks. Published by Elsevier Inc. on behalf of the American Society for Blood and Marrow Transplantation.
C1 [Khan, Nicholas E.; Alter, Blanche P.] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,Room 6E452, Bethesda, MD 20850 USA.
[Rosenberg, Philip S.] NCI, Biostat Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Alter, BP (reprint author), NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,Room 6E452, Bethesda, MD 20850 USA.
EM alterb@mail.nih.gov
FU Intramural Research Program of the National Cancer Institute of the
National Institutes of Health
FX This research was supported in part by the Intramural Research Program
of the National Cancer Institute of the National Institutes of Health.
NR 23
TC 1
Z9 1
U1 2
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
EI 1523-6536
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD OCT
PY 2016
VL 22
IS 10
BP 1888
EP 1892
DI 10.1016/j.bbmt.2016.06.018
PG 5
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA DY3BG
UT WOS:000384965200022
PM 27345141
ER
PT J
AU Doyle, M
Pohost, GM
Merz, CNB
Shaw, LJ
Sopko, G
Rogers, WJ
Sharaf, BL
Pepine, CJ
Thompson, DV
Rayarao, G
Tauxe, L
Kelsey, SF
Biederman, RWW
AF Doyle, Mark
Pohost, Gerald M.
Merz, C. Noel Bairey
Shaw, Leslee J.
Sopko, George
Rogers, William J.
Sharaf, Barry L.
Pepine, Carl J.
Thompson, Diane V.
Rayarao, Geetha
Tauxe, Lindsey
Kelsey, Sheryl F.
Biederman, Robert W. W.
TI Use of bio-informatics assessment schema (BIAS) to improve diagnosis and
prognosis of myocardial perfusion data: results from the NHLBI-sponsored
women's ischemia syndrome evaluation (WISE)
SO CARDIOVASCULAR DIAGNOSIS AND THERAPY
LA English
DT Article
DE Modeling; prognosis; diagnosis; myocardial perfusion imaging (MPI);
women
ID CARDIOVASCULAR MAGNETIC-RESONANCE; CORONARY-ARTERY-DISEASE; FEASIBILITY;
RESERVE; SPECT; FLOW
AB Background: We introduce an algorithmic approach to optimize diagnostic and prognostic value of gated cardiac single photon emission computed tomography (SPECT) and magnetic resonance (MR) myocardial perfusion imaging (MPI) modalities in women with suspected myocardial ischemia. The novel approach: bioinformatics assessment schema (BIAS) forms a mathematical model utilizing MPI data and cardiac metrics generated by one modality to predict the MPI status of another modality. The model identifies cardiac features that either enhance or mask the image-based evidence of ischemia. For each patient, the BIAS model value is used to set an appropriate threshold for the detection of ischemia.
Methods: Women (n=130), with symptoms and signs of suspected myocardial ischemia, underwent MPI assessment for regional perfusion defects using two different modalities: gated SPECT and MR. To determine perfusion status, MR data were evaluated qualitatively (MRIQL) and semi-quantitatively (MRISQ) while SPECT data were evaluated using conventional clinical criteria. Evaluators were masked to results of the alternate modality. These MPI status readings were designated "original". Two regression models designated "BIAS" models were generated to model MPI status obtained with one modality (e.g., MRI) compared with a second modality (e.g., SPECT), but importantly, the BIAS models did not include the primary Original MPI reading of the predicting modality. Instead, the BIAS models included auxiliary measurements like left ventricular chamber volumes and myocardial wall thickness. For each modality, the BIAS model was used to set a progressive threshold for interpretation of MPI status. Women were then followed for 38 +/- 14 months for the development of a first major adverse cardiovascular event [MACE: CV death, nonfatal myocardial infarction (MI) or hospitalization for heart failure]. Original and BIAS-augmented perfusion status were compared in their ability to detect coronary artery disease (CAD) and for prediction of MACE.
Results: Adverse events occurred in 14 (11%) women and CAD was present in 13 (10%). There was a positive correlation of maximum coronary artery stenosis and BIAS score for MRI and SPECT (P<0.001). Receiver operator characteristic (ROC) analysis was conducted and showed an increase in the area under the curve of the BIAS-augmented MPI interpretation of MACE vs. the original for MRISQ (0.78 vs. 0.54), MRIQL (0.78 vs. 0.64), SPECT (0.82 vs. 0.63) and the average of the three readings (0.80 +/- 0.02 vs. 0.60 +/- 0.05, P<0.05).
Conclusions: Increasing values of the BIAS score generated by both MRI and SPECT corresponded to the increasing prevalence of CAD and MACE. The BIAS-augmented detection of ischemia better predicted MACE compared with the Original reading for the MPI data for both MRI and SPECT.
C1 [Doyle, Mark; Thompson, Diane V.; Rayarao, Geetha; Biederman, Robert W. W.] Allegheny Gen Hosp, Pittsburgh, PA 15212 USA.
[Pohost, Gerald M.] Univ Southern Calif, Keck Med Ctr, Los Angeles, CA USA.
[Merz, C. Noel Bairey; Shaw, Leslee J.] Cedars Sinai Heart Inst, Barbra Streisand Womens Heart Ctr, Los Angeles, CA USA.
[Sopko, George] NHLBI, NIH, Bldg 10, Bethesda, MD 20892 USA.
[Rogers, William J.; Tauxe, Lindsey] Univ Alabama Birmingham, Birmingham, AL USA.
[Sharaf, Barry L.] Brown Univ, Providence, RI 02912 USA.
[Pepine, Carl J.] Univ Florida, Gainesville, FL USA.
[Kelsey, Sheryl F.] Univ Pittsburgh, Grad Sch Publ Hlth, Pittsburgh, PA USA.
RP Doyle, M (reprint author), Allegheny Gen Hosp, Div Cardiol, CV MRI Ctr, 320 East North Ave, Pittsburgh, PA 15212 USA.
EM mdoyle@wpahs.org
FU NHLBI NIH HHS [N01 HV068161, N01 HV068164, N01HV68162, N01HV68163, R01
HL073412]
NR 16
TC 0
Z9 0
U1 2
U2 2
PU AME PUBL CO
PI SHEUNG WAN
PA ROOM 604 6-F HOLLYWOOD CENTER, 77-91, QUEENS ROAD, SHEUNG WAN, HONG KONG
00000, PEOPLES R CHINA
SN 2223-3652
EI 2223-3660
J9 CARDIOVASC DIAGN THE
JI Cardiovisc. Diagn. Ther.
PD OCT
PY 2016
VL 6
IS 5
BP 424
EP U9
DI 10.21037/cdt.2016.03.11
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA DX6KS
UT WOS:000384493200003
PM 27747165
ER
PT J
AU Morkl, S
Muller, NJ
Blesl, C
Wilkinson, L
Tmava, A
Wurm, W
Holl, AK
Painold, A
AF Moerkl, Sabrina
Mueller, Nicole J.
Blesl, Claudia
Wilkinson, Leonora
Tmava, Adelina
Wurm, Walter
Holl, Anna K.
Painold, Annamaria
TI Problem solving, impulse control and planning in patients with early-
and late-stage Huntington's disease
SO EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE
LA English
DT Article
DE Huntington's disease; Executive function; Tower of London;
Neuropsychology; Disease severity
ID DECISION-MAKING; LONDON TASK; SCHIZOPHRENIA; COMPENSATION; PROGRESSION;
DIAGNOSIS; PATHOLOGY; MEMORY; TOWER; HD
AB Sub-domains of executive functions, including problems with planning, accuracy, impulsivity, and inhibition, are core features of Huntington's disease. It is known that the decline of cognitive function in Huntington's disease is related to the anatomical progression of pathology in the basal ganglia. However, it remains to be determined whether the severity of executive dysfunction depends on the stage of the disease. To examine the severity of sub-domains of executive dysfunction in early- and late-stage Huntington's disease, we studied performance in the Tower of London task of two groups of Huntington's disease patients (Group 1: early, n = 23, and Group 2: late stage, n = 29), as well as a third group of age, education, and IQ matched healthy controls (n = 34). During the task, we measured the total number of problems solved, total planning time, and total number of breaks taken. One aspect of executive function indexed by the number of solved problems seems to progress in the course of the disease. Late-stage Huntington's disease patients scored significantly worse than early-stage patients and controls, and early-stage patients scored significantly worse than controls on this measure of accuracy. In contrast, late- and early-stage HD patients did not differ in terms of planning time and number of breaks. Early- and late-stage HD pathology has a different impact on executive sub-domains. While accuracy differs between early- and late-stage HD patients, other domains like planning time and number of breaks do not. Striatal degeneration, which is a characteristic feature of the disease, might not affect all aspects of executive function in HD.
C1 [Moerkl, Sabrina; Mueller, Nicole J.; Blesl, Claudia; Tmava, Adelina; Wurm, Walter; Holl, Anna K.; Painold, Annamaria] Med Univ Graz, Dept Psychiat, Auenbruggerpl 31-1, A-8036 Graz, Austria.
[Wilkinson, Leonora] NINDS, Behav Neurol Unit, NIH, 10 Ctr Dr,MSC 1440, Bethesda, MD 20892 USA.
RP Blesl, C (reprint author), Med Univ Graz, Dept Psychiat, Auenbruggerpl 31-1, A-8036 Graz, Austria.
EM claudia.blesl@medunigraz.at
FU Medical University of Graz
FX Open access funding provided by Medical University of Graz. We express
our kind appreciation to all the participants of the study.
NR 36
TC 0
Z9 0
U1 8
U2 8
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0940-1334
EI 1433-8491
J9 EUR ARCH PSY CLIN N
JI Eur. Arch. Psych. Clin. Neurosci.
PD OCT
PY 2016
VL 266
IS 7
BP 663
EP 671
DI 10.1007/s00406-016-0707-4
PG 9
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA DY5TY
UT WOS:000385167700009
PM 27372072
ER
PT J
AU Li, DX
Ferrada, MA
Avdic, E
Tamma, PD
Cosgrove, SE
AF Li, David X.
Ferrada, Marcela A.
Avdic, Edina
Tamma, Pranita D.
Cosgrove, Sara E.
TI Sustained Impact of an Antibiotic Stewardship Intervention for
Community-Acquired Pneumonia
SO INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY
LA English
DT Article
ID IMPLEMENTATION
AB Antibiotic stewardship interventions targeting community-acquired pneumonia have been successful in reducing antibiotic overuse in the short term, but the sustainability of their effects has not been investigated. We report that improvements in antibiotic use due to a syndrome-focused intervention for community-acquired pneumonia were sustained 3 years later without additional intervention.
C1 [Li, David X.; Ferrada, Marcela A.; Cosgrove, Sara E.] Johns Hopkins Univ, Sch Med, Div Infect Dis, Baltimore, MD 21205 USA.
[Ferrada, Marcela A.] NIH, Dept Crit Care Med, Bldg 10, Bethesda, MD 20892 USA.
[Avdic, Edina] Johns Hopkins Univ Hosp, Dept Pharm, Baltimore, MD 21287 USA.
[Tamma, Pranita D.] Johns Hopkins Univ, Sch Med, Div Pediat Infect Dis, Baltimore, MD USA.
RP Cosgrove, SE (reprint author), Johns Hopkins Univ Hosp, 600 N Wolfe St,Halsted 827, Baltimore, MD 21287 USA.
EM scosgro1@jhmi.edu
FU Pfizer Grants for Learning and Change; Joint Commission
FX Pfizer Grants for Learning and Change and the Joint Commission (grant to
P.D.T., E.A., and S.E.C.).
NR 9
TC 0
Z9 0
U1 2
U2 2
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0899-823X
EI 1559-6834
J9 INFECT CONT HOSP EP
JI Infect. Control Hosp. Epidemiol.
PD OCT
PY 2016
VL 37
IS 10
BP 1243
EP 1246
DI 10.1017/ice.2016.165
PG 4
WC Public, Environmental & Occupational Health; Infectious Diseases
SC Public, Environmental & Occupational Health; Infectious Diseases
GA DY4GS
UT WOS:000385057600016
PM 27498601
ER
PT J
AU Sy, AA
Kim, WS
Chen, J
Shen, Y
Tao, C
Lee, JS
AF Sy, A. A.
Kim, W. S.
Chen, J.
Shen, Y.
Tao, C.
Lee, J. S.
TI Acculturation levels and personalizing orthognathic surgery for the
Asian American patient
SO INTERNATIONAL JOURNAL OF ORAL AND MAXILLOFACIAL SURGERY
LA English
DT Article
DE facial aesthetics; ethnic variation; Suinn-Lew survey; Western
aesthetics; customized orthognathic treatment planning
ID HEALTH-CARE; ATTRACTIVENESS; QUALITY
AB This study was performed to investigate whether the level of acculturation among Asians living in the USA plays a significant role in their opinion of facial profiles. One hundred and ninety-eight Asian American subjects were asked to complete a pre-validated survey to measure their level of acculturation and to evaluate four sets of pictures that displayed a class II male, class II female, class III male, and class III female. Each set consisted of three lateral profile pictures: an initial unaltered photo, a picture simulating a flatter profile (orthodontic camouflage in class II; mandibular setback in class III), and a picture simulating a fuller profile (mandibular advancement in class II; maxillary advancement in class III). For the class II male, subjects who were more acculturated indicated that a flatter profile (orthodontic camouflage) was less attractive. For the class II female, higher acculturated subjects chose expansive treatment (mandibular advancement) as more aesthetic compared to the less acculturated subjects. Each of these scenarios had statistically significant odds ratios. In general, highly acculturated subjects preferred a fuller facial profile, while low acculturated subjects preferred a flatter facial profile appearance, except for the class III female profile, which did not follow this trend.
C1 [Sy, A. A.; Lee, J. S.] UCSF Oral & Maxillofacial Surg, Box 0440,521 Parnassus Ave,Clin Sci Room 522C, San Francisco, CA 94143 USA.
[Kim, W. S.] Columbia Univ, Oral & Maxillofacial Surg, New York, NY USA.
[Shen, Y.] Washington St, Daly City, CA USA.
[Lee, J. S.] NIDCR, NIH, Bethesda, MD USA.
RP Sy, AA (reprint author), UCSF Oral & Maxillofacial Surg, Box 0440,521 Parnassus Ave,Clin Sci Room 522C, San Francisco, CA 94143 USA.
EM Aldrich.sy@ucsf.edu
OI Kim, William/0000-0001-7693-3454
FU Oral and Maxillofacial Surgery Foundation Student Research Fund
FX This research was supported by the Oral and Maxillofacial Surgery
Foundation Student Research Fund.
NR 26
TC 0
Z9 0
U1 3
U2 3
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0901-5027
EI 1399-0020
J9 INT J ORAL MAX SURG
JI Int. J. Oral Maxillofac. Surg.
PD OCT
PY 2016
VL 45
IS 10
BP 1201
EP 1208
DI 10.1016/j.ijom.2016.04.013
PG 8
WC Dentistry, Oral Surgery & Medicine; Surgery
SC Dentistry, Oral Surgery & Medicine; Surgery
GA DY1MB
UT WOS:000384858000003
PM 27197783
ER
PT J
AU Yoneyama, K
Donekal, S
Venkatesh, BA
Wu, CO
Liu, CY
Nacif, MS
Armstrong, A
Gomes, AS
Hundley, WG
McClelland, RL
Bluemke, DA
Lima, JAG
AF Yoneyama, Kihei
Donekal, Sirisha
Venkatesh, Bharath A.
Wu, Colin O.
Liu, Chia-Ying
Nacif, Marcelo Souto
Armstrong, Anderson
Gomes, Antoinette S.
Hundley, W. Gregory
McClelland, Robyn L.
Bluemke, David A.
Lima, Joao A. G.
TI Natural History of Myocardial Function in an Adult Human Population
Serial Longitudinal Observations From MESA
SO JACC-CARDIOVASCULAR IMAGING
LA English
DT Article
DE aging; heart failure; hypertension; left ventricular; torsion
ID LEFT-VENTRICULAR HYPERTROPHY; HYPERTENSIVE HEART-DISEASE; CARDIAC
MAGNETIC-RESONANCE; ASYMPTOMATIC INDIVIDUALS; CARDIOVASCULAR EVENTS;
ATHEROSCLEROSIS MESA; PROGNOSTIC VALUE; BLOOD-PRESSURE; MIDDLE-AGE;
DYSFUNCTION
AB OBJECTIVES The aim of this longitudinal study was to define the determinants of aging-related left ventricular (LV) remodeling and function in a large multiethnic population.
BACKGROUND The influence of risk factor exposure on myocardial remodeling and function in humans across adult life remains incompletely understood. MESA (Multi-Ethnic Study of Atherosclerosis) is a Longitudinal population-based cohort of asymptomatic adults at baseline.
METHODS We examined 757 participants who were free of clinical cardiovascular disease and underwent tagged cardiac magnetic resonance both at baseline and at the 10-year follow-up as part of the MESA study. LV remodeling, circumferential shortening (CS), and torsion were assessed by tagged cardiac magnetic resonance. Multivariable linear regression was used to determine the association of changes in risk factors with changes in cardiac geometry and function.
RESULTS The mean age of participants was 63 9 years at baseline; 50% were women. Overall, the LV mass-to volume ratio increased by 10% over 10 years (p < 0.01). CS was unchanged (17.8% to 17.9%, p = 0.246), whereas torsion increased by 13% (3.8 degrees/cm to 4.3 degrees/cm, p < 0.001). Increased systolic blood pressure was associated with reduced CS (-0.02%/mm Hg, p < 0.01). Participants who remained on antihypertensive therapy during the whole study had a greater decrease in LV mass-to-volume ratio (-0.045 vs. no medication, p < 0.05) with a greater increase in CS (0.78% vs. no medication, p < 0.01). Moreover, greater LV mass at baseline was significantly associated with reduced CS (-0.02%/g, p < 0.01) and torsion (-0.02 degrees/cm/g, p < 0.01) independently of risk factors.
CONCLUSIONS Longitudinal observation demonstrates that LV mass and worsening risk factors are fundamental determinants of reduced regional myocardial shortening over 10 years. Increased torsion of the myocardial wall is seen with progressive concentric remodeling and may explain why systolic function is maintained with aging. (C) 2016 by the American College of Cardiology Foundation.
C1 [Yoneyama, Kihei; Donekal, Sirisha; Venkatesh, Bharath A.; Nacif, Marcelo Souto; Armstrong, Anderson; Lima, Joao A. G.] Johns Hopkins Univ, Dept Cardiol, Baltimore, MD USA.
[Yoneyama, Kihei] St Marianna Univ, Sch Med, Kawasaki, Kanagawa, Japan.
[Wu, Colin O.] NHLBI, Off Biostat Res, Bldg 10, Bethesda, MD 20892 USA.
[Liu, Chia-Ying; Nacif, Marcelo Souto; Bluemke, David A.] Natl Inst Biomed Imaging & Bioengn, NIH, Ctr Clin, Bethesda, MD USA.
[Gomes, Antoinette S.] Univ Calif Los Angeles, Sch Med, Dept Radiol, Los Angeles, CA 90024 USA.
[Hundley, W. Gregory] Wake Forest Univ Hlth Sci, Dept Internal Med Cardiol, Winston Salem, NC USA.
[McClelland, Robyn L.] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
RP Lima, JAG (reprint author), Johns Hopkins Univ, Johns Hopkins Hosp, Div Cardiol, Blalock 524D1,600 North Wolfe St, Baltimore, MD 21287 USA.
EM jlima@jhmi.edu
OI 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, N01-HC-95169]; National Center
for Research Resources [UL1-TR-000040, UL1-TR-001079]
FX This research was supported by contracts 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, and N01-HC-95169 from the
National Heart, Lung, and Blood Institute and by grants UL1-TR-000040
and UL1-TR-001079 from the National Center for Research Resources. The
authors have reported that they have no relationships relevant to the
contents of this paper to disclose.
NR 37
TC 2
Z9 2
U1 1
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1936-878X
EI 1876-7591
J9 JACC-CARDIOVASC IMAG
JI JACC-Cardiovasc. Imag.
PD OCT
PY 2016
VL 9
IS 10
BP 1164
EP 1173
DI 10.1016/j.jcmg.2016.01.038
PG 10
WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical
Imaging
SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine &
Medical Imaging
GA DY6JO
UT WOS:000385212400005
PM 27639760
ER
PT J
AU Lancaster, C
Pristatsky, P
Hoang, VM
Casimiro, DR
Schwartz, RM
Rustandi, R
Ha, S
AF Lancaster, Catherine
Pristatsky, Pavlo
Hoang, Van M.
Casimiro, Danilo R.
Schwartz, Richard M.
Rustandi, Richard
Ha, Sha
TI Characterization of N-glycosylation profiles from mammalian and insect
cell derived chikungunya VLP
SO JOURNAL OF CHROMATOGRAPHY B-ANALYTICAL TECHNOLOGIES IN THE BIOMEDICAL
AND LIFE SCIENCES
LA English
DT Article
DE Chikungunya; Vaccine; VLP; Glycosylation; HILIC
ID PARTICLE VACCINE; NEUTRALIZING ANTIBODIES; VIRAL HEMAGGLUTININ;
AEDES-ALBOPICTUS; VIRUS; CULTURE; IMMUNOGENICITY; GLYCOPROTEINS;
PATTERNS; MOSQUITO
AB Chikungunya virus (CHIKV) is a mosquito-borne alphavirus that causes severe arthralgia. The envelope of CHIKV is composed of 240 copies of two glycoproteins: El and E2. In this work, we have characterized the N-glycosylation patterns of CHIKV virus-like particles (VLP5), containing both El and E2 proteins, derived from mammalian and insect cells using hydrophilic interaction liquid chromatography (HILIC) with fluorescence (FL) and mass spectrometry (MS) detection. While HEK293 derived CHIKV VLPs contain oligomannose, hybrid and complex glycans, VLPs derived from SfBasic predominantly contain oligomannose glycans. This strong host dependence of N-glycosylation pattern resembles other alphaviruses such as SINV. The VLPs from HEK293 and SfBasic, with significantly different N-glycosylation profiles, are valuable reagents enabling future in-depth correlation studies between immunogenicity and glycosylation. In addition, the characterization tools presented here allow one to monitor glycosylation during vaccine process development and ensure process consistency. (C) 2016 Published by Elsevier B.V.
C1 [Lancaster, Catherine; Pristatsky, Pavlo; Hoang, Van M.; Casimiro, Danilo R.; Rustandi, Richard; Ha, Sha] Merck Res Labs, Vaccine Bioproc Res & Dev, West Point, PA 19486 USA.
[Schwartz, Richard M.] NIAID, Vaccine Prod Program, Vaccine Res Ctr, NIH, Gaithersburg, MD 20878 USA.
RP Ha, S (reprint author), Merck Res Labs, Vaccine Bioproc Res & Dev, West Point, PA 19486 USA.
EM sha_ha@merck.com
NR 30
TC 0
Z9 0
U1 4
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1570-0232
EI 1873-376X
J9 J CHROMATOGR B
JI J. Chromatogr. B
PD OCT 1
PY 2016
VL 1032
SI SI
BP 218
EP 223
DI 10.1016/j.jchromb.2016.04.025
PG 6
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA DY1LV
UT WOS:000384857400024
PM 27157808
ER
PT J
AU Gordon, SN
Liyanage, NPM
Doster, MN
Vaccari, M
Vargas-Inchaustegui, DA
Pegu, P
Schifanella, L
Shen, XY
Tomaras, GD
Rao, M
Billings, EA
Schwartz, J
Prado, I
Bobb, K
Zhang, WL
Montefiori, DC
Foulds, KE
Ferrari, G
Robert-Guroff, M
Roederer, M
Phan, TB
Forthal, DN
Stablein, DM
Phogat, S
Venzon, DJ
Fouts, T
Franchini, G
AF Gordon, Shari N.
Liyanage, Namal P. M.
Doster, Melvin N.
Vaccari, Monica
Vargas-Inchaustegui, Diego A.
Pegu, Poonam
Schifanella, Luca
Shen, Xiaoying
Tomaras, Georgia D.
Rao, Mangala
Billings, Erik A.
Schwartz, Jennifer
Prado, Ilia
Bobb, Kathryn
Zhang, Wenlei
Montefiori, David C.
Foulds, Kathryn E.
Ferrari, Guido
Robert-Guroff, Marjorie
Roederer, Mario
Phan, Tran B.
Forthal, Donald N.
Stablein, Donald M.
Phogat, Sanjay
Venzon, David J.
Fouts, Timothy
Franchini, Genoveffa
TI Boosting of ALVAC-SIV Vaccine-Primed Macaques with the CD4-SIVgp120
Fusion Protein Elicits Antibodies to V2 Associated with a Decreased Risk
of SIVmac251 Acquisition
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID DEPENDENT CELLULAR CYTOTOXICITY; IMMUNODEFICIENCY VIRUS SIV; SIMIAN
IMMUNODEFICIENCY; RHESUS MACAQUES; HIV-1 VACCINE; MEDIATED CYTOTOXICITY;
SHIV CHALLENGE; GAG/POL/NEF VACCINE; ENVELOPE PROTEIN; EFFICACY TRIAL
AB The recombinant ALVAC vaccine coupled with the monomeric gp120/alum protein have decreased the risk of HIV and SIV acquisition. Ab responses to the V1/V2 regions have correlated with a decreased risk of virus acquisition in both humans and macaques. We hypothesized that the breadth and functional profile of Abs induced by an ALVAC/envelope protein regimen could be improved by substituting the monomeric gp120 boost, with the full-length single-chain (FLSC) protein. FLSC is a CD4-gp120 fusion immunogen that exposes cryptic gp120 epitopes to the immune system. We compared the immunogenicity and relative efficiency of an ALVAC-SIV vaccine boosted either with bivalent FLSC proteins or with monomeric gp120 in alum. FLSC was superior to monomeric gp120 in directing Abs to the C3 alpha 2 helix, the V5 loop, and the V3 region that contains the putative CCR5 binding site. In addition, FLSC boosting elicited significantly higher binding Abs to V2 and increased both the Ab-dependent cellular cytotoxicity activity and the breadth of neutralizing Abs. However, the FLSC vaccine regimen demonstrated only a trend in vaccine efficacy, whereas the monomeric gp120 regimen significantly decreased the risk of SIVmac251 acquisition. In both vaccine regimens, anti-V2 Abs correlated with a decreased risk of virus acquisition but differed with regard to systemic or mucosal origin. In the FLSC regimen, serum Abs to V2 correlated, whereas in the monomeric gp120 regimen, V2 Abs in rectal secretions, the site of viral challenge, were associated with efficacy.
C1 [Gordon, Shari N.; Liyanage, Namal P. M.; Doster, Melvin N.; Vaccari, Monica; Pegu, Poonam; Schifanella, Luca; Franchini, Genoveffa] NCI, Anim Models & Vaccine Sect, NIH, 41 Lib Dr,Bldg 41,Room D804, Bethesda, MD 20892 USA.
[Vargas-Inchaustegui, Diego A.; Robert-Guroff, Marjorie] NCI, Immune Biol Retroviral Infect Sect, Vaccine Branch, Bethesda, MD 20892 USA.
[Shen, Xiaoying; Tomaras, Georgia D.; Montefiori, David C.; Ferrari, Guido] Duke Univ, Med Ctr, Durham, NC 27710 USA.
[Rao, Mangala; Billings, Erik A.] Walter Reed Army Inst Res, US Mil HIV Res Program, Silver Spring, MD 20910 USA.
[Schwartz, Jennifer; Prado, Ilia; Bobb, Kathryn; Zhang, Wenlei; Fouts, Timothy] Profectus BioSci Inc, Baltimore, MD 21224 USA.
[Foulds, Kathryn E.; Roederer, Mario] NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Phan, Tran B.; Forthal, Donald N.] Univ Calif Irvine, Div Infect Dis, Dept Med, Sch Med, Irvine, CA 92868 USA.
[Stablein, Donald M.] Emmes Corp, Rockville, MD 20850 USA.
[Phogat, Sanjay] Sanofi Pasteur, Swiftwater, PA 18370 USA.
[Venzon, David J.] NCI, Biostat & Data Management Sect, NIH, Bethesda, MD 20892 USA.
RP Franchini, G (reprint author), NCI, Anim Models & Vaccine Sect, NIH, 41 Lib Dr,Bldg 41,Room D804, Bethesda, MD 20892 USA.
EM franchig@mail.nih.gov
FU Intramural NIH HHS [Z01 BC005688-17]
NR 53
TC 0
Z9 0
U1 2
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD OCT 1
PY 2016
VL 197
IS 7
BP 2726
EP 2737
DI 10.4049/jimmunol.1600674
PG 12
WC Immunology
SC Immunology
GA DY3OX
UT WOS:000385004600022
PM 27591322
ER
PT J
AU Roberts, LM
Crane, DD
Wehrly, TD
Fletcher, JR
Jones, BD
Bosio, CM
AF Roberts, Lydia M.
Crane, Deborah D.
Wehrly, Tara D.
Fletcher, Joshua R.
Jones, Bradley D.
Bosio, Catharine M.
TI Inclusion of Epitopes That Expand High-Avidity CD4(+) T Cells Transforms
Subprotective Vaccines to Efficacious Immunogens against Virulent
Francisella tularensis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID RESPIRATORY VIRUS-INFECTIONS; TULAREMIA VACCINES; PROTECTIVE IMMUNITY;
INTERFERON-GAMMA; C57BL/6 MICE; IFN-GAMMA; LVS; PULMONARY; LIVE;
IDENTIFICATION
AB T cells are the immunological cornerstone in host defense against infections by intracellular bacterial pathogens, such as virulent Francisella tularensis spp. tularensis (Ftt). The general paucity of novel vaccines for Ftt during the past 60 y can, in part, be attributed to the poor understanding of immune parameters required to survive infection. Thus, we developed a strategy utilizing classical immunological tools to elucidate requirements for effective adaptive immune responses directed against Ftt. Following generation of various Francisella strains expressing well-characterized lymphocytic choriomeningitis virus epitopes, we found that survival correlated with persistence of Ag-specific CD4(+) T cells. Function of these cells was confirmed in their ability to more effectively control Ftt replication in vitro. The importance of understanding the Ag-specific response was underscored by our observation that inclusion of an epitope that elicits high-avidity CD4(+) T cells converted a poorly protective vaccine to one that engenders 100% protection. Taken together, these data suggest that improved efficacy of current tularemia vaccine platforms will require targeting appropriate Ag-specific CD4(+) T cell responses and that elucidation of Francisella epitopes that elicit high-avidity CD4(+) T cell responses, specifically in humans, will be required for successful vaccine development.
C1 [Roberts, Lydia M.; Crane, Deborah D.; Wehrly, Tara D.; Bosio, Catharine M.] NIAID, Immun Pulm Pathogens Sect, Bacteriol Lab, Rocky Mt Labs,NIH, 903 S 4th St, Hamilton, MT 59840 USA.
[Fletcher, Joshua R.; Jones, Bradley D.] Univ Iowa, Carver Coll Med, Dept Microbiol, Iowa City, IA 52242 USA.
RP Bosio, CM (reprint author), NIAID, Immun Pulm Pathogens Sect, Bacteriol Lab, Rocky Mt Labs,NIH, 903 S 4th St, Hamilton, MT 59840 USA.
EM bosioc@niaid.nih.gov
FU Intramural NIH HHS [Z01 AI001013-02]; NIAID NIH HHS [HHSN272201300006C]
NR 38
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD OCT 1
PY 2016
VL 197
IS 7
BP 2738
EP 2747
DI 10.4049/jimmunol.1600879
PG 10
WC Immunology
SC Immunology
GA DY3OX
UT WOS:000385004600023
PM 27543611
ER
PT J
AU Gazzinelli-Guimaraes, PH
Bonne-Annee, S
Fujiwara, RT
Santiago, HC
Nutman, TB
AF Gazzinelli-Guimaraes, Pedro H.
Bonne-Annee, Sandra
Fujiwara, Ricardo T.
Santiago, Helton C.
Nutman, Thomas B.
TI Allergic Sensitization Underlies Hyperreactive Antigen-Specific CD4(+) T
Cell Responses in Coincident Filarial Infection
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID TROPICAL PULMONARY EOSINOPHILIA; SPIRALIS NEWBORN LARVAE;
ASCARIS-LUMBRICOIDES; IGE RESPONSES; LYMPHATIC FILARIASIS; HELMINTH
INFECTIONS; SCHISTOSOMA-MANSONI; NECATOR-AMERICANUS; IMMUNOGLOBULIN-E;
SCHOOL-CHILDREN
AB Among the various hypotheses put forward to explain the modulatory influence of helminth infection on allergic effector responses in humans, the IL-10-induced suppression of Th2-associated responses has been the leading candidate. To explore this helminth/allergy interaction more fully, parasite-and allergen-specific CD4(+) T cell responses in 12 subjects with filarial infections, and coincident allergic sensitization (filarial [Fil](+)allergy [A](+)) were compared with the responses to three appropriate control groups (Fil(-)A(-) [n = 13], Fil(-)A(+) [n = 12], Fil(+)A(-) [n = 11]). The most important findings revealed that Fil(+)A(+) had marked (p < 0.0001 for all cytokines) increases in parasite Ag-driven Th2 (IL-4, IL-5, IL-13), Th9 (IL-9), and the regulatory (IL-10) cytokines when compared with Fil(+)A(-). Moreover, using multiparameter flow cytometry, filarial parasite Ag induced a marked increase in not only the frequency of CD4(+) T cells producing IL-4, IL-5, IL-2, and TNF-alpha in Fil(+)A(+) when compared with Fil(+)A(-) patients, but also in the frequencies of polyfunctional Th2-like (CD4(+)IL-4(+)IL-5(+) and CD4(+)IL-2(+)IL-4(+)IL-5(+)TNF-alpha(+)) cells. The Th2-associated responses seen in the Fil(+)A(+) group were correlated with serum IgE levels (p < 0.01, r = 0.5165 for IL-4; p < 0.001, r = 0.5544 for IL-5; and p < 0.001, r = 0.4901 for IL-13) and levels of circulating eosinophils (p < 0.0116, r = 0.5656) and their degranulation/activation products (major basic protein [p < 0.001, r = 0.7353] and eosinophil-derived neurotoxin [p < 0.01, r = 0.7059]). CD4(+) responses to allergen were not different (to a large extent) among the groups. Taken together, our data suggest that allergic sensitization coincident with filarial infection drives parasite Ag-specific T cell hyperresponsiveness, which is characterized largely by an augmented Th2-dominated immune response.
C1 [Gazzinelli-Guimaraes, Pedro H.; Bonne-Annee, Sandra; Nutman, Thomas B.] NIAID, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Gazzinelli-Guimaraes, Pedro H.; Fujiwara, Ricardo T.] Univ Fed Minas Gerais, Inst Biol Sci, Dept Parasitol, BR-31270901 Belo Horizonte, MG, Brazil.
[Santiago, Helton C.] Univ Fed Minas Gerais, Inst Biol Sci, Dept Immunol & Biochem, BR-31270901 Belo Horizonte, MG, Brazil.
RP Nutman, TB (reprint author), NIAID, Parasit Dis Lab, NIH, 4 Ctr Dr,Bldg 4,Room B1-03, Bethesda, MD 20892 USA.
EM tnutman@niaid.nih.gov
RI Gazzinelli-Guimaraes, Pedro Henrique/E-7693-2013; Fujiwara,
Ricardo/J-7579-2012
OI Gazzinelli-Guimaraes, Pedro Henrique/0000-0003-4932-2206; Fujiwara,
Ricardo/0000-0002-4713-575X
FU Intramural NIH HHS [Z01 AI000197-28]
NR 76
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD OCT 1
PY 2016
VL 197
IS 7
BP 2772
EP 2779
DI 10.4049/jimmunol.1600829
PG 8
WC Immunology
SC Immunology
GA DY3OX
UT WOS:000385004600026
PM 27566825
ER
PT J
AU Chan, YN
Boesch, AW
Osei-Owusu, NY
Emileh, A
Crowley, AR
Cocklin, SL
Finstad, SL
Linde, CH
Howell, RA
Zentner, I
Cocklin, S
Miles, AR
Eckman, JW
Alter, G
Schmitz, JE
Ackerman, ME
AF Chan, Ying N.
Boesch, Austin W.
Osei-Owusu, Nana Y.
Emileh, Ali
Crowley, Andrew R.
Cocklin, Sarah L.
Finstad, Samantha L.
Linde, Caitlyn H.
Howell, Rebecca A.
Zentner, Isaac
Cocklin, Simon
Miles, Adam R.
Eckman, Joshua W.
Alter, Galit
Schmitz, Joern E.
Ackerman, Margaret E.
TI IgG Binding Characteristics of Rhesus Macaque Fc gamma R
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID HIGH-THROUGHPUT; PROTECTIVE EFFICACY; ANTIBODY; AFFINITY; RECEPTOR; HIV;
COMPLEMENT; CHALLENGES; SUBCLASSES; VACCINES
AB Indian rhesus macaques (Macaca mulatta) are routinely used in preclinical studies to evaluate therapeutic Abs and candidate vaccines. The efficacy of these interventions in many cases is known to rely heavily on the ability of Abs to interact with a set of Ab Fc gamma R expressed on innate immune cells. Yet, despite their presumed functional importance, M. mulatta Ab receptors are largely uncharacterized, posing a fundamental limit to ensuring accurate interpretation and translation of results from studies in this model. In this article, we describe the binding characteristics of the most prevalent allotypic variants of M. mulatta FcgR for binding to both human and M. mulatta IgG of varying subclasses. The resulting determination of the affinity, specificity, and glycan sensitivity of these receptors promises to be useful in designing and evaluating studies of candidate vaccines and therapeutic Abs in this key animal model and exposes significant evolutionary divergence between humans and macaques.
C1 [Chan, Ying N.; Boesch, Austin W.; Emileh, Ali; Ackerman, Margaret E.] Dartmouth Coll, Thayer Sch Engn, Hanover, NH 03755 USA.
[Osei-Owusu, Nana Y.; Crowley, Andrew R.; Ackerman, Margaret E.] Dartmouth Coll, Mol & Cellular Biol Program, Hanover, NH 03755 USA.
[Cocklin, Sarah L.; Finstad, Samantha L.; Linde, Caitlyn H.; Howell, Rebecca A.; Schmitz, Joern E.] Harvard Med Sch, Ctr Virol & Vaccine Res, Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA.
[Zentner, Isaac; Cocklin, Simon] Drexel Univ, Coll Med, Dept Biochem & Mol Biol, Philadelphia, PA 19102 USA.
[Miles, Adam R.; Eckman, Joshua W.] Wasatch Microfluid, Salt Lake City, UT 84103 USA.
[Linde, Caitlyn H.; Alter, Galit] Ragon Inst MGH MIT & Harvard, Cambridge, MA 02139 USA.
[Finstad, Samantha L.] NIH, Off AIDS Res, Bldg 10, Bethesda, MD 20892 USA.
[Schmitz, Joern E.] Fraunhofer Inst Mol Biol & Appl Ecol, Dept Immunotherapy, Aachen, Germany.
RP Ackerman, ME (reprint author), Dartmouth Coll, 14 Engn Dr, Hanover, NH 03755 USA.
EM margaret.e.ackerman@dartmouth.edu
FU NIAID NIH HHS [HHSN272201100023C, P01 AI120756, R01 AI102691, R56
AI097315, UM1 AI100645]
NR 30
TC 1
Z9 1
U1 1
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD OCT 1
PY 2016
VL 197
IS 7
BP 2936
EP 2947
DI 10.4049/jimmunol.1502252
PG 12
WC Immunology
SC Immunology
GA DY3OX
UT WOS:000385004600042
PM 27559046
ER
PT J
AU Absinta, M
Reich, DS
Filippi, M
AF Absinta, Martina
Reich, Daniel S.
Filippi, Massimo
TI Spring cleaning: time to rethink imaging research lines in MS?
SO JOURNAL OF NEUROLOGY
LA English
DT Review
DE Multiple sclerosis; Neuroimaging; Biomarkers
ID MULTIPLE-SCLEROSIS LESIONS; OPTICAL COHERENCE TOMOGRAPHY; REGIONAL
HIPPOCAMPAL ATROPHY; WHITE-MATTER LESIONS; BLOOD-BRAIN-BARRIER;
CORTICAL-LESIONS; IN-VIVO; 7 TESLA; COGNITIVE IMPAIRMENT; SPINAL-CORD
AB Together with recently advanced MRI technological capability, new needs and updated questions are emerging in imaging research in multiple sclerosis (MS), especially with respect to the identification of novel in vivo biomarkers of MS-relevant pathological processes. Expected benefits will involve approaches to diagnosis and clinical classification. In detail, three main points of discussion are addressed in this review: (1) new imaging biomarkers (centrifugal/centripetal lesion enhancement, central vein, paramagnetic rims at the lesion edge, subpial cortical demyelination); (2) thinking about high-resolution MR from a pathological perspective (from postmortem to in vivo staging); and (3) the clinical utility of quantitative MRI. In this context, research efforts should increasingly be focused on the direct in vivo visualization of "hidden" inflammation, beyond what can be detected with conventional gadolinium-based methods, as well as remyelination and repair, since these are likely to represent critical pathological processes and potential therapeutic targets. Concluding remarks concern the limitations, challenges, and ultimately clinical role of non-conventional MRI techniques.
C1 [Absinta, Martina; Filippi, Massimo] Univ Vita Salute San Raffaele, Inst Expt Neurol, San Raffaele Sci Inst, Hosp San Raffaele,Neuroimaging Res Unit,Div Neuro, Via Olgettina 60, I-20132 Milan, Italy.
[Absinta, Martina; Reich, Daniel S.] NINDS, Translat Neuroradiol Unit, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
RP Filippi, M (reprint author), Univ Vita Salute San Raffaele, Inst Expt Neurol, San Raffaele Sci Inst, Hosp San Raffaele,Neuroimaging Res Unit,Div Neuro, Via Olgettina 60, I-20132 Milan, Italy.
EM filippi.massimo@hsr.it
OI Filippi, Massimo/0000-0002-5485-0479
FU Intramural Research Program of NINDS, NIH
FX Special thanks to Prof. Andrea Falini (Head of the Department of
Neuroradiology, San Raffaele Hospital), Dr. Vittorio Martinelli (Head of
Clinical Trials Unit, Division of Neuroscience, San Raffaele Hospital),
and Dr. Pascal Sati and Dr. Govind Nair (staff scientists, NINDS, NIH)
for valuable advice, assistance with MRI data
acquisition/post-processing, and help in figures' preparation. This work
was supported in part by the Intramural Research Program of NINDS, NIH.
NR 116
TC 0
Z9 0
U1 3
U2 3
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0340-5354
EI 1432-1459
J9 J NEUROL
JI J. Neurol.
PD OCT
PY 2016
VL 263
IS 10
BP 1893
EP 1902
DI 10.1007/s00415-016-8060-0
PG 10
WC Clinical Neurology
SC Neurosciences & Neurology
GA DY5WA
UT WOS:000385173900001
PM 26886204
ER
PT J
AU Buch, S
Chivero, ET
Hoare, J
Jumare, J
Nakasujja, N
Mudenda, V
Paul, R
Kanmogne, GD
Sacktor, N
Wood, C
Royal, W
Joseph, J
AF Buch, Shilpa
Chivero, Ernest T.
Hoare, Jackie
Jumare, Jibreel
Nakasujja, Noeline
Mudenda, Victor
Paul, Robert
Kanmogne, Georgette D.
Sacktor, Ned
Wood, Charles
Royal, Walter
Joseph, Jeymohan
TI Proceedings from the NIMH symposium on "NeuroAIDS in Africa:
neurological and neuropsychiatric complications of HIV"
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Article
DE Human immunodeficiency virus (HIV); HIV-associated neurocognitive
disorders (HAND); NeuroAIDS
ID COGNITIVE IMPAIRMENT; TAT; DISORDERS; THERAPY; DISEASE; HAART
AB Despite major advances in HIV-1 treatment, the prevalence of HIV-associated neurocognitive disorders (HAND) remains a problem, particularly as individuals on suppressive treatment continue to live longer. To facilitate discussion on emerging and future directions in HAND research, a meeting was held in Durban, South Africa in March 2015 as part of the Society of Neuroscientists of Africa (SONA) conference. The objective of the meeting was to assess the impact of HIV subtype diversity on HAND and immunological dysfunction. The meeting brought together international leaders in the area of neurological complications of HIV-1 infection with special focus on the African population. Research presentations indicated that HAND was highly prevalent and that inflammatory cytokines and immune-activation played important roles in progression of neurocognitive impairment. Furthermore, children on antiretroviral therapy were also at risk for developing neurocognitive impairment. With respect to the effect of HIV-1 subtype diversity, analyses of HIV-1 clade C infection among South Africans revealed that clade C infection induced cognitive impairment that was independent of the substitution in HIV-1 Trans-Activator of Transcription (Tat; C31S). At the cellular level, a Zambian study showed that clade C infection resulted in reduced brain cell death compared with clade B infection suggesting clade specific variations in mediating brain cell injury. Furthermore, ex vivo Tat protein from clade CRF02_AG, prevalent in West/ Central Africa, exhibited reduced disruption of brain endothelium compared with clade B Tat protein. Discussions shed light on future research directions aimed at understanding biomarkers and disease mechanisms critical for HAND.
C1 [Buch, Shilpa; Chivero, Ernest T.; Kanmogne, Georgette D.] Univ Nebraska Med Ctr, Omaha, NE 68198 USA.
[Hoare, Jackie] Univ Cape Town, Cape Town, South Africa.
[Jumare, Jibreel; Royal, Walter] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[Nakasujja, Noeline] Makerere Univ, Kampala, Uganda.
[Mudenda, Victor] Univ Zambia, Lusaka, Zambia.
[Paul, Robert] Univ Missouri, St Louis, MO 63121 USA.
[Sacktor, Ned] Johns Hopkins Univ, Baltimore, MD USA.
[Wood, Charles] Univ Nebraska, Lincoln, NE USA.
[Joseph, Jeymohan] NIMH, Div AIDS Res, NIH, Bethesda, MD 20892 USA.
RP Buch, S (reprint author), Univ Nebraska Med Ctr, Omaha, NE 68198 USA.; Joseph, J (reprint author), NIMH, Div AIDS Res, NIH, Bethesda, MD 20892 USA.
EM sbuch@unmc.edu; jjeymoha@mail.nih.gov
FU National Institutes of Health [MH094160, DA036157]
FX The authors acknowledge funding from National Institutes of Health:
MH094160 (to GDK); DA036157 (to SB).
NR 16
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 2016
VL 22
IS 5
BP 699
EP 702
DI 10.1007/s13365-016-0467-y
PG 4
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA DY4JM
UT WOS:000385064800020
PM 27473196
ER
PT J
AU Lindenberg, L
Ahlman, M
Turkbey, B
Mena, E
Choyke, P
AF Lindenberg, Liza
Ahlman, Mark
Turkbey, Baris
Mena, Esther
Choyke, Peter
TI Evaluation of Prostate Cancer with PET/MRI
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE multiparametric MRI; PET/MRI; prostate cancer
ID SEMINAL-VESICLE INVASION; PLANAR BONE-SCINTIGRAPHY; INTEGRATED
WHOLE-BODY; FUSION-GUIDED BIOPSY; EXTRACAPSULAR EXTENSION;
INITIAL-EXPERIENCE; F-18-DCFBC PET/CT; CHOLINE-PET/CT; METASTASES; MRI
AB In the ongoing effort to understand and cure prostate cancer, imaging modalities are constantly evolving to assist in clinical decisions. Multiparametric MRI can be used to direct prostate biopsies, improve diagnostic yield, and help clinicians make more accurate decisions. PET is superior in providing biologic information about the cancer and is sensitive and highly specific. Integrated PET/MRI is a welcome technical advance with great potential to influence the diagnosis and management of prostate cancer in clinical practice.
C1 [Lindenberg, Liza; Turkbey, Baris; Choyke, Peter] NCI, Mol Imaging Program, Ctr Canc Res, NIH, Bldg 10,Room B3B402 MS 1088,10 Ctr Dr, Bethesda, MD 20892 USA.
[Ahlman, Mark] NIH, Dept Radiol & Imaging Sci, Ctr Clin, Bldg 10, Bethesda, MD 20892 USA.
[Mena, Esther] Johns Hopkins Med Inst, Russell H Morgan Dept Radiol & Radiol Sci, 600 N Wolfe St, Baltimore, MD 21205 USA.
RP Lindenberg, L (reprint author), NCI, Mol Imaging Program, Ctr Canc Res, NIH, Bldg 10,Room B3B402 MS 1088,10 Ctr Dr, Bethesda, MD 20892 USA.
EM liza.lindenberg@mail.nih.gov
NR 51
TC 2
Z9 2
U1 3
U2 3
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD OCT
PY 2016
VL 57
SU 3
BP 111S
EP 116S
DI 10.2967/jnumed.115.169763
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA DY3AB
UT WOS:000384962100019
PM 27694163
ER
PT J
AU Kiess, AP
Minn, I
Vaidyanathan, G
Hobbs, RF
Josefsson, A
Shen, C
Brummet, M
Chen, Y
Choi, J
Koumarianou, E
Baidoo, K
Brechbiel, MW
Mease, RC
Sgouros, G
Zalutsky, MR
Pomper, MG
AF Kiess, Ana P.
Minn, Il
Vaidyanathan, Ganesan
Hobbs, Robert F.
Josefsson, Anders
Shen, Colette
Brummet, Mary
Chen, Ying
Choi, Jaeyeon
Koumarianou, Eftychia
Baidoo, Kwamena
Brechbiel, Martin W.
Mease, Ronnie C.
Sgouros, George
Zalutsky, Michael R.
Pomper, Martin G.
TI (2S)-2-(3-(1-Carboxy-5-(4-At-211-Astatobenzamido)Pentyl)
Ureido)-Pentanedioic Acid for PSMA-Targeted alpha-Particle
Radiopharmaceutical Therapy
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE oncology: GU; radionuclide therapy; radiopharmaceuticals; alpha emitter;
astatine; prostate cancer; prostate-specific membrane antigen; radiation
dosimetry
ID METASTATIC PROSTATE-CANCER; MALIGNANT HUMAN TISSUES; MEMBRANE ANTIGEN
PSMA; SURVIVAL; RADIOIMMUNOTHERAPY; EXPRESSION; INHIBITORS; F-18-DCFBC;
DOSIMETRY; SERIES
AB Alpha-particle emitters have a high linear energy transfer and short range, offering the potential for treating micrometastases while sparing normal tissues. We developed a urea-based, At-211-labeled small molecule targeting prostate-specific membrane antigen (PSMA) for the treatment of micrometastases due to prostate cancer (PC). Methods: PSMA-targeted (2S)-2-(3-(1-carboxy-5-(4-At-211-astatobenzami do) pentyl)ureido)-pentanedioic acid (At-211-6) was synthesized. Cellular uptake and clonogenic survival were tested in PSMA-positive (PSMA+) PC3 PIP and PSMA-negative (PSMA-) PC3 flu human PC cells after At-211-6 treatment. The antitumor efficacy of At-211-6 was evaluated in mice bearing PSMA+ PC3 PIP and PSMA- PC3 flu flank xenografts at a 740-kBq dose and in mice bearing PSMA+, luciferase-expressing PC3-ML micrometastases. Biodistribution was determined in mice bearing PSMA+ PC3 PIP and PSMA(-) PC3 flu flank xenografts. Suborgan distribution was evaluated using alpha-camera images, and microscale dosimetry was modeled. Longterm toxicity was assessed in mice for 12 mo. Results: At-211-6 treatment resulted in PSMA-specific cellular uptake and decreased clonogenic survival in PSMA+ PC3 PIP cells and caused significant tumor growth delay in PSMA+ PC3 PIP flank tumors. Significantly improved survival was achieved in the newly developed PSMA+ micrometastatic PC model. Biodistribution showed uptake of At-211-6 in PSMA+ PC3 PIP tumors and in kidneys. Microscale kidney dosimetry based on alpha-camera images and a nephron model revealed hot spots in the proximal renal tubules. Long-term toxicity studies confirmed that the dose-limiting toxicity was late radiation nephropathy. Conclusion: PSMA-targeted At-211-6 alpha-particle radiotherapy yielded significantly improved survival in mice bearing PC micrometastases after systemic administration. At-211-6 also showed uptake in renal proximal tubules resulting in late nephrotoxicity, highlighting the importance of long-term toxicity studies and microscale dosimetry.
C1 [Kiess, Ana P.; Hobbs, Robert F.; Shen, Colette; Sgouros, George; Pomper, Martin G.] Johns Hopkins Univ, Sch Med, Dept Radiat Oncol & Mol Radiat Sci, Baltimore, MD USA.
[Minn, Il; Josefsson, Anders; Brummet, Mary; Chen, Ying; Mease, Ronnie C.; Sgouros, George; Pomper, Martin G.] Johns Hopkins Univ, Sch Med, Russell H Morgan Dept Radiol & Radiol Sci, Baltimore, MD USA.
[Vaidyanathan, Ganesan; Choi, Jaeyeon; Koumarianou, Eftychia; Zalutsky, Michael R.] Duke Univ, Med Ctr, Dept Radiol, Durham, NC 27710 USA.
[Baidoo, Kwamena; Brechbiel, Martin W.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Pomper, MG (reprint author), Johns Hopkins Med Sch, 1550 Orleans St,492 CRB 2, Baltimore, MD 21287 USA.
EM mpomper@jhmi.edu
FU NIH [CA116477, CA184228, CA134675, CA183031, CA157542, EB005324];
Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research
FX The costs of publication of this article were defrayed in part by the
payment of page charges. Therefore, and solely to indicate this fact,
this article is hereby marked "advertisement" in accordance with 18 USC
section 1734. This work was supported by NIH CA116477, CA184228,
CA134675, CA183031, CA157542, and EB005324 and in part by the Intramural
Research Program of the NIH, National Cancer Institute, Center for
Cancer Research. No other potential conflict of interest relevant to
this article was reported.
NR 32
TC 2
Z9 2
U1 15
U2 15
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD OCT
PY 2016
VL 57
IS 10
BP 1569
EP 1575
DI 10.2967/jnumed.116.174300
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA DY2ZZ
UT WOS:000384961900022
PM 27230930
ER
PT J
AU Von Korff, M
Scher, AI
Helmick, C
Carter-Pokras, O
Dodick, DW
Goulet, J
Hamill-Ruth, R
LeResche, L
Porter, L
Tait, R
Terman, G
Veasley, C
Mackey, S
AF Von Korff, Michael
Scher, Ann I.
Helmick, Charles
Carter-Pokras, Olivia
Dodick, David W.
Goulet, Joseph
Hamill-Ruth, Robin
LeResche, Linda
Porter, Linda
Tait, Raymond
Terman, Gregory
Veasley, Christin
Mackey, Sean
TI United States National Pain Strategy for Population Research: Concepts,
Definitions, and Pilot Data
SO JOURNAL OF PAIN
LA English
DT Article
DE Chronic pain; epidemiology; health services research; prevalence;
electronic databases
ID CROSS-SECTIONAL SURVEY; CHRONIC BACK-PAIN; SEVERITY; MODERATE; PATIENT;
MILD; COMORBIDITY; PREVALENCE; DISABILITY; ARTHRITIS
AB National Pain Strategy population research objectives include: estimating chronic pain prevalence, studying pain treatment with electronic health care data, and developing metrics to assess progress in reducing chronic pain impact. In this article, the National Pain Strategy Population Research Workgroup reviews concepts relevant to achieving these aims. High-impact chronic pain was defined as persistent pain with substantial restriction of life activities lasting 6 months or more. In pilot work, we tested a brief assessment of high-impact chronic pain, and used electronic health records data to describe pain-related health care. A mail survey of adult health plan enrollees (N = 770) reported that 14% had high-impact chronic pain. Relative to persons with lower-impact chronic pain, those with high-impact chronic pain were more often frequent users of health care for pain, reported lower quality of life, greater pain-related interference with activities, and more often reported pain at multiple anatomic locations. Analyses of health care data (N = 289,464) reported that pain patients had higher health care costs compared with others and that pain services were typically delivered in primary care. These results support the feasibility of developing data on chronic pain through national health interview surveys and large electronic health care databases.
Perspective: Pilot analyses supported the feasibility of brief chronic pain assessments suitable for national health surveys and use of electronic health care databases to develop data regarding trends in the delivery of pain treatments, costs, and effectiveness. These methods are relevant to achieving the aims of the US National Pain Strategy. (C) 2016 by the American Pain Society
C1 [Von Korff, Michael] Grp Hlth Res Inst, 1730 Minor Ave,Suite 1600, Seattle, WA 98101 USA.
[Scher, Ann I.] Uniformed Serv Univ Hlth Sci, Dept Prevent Med & Biostat, Bethesda, MD 20814 USA.
[Helmick, Charles] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Carter-Pokras, Olivia] Univ Maryland, Sch Publ Hlth, College Pk, MD 20742 USA.
[Dodick, David W.] Mayo Clin, Coll Med, Phoenix, AZ USA.
[Goulet, Joseph] Yale Univ, Sch Med, New Haven, CT USA.
[Hamill-Ruth, Robin] Univ Virginia Hlth Syst, Charlottesville, VA USA.
[LeResche, Linda] Univ Washington, Sch Dent, Seattle, WA 98195 USA.
[Porter, Linda] NINDS, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
[Tait, Raymond] St Louis Univ, Sch Med, Dept Psychiat, St Louis, MO 63103 USA.
[Terman, Gregory] Univ Washington, Sch Med, Seattle, WA 98195 USA.
[Veasley, Christin] Chron Pain Res Alliance, Milwaukee, WI USA.
[Mackey, Sean] Stanford Univ, Sch Med, Palo Alto, CA 94304 USA.
RP Von Korff, M (reprint author), Grp Hlth Res Inst, 1730 Minor Ave,Suite 1600, Seattle, WA 98101 USA.
EM vonkorff.m@ghc.org
OI Goulet, Joseph/0000-0002-0842-804X
FU NINDS; IH Inter-Agency Pain Research Coordinating Committee [AG034181];
Pfizer Inc.; Healthlogix; Haymarket Media Group, Ltd.; SAGE Publishing;
Synergy; Allergan; Lippincott Williams Wilkins; Oxford University Press;
Cambridge University Press
FX The pilot data collection reported in this paper was supported by a
supplemental award from NINDS and the NIH Inter-Agency Pain Research
Coordinating Committee to a National Institute on Aging grant (AG034181,
Von Korff, Principal Investigator).; Dr. Von Korff is the Principal
Investigator of grants to GHRI from Pfizer Inc. that concern opioids.
Dr. Scher is an advisory board member and consultant for Allergan. Dr.
Tait's spouse serves on the speaker's bureau for Lilly Pharmaceuticals.
David W. Dodick, MD, in the past 12 months, has served on advisory
boards and has consulted for Allergan, Amgen, Alder, CoLucid, Merck,
ENeura, Eli Lilly & Company, Autonomic Technologies, Teva, Tonix,
Novartis, Supernus, ScionNeurostim, Boston Scientific. Within the past
12 months, Dr. Dodick has received royalties, funding for travel,
speaking, or editorial activities from the following: Healthlogix,
Haymarket Media Group, Ltd., SAGE Publishing, Synergy, Allergan,
Lippincott Williams & Wilkins, Oxford University Press, and Cambridge
University Press; he serves as Editor-in-Chief of Cephalalgia and on the
editorial boards of The Neurologist, Lancet Neurology, and Postgraduate
Medicine. The remaining authors report no conflicts.
NR 41
TC 1
Z9 1
U1 4
U2 4
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 1526-5900
J9 J PAIN
JI J. Pain
PD OCT
PY 2016
VL 17
IS 10
BP 1068
EP 1080
DI 10.1016/j.jpain.2016.06.009
PG 13
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA DY1SF
UT WOS:000384874000003
PM 27377620
ER
PT J
AU Ruiz-Rodado, V
Nicoli, ER
Probert, F
Smith, DA
Morris, L
Wassif, CA
Platt, FM
Grootveld, M
AF Ruiz-Rodado, Victor
Nicoli, Elena-Raluca
Probert, Fay
Smith, David A.
Morris, Lauren
Wassif, Christopher A.
Platt, Frances M.
Grootveld, Martin
TI H-1 NMR-Linked Metabolomics Analysis of Liver from a Mouse Model of
NP-C1 Disease
SO JOURNAL OF PROTEOME RESEARCH
LA English
DT Article
DE NP-Cl disease; liver damage/dysfunction; fibrosis-cirrhosis; NMR-based
metabolomics; biomarkers; amino acid biosynthesis and metabolism;
nicotinate and niacinamide metabolism; 3-hydroxyphenylacetate; metabolic
pathway analysis
ID NIEMANN-PICK-DISEASE; CHAIN AMINO-ACIDS; C DISEASE; GLUTATHIONE
METABOLISM; METABONOMIC APPROACH; URINARY-EXCRETION; STORAGE DISORDER;
PHENOLIC-ACIDS; RANDOM FORESTS; MURINE MODEL
AB Clinical manifestations of Niemann-Pick type Cl (NP-C1) disease include neonatal hepatosplenomegaly and in some patients progressive liver dysfunction and failure. This study involved a H-1 NMR-linked metabolomics analysis of liver samples collected from a NP-C1 disease mutant mouse model in order to explore time-dependent imbalances in metabolic pathways associated with NP-C1 liver dysfunction, including fibrosis. NP-Cl mutant (Npc1(-/-); NP-C1), control (Npcl(+/+); WT), and NP-C1 heterozygous mice (Npc1(+/-); HET) were generated from heterozygote matings. Aqueous extracts of these liver samples collected at time points of 3, 6, 9, and 11 weeks were subjected to high-resolution NMR analysis, and multivariate (MV) metabolomics analyses of data sets acquired were performed. A MV random forests (RFs) model effectively discriminated between NP-C1 and a combined WT/HET hepatic NMR profiles with very high predictive accuracy and reliability. Key distinguishing features included significant upregulations in the hepatic concentrations of phenylalanine, tyrosine, glutamate, lysine/ornithine, valine, threonine, and hypotaurine/methionine, and diminished levels of nicotinate/niacinamide, inosine, phosphoenolpyruvate, and 3-hydroxyphenylacetate. Quantitative pathway topological analysis confirmed that imbalances in tyrosine biosynthesis, and hepatic phenylalanine, tyrosine, glutamate/glutamine, and nicotinate/niacinamide metabolism were involved in the pathogenesis of NP-C1 disease-associated liver dysfunction/damage. H-1 NMR-linked metabolomics analysis provides valuable biomarker information regarding hepatic dysfunction or damage in NP-C1 disease.
C1 [Ruiz-Rodado, Victor; Probert, Fay; Grootveld, Martin] De Montfort Univ, Leicester Sch Pharm, Leicester LE1 9BH, Leics, England.
[Nicoli, Elena-Raluca; Smith, David A.; Morris, Lauren; Wassif, Christopher A.; Platt, Frances M.] Univ Oxford, Dept Pharmacol, Mansfield Rd, Oxford OX1 3QT, England.
[Wassif, Christopher A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD 20892 USA.
RP Grootveld, M (reprint author), De Montfort Univ, Leicester Sch Pharm, Leicester LE1 9BH, Leics, England.
EM mgrootveld@dmu.ac.uk
FU SPARKS Medical Charity for Children's Health; Action Medical research;
Niemann-Pick Research Foundation
FX We are very grateful to the SPARKS Medical Charity for Children's Health
for providing funding for a Research Fellowship to F.P. and the Hope
Against Cancer Charity and De Montfort University, Leicester, for the
provision of doctoral training bursaries to V.R-R. E.-R.N. is supported
by Action Medical research, and D.S. is supported by the Niemann-Pick
Research Foundation. F.M.P. is a Royal Society Wolfson Research Merit
Award holder.
NR 90
TC 0
Z9 0
U1 3
U2 3
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 2016
VL 15
IS 10
BP 3511
EP 3527
DI 10.1021/acs.jproteome.6b00238
PG 17
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA DY4FJ
UT WOS:000385054100007
PM 27503774
ER
PT J
AU Park, S
Thompson, FE
McGuire, LC
Pan, LP
Galuska, DA
Blanck, HM
AF Park, Sohyun
Thompson, Frances E.
McGuire, Lisa C.
Pan, Liping
Galuska, Deborah A.
Blanck, Heidi M.
TI Sociodemographic and Behavioral Factors Associated with Added Sugars
Intake among US Adults
SO JOURNAL OF THE ACADEMY OF NUTRITION AND DIETETICS
LA English
DT Article
DE Added sugars; Sugar-sweetened beverages; Sweet food; Sociodemographic
characteristics; Behaviors
ID SWEETENED BEVERAGE INTAKE; FAMILY-HISTORY; CIGARETTE-SMOKING; TASTE
INTENSITY; YOUNG-ADULTS; HEALTH; ALCOHOLISM; STATES; CONSUMPTION;
ADDICTION
AB Background Reducing added sugars intake is one, of the Healthy People 2020 objectives. High added sugars intake may be associated with adverse health consequences.
Objective This cross-sectional study identified sociodemographic and behavioral characteristics associated With added sugars intake among US adults (18 years and older) using the 2010 National Health Interview Survey data (n=24,967).
Methods The outcome variable was added sugars intake from foods and beverages using scoring algorithms to convert dietary screener frequency responses on nine items to estimates of individual dietary intake of added sugars in teaspoons per day. Added sugars intake was categorized into tertiles (lowest, middle, highest) stratified by sex. The explanatory variables were sociodemographic and behavioral characteristics. Multinomial logistic regression was used to estimate the adjusted odds ratios for the highest and middle tertile added sugars intake groups as compared with the lowest tertile group.
Results Estimated median added sugars intake was 17.6 tsp/d for men and 11.7 tsp/d for women. For men and women, those who had significantly greater odds for being in the highest tertile of added sugars intake (men: >= 22.0 tsp/d; women: >= 14.6 tsp/d) were younger, less educated, had lower income, were less physically active, were current smokers, and were former or current infrequent/light drinkers, whereas non-Hispanic other/multiracial and those living in the West had significantly lower odds for being in the highest tertile of added sugars intake. Different patterns were found by sex. Non-Hispanic black men had lower odds for being in the highest tertile of added sugars intake, whereas non-Hispanic black women had greater odds for being in the highest tertile.
Conclusions One in three men consumed >= 22.0 tsp added sugars and one in three women consumed >= 14.6 tsp added sugars daily. Higher added sugars intake was associated with various sociodemographic and behavioral characteristics; this information can inform efforts to design programs and policies specific to high-intake populations.
C1 [Park, Sohyun; Pan, Liping; Galuska, Deborah A.; Blanck, Heidi M.] Ctr Dis Control & Prevent, Div Nutr Phys Act & Obes, Natl Ctr Chron Dis Prevent & Hlth Promot, 4770 Buford Hwy NE,Mailstop F77, Atlanta, GA 30341 USA.
[McGuire, Lisa C.] Ctr Dis Control & Prevent, Div Populat Hlth, Natl Ctr Chron Dis Prevent & Hlth Promot, Atlanta, GA USA.
[Thompson, Frances E.] NCI, Risk Factor Assessment Branch, Epidemiol & Genom Res Program, Div Canc Control & Populat Sci,NIH, Bethesda, MD 20892 USA.
RP Park, S (reprint author), Ctr Dis Control & Prevent, Div Nutr Phys Act & Obes, Natl Ctr Chron Dis Prevent & Hlth Promot, 4770 Buford Hwy NE,Mailstop F77, Atlanta, GA 30341 USA.
EM spark3@cdc.gov
FU Intramural CDC HHS [CC999999]
NR 36
TC 0
Z9 0
U1 8
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 2212-2672
EI 2212-2680
J9 J ACAD NUTR DIET
JI J. Acad. Nutr. Diet.
PD OCT
PY 2016
VL 116
IS 10
BP 1589
EP 1598
DI 10.1016/j.jand.2016.04.012
PG 10
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA DY4GI
UT WOS:000385056600008
PM 27236642
ER
PT J
AU Lu, GY
Ren, L
Kolagunda, A
Wang, XL
Turkbey, IB
Choyke, PL
Kambhamettu, C
AF Lu, Guoyu
Ren, Li
Kolagunda, Abhishek
Wang, Xiaolong
Turkbey, Ismail B.
Choyke, Peter L.
Kambhamettu, Chandra
TI Representing 3D shapes based on implicit surface functions learned from
RBF neural networks
SO JOURNAL OF VISUAL COMMUNICATION AND IMAGE REPRESENTATION
LA English
DT Article
DE 3D shape presentation; Radial basis function; Neural network; 3D
reconstruction
ID RECONSTRUCTION; KERNELS
AB We propose to represent the shape of 3D objects using a neural network classifier. The 3D shape is learned from a neural network, where Radial Basis Function (RBF) is applied as the activation function for each perceptron. The implicit functions derived from the neural network is a combination of radial basis functions, which can represent complex shapes. The use of RBF provides a rotation, translation and scaling invariant feature to represent the shape. We conduct experiments on a new prostate dataset and public datasets. Our testing results show that our neural network -based method can accurately represent various shapes. (C) 2016 Elsevier Inc. All rights reserved.
C1 [Lu, Guoyu; Ren, Li; Kolagunda, Abhishek; Wang, Xiaolong; Kambhamettu, Chandra] Univ Delaware, Dept Comp & Informat Sci, Newark, DE 19716 USA.
[Turkbey, Ismail B.; Choyke, Peter L.] NCI, NIH, Bethesda, MD 20892 USA.
RP Lu, GY (reprint author), Univ Delaware, Dept Comp & Informat Sci, Newark, DE 19716 USA.
EM luguoyu@udel.edu
NR 35
TC 0
Z9 0
U1 5
U2 5
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1047-3203
EI 1095-9076
J9 J VIS COMMUN IMAGE R
JI J. Vis. Commun. Image Represent.
PD OCT
PY 2016
VL 40
BP 852
EP 860
DI 10.1016/j.jvcir.2016.08.014
PN B
PG 9
WC Computer Science, Information Systems; Computer Science, Software
Engineering
SC Computer Science
GA DX5CY
UT WOS:000384398600039
ER
PT J
AU Brown, P
AF Brown, Patricia
TI A Word from OLAW
SO LAB ANIMAL
LA English
DT Editorial Material
C1 [Brown, Patricia] NIH, OLAW, OER, OD,HHS, Bethesda, MD 20892 USA.
RP Brown, P (reprint author), NIH, OLAW, OER, OD,HHS, Bethesda, MD 20892 USA.
NR 2
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0093-7355
EI 1548-4475
J9 LAB ANIMAL
JI Lab Anim.
PD OCT
PY 2016
VL 45
IS 10
BP 356
EP 356
PG 1
WC Veterinary Sciences
SC Veterinary Sciences
GA DY4FU
UT WOS:000385055200016
PM 27654683
ER
PT J
AU Blankenship-Paris, TL
Dutton, JW
Goulding, DR
Mcgee, CA
Kissling, GE
Myers, PH
AF Blankenship-Paris, Terry L.
Dutton, John W.
Goulding, David R.
McGee, Christopher A.
Kissling, Grace E.
Myers, Page H.
TI Evaluation of buprenorphine hydrochloride Pluronica (R) gel formulation
in male C57BL/6NCrl mice
SO LAB ANIMAL
LA English
DT Article
ID SUSTAINED-RELEASE BUPRENORPHINE; RATS RATTUS-NORVEGICUS;
ORALLY-ADMINISTERED BUPRENORPHINE; CORTICOSTERONE LEVELS; POSTOPERATIVE
ANALGESICS; VOLUNTARY INGESTION; INCISIONAL PAIN; DRUG-RELEASE;
BODY-WEIGHT; 2 STRAINS
AB Providing adequate analgesia while minimizing handling and stress post-surgery can be challenging. Recently, there have been commercial products made available for providing long acting analgesia in rodents. However, we find there are limitations for use in mice due to the viscosity of the product and the small dosing volumes needed. This project evaluated an in-house compounded formulation of buprenorphine easily made in the laboratory using pharmaceutical. grade products. The release of buprenorphine was evaluated when compounded with two types of hydrogels (Pluronic (R) F-127 and F-68). Mice given buprenorphine in hydrogel (BP) demonstrated higher serum levels of buprenorphine for a longer period of time compared to mice given standard buprenorphine (Bup). However, the rate of decline in serum levels between the groups was similar; thus, it is more likely that the higher buprenorphine concentration seen in the BP group is due to the higher dose of buprenorphine given, rather than a slower release of product. Feed consumption was decreased in both groups one day after dosing; however, there was no difference in body weights. Increased activity in the open field was observed with both buprenorphine formulations, and lipemia was observed in mice given BP which persisted to at least 96 h. Based on our results, we conclude that this formulation did not sustain the release of buprenorphine or eliminate the increased activity commonly seen in mice given buprenorphine. In addition, the lipemia may confound research parameters, especially in cardiac studies and lipid metabolism studies. Therefore, we cannot recommend this formulation for use.
C1 [Blankenship-Paris, Terry L.; Goulding, David R.; McGee, Christopher A.; Myers, Page H.] NIEHS, Vet Med Sect, Comparat Med Branch, NIH,DHHS, POB 12233, Res Triangle Pk, NC 27709 USA.
[Dutton, John W.] Texas Biomed Res Inst, Southwest Natl Primate Res Ctr, San Antonio, TX USA.
[Kissling, Grace E.] NIEHS, Biostat & Computat Biol Branch, NIH, DHHS, Res Triangle Pk, NC USA.
RP Blankenship-Paris, TL (reprint author), NIEHS, Vet Med Sect, Comparat Med Branch, NIH,DHHS, POB 12233, Res Triangle Pk, NC 27709 USA.
EM blanken1@niehs.nih.gov
FU Intramural Research Program of the National Institutes of Health;
National Institute of Environmental Health Sciences
FX This research was supported by the Intramural Research Program of the
National Institutes of Health and the National Institute of
Environmental Health Sciences. This article may be the work product of
an employee or group of employees of the National Institute of
Environmental Health Sciences (NIEHS), National Institutes of Health
(NIH), however, the statements, opinions or conclusions contained herein
do not necessarily represent the statements, opinions or conclusions of
NIEHS, NIH or the United States government.
NR 66
TC 0
Z9 0
U1 2
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0093-7355
EI 1548-4475
J9 LAB ANIMAL
JI Lab Anim.
PD OCT
PY 2016
VL 45
IS 10
BP 370
EP 379
PG 10
WC Veterinary Sciences
SC Veterinary Sciences
GA DY4FU
UT WOS:000385055200021
PM 27654688
ER
PT J
AU Johnson, C
Pinal-Fernandez, I
Parikh, R
Paik, J
Albayda, J
Mammen, AL
Christopher-Stine, L
Danoff, S
AF Johnson, Cheilonda
Pinal-Fernandez, Iago
Parikh, Radhika
Paik, Julie
Albayda, Jemima
Mammen, Andrew L.
Christopher-Stine, Lisa
Danoff, Sonye
TI Assessment of Mortality in Autoimmune Myositis With and Without
Associated Interstitial Lung Disease
SO LUNG
LA English
DT Article
DE Survival; Interstitial lung disease; Idiopathic inflammatory myopathy;
Dermatomyositis; Polymyositis; Clinically amyopathic dermatomyositis
ID IDIOPATHIC INFLAMMATORY MYOPATHIES; AMYOPATHIC DERMATOMYOSITIS;
POLYMYOSITIS; SURVIVAL; TERM
AB Among patients with autoimmune myositis, associated interstitial lung disease (MA-ILD) is a known contributor of excess morbidity and mortality. Recent data on survival in idiopathic inflammatory myopathies originate primarily in Asia and Europe and vary widely. We sought to examine mortality in a large U.S. myositis cohort focusing in particular on the impact of associated ILD.
A cross-sectional analysis of participants from the Johns Hopkins Myositis Center with autoimmune myositis (polymyositis [PM], dermatomyositis [DM], or clinically amyopathic dermatomyositis [CADM]) was conducted. The primary outcome assessed was all-cause mortality. Cumulative mortality rates were estimated using the Kaplan-Meier test; the Cox proportional hazards model was used to compare group differences in survival.
Eight hundred and thirty-one participants were included with a median follow-up time of 4.5 years. Four hundred thirty-eight (53 %) had PM, 362 (43 %) had DM, and 31 (4 %) had CADM. Ninety-four (11 %) participants had clinically evident ILD. Overall, 51 participants died (6 %). In those without ILD, the survival rates at 1, 5, and 10 years were 99, 95, and 90 %, respectively. In those with ILD, the survival rates at 1, 5, and 10 years were 97, 91, and 81 %, respectively. The risk of death was statistically significantly higher among participants with ILD compared to those without ILD (HR 2.13. 95 % CI 1.06-4.25; p = 0.03).
We analyzed one of the largest known cohorts of patients with autoimmune myositis and found significantly higher mortality rates among those with clinically evident ILD compared to those without clinically evident ILD. Our results suggest that ILD remains an important and significant source of mortality in patients with inflammatory myopathies and as such should be screened for and treated aggressively.
C1 [Johnson, Cheilonda; Danoff, Sonye] Johns Hopkins Univ, Sch Med, Div Pulm & Crit Care Med, 1830 E Monument St Suite 500, Baltimore, MD 21224 USA.
[Pinal-Fernandez, Iago; Mammen, Andrew L.] NIAMSD, Muscle Dis Unit, Lab Muscle Stem Cells & Gene Express, NIH, Bethesda, MD 20892 USA.
[Parikh, Radhika] Univ Vermont, Div Pulm & Crit Care Med, Med Ctr, Burlington, VT 05401 USA.
[Paik, Julie; Albayda, Jemima; Christopher-Stine, Lisa] Johns Hopkins Univ, Div Rheumatol, Sch Med, Baltimore, MD 21224 USA.
[Mammen, Andrew L.] Johns Hopkins Univ, Dept Neurol, Sch Med, Baltimore, MD 21224 USA.
RP Danoff, S (reprint author), Johns Hopkins Univ, Sch Med, Div Pulm & Crit Care Med, 1830 E Monument St Suite 500, Baltimore, MD 21224 USA.
EM sdanoff@jhmi.edu
FU Huayi and Siuling Zhang Discovery Fund
FX This study was financially supported by The Huayi and Siuling Zhang
Discovery Fund.
NR 25
TC 2
Z9 2
U1 2
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0341-2040
EI 1432-1750
J9 LUNG
JI Lung
PD OCT
PY 2016
VL 194
IS 5
BP 733
EP 737
DI 10.1007/s00408-016-9896-x
PG 5
WC Respiratory System
SC Respiratory System
GA DY5OG
UT WOS:000385148500004
PM 27166633
ER
PT J
AU Fulton, JE
Carlson, SA
Ainsworth, BE
Berrigan, D
Carlson, C
Dorn, JM
Heath, GW
Kohl, HW
Lee, IM
Lee, SM
Masse, LC
Morrow, JR
Gabriel, KP
Pivarnik, JM
Pronk, NP
Rodgers, AB
Saelens, BE
Sallis, JF
Troiano, RP
Tudor-Locke, C
Wendel, A
AF Fulton, Janet E.
Carlson, Susan A.
Ainsworth, Barbara E.
Berrigan, David
Carlson, Cynthia
Dorn, Joan M.
Heath, Gregory W.
Kohl, Harold W., III
Lee, I-Min
Lee, Sarah M.
Masse, Louise C.
Morrow, James R., Jr.
Gabriel, Kelley Pettee
Pivarnik, James M.
Pronk, Nicolaas P.
Rodgers, Anne B.
Saelens, Brian E.
Sallis, James F.
Troiano, Richard P.
Tudor-Locke, Catrine
Wendel, Arthur
TI Strategic Priorities for Physical Activity Surveillance in the United
States
SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
LA English
DT Article
DE POPULATION HEALTH; MONITORING; EPIDEMIOLOGY; RECOMMENDATIONS; EXERCISE
ID GOOGLE STREET VIEW; NEIGHBORHOOD ENVIRONMENTS; SELF-REPORT; SEDENTARY
BEHAVIOR; ADULTS; ACCELEROMETER; PREVALENCE; FITNESS; TRENDS; AUDIT
AB Purpose Develop strategic priorities to guide future physical activity surveillance in the United States.
Methods The Centers for Disease Control and Prevention and the American College of Sports Medicine convened a scientific roundtable of physical activity and measurement experts. Participants summarized the current state of aerobic physical activity surveillance for adults, focusing on practice and research needs in three areas: 1) behavior, 2) human movement, and 3) community supports. Needs and challenges for each area were identified. At the conclusion of the meeting, experts identified one overarching strategy and five strategic priorities to guide future surveillance.
Results The identified overarching strategy was to develop a national plan for physical activity surveillance similar to the U.S. National Physical Activity Plan for promotion. The purpose of the plan would be to enhance coordination and collaboration within and between sectors, such as transportation and public health, and to address specific strategic priorities identified at the roundtable. These strategic priorities were used 1) to identify and prioritize physical activity constructs; 2) to assess the psychometric properties of instruments for physical activity surveillance; 3) to provide training and technical assistance for those collecting, analyzing, or interpreting surveillance data; 4) to explore accessing data from alternative sources; and 5) to improve communication, translation, and dissemination about estimates of physical activity from surveillance systems.
Conclusion This roundtable provided strategic priorities for physical activity surveillance in the United States. A first step is to develop a national plan for physical activity surveillance that would provide an operating framework from which to execute these priorities.
C1 [Fulton, Janet E.; Carlson, Susan A.; Dorn, Joan M.; Lee, Sarah M.] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Ainsworth, Barbara E.] Arizona State Univ, Phoenix, AZ USA.
[Berrigan, David; Troiano, Richard P.] NCI, Bethesda, MD 20892 USA.
[Carlson, Cynthia] Merrimack Coll, N Andover, MA 01845 USA.
[Carlson, Cynthia] MA England Coll, Henniker, NH USA.
[Heath, Gregory W.] Univ Tennessee, Chattanooga, TN USA.
[Kohl, Harold W., III; Gabriel, Kelley Pettee] Univ Texas Hlth Sci Ctr Houston, Sch Publ Hlth, Austin Reg Campus, Austin, TX USA.
[Kohl, Harold W., III] Univ Texas Austin, Austin, TX 78712 USA.
[Lee, I-Min; Pronk, Nicolaas P.] Harvard Univ, Boston, MA 02115 USA.
[Masse, Louise C.] Univ British Columbia, Vancouver, BC, Canada.
[Masse, Louise C.] British Columbia Childrens Hosp, Child & Family Res Inst, Vancouver, BC, Canada.
[Morrow, James R., Jr.] Univ North Texas, Denton, TX USA.
[Pivarnik, James M.] Michigan State Univ, E Lansing, MI 48824 USA.
[Pronk, Nicolaas P.] HealthPartners, Minneapolis, MN USA.
[Rodgers, Anne B.] Ctr Dis Control & Prevent, Falls Church, VA USA.
[Saelens, Brian E.] Univ Washington, Seattle, WA 98195 USA.
[Saelens, Brian E.] Seattle Childrens Res Inst, Seattle, WA USA.
[Sallis, James F.] Univ Calif Calif, La Jolla, CA USA.
[Tudor-Locke, Catrine] Univ Massachusetts, Amherst, MA 01003 USA.
[Wendel, Arthur] Agcy Tox Subst & Dis Registry, Atlanta, GA USA.
RP Fulton, JE (reprint author), Ctr Dis Control & Prevent, Div Nutr Phys Act & Obes, 4770 Buford Highway NE,MS F-77, Atlanta, GA 30341 USA.
EM jkf2@cdc.gov
FU Child and Family Research Institute at the British Columbia Children's
Hospital
FX LCM received salary support from the Child and Family Research Institute
at the British Columbia Children's Hospital.
NR 68
TC 1
Z9 1
U1 7
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0195-9131
EI 1530-0315
J9 MED SCI SPORT EXER
JI Med. Sci. Sports Exerc.
PD OCT
PY 2016
VL 48
IS 10
BP 2057
EP 2069
DI 10.1249/MSS.0000000000000989
PG 13
WC Sport Sciences
SC Sport Sciences
GA DX3TZ
UT WOS:000384298800024
PM 27187094
ER
PT J
AU Esmail, H
Lai, RP
Lesosky, M
Wilkinson, KA
Graham, CM
Coussens, AK
Oni, T
Warwick, JM
Said-Hartley, Q
Koegelenberg, CF
Walzl, G
Flynn, JL
Young, DB
Barry, CE
O'Garra, A
Wilkinson, RJ
AF Esmail, Hanif
Lai, Rachel P.
Lesosky, Maia
Wilkinson, Katalin A.
Graham, Christine M.
Coussens, Anna K.
Oni, Tolu
Warwick, James M.
Said-Hartley, Qonita
Koegelenberg, Coenraad F.
Walzl, Gerhard
Flynn, JoAnne L.
Young, Douglas B.
Barry, Clifton E., III
O'Garra, Anne
Wilkinson, Robert J.
TI Characterization of progressive HIV-associated tuberculosis using
2-deoxy-2-[F-18] fluoro-D-glucose positron emission and computed
tomography
SO NATURE MEDICINE
LA English
DT Article
ID PULMONARY TUBERCULOSIS; ACTIVE TUBERCULOSIS; FUTURE-PROSPECTS;
INFECTION; PREVALENCE; STRATEGIES; DISEASE; ADULTS; LUNG
AB Tuberculosis is classically divided into states of latent infection and active disease. Using combined positron emission and computed tomography in 35 asymptomatic, antiretroviral-therapy-naive, HIV-1-infected adults with latent tuberculosis, we identified ten individuals with pulmonary abnormalities suggestive of subclinical, active disease who were substantially more likely to progress to clinical disease. Our findings challenge the conventional two-state paradigm and may aid future identification of biomarkers that are predictive of progression.
C1 [Esmail, Hanif; Young, Douglas B.; Wilkinson, Robert J.] Imperial Coll London, Dept Med, London, England.
[Esmail, Hanif; Lesosky, Maia; Wilkinson, Katalin A.; Coussens, Anna K.; Oni, Tolu; Barry, Clifton E., III; Wilkinson, Robert J.] Univ Cape Town, Inst Infect Dis & Mol Med, Clin Infect Dis Res Initiat, Cape Town, South Africa.
[Esmail, Hanif] Univ Oxford, Radcliffe Dept Med, Oxford, England.
[Lai, Rachel P.; Wilkinson, Katalin A.; Graham, Christine M.; Young, Douglas B.; O'Garra, Anne; Wilkinson, Robert J.] Francis Crick Inst Mill Hill Lab, London, England.
[Lesosky, Maia] Univ Cape Town, Sch Publ Hlth & Family Med, Div Epidemiol & Biostat, Cape Town, South Africa.
[Warwick, James M.] Univ Stellenbosch, Dept Med Imaging & Clin Oncol, Cape Town, South Africa.
[Said-Hartley, Qonita] Groote Schuur Hosp, Dept Radiol, Cape Town, South Africa.
[Koegelenberg, Coenraad F.; Walzl, Gerhard] Univ Stellenbosch, Dept Med, Cape Town, South Africa.
[Walzl, Gerhard; Barry, Clifton E., III] Univ Stellenbosch, Dept Biomed Sci, Fac Med & Hlth Sci, Cape Town, South Africa.
[Flynn, JoAnne L.] Univ Pittsburgh, Sch Med, Dept Microbiol & Mol Genet, Pittsburgh, PA USA.
[Barry, Clifton E., III] NIAID, TB Res Sect, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Barry, Clifton E., III] Univ Cape Town, Dept Pathol, Cape Town, South Africa.
[O'Garra, Anne] Imperial Coll London, Natl Heart & Lung Inst, London, England.
RP Esmail, H; Wilkinson, RJ (reprint author), Imperial Coll London, Dept Med, London, England.; Esmail, H; Wilkinson, RJ (reprint author), Univ Cape Town, Inst Infect Dis & Mol Med, Clin Infect Dis Res Initiat, Cape Town, South Africa.; Esmail, H (reprint author), Univ Oxford, Radcliffe Dept Med, Oxford, England.; Wilkinson, RJ (reprint author), Francis Crick Inst Mill Hill Lab, London, England.
EM hanif.esmail@ndcls.ox.ac.uk; r.j.wilkinson@imperial.ac.uk
OI Esmail, Hanif/0000-0002-4278-9316; Lesosky, Maia/0000-0002-2026-958X;
Coussens, Anna/0000-0002-7086-2621
FU Wellcome Trust [090170, 104803]; Bill and Melinda Gates
Foundation-Wellcome Trust Grand challenges in Global Health [37822]; US
National Institutes of Health (NIH) [R01 HL106804]; intramural research
program of the NIH-NIAID; European Union [FP& HEALTH F3-2012-305578];
National Research Foundation of South Africa [96841]; Research Councils
of the UK via the Francis Crick Institute [10218, U117565642]; Medical
Research Council of South Africa (Strategic Health Innovations
partnership)
FX This work was funded by the Wellcome Trust (grant no. 090170 (H.E.) and
104803 (R.J.W.)), the Bill and Melinda Gates Foundation-Wellcome Trust
Grand challenges in Global Health (grant no. 37822; D.B.Y.), the US
National Institutes of Health (NIH) (grant no. R01 HL106804; J.L.F.) and
the intramural research program of the NIH-NIAID (C.E.B.). R.J.W. also
received support from the European Union (grant no. FP& HEALTH
F3-2012-305578), the National Research Foundation of South Africa (grant
no. 96841), the Research Councils of the UK via the Francis Crick
Institute (grant no. 10218 and U117565642) and the Medical Research
Council of South Africa (Strategic Health Innovations partnership).
NR 20
TC 5
Z9 5
U1 2
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD OCT
PY 2016
VL 22
IS 10
BP 1090
EP 1093
DI 10.1038/nm.4161
PG 4
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA DY1RQ
UT WOS:000384872500011
PM 27595321
ER
PT J
AU Malherbe, ST
Shenai, S
Ronacher, K
Loxton, AG
Dolganov, G
Kriel, M
Van, T
Chen, RY
Warwick, J
Via, LE
Song, T
Lee, M
Schoolnik, G
Tromp, G
Alland, D
Barry, CE
Winter, J
Walzl, G
AF Malherbe, Stephanus T.
Shenai, Shubhada
Ronacher, Katharina
Loxton, Andre G.
Dolganov, Gregory
Kriel, Magdalena
Tran Van
Chen, Ray Y.
Warwick, James
Via, Laura E.
Song, Taeksun
Lee, Myungsun
Schoolnik, Gary
Tromp, Gerard
Alland, David
Barry, Clifton E., III
Winter, Jill
Walzl, Gerhard
CA Catalysis TB-Biomarker Consortium
TI Persisting positron emission tomography lesion activity and
Mycobacterium tuberculosis mRNA after tuberculosis cure
SO NATURE MEDICINE
LA English
DT Article
ID PULMONARY TUBERCULOSIS; RECURRENT TUBERCULOSIS; THERAPEUTIC RESPONSE;
SHORTENING TREATMENT; COMPUTED-TOMOGRAPHY; CULTURE CONVERSION;
RISK-FACTORS; RELAPSE; REINFECTION; IMPAIRMENT
AB The absence of a gold standard to determine when antibiotics induce a sterilizing cure has confounded the development of new approaches to treat pulmonary tuberculosis (PTB). We detected positron emission tomography and computerized tomography (PET-CT) imaging response patterns consistent with active disease, along with the presence of Mycobacterium tuberculosis (MTB) mRNA in sputum and bronchoalveolar lavage samples, in a substantial proportion of adult, HIV-negative patients with PTB after a standard 6-month treatment plus 1 year follow-up, including patients with a durable cure and others who later developed recurrent disease. The presence of MTB mRNA in the context of nonresolving and intensifying lesions on PET-CT images might indicate ongoing transcription, suggesting that even apparently curative treatment for PTB may not eradicate all of the MTB bacteria in most patients. This suggests an important complementary role for the immune response in maintaining a disease-free state. Sterilizing drugs or host-directed therapies, and better treatment response markers, are probably needed for the successful development of improved and shortened PTB-treatment strategies.
C1 [Malherbe, Stephanus T.; Ronacher, Katharina; Loxton, Andre G.; Kriel, Magdalena; Tromp, Gerard; Barry, Clifton E., III; Walzl, Gerhard] Univ Stellenbosch, Natl Res Fdn Ctr Excellence Biomed TB Res, Dept Sci & Technol, Cape Town, South Africa.
[Malherbe, Stephanus T.; Ronacher, Katharina; Loxton, Andre G.; Kriel, Magdalena; Tromp, Gerard; Barry, Clifton E., III; Walzl, Gerhard] Univ Stellenbosch, Fac Med & Hlth Sci, Div Mol Biol & Human Genet, South African Med Res Council,Ctr TB Res, Cape Town, South Africa.
[Shenai, Shubhada] Rutgers New Jersey Med Sch, Dept Med, Ctr Emerging Pathogens, Newark, NJ USA.
[Dolganov, Gregory; Tran Van] Stanford Univ, Dept Microbiol & Immunol, Sch Med, Stanford, CA 94305 USA.
[Chen, Ray Y.; Via, Laura E.] NIAID, TB Res Sect, Lab Clin Infect Dis, Div Intramural Res,NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Warwick, James] Tygerberg Acad Hosp, Western Cape Acad Positron Emiss Tomog Computed T, Cape Town, South Africa.
[Warwick, James] Univ Stellenbosch, Div Nucl Med, Dept Med Imaging & Clin Oncol, Fac Med & Hlth Sci, Cape Town, South Africa.
[Via, Laura E.; Barry, Clifton E., III] Univ Cape Town, Inst Infect Dis & Mol Med, Dept Clin Lab Sci, Cape Town, South Africa.
[Song, Taeksun; Lee, Myungsun] Int TB Res Ctr, Seoul, South Korea.
[Winter, Jill] Catalysis Fdn Hlth, Emeryville, CA USA.
Natl Med Ctr, Seoul, South Korea.
NIAID, Biostat Res Branch, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
Univ Stellenbosch, Divis Pulmonol, Fac Med & Hlth Sci, Cape Town, South Africa.
Univ Stellenbosch, Fac Med & Hlth Sci, Med Imaging & Clin Oncol, Div Radiodiag, Cape Town, South Africa.
RP Malherbe, ST (reprint author), Univ Stellenbosch, Natl Res Fdn Ctr Excellence Biomed TB Res, Dept Sci & Technol, Cape Town, South Africa.; Malherbe, ST (reprint author), Univ Stellenbosch, Fac Med & Hlth Sci, Div Mol Biol & Human Genet, South African Med Res Council,Ctr TB Res, Cape Town, South Africa.
EM malherbe@sun.ac.za
FU Catalysis Foundation for Health (CFH); Division of Intramural Research,
National Institute of Allergy and Infectious Diseases; National
Institute of Allergy and Infectious Diseases, International
Collaborations in Infectious Disease Research
FX Funding was provided by grants from the Catalysis Foundation for Health
(CFH) (G.W., C.E.B. and D.A.) the Division of Intramural Research,
National Institute of Allergy and Infectious Diseases (C.E.B.) and the
National Institute of Allergy and Infectious Diseases, International
Collaborations in Infectious Disease Research (G.W.), as well as by a
bursary from the South African National Research Fund and the Medical
Research Council's Clinician Scholarship Program (S.T.M.). We thank our
participants for their willingness to take part in this study. We
acknowledge R. Thayer and M. Urdea of CFH, the staff at the Stellenbosch
University Immunology Research Group, the International TB Research
Center (Seoul), the Western Cape Academic PET-CT Centre, Ithemba LABS,
Tygerberg Academic Hospital's Nuclear Medicine Department and
Pulmonology Unit, as well as the managers and healthcare providers from
the City of Cape Town Health Department for assistance with the
recruitment of participants and sample collection.
NR 52
TC 3
Z9 3
U1 2
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD OCT
PY 2016
VL 22
IS 10
BP 1094
EP 1100
DI 10.1038/nm.4177
PG 7
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA DY1RQ
UT WOS:000384872500012
PM 27595324
ER
PT J
AU Xu, M
Lee, EM
Wen, ZX
Cheng, YC
Huang, WK
Qian, XY
Julia, TCW
Kouznetsova, J
Ogden, SC
Hammack, C
Jacob, F
Nguyen, HN
Itkin, M
Hanna, C
Shinn, P
Allen, C
Michael, SG
Simeonov, A
Huang, WW
Christian, KM
Goate, A
Brennand, KJ
Huang, RL
Xia, MH
Ming, GL
Zheng, W
Song, HJ
Tang, HL
AF Xu, Miao
Lee, Emily M.
Wen, Zhexing
Cheng, Yichen
Huang, Wei-Kai
Qian, Xuyu
Julia, T. C. W.
Kouznetsova, Jennifer
Ogden, Sarah C.
Hammack, Christy
Jacob, Fadi
Ha Nam Nguyen
Itkin, Misha
Hanna, Catherine
Shinn, Paul
Allen, Chase
Michael, Samuel G.
Simeonov, Anton
Huang, Wenwei
Christian, Kimberly M.
Goate, Alison
Brennand, Kristen J.
Huang, Ruili
Xia, Menghang
Ming, Guo-li
Zheng, Wei
Song, Hongjun
Tang, Hengli
TI Identification of small-molecule inhibitors of Zika virus infection and
induced neural cell death via a drug repurposing screen
SO NATURE MEDICINE
LA English
DT Article
ID CDK9 INHIBITORS; APPROVED DRUGS; MICE; TRANSMISSION; REPLICATION;
ORGANOIDS; NICLOSAMIDE; THERAPY; FIT-039; BIOLOGY
AB In response to the current global health emergency posed by the Zika virus (ZIKV) outbreak and its link to microcephaly and other neurological conditions, we performed a drug repurposing screen of similar to 6,000 compounds that included approved drugs, clinical trial drug candidates and pharmacologically active compounds; we identified compounds that either inhibit ZIKV infection or suppress infection-induced caspase-3 activity in different neural cells. A pan-caspase inhibitor, emricasan, inhibited ZIKV-induced increases in caspase-3 activity and protected human cortical neural progenitors in both monolayer and three-dimensional organoid cultures. Ten structurally unrelated inhibitors of cyclin-dependent kinases inhibited ZIKV replication. Niclosamide, a category B anthelmintic drug approved by the US Food and Drug Administration, also inhibited ZIKV replication. Finally, combination treatments using one compound from each category (neuroprotective and antiviral) further increased protection of human neural progenitors and astrocytes from ZIKV-induced cell death. Our results demonstrate the efficacy of this screening strategy and identify lead compounds for anti-ZIKV drug development.
C1 [Xu, Miao; Kouznetsova, Jennifer; Itkin, Misha; Shinn, Paul; Michael, Samuel G.; Simeonov, Anton; Huang, Wenwei; Huang, Ruili; Xia, Menghang; Zheng, Wei] NIH, Natl Ctr Adv Translat, Bldg 10, Bethesda, MD 20892 USA.
[Xu, Miao] Zhejiang Univ, Sch Med, Sir Run Run Shaw Hosp, Hangzhou, Zhejiang, Peoples R China.
[Lee, Emily M.; Cheng, Yichen; Ogden, Sarah C.; Hammack, Christy; Hanna, Catherine; Allen, Chase; Tang, Hengli] Florida State Univ, Dept Biol Sci, B-157, Tallahassee, FL 32306 USA.
[Wen, Zhexing] Emory Univ, Sch Med, Dept Psychiat & Behav Sci, Atlanta, GA USA.
[Wen, Zhexing] Emory Univ, Sch Med, Dept Cell Biol, Atlanta, GA USA.
[Wen, Zhexing] Emory Univ, Sch Med, Dept Neurol, Atlanta, GA 30322 USA.
[Wen, Zhexing; Huang, Wei-Kai; Qian, Xuyu; Jacob, Fadi; Ha Nam Nguyen; Christian, Kimberly M.; Ming, Guo-li; Song, Hongjun] Johns Hopkins Univ, Sch Med, Inst Cell Engn, Baltimore, MD 21218 USA.
[Huang, Wei-Kai] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA.
[Qian, Xuyu; Ming, Guo-li; Song, Hongjun] Johns Hopkins Univ, Sch Med, Biomed Engn Grad Program, Baltimore, MD 21218 USA.
[Julia, T. C. W.; Goate, Alison] Icahn Sch Med Mt Sinai, Dept Neurosci, New York, NY 10029 USA.
[Jacob, Fadi; Ming, Guo-li; Song, Hongjun] Johns Hopkins Univ, Sch Med, Solomon H Snyder Dept Neurosci, Baltimore, MD 21218 USA.
[Ha Nam Nguyen; Christian, Kimberly M.; Ming, Guo-li; Song, Hongjun] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA.
[Brennand, Kristen J.] Icahn Sch Med Mt Sinai, Dept Psychiat, New York, NY 10029 USA.
[Ming, Guo-li] Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA.
[Ming, Guo-li; Song, Hongjun] Johns Hopkins Univ, Sch Med, Kavli Neurosci Discovery Inst, Baltimore, MD 21218 USA.
RP Zheng, W (reprint author), NIH, Natl Ctr Adv Translat, Bldg 10, Bethesda, MD 20892 USA.; Tang, HL (reprint author), Florida State Univ, Dept Biol Sci, B-157, Tallahassee, FL 32306 USA.; Ming, GL; Song, HJ (reprint author), Johns Hopkins Univ, Sch Med, Inst Cell Engn, Baltimore, MD 21218 USA.; Ming, GL; Song, HJ (reprint author), Johns Hopkins Univ, Sch Med, Biomed Engn Grad Program, Baltimore, MD 21218 USA.; Song, HJ (reprint author), Johns Hopkins Univ, Sch Med, Solomon H Snyder Dept Neurosci, Baltimore, MD 21218 USA.; Ming, GL; Song, HJ (reprint author), Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA.; Ming, GL (reprint author), Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA.; Ming, GL; Song, HJ (reprint author), Johns Hopkins Univ, Sch Med, Kavli Neurosci Discovery Inst, Baltimore, MD 21218 USA.
EM gming1@jhmi.edu; wzheng@mail.nih.gov; shongju1@jhmi.edu;
tang@bio.fsu.edu
RI Brennand, Kristen/J-8704-2012; Zheng, Wei/J-8889-2014;
OI Brennand, Kristen/0000-0003-0993-5956; Zheng, Wei/0000-0003-1034-0757;
Qian, Xuyu/0000-0001-5944-3816
FU Intramural Research Program of the National Center for Advancing
Translational Sciences, National Institutes of Health (NIH); Florida
State University; Emory University; Brain and Behavior Research
Foundation; New York Stem Cell Foundation; Maryland Stem Cell Research
Fund; Simons Foundation Autism Research Initiative [308988]; NIH
[NS048271, NS095348, MH105128, NS047344, NS097206, MH106434, MH101454,
MH106056, AG005138, AG046170, AI119530]
FX We thank R. Tesh and P.-Y. Shi (University of Texas Medical Branch) and
the World Reference Center for Emerging Viruses and Arboviruses (WRCEVA)
for the FSS-13025 isolate of ZIKV, and D. Meckes (Florida State
University) for the glioblastoma SNB-19 cell line. We also thank L. Liu
and Y. Cai for technical support. This work was supported by the
Intramural Research Program of the National Center for Advancing
Translational Sciences, National Institutes of Health (NIH) (W.Z.), ZIKV
seed funding from Florida State University (H.T.), a start-up fund from
Emory University (Z.W.), the Brain and Behavior Research Foundation
(K.J.B.), the New York Stem Cell Foundation (K.J.B.), the Maryland Stem
Cell Research Fund (G.M. and H.S.), the Simons Foundation Autism
Research Initiative (award no. 308988; H.S.), and partially by NIH
grants NS048271 (G.M.), NS095348 (G.M.), MH105128 (G.M.), NS047344
(H.S.), NS097206 (H.S.), MH106434 (H.S.), MH101454 (K.J.B.), MH106056
(K.J.B.), AG005138 (K.J.B.), AG046170 (K.J.B.) and AI119530 (H.T.).
NR 59
TC 23
Z9 23
U1 121
U2 121
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD OCT
PY 2016
VL 22
IS 10
BP 1101
EP 1107
DI 10.1038/nm.4184
PG 7
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA DY1RQ
UT WOS:000384872500013
PM 27571349
ER
PT J
AU Blackshaw, S
Venkataraman, A
Irizarry, J
Yang, K
Anderson, S
Campbell, E
Gatlin, CL
Freeman, NL
Basavappa, R
Stewart, R
Loss, MA
Pino, I
Zhu, H
Bader, JS
AF Blackshaw, Seth
Venkataraman, Anand
Irizarry, Jose
Yang, Kun
Anderson, Stephen
Campbell, Elliot
Gatlin, Christine L.
Freeman, Nancy L.
Basavappa, Ravi
Stewart, Randall
Loss, Michael A.
Pino, Ignacio
Zhu, Heng
Bader, Joel S.
TI The NIH Protein Capture Reagents Program (PCRP): a standardized protein
affinity reagent toolbox
SO NATURE METHODS
LA English
DT Letter
ID ANTIBODIES
C1 [Blackshaw, Seth; Venkataraman, Anand] Johns Hopkins Univ, Solomon H Snyder Dept Neurosci, Baltimore, MD 21218 USA.
[Blackshaw, Seth] Johns Hopkins Univ, Dept Neurol, Baltimore, MD 21218 USA.
[Blackshaw, Seth] Johns Hopkins Univ, Dept Ophthalmol, Baltimore, MD 21218 USA.
[Blackshaw, Seth; Zhu, Heng; Bader, Joel S.] Johns Hopkins Univ, Ctr Human Syst Biol, Baltimore, MD 21218 USA.
[Blackshaw, Seth] Johns Hopkins Univ, Inst Cell Engn, Baltimore, MD 21218 USA.
[Irizarry, Jose; Pino, Ignacio] CDI Labs, Guanajibo Res & Innovat Pk, Mayaguez, PR USA.
[Yang, Kun] Johns Hopkins Univ, Dept Biomed Engn, Baltimore, MD USA.
[Anderson, Stephen; Campbell, Elliot] Rutgers State Univ, Dept Mol Biol & Biochem, New Brunswick, NJ USA.
[Anderson, Stephen; Campbell, Elliot] Ctr Adv Biotechnol & Med, Piscataway, NJ USA.
[Gatlin, Christine L.] NHGRI, Bethesda, MD 20892 USA.
[Gatlin, Christine L.; Freeman, Nancy L.; Basavappa, Ravi; Stewart, Randall] NIH, Bldg 10, Bethesda, MD 20892 USA.
[Freeman, Nancy L.] NIDCD, Div Sci Programs, Bethesda, MD USA.
[Basavappa, Ravi] NIH, Off Strateg Coordinat, Off Director, Bldg 10, Bethesda, MD 20892 USA.
[Stewart, Randall] NINDS, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
[Loss, Michael A.] Leidos Biomed Res Inc, Frederick Natl Lab Canc Res, Adv Biomed Comp Ctr, Frederick, MD USA.
[Zhu, Heng] Johns Hopkins Univ, Dept Pharmacol, Baltimore, MD USA.
[Bader, Joel S.] Ctr Neurosci, Bethesda, MD USA.
RP Blackshaw, S (reprint author), Johns Hopkins Univ, Solomon H Snyder Dept Neurosci, Baltimore, MD 21218 USA.; Blackshaw, S (reprint author), Johns Hopkins Univ, Dept Neurol, Baltimore, MD 21218 USA.; Blackshaw, S (reprint author), Johns Hopkins Univ, Dept Ophthalmol, Baltimore, MD 21218 USA.; Blackshaw, S (reprint author), Johns Hopkins Univ, Ctr Human Syst Biol, Baltimore, MD 21218 USA.; Blackshaw, S (reprint author), Johns Hopkins Univ, Inst Cell Engn, Baltimore, MD 21218 USA.
EM sblack@jhmi.edu
NR 6
TC 0
Z9 0
U1 3
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1548-7091
EI 1548-7105
J9 NAT METHODS
JI Nat. Methods
PD OCT
PY 2016
VL 13
IS 10
BP 805
EP 806
DI 10.1038/nmeth.4013
PG 2
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA DY6CV
UT WOS:000385194600005
PM 27684578
ER
PT J
AU Uhlen, M
Bandrowski, A
Carr, S
Edwards, A
Ellenberg, J
Lundberg, E
Rimm, DL
Rodriguez, H
Hiltke, T
Snyder, M
Yamamoto, T
AF Uhlen, Mathias
Bandrowski, Anita
Carr, Steven
Edwards, Aled
Ellenberg, Jan
Lundberg, Emma
Rimm, David L.
Rodriguez, Henry
Hiltke, Tara
Snyder, Michael
Yamamoto, Tadashi
TI A proposal for validation of antibodies
SO NATURE METHODS
LA English
DT Article
ID ASSAYS; LOCALIZATION; MICROARRAYS; PROTEINS; CELLS
AB We convened an ad hoc International Working Group for Antibody Validation in order to formulate the best approaches for validating antibodies used in common research applications and to provide guidelines that ensure antibody reproducibility. We recommend five conceptual 'pillars' for antibody validation to be used in an application-specific manner.
C1 [Uhlen, Mathias; Lundberg, Emma] KTH Royal Inst Technol, Sch Biotechnol, Sci Life Lab, Stockholm, Sweden.
[Bandrowski, Anita] Univ Calif San Diego, Ctr Res Biol Syst, San Diego, CA 92103 USA.
[Carr, Steven] Broad Inst Massachusetts Inst Technol & Harvard U, Prote Platform, Cambridge, MA USA.
[Edwards, Aled] Univ Toronto, Struct Genom Consortium, Toronto, ON, Canada.
[Ellenberg, Jan] European Mol Biol Lab, Cell Biol & Biophys Unit, Heidelberg, Germany.
[Rimm, David L.] Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06510 USA.
[Rodriguez, Henry; Hiltke, Tara] NCI, Off Canc Clin Prote Res, NIH, Bethesda, MD 20892 USA.
[Snyder, Michael] Stanford Univ, Dept Genet, Sch Med, Stanford, CA 94305 USA.
[Yamamoto, Tadashi] Niigata Univ, Biofluid Biomarker Ctr, Niigata, Japan.
RP Uhlen, M (reprint author), KTH Royal Inst Technol, Sch Biotechnol, Sci Life Lab, Stockholm, Sweden.
EM mathias.uhlen@scilifelab.se
OI Bandrowski, Anita/0000-0002-5497-0243; Ellenberg,
Jan/0000-0001-5909-701X; Uhlen, Mathias/0000-0002-4858-8056
NR 20
TC 7
Z9 7
U1 14
U2 14
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1548-7091
EI 1548-7105
J9 NAT METHODS
JI Nat. Methods
PD OCT
PY 2016
VL 13
IS 10
BP 823
EP +
DI 10.1038/NMETH.3995
PG 6
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA DY6CV
UT WOS:000385194600015
PM 27595404
ER
PT J
AU Arveson, I
Shelton, M
Tonkura, F
Bendixen, R
Meilleur, K
AF Arveson, I.
Shelton, M.
Tonkura, F.
Bendixen, R.
Meilleur, K.
TI Development of a proxy motor outcome measurement scale in young children
with neuromuscular disorders
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 21st International Congress of the World-Muscle-Society
CY OCT 04-08, 2016
CL Granada, SPAIN
SP World Muscle Soc
C1 [Arveson, I.; Shelton, M.; Tonkura, F.; Meilleur, K.] NIH, Bldg 10, Bethesda, MD 20892 USA.
[Bendixen, R.] Univ Pittsburgh, Pittsburgh, PA 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
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2016
VL 26
SU 2
MA P.207
BP S148
EP S148
DI 10.1016/j.nmd.2016.06.227
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA DY0ME
UT WOS:000384790100217
ER
PT J
AU Arveson, I
Witherspoon, J
Drinkard, B
Waite, M
Razaqyar, M
Tounkara, E
Elliott, J
Shelton, M
Jain, M
Bonnemann, C
Meilleur, K
AF Arveson, I.
Witherspoon, J.
Drinkard, B.
Waite, M.
Razaqyar, M.
Tounkara, E.
Elliott, J.
Shelton, M.
Jain, M.
Bonnemann, C.
Meilleur, K.
TI Antioxidant therapy in RYR1-related myopathies
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 21st International Congress of the World-Muscle-Society
CY OCT 04-08, 2016
CL Granada, SPAIN
SP World Muscle Soc
C1 [Arveson, I.; Witherspoon, J.; Drinkard, B.; Waite, M.; Razaqyar, M.; Tounkara, E.; Elliott, J.; Shelton, M.; Jain, M.; Bonnemann, C.; Meilleur, K.] NIH, Bldg 10, 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
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2016
VL 26
SU 2
MA P.166
BP S137
EP S137
DI 10.1016/j.nmd.2016.06.186
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA DY0ME
UT WOS:000384790100176
ER
PT J
AU Bharucha-Goebel, D
Collins, J
Hu, Y
Foley, AR
Donkervoort, S
Leach, M
Dastgir, N
Vuillerot, C
Meilleur, K
Jain, M
Waite, M
Jacobson, S
Gordish, H
Rutkowski, A
Hoffman, E
Hathout, Y
Bonnemann, C
AF Bharucha-Goebel, D.
Collins, J.
Hu, Y.
Foley, A. Reghan
Donkervoort, S.
Leach, M.
Dastgir, N.
Vuillerot, C.
Meilleur, K.
Jain, M.
Waite, M.
Jacobson, S.
Gordish, H.
Rutkowski, A.
Hoffman, E.
Hathout, Y.
Bonnemann, C.
TI Serum biomarker discovery for congenital muscular dystrophies
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 21st International Congress of the World-Muscle-Society
CY OCT 04-08, 2016
CL Granada, SPAIN
SP World Muscle Soc
C1 [Bharucha-Goebel, D.; Hu, Y.; Foley, A. Reghan; Donkervoort, S.; Leach, M.; Meilleur, K.; Jain, M.; Waite, M.; Bonnemann, C.] NIH, Bldg 10, Bethesda, MD 20892 USA.
[Bharucha-Goebel, D.; Leach, M.] Natl Inst Childrens Natl Hlth Syst, Bethesda, MD USA.
[Collins, J.] Mercy Clin, Springfield, MO USA.
[Dastgir, N.] Columbia Univ, Med Ctr, New York, NY USA.
[Vuillerot, C.] Hosp Civils Lyon, Lyon, France.
[Jacobson, S.] Cincinnati Childrens Hosp Ctr, Cincinnati, OH USA.
[Gordish, H.] Childrens Natl Hlth Syst, Washington, DC USA.
[Rutkowski, A.] Cure CMD, Torrance, CA USA.
[Hoffman, E.; Hathout, Y.] Childrens Natl Hlth Syst CRI, Washington, DC 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
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2016
VL 26
SU 2
MA P.345
BP S189
EP S189
DI 10.1016/j.nmd.2016.06.374
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA DY0ME
UT WOS:000384790100363
ER
PT J
AU Butterfield, R
Dunn, D
Hu, Y
Bonnernann, C
Weiss, R
AF Butterfield, R.
Dunn, D.
Hu, Y.
Bonnernann, C.
Weiss, R.
TI Transcriptome profiling identifies key pathways important in collagen VI
related muscular dystrophies including differences between patients with
dominant negative vs. null mutations
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 21st International Congress of the World-Muscle-Society
CY OCT 04-08, 2016
CL Granada, SPAIN
SP World Muscle Soc
C1 [Butterfield, R.; Dunn, D.; Weiss, R.] Univ Utah, Salt Lake City, UT USA.
[Hu, Y.; Bonnernann, C.] NIH, Bldg 10, 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
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2016
VL 26
SU 2
MA P.342
BP S188
EP S189
DI 10.1016/j.nmd.2016.06.371
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA DY0ME
UT WOS:000384790100360
ER
PT J
AU Carrillo, N
Huizing, M
Quintana, M
Slota, C
Malicdan, M
Khatami, H
Berry, S
Gahl, W
AF Carrillo, N.
Huizing, M.
Quintana, M.
Slota, C.
Malicdan, M.
Khatami, H.
Berry, S.
Gahl, W.
TI Therapeutic development of ManNAc for GNE myopathy
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 21st International Congress of the World-Muscle-Society
CY OCT 04-08, 2016
CL Granada, SPAIN
SP World Muscle Soc
C1 [Carrillo, N.; Huizing, M.; Slota, C.; Malicdan, M.; Gahl, W.] NIH, Bldg 10, Bethesda, MD 20892 USA.
[Quintana, M.; Berry, S.] Berry Consultants, Austin, TX USA.
[Khatami, H.] Escala Therapeut, New York, NY 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
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2016
VL 26
SU 2
MA P.283
BP S172
EP S172
DI 10.1016/j.nmd.2016.06.313
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA DY0ME
UT WOS:000384790100302
ER
PT J
AU Rubio, RD
Martinez, A
Poza, J
Bragado, FG
Jerico, I
van der Ven, P
Furst, D
Romero, N
Goldfarb, L
Olive, M
AF Dominguez Rubio, R.
Martinez, A.
Poza, J.
Garcia Bragado, F.
Jerico, I.
van der Ven, P.
Fuerst, D.
Romero, N.
Goldfarb, L.
Olive, M.
TI Intranuclear protein aggregation in myofibrillar myopathies
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 21st International Congress of the World-Muscle-Society
CY OCT 04-08, 2016
CL Granada, SPAIN
SP World Muscle Soc
C1 [Dominguez Rubio, R.; Martinez, A.; Olive, M.] IDIBELL Hosp Bellvitge, Lhospitalet De Llobregat, Spain.
[Poza, J.] Hosp Donostia, San Sebastian, Spain.
[Garcia Bragado, F.] Hosp Virgen del Camino, Pamplona, Spain.
[Jerico, I.] Complejo Hosp Navarra, Pamplona, Spain.
[van der Ven, P.; Fuerst, D.] Univ Bonn, Inst Cell Biol, Bonn, Germany.
[Romero, N.] GHU Pitie Salpetriere, Inst Myol, Paris, France.
[Goldfarb, L.] NIH, Bldg 10, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 2
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2016
VL 26
SU 2
MA P.352
BP S191
EP S191
DI 10.1016/j.nmd.2016.06.381
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA DY0ME
UT WOS:000384790100370
ER
PT J
AU Foley, AR
Cocanougher, B
Flynn, L
Yun, P
Jain, M
Waite, M
Vasavada, R
de Chastonay, S
Donkervoort, S
Bonnemann, C
AF Foley, A. Reghan
Cocanougher, B.
Flynn, L.
Yun, P.
Jain, M.
Waite, M.
Vasavada, R.
de Chastonay, S.
Donkervoort, S.
Bonnemann, C.
TI MTM1-related myopathy carrier females manifest significant skeletal
asymmetries and a spectrum of muscle involvement
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 21st International Congress of the World-Muscle-Society
CY OCT 04-08, 2016
CL Granada, SPAIN
SP World Muscle Soc
C1 [Foley, A. Reghan; Flynn, L.; Yun, P.; Donkervoort, S.; Bonnemann, C.] NINDS, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
[Cocanougher, B.] Howard Hughes Med Inst, Ashburn, VA USA.
[Jain, M.; Waite, M.; Vasavada, R.] NIH, Bethesda, MD USA.
[de Chastonay, S.] Cure CMD, Torrance, CA 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
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2016
VL 26
SU 2
MA P.93
BP S117
EP S117
DI 10.1016/j.nmd.2016.06.115
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA DY0ME
UT WOS:000384790100105
ER
PT J
AU Korinthenberg, R
Schorling, D
Rost, S
Krueger, M
Beytia, M
Mueller, C
Bonnemann, C
Kirschner, J
AF Korinthenberg, R.
Schorling, D.
Rost, S.
Krueger, M.
Beytia, M.
Mueller, C.
Bonnemann, C.
Kirschner, J.
TI Severe congenital myopathy with myasthenic features and lethal
neurodegeneration - A new ALG14-related phenotype?
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 21st International Congress of the World-Muscle-Society
CY OCT 04-08, 2016
CL Granada, SPAIN
SP World Muscle Soc
C1 [Korinthenberg, R.; Schorling, D.; Krueger, M.; Kirschner, J.] Univ Med Ctr Freiburg, Freiburg, Germany.
[Rost, S.; Beytia, M.; Mueller, C.] Univ Wurzburg, D-97070 Wurzburg, Germany.
[Bonnemann, C.] NIH, Bldg 10, 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
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2016
VL 26
SU 2
MA P.77
BP S112
EP S112
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA DY0ME
UT WOS:000384790100089
ER
PT J
AU Malicdan, M
Leoyklang, P
Ciccone, C
Carrillo, N
Huizing, M
Gahl, W
AF Malicdan, M.
Leoyklang, P.
Ciccone, C.
Carrillo, N.
Huizing, M.
Gahl, W.
TI GNE myopathy biomarkers: Essential for diagnosis and response to therapy
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 21st International Congress of the World-Muscle-Society
CY OCT 04-08, 2016
CL Granada, SPAIN
SP World Muscle Soc
C1 [Malicdan, M.; Leoyklang, P.; Ciccone, C.; Carrillo, N.; Huizing, M.; Gahl, W.] NHGRI, 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
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2016
VL 26
SU 2
MA P.276
BP S170
EP S170
DI 10.1016/j.nmd.2016.06.306
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA DY0ME
UT WOS:000384790100295
ER
PT J
AU Miyakawa, M
Cho, A
Malicdan, M
Nishino, I
Noguchi, S
AF Miyakawa, M.
Cho, A.
Malicdan, M.
Nishino, I.
Noguchi, S.
TI S-nitrosylation of muscle contractile proteins and metabolic enzymes
causes muscle atrophy and weakness in GNE myopathy
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 21st International Congress of the World-Muscle-Society
CY OCT 04-08, 2016
CL Granada, SPAIN
SP World Muscle Soc
C1 [Miyakawa, M.; Nishino, I.; Noguchi, S.] Natl Inst Neurosci, Kodaira, Tokyo, Japan.
[Cho, A.] Ewha Womans Univ, Sch Med, Seoul, South Korea.
[Malicdan, M.] NHGRI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2016
VL 26
SU 2
MA P.281
BP S171
EP S172
DI 10.1016/j.nmd.2016.06.311
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA DY0ME
UT WOS:000384790100300
ER
PT J
AU Oates, E
Yau, K
Donkervoort, S
Swanson, L
Brammah, S
Topf, A
Richard, I
Ferreiro, A
Hoffman, E
Bushby, K
Straub, V
Udd, B
Lek, M
MacArthur, D
Granzier, H
Beggs, A
Bonnemann, C
North, K
Davis, M
Laing, N
AF Oates, E.
Yau, K.
Donkervoort, S.
Swanson, L.
Brammah, S.
Topf, A.
Richard, I.
Ferreiro, A.
Hoffman, E.
Bushby, K.
Straub, V.
Udd, B.
Lek, M.
MacArthur, D.
Granzier, H.
Beggs, A.
Bonnemann, C.
North, K.
Davis, M.
Laing, N.
TI Analysis of a large international cohort confirms that recessively
inherited loss-of-function TTN mutations cause prenatal or infant-onset
muscle disease, often complicated by early cardiorespiratory involvement
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 21st International Congress of the World-Muscle-Society
CY OCT 04-08, 2016
CL Granada, SPAIN
SP World Muscle Soc
C1 [Oates, E.] Inst Neurosci & Muscle Res, Sydney, NSW, Australia.
[Yau, K.; Laing, N.] Univ Western Australia, Perth, WA, Australia.
[Donkervoort, S.; Bonnemann, C.] NIH, Bldg 10, Bethesda, MD 20892 USA.
[Swanson, L.; Beggs, A.] Harvard Med Sch, Boston Childrens Hosp, Boston, MA USA.
[Brammah, S.] Concord Repatriat Gen Hosp, Sydney, NSW, Australia.
[Topf, A.; Bushby, K.; Straub, V.] Univ Newcastle, Newcastle Upon Tyne, Tyne & Wear, England.
[Richard, I.] Genethon, Evry, France.
[Ferreiro, A.] Univ Paris, Sorbonne, Diderot, Paris, France.
[Hoffman, E.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Hoffman, E.] George Washington Univ, Washington, DC USA.
[Udd, B.] Tampere Univ, Tampere, Finland.
[Udd, B.] Univ Hosp, Tampere, Finland.
[Lek, M.; MacArthur, D.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Lek, M.; MacArthur, D.] Broad Inst Harvard & MIT, Boston, MA USA.
[Granzier, H.] Univ Arizona, Tucson, AZ USA.
[North, K.] Royal Childrens Hosp, Melbourne, Vic, Australia.
[Davis, M.] Royal Perth Hosp, Perth, WA, Australia.
RI North, Kathryn/K-6476-2012
OI North, Kathryn/0000-0003-0841-8009
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
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2016
VL 26
SU 2
MA S.O.2
BP S89
EP S89
DI 10.1016/j.nmd.2016.06.018
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA DY0ME
UT WOS:000384790100008
ER
PT J
AU Punetha, J
Kesari, A
Hoffman, E
Gos, M
Kaminska, A
Kostera-Pruszczyk, A
Hu, Y
Zou, Y
Bonnemann, C
Jedrzejowska, M
AF Punetha, J.
Kesari, A.
Hoffman, E.
Gos, M.
Kaminska, A.
Kostera-Pruszczyk, A.
Hu, Y.
Zou, Y.
Bonnemann, C.
Jedrzejowska, M.
TI A novel COL12A1 variant expands the clinical picture for a collagen
XII-related myopathy
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 21st International Congress of the World-Muscle-Society
CY OCT 04-08, 2016
CL Granada, SPAIN
SP World Muscle Soc
C1 [Punetha, J.; Kesari, A.; Hoffman, E.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Gos, M.] Inst Mother & Child Hlth, Warsaw, Poland.
[Kaminska, A.; Kostera-Pruszczyk, A.] Med Univ Warsaw, Warsaw, Poland.
[Hu, Y.; Zou, Y.; Bonnemann, C.] NINDS, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
[Jedrzejowska, M.] Mossakowski Med Res Ctr, Warsaw, Poland.
NR 0
TC 0
Z9 0
U1 3
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2016
VL 26
SU 2
MA P.344
BP S189
EP S189
DI 10.1016/j.nmd.2016.06.373
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA DY0ME
UT WOS:000384790100362
ER
PT J
AU Razaqyar, M
Butrum, J
Witherspoon, J
Tounkara, F
Shelton, M
Elliott, J
Arveson, I
Meilleur, K
AF Razaqyar, M.
Butrum, J.
Witherspoon, J.
Tounkara, F.
Shelton, M.
Elliott, J.
Arveson, I.
Meilleur, K.
TI Qualitative comparison of healthy versus affected muscles by ultrasound
imaging in RYR1-related myopathies
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 21st International Congress of the World-Muscle-Society
CY OCT 04-08, 2016
CL Granada, SPAIN
SP World Muscle Soc
C1 [Razaqyar, M.; Butrum, J.; Witherspoon, J.; Tounkara, F.; Shelton, M.; Elliott, J.; Arveson, I.; Meilleur, K.] NIH, Bldg 10, 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
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2016
VL 26
SU 2
MA P.28
BP S98
EP S98
DI 10.1016/j.nmd.2016.06.050
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA DY0ME
UT WOS:000384790100040
ER
PT J
AU Witherspoon, J
Drinkard, B
Arveson, I
Stockman, M
Jain, M
Meilleur, K
AF Witherspoon, J.
Drinkard, B.
Arveson, I.
Stockman, M.
Jain, M.
Meilleur, K.
TI Skeletal muscle oxygenation in adults with RYR1-related myopathies:
Exploratory study
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 21st International Congress of the World-Muscle-Society
CY OCT 04-08, 2016
CL Granada, SPAIN
SP World Muscle Soc
C1 [Witherspoon, J.; Drinkard, B.; Arveson, I.; Stockman, M.; Jain, M.; Meilleur, K.] NIH, Bldg 10, 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
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2016
VL 26
SU 2
MA P.160
BP S135
EP S135
DI 10.1016/j.nmd.2016.06.180
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA DY0ME
UT WOS:000384790100170
ER
PT J
AU Zou, Y
Donkervoort, S
Salo, A
Barnes, A
Hu, Y
Foley, AR
Makareeva, E
Leach, M
Dastgir, J
Cohn, R
DiNonno, W
Leikin, S
Marini, J
Myllyharju, J
Bonnemann, C
AF Zou, Y.
Donkervoort, S.
Salo, A.
Barnes, A.
Hu, Y.
Foley, A. Reghan
Makareeva, E.
Leach, M.
Dastgir, J.
Cohn, R.
DiNonno, W.
Leikin, S.
Marini, J.
Myllyharju, J.
Bonnemann, C.
TI P4HA1 mutations cause a unique congenital disorder of connective tissue
involving tendon, bone, muscle and the eye
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 21st International Congress of the World-Muscle-Society
CY OCT 04-08, 2016
CL Granada, SPAIN
SP World Muscle Soc
C1 [Zou, Y.; Donkervoort, S.; Hu, Y.; Foley, A. Reghan; Leach, M.; Dastgir, J.; Bonnemann, C.] NINDS, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
[Salo, A.; Myllyharju, J.] Bioctr Oulu, Oulu Ctr Cell Matrix Res, Oulu, Finland.
[Barnes, A.; Makareeva, E.; Leikin, S.; Marini, J.] NICHD, NIH, Bethesda, MD USA.
[Cohn, R.] Hosp Sick Children, Toronto, ON, Canada.
[DiNonno, W.] Eastern Virginia Med Sch, Norfolk, VA 23501 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
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2016
VL 26
SU 2
MA G.O.21
BP S211
EP S212
DI 10.1016/j.nmd.2016.06.455
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA DY0ME
UT WOS:000384790100444
ER
PT J
AU de Jesus, AA
Goldbach-Mansky, R
AF de Jesus, A. A.
Goldbach-Mansky, R.
TI Genetically defined autoinflammatory diseases
SO ORAL DISEASES
LA English
DT Review
DE autoinflammatory diseases; inflammatory diseases; immune defects;
immunology; rheumatology; IL-1; Type I interferon
ID FAMILIAL MEDITERRANEAN FEVER; SINGLETON-MERTEN SYNDROME; RECURRENT
MULTIFOCAL OSTEOMYELITIS; PEDIATRIC GRANULOMATOUS ARTHRITIS; CONGENITAL
SIDEROBLASTIC ANEMIA; MACROPHAGE ACTIVATION SYNDROME; JUVENILE
IDIOPATHIC ARTHRITIS; INFLAMMATORY-BOWEL-DISEASE; STEM-CELL
TRANSPLANTATION; DEVELOPMENTAL DELAY SIFD
AB Autoinflammatory diseases are hyperinflammatory, immune dysregulatory conditions that typically present in early childhood with fever and rashes and disease-specific patterns of organ inflammation. This review provides a historic background of autoinflammatory disease research, an overview of the currently genetically defined autoinflammatory diseases, and insights into treatment strategies derived from understanding of the disease pathogenesis. The integrative assessment of autoinflammatory conditions led to the identification of innate pro-inflammatory cytokine amplification loops' as the cause of the systemic and organ-specific disease manifestations, which initially centered around increased IL-1 production and signaling. More recently, additional innate pro-inflammatory cytokine amplification loops resulting in increased Type I IFN, IL-17, IL-18, or IL-36 signaling or production have led to the successful use of targeted therapies in some of these conditions. Clinical findings such as fever patterns, type of skin lesions, genetic mutation testing, and the prevalent cytokine abnormalities can be used to group autoinflammatory diseases.
C1 [de Jesus, A. A.; Goldbach-Mansky, R.] Natl Inst Arthrit Musculoskeletal & Skin Dis NIAM, Translat Autoinflammatory Dis Sect, NIH, Bethesda, MD USA.
RP Goldbach-Mansky, R (reprint author), Natl Inst Arthrit Musculoskeletal & Skin Dis NIAM, Translat Autoinflammatory Dis Sect, Ctr Clin, NIH, Bldg 10 Room 6D47-B,10 Ctr Dr, Bethesda, MD 20814 USA.
EM goldbacr@arb.niams.nih.gov
FU Intramural NIH HHS [Z01 AR041138-06]
NR 82
TC 0
Z9 0
U1 5
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1354-523X
EI 1601-0825
J9 ORAL DIS
JI Oral Dis.
PD OCT
PY 2016
VL 22
IS 7
BP 591
EP 604
DI 10.1111/odi.12448
PG 14
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA DW4MS
UT WOS:000383617900003
PM 26837051
ER
PT J
AU Shaikh, N
Hoberman, A
Keren, R
Ivanova, A
Ziessman, HA
Cui, G
Mattoo, TK
Bhatnagar, S
Nadkarni, MD
Moxey-Mims, M
Primack, WA
AF Shaikh, Nader
Hoberman, Alejandro
Keren, Ron
Ivanova, Anastasia
Ziessman, Harvey A.
Cui, Gang
Mattoo, Tej K.
Bhatnagar, Sonika
Nadkarni, Milan D.
Moxey-Mims, Marva
Primack, William A.
TI Utility of sedation for young children undergoing dimercaptosuccinic
acid renal scans
SO PEDIATRIC RADIOLOGY
LA English
DT Article
DE Anxiolytic; Children; Dimercaptosuccinic acid; Renal scintigraphy;
Sedation; Ultrasound; Voiding cystourethrogram
ID VOIDING CYSTOURETHROGRAPHY; ORAL MIDAZOLAM; VESICOURETERAL REFLUX;
NITROUS-OXIDE; DOUBLE-BLIND; DISTRESS; EFFICACY; PREMEDICATION; SAFETY
AB No studies have examined whether use of sedation during a Tc-99 m dimercaptosuccinic acid (DMSA) renal scan reduces patient discomfort.
To compare discomfort level during a DMSA scan to the discomfort level during other frequently performed uroradiologic tests, and to determine whether use of sedation during a DMSA scan modifies the level of discomfort.
We examined the discomfort level in 798 children enrolled in the Randomized Intervention for children with Vesicoureteral Reflux (RIVUR) and Careful Urinary Tract Infection Evaluation (CUTIE) studies by asking parents to rate their child's discomfort level with each procedure on a scale from 0 to 10. We compared discomfort during the DMSA scan and the DMSA image quality between centers in which sedation was used > 90% of the time (sedation centers), centers in which sedation was used < 10% of the time (non-sedation centers), and centers in which sedation was used on a case-by-case basis (selective centers).
Mean discomfort level was highest for voiding cystourethrogram (6.4), followed by DMSA (4.0), followed by ultrasound (2.4; P < 0.0001). Mean discomfort level during the DMSA scan was significantly higher at non-sedation centers than at selective centers (P < 0.001). No difference was apparent in discomfort level during the DMSA scan between sedation centers and selective centers (P=0.12), or between the sedation centers and non-sedation centers (P=0.80). There were no differences in the proportion with uninterpretable DMSA scans according to sedation use.
Selective use of sedation in children 12-36 months of age can reduce the discomfort level experienced during a DMSA scan.
C1 [Shaikh, Nader; Hoberman, Alejandro; Bhatnagar, Sonika] Univ Pittsburgh, Sch Med, Childrens Hosp Pittsburgh UPMC, Div Gen Acad Pediat, One Childrens Hosp Dr,4401 Penn Ave, Pittsburgh, PA 15224 USA.
[Keren, Ron] Childrens Hosp Philadelphia, Ctr Pediat Clin Effectiveness, Div Gen Pediat, Philadelphia, PA 19104 USA.
[Ivanova, Anastasia] Univ N Carolina, Dept Biostat, Chapel Hill, NC USA.
[Ziessman, Harvey A.] Johns Hopkins Univ, Dept Radiol, Baltimore, MD USA.
[Cui, Gang] Univ N Carolina, Collaborat Studies Coordinating Ctr, Chapel Hill, NC USA.
[Mattoo, Tej K.] Wayne State Univ, Sch Med, Childrens Hosp Michigan, Div Nephrol & Hypertens, Detroit, MI USA.
[Nadkarni, Milan D.] Wake Forest Sch Med, Brenner Childrens Hosp, Pediat Emergency Dept, Winston Salem, NC USA.
[Moxey-Mims, Marva] NIDDK, NIH, Bethesda, MD 20892 USA.
[Primack, William A.] Univ N Carolina, Kidney Ctr, Chapel Hill, NC USA.
RP Shaikh, N (reprint author), Univ Pittsburgh, Sch Med, Childrens Hosp Pittsburgh UPMC, Div Gen Acad Pediat, One Childrens Hosp Dr,4401 Penn Ave, Pittsburgh, PA 15224 USA.
EM nader.shaikh@chp.edu
FU NIDDK NIH HHS [U01 DK074059]
NR 15
TC 0
Z9 0
U1 2
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0301-0449
EI 1432-1998
J9 PEDIATR RADIOL
JI Pediatr. Radiol.
PD OCT
PY 2016
VL 46
IS 11
BP 1573
EP 1578
DI 10.1007/s00247-016-3649-0
PG 6
WC Pediatrics; Radiology, Nuclear Medicine & Medical Imaging
SC Pediatrics; Radiology, Nuclear Medicine & Medical Imaging
GA DY5WX
UT WOS:000385176200011
PM 27287454
ER
PT J
AU Lopez, G
Bayulkem, K
Hallett, M
AF Lopez, G.
Bayulkem, K.
Hallett, M.
TI Progressive supranuclear palsy (PSP): Richardson syndrome and other PSP
variants
SO ACTA NEUROLOGICA SCANDINAVICA
LA English
DT Review
DE atypical parkinsonism; phenomenology; progressive supranuclear palsy;
Richardson syndrome; tauopathy
ID PRIMARY LATERAL SCLEROSIS; CORTICOBASAL DEGENERATION; FRONTOTEMPORAL
DEMENTIA; ESSENTIAL TREMOR; NONFLUENT APHASIA; PARKINSONISM; DIAGNOSIS;
CRITERIA; APRAXIA; SPEECH
AB Phenotypic heterogeneity of progressive supranuclear palsy (PSP) has been increasingly reported in the literature and can be the source of incorrect clinical diagnosis particularly in the early stages of the disease when the classically associated symptoms of early falls and supranuclear gaze palsy may not be apparent. In addition to Richardson syndrome (RS), several atypical clinical phenotypes have been described. Advances in genetic, neuroimaging, and biochemical/molecular technologies contribute to the identification of these clinical subtypes in the context of typical PSP pathological findings. Our goal is to review the phenomenology reported in the literature that is associated with confirmed histopathological changes consistent with a PSP diagnosis and to highlight the clinical spectrum of PSP. A systematic review of the literature in PubMed through July 2015 using MeSH terms and key words related to PSP was conducted. Articles describing PSP classifications, diagnostic criteria, and case reports were reviewed and summarized. Additional PSP phenotypes not seen in recent clinicopathological studies are included. These include primary lateral sclerosis, pallido-nigro-luysian degeneration, axonal dystrophy, and multiple system atrophy in the spectrum of atypical PSP variants beyond the traditionally classified PSP subtypes. This review is intended to help with the diagnostic challenges of atypical PSP variants. We believe that large multicenter clinicopathological studies will help expand our understanding of etiology and specific mechanisms of neurodegeneration and will aid in the appropriate interpretation of outcomes when conducting clinical and basic science research.
C1 [Lopez, G.] NHGRI, Sect Mol Neurogenet, Med Genet Branch, Intramural Res Program,NIH, Bethesda, MD 20892 USA.
[Bayulkem, K.; Hallett, M.] NINDS, Human Motor Control Sect, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
RP Lopez, G (reprint author), NHGRI, Sect Mol Neurogenet, Med Genet Branch, Intramural Res Program,NIH, Bethesda, MD 20892 USA.
EM glopez@mail.nih.gov
NR 45
TC 0
Z9 0
U1 5
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0001-6314
EI 1600-0404
J9 ACTA NEUROL SCAND
JI Acta Neurol. Scand.
PD OCT
PY 2016
VL 134
IS 4
BP 242
EP 249
DI 10.1111/ane.12546
PG 8
WC Clinical Neurology
SC Neurosciences & Neurology
GA DW4OI
UT WOS:000383622300001
PM 27070344
ER
PT J
AU Doussau, A
Grady, C
AF Doussau, Adelaide
Grady, Christine
TI The Ethics of Studying Financial Incentives in Public Health
Implementation: Study Design Challenges
SO AMERICAN JOURNAL OF BIOETHICS
LA English
DT Editorial Material
ID CLUSTER RANDOMIZED-TRIAL
C1 [Doussau, Adelaide; Grady, Christine] NIH, 10 Ctr Dr,Bldg 10, Bethesda, MD 20892 USA.
RP Doussau, A (reprint author), NIH, Dept Bioeth, Ctr Clin, Bioeth, 10 Ctr Dr,Bldg 10, Bethesda, MD 20892 USA.
EM adelaide.doussau@gmail.com
NR 10
TC 0
Z9 0
U1 1
U2 1
PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND
SN 1526-5161
EI 1536-0075
J9 AM J BIOETHICS
JI Am. J. Bioeth.
PD OCT
PY 2016
VL 16
IS 10
BP 78
EP 80
DI 10.1080/15265161.2016.1214322
PG 3
WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical
SC Social Sciences - Other Topics; Medical Ethics; Social Issues;
Biomedical Social Sciences
GA DX6ZU
UT WOS:000384536000031
PM 27653414
ER
PT J
AU Rosenkrantz, AB
Oto, A
Turkbey, B
Westphalen, AC
AF Rosenkrantz, Andrew B.
Oto, Aytekin
Turkbey, Baris
Westphalen, Antonio C.
TI Reply to "Standardizing Biparametric MRI to Simplify and Improve
Prostate Imaging Reporting and Data System, Version 2, in Prostate
Cancer Management"
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Letter
ID PI-RADS; BIOPSY
C1 [Rosenkrantz, Andrew B.] NYU, Langone Med Ctr, Sch Med, New York, NY 10012 USA.
[Oto, Aytekin] Univ Chicago, Chicago, IL 60637 USA.
[Turkbey, Baris] NCI, NIH, Bethesda, MD 20892 USA.
[Westphalen, Antonio C.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
RP Rosenkrantz, AB (reprint author), NYU, Langone Med Ctr, Sch Med, New York, NY 10012 USA.
NR 6
TC 0
Z9 0
U1 0
U2 0
PU AMER ROENTGEN RAY SOC
PI RESTON
PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA
SN 0361-803X
EI 1546-3141
J9 AM J ROENTGENOL
JI Am. J. Roentgenol.
PD OCT
PY 2016
VL 207
IS 4
BP W76
EP W76
DI 10.2214/AJR.16.16563
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA DX7LF
UT WOS:000384568100008
ER
PT J
AU Costa, VD
Kakalios, LC
Averbeck, BB
AF Costa, Vincent D.
Kakalios, Laura C.
Averbeck, Bruno B.
TI Blocking Serotonin but Not Dopamine Reuptake Alters Neural Processing
During Perceptual Decision Making
SO BEHAVIORAL NEUROSCIENCE
LA English
DT Article
DE serotonin; dopamine; impulsivity; perceptual inference; drift diffusion
model
ID CENTRAL 5-HT DEPLETION; PARKINSONS-DISEASE; DELAYED REWARDS;
REACTION-TIME; IMPULSIVITY; NEURONS; PERFORMANCE; ACTIVATION; BEHAVIOR;
RATS
AB Dopamine and serotonin have opponent interactions on aspects of impulsivity. Therefore we wanted to test the hypothesis that dopamine and serotonin would have opposing effects on speed-accuracy trade offs in a perceptual decision making task. Unlike other behavioral measures of impulsivity, perceptual decision making allows us to determine whether decreasing premature responses, often interpreted as decreased impulsivity, corresponds to increased behavioral performance. We administered GBR-12909 (a dopamine transporter blocker), escitalopram (a serotonin transporter blocker), or saline in separate sessions to 3 rhesus macaques. We found that animals had slower reaction times (RTs) on escitalopram than on GBR-12909 or saline. However, they were also least accurate on escitalopram. Animals were faster, although nonsignificantly, on GBR than saline and had equivalent accuracy. Administration of GBR-12909 did cause animals to be faster in error trials than correct trials. Therefore, from the point of view of RTs the animals were less impulsive on escitalopram. However, the decreased accuracy of the monkeys shows that they were not able to make use of their slower response times to make more accurate decisions. Therefore, impulsivity was reduced on escitalopram, but at the expense of a slower information-processing rate in the perceptual inference task.
C1 [Costa, Vincent D.; Kakalios, Laura C.; Averbeck, Bruno B.] NIMH, Neuropsychol Lab, NIH, Bldg 49,Room 1B80,49 Convent Dr,MSC 4415, Bethesda, MD 20892 USA.
RP Averbeck, BB (reprint author), NIMH, Neuropsychol Lab, NIH, Bldg 49,Room 1B80,49 Convent Dr,MSC 4415, Bethesda, MD 20892 USA.
EM bruno.averbeck@nih.gov
OI Costa, Vincent/0000-0002-5412-8945
FU Intramural Research Program of the National Institute of Mental Health
FX This work was supported by the Intramural Research Program of the
National Institute of Mental Health.
NR 37
TC 0
Z9 0
U1 4
U2 4
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0735-7044
EI 1939-0084
J9 BEHAV NEUROSCI
JI Behav. Neurosci.
PD OCT
PY 2016
VL 130
IS 5
BP 461
EP 468
DI 10.1037/bne0000162
PG 8
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA DX6XR
UT WOS:000384529900001
PM 27513807
ER
PT J
AU Castillo, JJ
Garcia-Sanz, R
Hatjiharissi, E
Kyle, RA
Leleu, X
McMaster, M
Merlini, G
Minnema, MC
Morra, E
Owen, RG
Poulain, S
Stone, MJ
Tam, C
Varettoni, M
Dimopoulos, MA
Treon, SP
Kastritis, E
AF Castillo, Jorge J.
Garcia-Sanz, Ramon
Hatjiharissi, Evdoxia
Kyle, Robert A.
Leleu, Xavier
McMaster, Mary
Merlini, Giampaolo
Minnema, Monique C.
Morra, Enrica
Owen, Roger G.
Poulain, Stephanie
Stone, Marvin J.
Tam, Constantine
Varettoni, Marzia
Dimopoulos, Meletios A.
Treon, Steven P.
Kastritis, Efstathios
TI Recommendations for the diagnosis and initial evaluation of patients
with Waldenstrom Macroglobulinaemia: A Task Force from the 8th
International Workshop on Waldenstrom Macroglobulinaemia
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE Waldenstrom macroglobulinaemia; anaemia; neuropathy; hyperviscosity;
Bing-Neel syndrome; amyloidosis
ID CONSENSUS PANEL RECOMMENDATIONS; IGM MONOCLONAL GAMMOPATHY; END RESULTS
DATABASE; BING-NEEL SYNDROME; MYD88 L265P; LYMPHOPLASMACYTIC LYMPHOMA;
CXCR4 MUTATIONS; HYPERVISCOSITY SYNDROME; GENOMIC LANDSCAPE; LIGHT-CHAIN
AB The diagnosis of Waldenstrom macroglobulinaemia (WM) can be challenging given the variety of signs and symptoms patients can present. Furthermore, once the diagnosis of WM is established, the initial evaluation should be thorough as well as appropriately directed. During the 8th International Workshop for WM in London, United Kingdom, a multi-institutional task force was formed to develop consensus recommendations for the diagnosis and initial evaluation of patients with WM. In this document, we present the results of the deliberations that took place to address these issues. We provide recommendations for history-taking and physical examination, laboratory studies, bone marrow aspiration and biopsy analysis and imaging studies. We also provide guidance on the initial evaluation of special situations, such as anaemia, hyperviscosity, neuropathy, Bing-Neel syndrome and amyloidosis. We hope these recommendations serve as a practical guidance to clinicians taking care of patients with a suspected or an established diagnosis of WM.
C1 [Castillo, Jorge J.; Treon, Steven P.] Harvard Med Sch, Dana Farber Canc Inst, Bing Ctr Waldenstrom Macroglobulinemia, 450 Brookline Ave,M221, Boston, MA 02215 USA.
[Garcia-Sanz, Ramon] Hosp Univ Salamanca, Salamanca, Spain.
[Hatjiharissi, Evdoxia] Theagene Hosp Thessaloniki, Dept Haematol, Thessaloniki, Greece.
[Kyle, Robert A.] Mayo Clin, Div Hematol, Rochester, MN USA.
[Leleu, Xavier] CHU Poitiers, La Mil Hosp, Poitiers, France.
[McMaster, Mary] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Merlini, Giampaolo] Univ Pavia, Fdn IRCCS Policlin San Matteo, Amyloidosis Res & Treatment Ctr, Pavia, Italy.
[Minnema, Monique C.] UMC Utrecht Canc Ctr, Dept Haematol, Utrecht, Netherlands.
[Morra, Enrica] Osped Niguarda Ca Granda, Div Haematol, Milan, Italy.
[Owen, Roger G.] Leeds Teaching Hosp NHS Trust, St Jamess Inst Oncol, Leeds, W Yorkshire, England.
[Poulain, Stephanie] Ctr Hosp Valenciennes, Serv Hematol Immunol Cytogenet, Valenciennes, France.
[Stone, Marvin J.] Baylor Charles Sammons Canc Ctr, Dept Oncol, Dallas, TX USA.
[Tam, Constantine] Univ Melbourne, Dept Haematol, Peter MacCallum Canc Ctr, Melbourne, Vic, Australia.
[Varettoni, Marzia] Univ Pavia, Fdn IRCCS Policlin San Matteo, Dept Haematol Oncol, Pavia, Italy.
[Dimopoulos, Meletios A.; Kastritis, Efstathios] Univ Athens, Dept Clin Therapeut, Sch Med, Athens, Greece.
RP Castillo, JJ (reprint author), Harvard Med Sch, Dana Farber Canc Inst, Bing Ctr Waldenstrom Macroglobulinemia, 450 Brookline Ave,M221, Boston, MA 02215 USA.
EM jorgej_castillo@dfci.harvard.edu
RI Garcia-Sanz, Ramon/B-7986-2017;
OI Garcia-Sanz, Ramon/0000-0003-4120-2787; Castillo,
Jorge/0000-0001-9490-7532
FU Abbvie; Gilead; Millennium; Pharmacyclics; Celgene; Janssen; Roche; Onyx
FX JJC received honoraria from Celgene and Pharmacyclics, and research
funding from Abbvie, Gilead, Millennium and Pharmacyclics. RGS received
honoraria from Bristol-Myers Squibb, Janssen and Takeda and. EH received
honoraria from Amgen, Gilead and Janssen. GM received honoraria from
GlaxoSmithKline, Janssen and Millennium-Takeda. RGO received honoraria
from Celgene, Janssen, Pharmacyclics and Roche, and research funding
from Celgene. CT received honoraria and research funding from Janssen
and Roche. MAD received honoraria from Amgen, Celgene, Janssen and
Novartis. SPT received research funding and/or honoraria from Gilead,
Janssen, Onyx and Pharmacyclics. EK received honoraria from Amgen,
Janssen and Takeda and. RAK, XL, MM, MCM, EM, SP, MJS, MV have no
conflict of interest to disclose.
NR 58
TC 2
Z9 2
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1048
EI 1365-2141
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD OCT
PY 2016
VL 175
IS 1
BP 77
EP 86
DI 10.1111/bjh.14196
PG 10
WC Hematology
SC Hematology
GA DY0TE
UT WOS:000384808300011
PM 27378193
ER
PT J
AU Schinasi, LH
Brown, EE
Camp, NJ
Wang, SS
Hofmann, JN
Chiu, BC
Miligi, L
Freeman, LEB
de Sanjose, S
Bernstein, L
Monnereau, A
Clavel, J
Tricot, GJ
Atanackovic, D
Cocco, P
Orsi, L
Dosman, JA
McLaughlin, JR
Purdue, MP
Cozen, W
Spinelli, JJ
de Roos, AJ
AF Schinasi, Leah H.
Brown, Elizabeth E.
Camp, Nicola J.
Wang, Sophia S.
Hofmann, Jonathan N.
Chiu, Brian C.
Miligi, Lucia
Freeman, Laura E. Beane
de Sanjose, Silvia
Bernstein, Leslie
Monnereau, Alain
Clavel, Jacqueline
Tricot, Guido J.
Atanackovic, Djordje
Cocco, Pierluigi
Orsi, Laurent
Dosman, James A.
McLaughlin, John R.
Purdue, Mark P.
Cozen, Wendy
Spinelli, John J.
de Roos, Anneclaire J.
TI Multiple myeloma and family history of lymphohaematopoietic cancers:
Results from the International Multiple Myeloma Consortium
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE multiple myeloma; epidemiology; lympho-haematopoietic malignancies;
family history; lymphoma
ID CHRONIC LYMPHOCYTIC-LEUKEMIA; MONOCLONAL GAMMOPATHY; UNDETERMINED
SIGNIFICANCE; HEMATOLOGIC MALIGNANCIES; 1ST-DEGREE RELATIVES; LYMPHOID
NEOPLASMS; RISK; OCCUPATION; VARIANTS; EXPOSURE
AB Family clusters of multiple myeloma (MM) suggest disease heritability. Nevertheless, patterns of inheritance and the importance of genetic versus environmental risk factors in MM aetiology remain unclear. We pooled data from eleven case-control studies from the International Multiple Myeloma Consortium to characterize the association of MM risk with having a first-degree relative with a history of a lympho-haematapoietic cancer. Unconditional logistic regression models, adjusted for study, sex, age and education level, were used to estimate associations between MM risk and having a first-degree relative with a history of non-Hodgkin lymphoma, Hodgkin lymphoma, leukaemia or MM. Sex, African American race/ethnicity and age were explored as effect modifiers. A total of 2843 cases and 11470 controls were included. MM risk was elevated in association with having a first-degree relative with any lympho-haematapoietic cancer (Odds Ratio (OR)=129, 95% Confidence Interval (CI): 108-155). The association was particularly strong for having a first-degree relative with MM (OR=190, 95% CI: 126-287), especially among men (OR=413, 95% CI: 217-785) and African Americans (OR=552, 95% CI: 187-1627).These results support the hypothesis that genetic inheritance plays a role in MM aetiology. Future studies are warranted to characterize interactions of genetic markers with environmental exposures.
C1 [Schinasi, Leah H.; de Roos, Anneclaire J.] Drexel Univ, Dornsife Sch Publ Hlth, Dept Environm & Occupat Hlth, Philadelphia, PA 19104 USA.
[Brown, Elizabeth E.] Univ Alabama Birmingham, Sch Publ Hlth, Dept Pathol, Birmingham, AL 35294 USA.
[Brown, Elizabeth E.] Univ Alabama Birmingham, Sch Publ Hlth, Ctr Comprehens Canc, Sch Med, Birmingham, AL 35294 USA.
[Camp, Nicola J.; Atanackovic, Djordje] Univ Utah, Sch Med, Div Hematol & Hematol Malignancies, Salt Lake City, UT USA.
[Wang, Sophia S.; Bernstein, Leslie] City Hope Natl Med Ctr, Beckman Res Inst, Dept Populat Sci, Div Canc Etiol, Duarte, CA USA.
[Hofmann, Jonathan N.; Freeman, Laura E. Beane; Purdue, Mark P.] NCI, Occupat & Environm Epidemiol Branch, Div Canc & Genet, Rockville, MD USA.
[Chiu, Brian C.] Univ Chicago, Dept Publ Hlth Sci, Chicago, IL 60637 USA.
[Miligi, Lucia] Inst Study & Prevent Canc, Unit Environm & Occupat Hlth, Florence, Italy.
[de Sanjose, Silvia] Catalan Inst Oncol, Canc Epidemiol Res Programme, Barcelona, Spain.
[Monnereau, Alain; Clavel, Jacqueline; Orsi, Laurent] INSERM, U1153, Epidemiol & Biostat Sorbonne Paris Cite Ctr CRESS, Epidemiol Childhood & Adolescent Canc Team EPICEA, Villejuif, France.
[Monnereau, Alain; Clavel, Jacqueline; Orsi, Laurent] Paris Descartes Univ, UMRS 1153, Epidemiol & Biostat Sorbonne Paris Cite Ctr CRESS, Paris, France.
[Tricot, Guido J.] Univ Iowa, Internal Med, Iowa City, IA USA.
[Cocco, Pierluigi] Univ Cagliari, Dept Publ Hlth Clin & Mol Med, Occupat Hlth Sect, Cagliari, Italy.
[Dosman, James A.] Univ Saskatchewan, Canadian Ctr Hlth & Safety Agr, Saskatoon, SK, Canada.
[McLaughlin, John R.] Publ Hlth Ontario, Toronto, ON, Canada.
[Cozen, Wendy] Univ Southern Calif, USC Keck Sch Med, Dept Prevent Med, Los Angeles, CA USA.
[Cozen, Wendy] Univ Southern Calif, USC Keck Sch Med, Dept Pathol, Los Angeles, CA USA.
[Spinelli, John J.] Univ British Columbia, Sch Populat & Publ Hlth, Canc Control Res, BC Canc Agcy, Vancouver, BC, Canada.
RP Schinasi, LH (reprint author), Drexel Univ, Sch Publ Hlth, Dept Environm & Occupat Hlth, Nesbitt Hall,3215 Market St, Philadelphia, PA 19104 USA.
EM lhs36@drexel.edu
RI Clavel, Jacqueline/Q-2750-2016; Beane Freeman, Laura/C-4468-2015
OI Clavel, Jacqueline/0000-0002-3616-7676; Beane Freeman,
Laura/0000-0003-1294-4124
FU National Institute of Environmental Health Sciences [R21 ES021592];
Intramural Research Program of the NIH; Association pour la Recherche
contre le Cancer; Fondation de France; AFSSET; NCI [U54CA118948,
R21CA155951, R25CA76023, R01CA186646]; NCI (University of Alabama at
Birmingham Comprehensive Cancer Center Support grant) [P30CA13148];
American Cancer Society [IRG60-001-47]
FX This study was supported by the National Institute of Environmental
Health Sciences grant R21 ES021592 (A.J.D.). The Connecticut Study and
the Population Health Study were supported in part by the Intramural
Research Program of the NIH. The ENGELA study (JC) was supported by
grants from the Association pour la Recherche contre le Cancer, the
Fondation de France, AFSSET and a donation from Faberge employees. The
work conducted by E.E. Brown was supported, in part, by grants from the
NCI (U54CA118948, R21CA155951, R25CA76023, R01CA186646, and the
University of Alabama at Birmingham Comprehensive Cancer Center Support
grant P30CA13148) and the American Cancer Society (IRG60-001-47).
NR 47
TC 0
Z9 0
U1 5
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1048
EI 1365-2141
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD OCT
PY 2016
VL 175
IS 1
BP 87
EP 101
DI 10.1111/bjh.14199
PG 15
WC Hematology
SC Hematology
GA DY0TE
UT WOS:000384808300012
PM 27330041
ER
PT J
AU Lewis, MD
Francisco, AF
Taylor, MC
Jayawardhana, S
Kelly, JM
AF Lewis, Michael D.
Francisco, Amanda Fortes
Taylor, Martin C.
Jayawardhana, Shiromani
Kelly, John M.
TI Host and parasite genetics shape a link between Trypanosoma cruzi
infection dynamics and chronic cardiomyopathy
SO CELLULAR MICROBIOLOGY
LA English
DT Article
ID CHRONIC-CHAGAS-CARDIOMYOPATHY; HEART-DISEASE; IMMUNE-SYSTEM;
LOOKING-BACK; INBRED MICE; AUTOIMMUNITY; PATHOGENESIS; MYOCARDITIS;
LESIONS; CLONES
AB Host and parasite diversity are suspected to be key factors in Chagas disease pathogenesis. Experimental investigation of underlying mechanisms is hampered by a lack of tools to detect scarce, pleiotropic infection foci. We developed sensitive imaging models to track Trypanosoma cruzi infection dynamics and quantify tissue-specific parasite loads, with minimal sampling bias. We used this technology to investigate cardiomyopathy caused by highly divergent parasite strains in BALB/c, C3H/HeN and C57BL/6 mice. The gastrointestinal tract was unexpectedly found to be the primary site of chronic infection in all models. Immunosuppression induced expansion of parasite loads in the gut and was followed by widespread dissemination. These data indicate that differential immune control of T. cruzi occurs between tissues and shows that the large intestine and stomach provide permissive niches for active infection. The end-point frequency of heart-specific infections ranged from 0% in TcVI-CLBR-infected C57BL/6 to 88% in TcI-JR-infected C3H/HeN mice. Nevertheless, infection led to fibrotic cardiac pathology in all models. Heart disease severity was associated with the model-dependent frequency of dissemination outside the gut and inferred cumulative heart-specific parasite loads. We propose a model of cardiac pathogenesis driven by periodic trafficking of parasites into the heart, occurring at a frequency determined by host and parasite genetics.
C1 [Lewis, Michael D.; Francisco, Amanda Fortes; Taylor, Martin C.; Jayawardhana, Shiromani; Kelly, John M.] London Sch Hyg & Trop Med, Dept Pathogen Mol Biol, Keppel St, London WC1E 7HT, England.
[Lewis, Michael D.] NIAID, Parasit Dis Lab, Bethesda, MD 20892 USA.
RP Lewis, MD (reprint author), London Sch Hyg & Trop Med, Dept Pathogen Mol Biol, Keppel St, London WC1E 7HT, England.; Lewis, MD (reprint author), NIAID, Parasit Dis Lab, Bethesda, MD 20892 USA.
EM michael.lewis@lshtm.ac.uk
FU Wellcome Trust [084175]; British Heart Foundation [PG/13/88/30556]; Bill
and Melinda Gates Foundation [OPPGH5337]; Drugs for Neglected Diseases
initiative (DNDi); EU Marie Curie Fellowship; NIAID, NIH
FX This work was supported by Wellcome Trust Grant 084175, British Heart
Foundation Grant PG/13/88/30556, Bill and Melinda Gates Foundation Grant
OPPGH5337 and the Drugs for Neglected Diseases initiative (DNDi). MDL is
currently supported by an EU Marie Curie Fellowship and the intramural
research programme of the NIAID, NIH. The authors thank LSHTM Biological
Services Facility staff for technical support, Bruce Branchini for the
PpyRE9h luciferase gene, Hernan Carrasco for the JR parasite stock,
Laura Muller and Monica Campos for experimental assistance, Cheryl
Whitehorn and Louisa Messenger for triatomine samples and Michael Miles
for valuable support, discussions and advice.
NR 61
TC 3
Z9 3
U1 2
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1462-5814
EI 1462-5822
J9 CELL MICROBIOL
JI Cell Microbiol.
PD OCT
PY 2016
VL 18
IS 10
BP 1429
EP 1443
DI 10.1111/cmi.12584
PG 15
WC Cell Biology; Microbiology
SC Cell Biology; Microbiology
GA DW4KS
UT WOS:000383612400009
PM 26918803
ER
PT J
AU Roudnitzky, N
Risso, D
Drayna, D
Behrens, M
Meyerhof, W
Wooding, SP
AF Roudnitzky, Natacha
Risso, Davide
Drayna, Dennis
Behrens, Maik
Meyerhof, Wolfgang
Wooding, Stephen P.
TI Copy Number Variation in TAS2R Bitter Taste Receptor Genes: Structure,
Origin, and Population Genetics
SO CHEMICAL SENSES
LA English
DT Article
DE bitter; evolution; genetic; genomic; natural selection; taste receptor
ID CELL-LINE PANEL; HUMAN GENOME; DEVELOPMENTAL DELAY; POSITIVE SELECTION;
ALLELIC VARIATION; EVOLUTION; SENSITIVITY; HUMANS; DIVERSITY;
VARIABILITY
AB Bitter taste receptor genes (TAS2Rs) harbor extensive diversity, which is broadly distributed across human populations and strongly associated with taste response phenotypes. The majority of TAS2R variation is composed of single-nucleotide polymorphisms. However, 2 closely positioned loci at 12p13, TAS2R43 and -45, harbor high-frequency deletion (Delta) alleles in which genomic segments are absent, resulting in copy number variation (CNV). To resolve their chromosomal structure and organization, we generated maps using long-range contig alignments and local sequencing across the TAS2R43-45 region. These revealed that the deletion alleles (43 Delta and 45 Delta) are 37.8 and 32.2 kb in length, respectively and span the complete coding region of each gene (similar to 1 kb) along with extensive up-and downstream flanking sequence, producing separate CNVs at the 2 loci. Comparisons with a chimpanzee genome, which contained intact homologs of TAS2R43, -45, and nearby TAS2Rs, indicated that the deletions evolved recently, through unequal recombination in a cluster of closely related loci. Population genetic analyses in 946 subjects from 52 worldwide populations revealed that copy number ranged from 0 to 2 at both TAS2R43 and TAS2R45, with 43 Delta and 45 Delta occurring at high global frequencies (0.33 and 0.18). Estimated recombination rates between the loci were low (rho = 2.7 x 10(-4); r = 6.6 x 10(-9)) and linkage disequilibrium was high (D' = 1.0), consistent with their adjacent genomic positioning and recent origin. Geographic variation pointed to an African origin for the deletions. However, no signatures of natural selection were found in population structure or integrated haplotype scores spanning the region, suggesting that patterns of diversity at TAS2R43 and -45 are primarily due to genetic drift.
C1 [Roudnitzky, Natacha; Behrens, Maik; Meyerhof, Wolfgang] German Inst Human Nutr Potsdam Rehbrucke, Dept Mol Genet, Arthur Scheunert Allee 114-116, D-14558 Nuthetal, Germany.
[Risso, Davide; Drayna, Dennis] NIDCD, NIH, Bethesda, MD 20892 USA.
[Wooding, Stephen P.] Univ Calif Merced, Hlth Sci Res Inst, 5200 North Lake Rd, Merced, CA 95343 USA.
RP Wooding, SP (reprint author), Univ Calif Merced, Hlth Sci Res Inst, 5200 North Lake Rd, Merced, CA 95343 USA.
EM swooding@ucmerced.edu
NR 64
TC 0
Z9 0
U1 18
U2 18
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0379-864X
EI 1464-3553
J9 CHEM SENSES
JI Chem. Senses
PD OCT
PY 2016
VL 41
IS 8
BP 3
EP 13
DI 10.1093/chemse/bjw067
PG 11
WC Behavioral Sciences; Food Science & Technology; Neurosciences;
Physiology
SC Behavioral Sciences; Food Science & Technology; Neurosciences &
Neurology; Physiology
GA DX5FZ
UT WOS:000384406500001
PM 27340135
ER
PT J
AU Papadakis, GZ
Millo, C
Sadowski, SM
Bagci, U
Patronas, NJ
AF Papadakis, Georgios Z.
Millo, Corina
Sadowski, Samira M.
Bagci, Ulas
Patronas, Nicholas J.
TI Epididymal Cystadenomas in von Hippel-Lindau Disease Showing Increased
Activity on Ga-68 DOTATATE PET/CT
SO CLINICAL NUCLEAR MEDICINE
LA English
DT Editorial Material
DE von Hippel-Lindau (VHL) disease; Ga-68 DOTATATE PET/CT; epididymal;
cystadenomas; somatostatin receptors imaging
ID CEREBELLAR HEMANGIOBLASTOMA; IMAGING FEATURES
AB von Hippel-Lindau (VHL) disease is a familial cancer syndrome characterized by the development of a variety of malignant and benign tumors, including epididymal cystadenomas. We report a case of a VHL patient with bilateral epididymal cystadenomas who was evaluated with Ga-68 DOTATATE PET/CT, showing intensely increased activity (SUVmax, 21.6) associated with the epididymal cystadenomas, indicating cell-surface overexpression of somatostatin receptors. The presented case supports the usefulness of somatostatin receptor imaging using Ga-68 DOTA-conjugated peptides for detection and follow-up of VHL manifestations, as well as surveillance of asymptomatic gene carriers.
C1 [Papadakis, Georgios Z.; Patronas, Nicholas J.] NCI, Radiol & Imaging Sci, Warren Grant Magnuson Clin Ctr, NIH, Bethesda, MD 20892 USA.
[Millo, Corina] NCI, Div Nucl Med, RADIS, Ctr Clin,NIH, Bethesda, MD 20892 USA.
[Sadowski, Samira M.] NCI, Endocrine Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Sadowski, Samira M.] Univ Hosp Geneva, Endocrine & Thorac Surg, Geneva, Switzerland.
[Bagci, Ulas] Univ Cent Florida, Dept Elect & Comp Sci, Ctr Comp Vis Res, Orlando, FL 32816 USA.
RP Patronas, NJ (reprint author), NIH, Radiol & Imaging Sci, Warren Grant Magnuson Clin Ctr, Bldg 10,Room 1C361X 10,Ctr Dr, Bethesda, MD 20814 USA.
EM NPatronas@cc.nih.gov
FU Intramural NIH HHS [Z99 CL999999]
NR 10
TC 2
Z9 2
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0363-9762
EI 1536-0229
J9 CLIN NUCL MED
JI Clin. Nucl. Med.
PD OCT
PY 2016
VL 41
IS 10
BP 781
EP 782
DI 10.1097/RLU.0000000000001314
PG 2
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA DX5WD
UT WOS:000384452500023
PM 27454594
ER
PT J
AU Papadakis, GZ
Millo, C
Sadowski, SM
Bagci, U
Patronas, NJ
AF Papadakis, Georgios Z.
Millo, Corina
Sadowski, Samira M.
Bagci, Ulas
Patronas, Nicholas J.
TI Endolymphatic Sac Tumor Showing Increased Activity on Ga-68 DOTATATE
PET/CT
SO CLINICAL NUCLEAR MEDICINE
LA English
DT Editorial Material
DE endolymphatic sac tumors; von Hippel-Lindau disease; Ga-68-DOTATATE
PET/CT; somatostatin receptors-imaging
ID HIPPEL-LINDAU-DISEASE
AB Endolymphatic sac tumors (ELSTs) are rare tumors arising from the epithelium of the endolymphatic sac and duct that can be either sporadic or associated with von Hippel-Lindau (VHL) disease. We report a case of a VHL patient with histologically proven residual ELST who underwent Ga-68 DOTATATE PET/CT showing increased activity (SUVmax, 6.29) by the ELST. The presented case of a VHL-associated ELST with increased Ga-68 DOTATATE uptake indicates cell-surface expression of somatostatin receptors by this tumor, suggesting the potential application of somatostatin receptor imaging using Ga-68 DOTA-conjugated peptides in the workup and management of these patients.
C1 [Papadakis, Georgios Z.; Patronas, Nicholas J.] NCI, Radiol & Imaging Sci, Warren Grant Magnuson Clin Ctr, NIH, Bethesda, MD 20892 USA.
[Millo, Corina] NCI, Div Nucl Med, RAD&IS, Ctr Clin,NIH, Bethesda, MD 20892 USA.
[Sadowski, Samira M.] NCI, Endocrine Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Sadowski, Samira M.] Univ Hosp Geneva, Endocrine & Thorac Surg, Geneva, Switzerland.
[Bagci, Ulas] Univ Cent Florida, Dept Elect & Comp Sci, Ctr Comp Vis Res, Orlando, FL 32816 USA.
RP Patronas, NJ (reprint author), NIH, Neuroradiol Sect, Warren Grant Magnuson Clin Ctr, Bldg 10,Room 1C361X 10,Ctr Dr, Bethesda, MD 20814 USA.
EM NPatronas@cc.nih.gov
FU Intramural NIH HHS [Z99 CL999999]
NR 12
TC 2
Z9 2
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0363-9762
EI 1536-0229
J9 CLIN NUCL MED
JI Clin. Nucl. Med.
PD OCT
PY 2016
VL 41
IS 10
BP 783
EP 784
DI 10.1097/RLU.0000000000001315
PG 2
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA DX5WD
UT WOS:000384452500024
PM 27454593
ER
PT J
AU Knickelbein, JE
Abbott, AB
Chew, EY
AF Knickelbein, Jared E.
Abbott, Akshar B.
Chew, Emily Y.
TI Fenofibrate and Diabetic Retinopathy
SO CURRENT DIABETES REPORTS
LA English
DT Review
DE Diabetic retinopathy; Diabetic macular edema; Fenofibrate
ID CONTROL-CARDIOVASCULAR-RISK; RANDOMIZED CONTROLLED-TRIAL; MACULAR EDEMA;
MELLITUS; PREVALENCE; COMPLICATIONS; RANIBIZUMAB; PROGRESSION;
DYSLIPIDEMIA; ASSOCIATION
AB Diabetic retinopathy, a common and sight-threatening microvascular complication of diabetes mellitus, is a leading cause of blindness among working-aged adults. Medical therapies including intensive control of hyperglycemia and hypertension have been shown to reduce the incidence and progression of diabetic retinopathy. The association of dyslipidemia and treatment with statins with diabetic retinopathy is inconsistent in epidemiologic studies. However, two recent randomized clinical trials have demonstrated beneficial effects of systemic fenofibrate therapy in reducing the progression of diabetic retinopathy independently of serum lipid levels. These findings suggest that fenofibrate may be an effective strategy for reducing the progression of diabetic retinopathy, thus reducing the large and growing public health burden of treating the sight-threatening complications of diabetic retinopathy.
C1 [Knickelbein, Jared E.; Abbott, Akshar B.; Chew, Emily Y.] NEI, NIH, 10 Ctr Dr,10-10D45, Bethesda, MD 20892 USA.
[Chew, Emily Y.] NEI, Div Epidemiol & Clin Applicat, Clin Trials Branch, NIH, Bldg 10 Clin Res Ctr,Room3-2531,10 Ctr Dr, Bethesda, MD 20892 USA.
RP Chew, EY (reprint author), NEI, NIH, 10 Ctr Dr,10-10D45, Bethesda, MD 20892 USA.; Chew, EY (reprint author), NEI, Div Epidemiol & Clin Applicat, Clin Trials Branch, NIH, Bldg 10 Clin Res Ctr,Room3-2531,10 Ctr Dr, Bethesda, MD 20892 USA.
EM Knickelbeinje@nei.nih.gov; akshar.abbott@nih.gov; echew@nei.nih.gov
FU Intramural Research Program of the NIH, NEI
FX This research was supported by the Intramural Research Program of the
NIH, NEI.
NR 45
TC 1
Z9 1
U1 2
U2 2
PU CURRENT MEDICINE GROUP
PI PHILADELPHIA
PA 400 MARKET STREET, STE 700, PHILADELPHIA, PA 19106 USA
SN 1534-4827
EI 1539-0829
J9 CURR DIABETES REP
JI Curr. Diabetes Rep.
PD OCT
PY 2016
VL 16
IS 10
AR 90
DI 10.1007/s11892-016-0786-7
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA DX7CG
UT WOS:000384543100002
PM 27525681
ER
PT J
AU Robinson, C
Collins, MT
Boyce, AM
AF Robinson, Cemre
Collins, Michael T.
Boyce, Alison M.
TI Fibrous Dysplasia/McCune-Albright Syndrome: Clinical and Translational
Perspectives
SO CURRENT OSTEOPOROSIS REPORTS
LA English
DT Review
DE Fibrous dysplasia; McCune-Albright syndrome; GNAS gene; G(s)alpha; FGF23
ID MARROW STROMAL CELLS; DENOSUMAB TREATMENT; ACTIVATING MUTATIONS;
INTRAVENOUS PAMIDRONATE; MONOZYGOTIC TWINS; SKELETAL LESIONS;
RANK-LIGAND; STEM-CELLS; G-PROTEIN; BONE
AB Fibrous dysplasia (FD) is an uncommon and debilitating skeletal disorder resulting in fractures, deformity, functional impairment, and pain. It arises from post-zygotic somatic activating mutations in GNAS, in the cAMP-regulating transcript alpha-subunit, G(s)alpha. Constitutive G(s) signaling results in activation of adenylyl cyclase and dysregulated cAMP production. In the skeleton, this leads to the development of FD lesions with abnormal bone matrix, trabeculae, and collagen, produced by undifferentiated mesenchymal cells. FD may occur in isolation or in combination with extraskeletal manifestations, including hyperfunctioning endocrinopathies and cafc-au-lait macules, termed McCune-Albright syndrome (MAS). This review summarizes current clinical and translational perspectives in FD/MAS, with an emphasis on FD pathogenesis, natural history, pre-clinical and clinical investigation, and future directions.
C1 [Robinson, Cemre; Collins, Michael T.; Boyce, Alison M.] Natl Inst Dent & Craniofacial Res, Sect Skeletal Disorders andMineral Homeostasis, Craniofacial & Skeletal Dis Branch, NIH, 30 Convent Dr Room 228 MSC 4320, Bethesda, MD 20892 USA.
[Boyce, Alison M.] Childrens Natl Hlth Syst, Div Endocrinol & Diabet, Washington, DC 20010 USA.
[Boyce, Alison M.] Childrens Natl Hlth Syst, Div Orthopaed & Sports Med, Bone Hlth Program, Washington, DC 20010 USA.
RP Boyce, AM (reprint author), Natl Inst Dent & Craniofacial Res, Sect Skeletal Disorders andMineral Homeostasis, Craniofacial & Skeletal Dis Branch, NIH, 30 Convent Dr Room 228 MSC 4320, Bethesda, MD 20892 USA.; Boyce, AM (reprint author), Childrens Natl Hlth Syst, Div Endocrinol & Diabet, Washington, DC 20010 USA.; Boyce, AM (reprint author), Childrens Natl Hlth Syst, Div Orthopaed & Sports Med, Bone Hlth Program, Washington, DC 20010 USA.
EM boyceam@mail.nih.gov
FU Intramural Research Program of the National Institute of Dental and
Craniofacial Research
FX This research was supported by the Intramural Research Program of the
National Institute of Dental and Craniofacial Research
NR 72
TC 1
Z9 1
U1 3
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1544-2241
J9 CURR OSTEOPOROS REP
JI Curr. Osteoporos. Rep.
PD OCT
PY 2016
VL 14
IS 5
BP 178
EP 186
DI 10.1007/s11914-016-0317-0
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA DX7DH
UT WOS:000384546100003
PM 27492469
ER
PT J
AU Provinciali, N
Suen, C
Dunn, BK
DeCensi, A
AF Provinciali, Nicoletta
Suen, Chen
Dunn, Barbara K.
DeCensi, Andrea
TI Raloxifene hydrochloride for breast cancer risk reduction in
postmenopausal women
SO EXPERT REVIEW OF CLINICAL PHARMACOLOGY
LA English
DT Article
DE Clinical trials; raloxifene; breast cancer risk; cancer prevention;
pharmacology
ID ESTROGEN-RECEPTOR MODULATOR; RANDOMIZED CONTROLLED-TRIAL; SURGICAL
ADJUVANT BREAST; CORONARY-HEART-DISEASE; BONE-MINERAL DENSITY; STAR P-2
TRIAL; PREMENOPAUSAL WOMEN; HORMONE-THERAPY; CLINICAL-TRIAL;
CARDIOVASCULAR EVENTS
AB Introduction: Raloxifene is an estrogen receptor modulator which competes with estrogens for binding to the estrogen receptor. Based on the results of the STAR (Study of Tamoxifen And Raloxifene) trial, raloxifene has been approved by the U.S. Food and Drug Administration for the reduction of breast cancer (BC) risk in postmenopausal women at increased risk.
Areas covered: This analysis reviews the activity of raloxifene and the clinical trials for non-BC indications which led to investigate its use as BC preventive agent. We review the trial establishing its efficacy for BC prevention and the meta-analyses including different SERMs for BC prevention.
Expert commentary: Compared with tamoxifen, raloxifene has shown a slightly lower efficacy in reducing BC risk and a better safety profile. Raloxifene also offers to postmenopausal women a benefit in terms of osteoporosis. Future research should investigate its use in premenopausal women and in association with other preventive agents.
C1 [Provinciali, Nicoletta; DeCensi, Andrea] EO Osped Galliera, Div Med Oncol, Mura Cappuccine 14, I-16128 Genoa, Italy.
[Suen, Chen; Dunn, Barbara K.] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
[DeCensi, Andrea] European Inst Oncol, Div Canc Prevent & Genet, Milan, Italy.
RP Provinciali, N (reprint author), EO Osped Galliera, Div Med Oncol, Mura Cappuccine 14, I-16128 Genoa, Italy.
EM nicoletta.provinciali@galliera.it
NR 67
TC 0
Z9 0
U1 5
U2 5
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1751-2433
EI 1751-2441
J9 EXPERT REV CLIN PHAR
JI Expert Rev. Clin. Pharmacol.
PD OCT
PY 2016
VL 9
IS 10
BP 1263
EP 1272
DI 10.1080/17512433.2016.1231575
PG 10
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA DX8MR
UT WOS:000384643500002
ER
PT J
AU Lynch, JA
Berse, B
Petkov, V
Filipski, K
Zhou, YJ
Khoury, MJ
Hassett, M
Freedman, AN
AF Lynch, Julie A.
Berse, Brygida
Petkov, Valentina
Filipski, Kelly
Zhou, Yingjun
Khoury, Muin J.
Hassett, Michael
Freedman, Andrew N.
TI Implementation of the 21-gene recurrence score test in the United States
in 2011
SO GENETICS IN MEDICINE
LA English
DT Article
DE breast cancer; cancer genomics; dissemination; equity; implementation
ID NEGATIVE BREAST-CANCER; GENE-EXPRESSION; ASSAY; POPULATION; ESTROGEN;
SUBTYPES; RISK; CHEMOTHERAPY; PATTERNS; WOMEN
AB Purpose: We examined hospital use of the 21-gene breast cancer test in the United States. We report state-level differences in utilization and propose a model for predicting implementation of -guideline-recommended genomic testing.
Methods: Genomic Health provided test orders for calendar year 2011. We summarized utilization at the hospital and state levels. Using logistic regression, we analyzed the association between the likelihood to order the test and the hospital's institutional and regional characteristics.
Results: In 2011, 45% of 4,712 acute-care hospitals ordered the test, which suggests that 25% of newly diagnosed invasive female breast cancer cases were tested. Significant predictors of testing included participation in National Cancer Institute (NCI) clinical research cooperative groups (odds ratio (OR) 3.73; 95% confidence interval, 2.96-4.70), advanced imaging (OR, 2.19; CI, 1.78-2.68), high-complexity laboratory (OR, 2.15; CI, 1.24-3.70), affiliation with a medical school (OR, 1.57; CI, 1.31-1.88), and reconstructive surgery (OR, 1.23; CI, 1.01-1.50). Significant regional predictors included metropolitan county (OR, 3.77; CI, 2.83-5.03), above-mean income (OR, 1.37; CI, 1.11-1.69), and education (OR, 1.26; CI, 1.03-1.54). Negative predictors included designation as a critical-access hospital (OR, 0.10; CI, 0.07-0.14) and distance from an NCI cancer center (OR, 0.998; CI, 0.997-0.999), with a 15% decrease in likelihood for every 100 miles.
Conclusion: Despite considerable market penetration of the test, there are significant regional and site-of-care differences in implementation, particularly in rural states.
C1 [Lynch, Julie A.] VA Salt Lake City Hlth Care Syst, Salt Lake City, UT 84148 USA.
[Lynch, Julie A.; Berse, Brygida] RTI Int, Durham, NC 27709 USA.
[Berse, Brygida] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Berse, Brygida] Vet Hlth Adm, Bedford, MA USA.
[Petkov, Valentina; Filipski, Kelly; Zhou, Yingjun; Freedman, Andrew N.] NCI, NIH, Bethesda, MD 20892 USA.
[Khoury, Muin J.] Ctr Dis Control & Prevent, Off Publ Hlth Genom, Atlanta, GA USA.
[Khoury, Muin J.] NCI, Epidemiol & Genom Res Program, NIH, Bethesda, MD 20892 USA.
[Hassett, Michael] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Hassett, Michael] Harvard Med Sch, Boston, MA USA.
RP Lynch, JA (reprint author), VA Salt Lake City Hlth Care Syst, Salt Lake City, UT 84148 USA.; Lynch, JA (reprint author), RTI Int, Durham, NC 27709 USA.
EM Julie.Lynch@va.gov
OI Lynch, Julie/0000-0003-0108-2127
FU National Cancer Institute
FX This research was conducted while J.A.L. was a postdoctoral fellow
within the Center for Healthcare Organization and Implementation
Research (CHOIR), a Veterans Administration Health Services Research &
Development Center of Excellence. She and B.B. are funded by the
National Cancer Institute through an Interagency Agreement. Preliminary
results were previously presented as a poster at the 49th American
Society of Clinical Oncology Annual Meeting, 31 May 20.
NR 34
TC 2
Z9 2
U1 2
U2 2
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 2016
VL 18
IS 10
BP 982
EP 990
DI 10.1038/gim.2015.218
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA DX8CN
UT WOS:000384615800013
PM 26890451
ER
PT J
AU Kelly, NR
Tanofsky-Kraff, M
Vannucci, A
Ranzenhofer, LM
Altschul, AM
Schvey, NA
Shank, LM
Brady, SM
Galescu, O
Kozlosky, M
Yanovski, SZ
Yanovski, JA
AF Kelly, Nichole R.
Tanofsky-Kraff, Marian
Vannucci, Anna
Ranzenhofer, Lisa M.
Altschul, Annie M.
Schvey, Natasha A.
Shank, Lisa M.
Brady, Sheila M.
Galescu, Ovidiu
Kozlosky, Merel
Yanovski, Susan Z.
Yanovski, Jack A.
TI Emotion Dysregulation and Loss-of-Control Eating in Children and
Adolescents
SO HEALTH PSYCHOLOGY
LA English
DT Article
DE emotion regulation; loss-of-control eating; binge eating; body mass; fat
mass
ID HANDLING MISSING DATA; BODY-MASS INDEX; SELF-REGULATION; ADULT OBESITY;
OVERWEIGHT CHILDREN; BEHAVIOR CHECKLIST; PUBERTAL STAGE; MEDIATING ROLE;
ENERGY-INTAKE; HIGH-RISK
AB Objective: To examine the associations among self-reported loss-of-control (LOC) eating, emotion dysregulation, body mass, and objective energy intake among youth. Emotion dysregulation may be 1 individual factor that promotes excess energy intake and increases in body mass among youth with LOC eating. Method: Children and adolescents (N = 230; 8 to 17 years) enrolled in a nonintervention study completed a structured interview to determine the presence or absence of self-reported LOC eating. Children's emotion dysregulation was assessed via parent-report with the Child Behavior Checklist. Youth also completed 2 test meals to capture "binge" and "normal" eating. Body composition was examined using air displacement plethysmography. Results: After controlling for relevant covariates, youth with self-reported LOC eating had higher parent-reported emotion dysregulation than those without LOC. Parent-reported emotion dysregulation was also associated with greater observed energy intake (after accounting for body mass), as well as higher fat mass. Emotion dysregulation also moderated associations between LOC status/gender and body mass variables; among youth with self-reported LOC eating and girls, those with high parent-described emotion dysregulation (vs. low) had significantly higher fat mass and BMIz. Conclusions: Data from the current study suggest that emotion dysregulation may play a role in energy intake and obesity, particularly among youth with self-reported LOC eating and girls. Additional studies are needed to identify the prospective mechanisms linking poor emotion regulation and LOC eating. These mechanisms, in turn, may inform future interventions targeting excess energy intake and obesity in pediatric samples.
C1 [Kelly, Nichole R.; Tanofsky-Kraff, Marian; Vannucci, Anna; Altschul, Annie M.; Schvey, Natasha A.; Shank, Lisa M.; Brady, Sheila M.; Galescu, Ovidiu; Kozlosky, Merel; Yanovski, Susan Z.; Yanovski, Jack A.] NIH, US Dept HHS, Bldg 10, Bethesda, MD 20892 USA.
[Kelly, Nichole R.; Tanofsky-Kraff, Marian; Vannucci, Anna; Schvey, Natasha A.; Shank, Lisa M.] Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA.
[Ranzenhofer, Lisa M.] Brown Univ, Miriam Hosp, Alpert Med Sch, Providence, RI USA.
RP Tanofsky-Kraff, M (reprint author), Uniformed Serv Univ Hlth Sci, Dept Med & Clin Psychol, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
EM marian.tanofsky-kraff@usuhs.edu
OI Shank, Lisa/0000-0002-6922-7946
FU USUHS [R072IC]; Intramural Research Program, NIH from the NICHD
[1ZIAHD000641]; NIMHD; Bench to Bedside Program; Office of Behavioral
and Social Sciences Research (OBSSR) of the NIH; NIMH [5F31MH095348];
Division of Nutrition Research Coordination, NIH
FX USUHS Grant R072IC (to Marian Tanofsky-Kraff). Intramural Research
Program, NIH, Grant 1ZIAHD000641 from the NICHD with supplemental
funding from NIMHD, the Bench to Bedside Program, the Office of
Behavioral and Social Sciences Research (OBSSR) of the NIH (to Jack A.
Yanovski), and NIMH 5F31MH095348 (to Lisa M. Ranzenhofer). Annie M.
Altschul is supported by the Division of Nutrition Research
Coordination, NIH.
NR 59
TC 0
Z9 0
U1 7
U2 7
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0278-6133
EI 1930-7810
J9 HEALTH PSYCHOL
JI Health Psychol.
PD OCT
PY 2016
VL 35
IS 10
BP 1110
EP 1119
DI 10.1037/hea0000389
PG 10
WC Psychology, Clinical; Psychology
SC Psychology
GA DX6XU
UT WOS:000384530200007
PM 27505194
ER
PT J
AU Xu, Y
Li, F
Zalzala, M
Xu, JS
Gonzalez, FJ
Adorini, L
Lee, YK
Yin, LY
Zhang, YQ
AF Xu, Yang
Li, Fei
Zalzala, Munaf
Xu, Jiesi
Gonzalez, Frank J.
Adorini, Luciano
Lee, Yoon-Kwang
Yin, Liya
Zhang, Yanqiao
TI Farnesoid X receptor activation increases reverse cholesterol transport
by modulating bile acid composition and cholesterol absorption in mice
SO HEPATOLOGY
LA English
DT Article
ID NEGATIVE FEEDBACK-REGULATION; FATTY LIVER-DISEASE; E-KNOCKOUT MICE;
NUCLEAR RECEPTOR; LIPID HOMEOSTASIS; IN-VIVO; METABOLISM; PATHWAYS; FXR;
ATHEROSCLEROSIS
AB Activation of farnesoid X receptor (FXR) markedly attenuates development of atherosclerosis in animal models. However, the underlying mechanism is not well elucidated. Here, we show that the FXR agonist, obeticholic acid (OCA), increases fecal cholesterol excretion and macrophage reverse cholesterol transport (RCT) dependent on activation of hepatic FXR. OCA does not increase biliary cholesterol secretion, but inhibits intestinal cholesterol absorption. OCA markedly inhibits hepatic cholesterol 7-alpha hydroxylase (Cyp7a1) and sterol 12 alpha-hydroxylase (Cyp8b1) partly through inducing small heterodimer partner, leading to reduced bile acid pool size and altered bile acid composition, with the alpha/beta-muricholic acid proportion in bile increased by 2.6-fold and taurocholic acid (TCA) level reduced by 71%. Overexpression of Cyp8b1 or concurrent overexpression of Cyp7a1 and Cyp8b1 normalizes TCA level, bile acid composition, and intestinal cholesterol absorption. Conclusion: Activation of FXR inhibits intestinal cholesterol absorption by modulation of bile acid pool size and composition, thus leading to increased RCT. Targeting hepatic FXR and/or bile acids may be useful for boosting RCT and preventing the development of atherosclerosis.
C1 [Xu, Yang; Zalzala, Munaf; Xu, Jiesi; Lee, Yoon-Kwang; Yin, Liya; Zhang, Yanqiao] Northeast Ohio Med Univ, Dept Integrat Med Sci, 4209 St,Route 44,POB 95, Rootstown, OH 44272 USA.
[Li, Fei; Gonzalez, Frank J.] NCI, Lab Metab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Zalzala, Munaf] Univ Baghdad, Coll Pharm, Dept Pharmacol & Toxicol, Baghdad, Iraq.
[Adorini, Luciano] Intercept Pharmaceut, New York, NY USA.
RP Yin, LY; Zhang, YQ (reprint author), Northeast Ohio Med Univ, Dept Integrat Med Sci, 4209 St,Route 44,POB 95, Rootstown, OH 44272 USA.
EM lyin@neomed.edu; yzhang@neomed.edu
FU NIH [R01HL103227, R01DK095895, R01DK102619]
FX This work was supported by NIH grants R01HL103227, R01DK095895, and
R01DK102619 (to Y.Z.).
NR 43
TC 2
Z9 2
U1 13
U2 13
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
IS 4
BP 1072
EP 1085
DI 10.1002/hep.28712
PG 14
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DX7FP
UT WOS:000384552300010
PM 27359351
ER
PT J
AU Bae, HR
Leung, PSC
Tsuneyama, K
Valencia, JC
Hodge, DL
Kim, S
Back, T
Karwan, M
Merchant, AS
Baba, N
Feng, DC
Park, O
Gao, B
Yang, GX
Gershwin, ME
Young, HA
AF Bae, Heekyong R.
Leung, Patrick S. C.
Tsuneyama, Koichi
Valencia, Julio C.
Hodge, Deborah L.
Kim, Seohyun
Back, Tim
Karwan, Megan
Merchant, Anand S.
Baba, Nobuyuki
Feng, Dechun
Park, Ogyi
Gao, Bin
Yang, Guo-Xiang
Gershwin, M. Eric
Young, Howard A.
TI Chronic Expression of Interferon-Gamma Leads to Murine Autoimmune
Cholangitis With a Female Predominance
SO HEPATOLOGY
LA English
DT Article
ID PRIMARY BILIARY-CIRRHOSIS; GENOME-WIDE ASSOCIATION; DIFFERENTIAL
GENE-EXPRESSION; ANTIMITOCHONDRIAL ANTIBODIES; T-CELLS; SUSCEPTIBILITY
LOCI; IMMUNE-RESPONSES; EPITHELIAL-CELLS; ANIMAL-MODELS; RISK-FACTORS
AB In most autoimmune diseases the serologic hallmarks of disease precede clinical pathology by years. Therefore, the use of animal models in defining early disease events becomes critical. We took advantage of a "designer" mouse with dysregulation of interferon gamma (IFN gamma) characterized by prolonged and chronic expression of IFN through deletion of the IFN gamma 3-untranslated region adenylate uridylate-rich element (ARE). The ARE-Del(-/-) mice develop primary biliary cholangitis (PBC) with a female predominance that mimics human PBC that is characterized by up-regulation of total bile acids, spontaneous production of anti-mitochondrial antibodies, and portal duct inflammation. Transfer of CD4 T cells from ARE-Del(-/-) to B6/Rag1(-/-) mice induced moderate portal inflammation and parenchymal inflammation, and RNA sequencing of liver gene expression revealed that up-regulated genes potentially define early stages of cholangitis. Interestingly, up-regulated genes specifically overlap with the gene expression signature of biliary epithelial cells in PBC, implying that IFN gamma may play a pathogenic role in biliary epithelial cells in the initiation stage of PBC. Moreover, differentially expressed genes in female mice have stronger type 1 and type 2 IFN gamma signaling and lymphocyte-mediated immune responses and thus may drive the female bias of the disease. Conclusion: Changes in IFN expression are critical for the pathogenesis of PBC.
C1 [Bae, Heekyong R.; Valencia, Julio C.; Hodge, Deborah L.; Kim, Seohyun; Back, Tim; Young, Howard A.] NCI, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21702 USA.
[Leung, Patrick S. C.; Yang, Guo-Xiang; Gershwin, M. Eric] Univ Calif Davis, Sch Med, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
[Tsuneyama, Koichi] Univ Tokushima, Inst Biomed Sci, Dept Pathol & Lab Med, Grad Sch, Tokushima, Japan.
[Karwan, Megan] NCI, Lab Anim Sci, Frederick, MD 21701 USA.
[Merchant, Anand S.] NCI, CCR Collaborat Bioinformat Core, Bethesda, MD 20892 USA.
[Baba, Nobuyuki] Kagawa Prefectural Cent Hosp, Cent Lab, Takamatsu, Kagawa, Japan.
[Feng, Dechun; Gao, Bin] NIAAA, Lab Liver Dis, Rockville, MD 20852 USA.
[Park, Ogyi] Johns Hopkins Univ, Sch Med, Russell H Morgan Dept Radiol & Radiol Sci, Baltimore, MD USA.
RP Young, HA (reprint author), NCI, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21702 USA.; Gershwin, ME (reprint author), Univ Calif Davis, Sch Med, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
FU National Institutes of Health grant [DK090019]
FX Supported in part by National Institutes of Health grant DK090019 (to
M.E.G.).
NR 44
TC 3
Z9 3
U1 4
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
IS 4
BP 1189
EP 1201
DI 10.1002/hep.28641
PG 13
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DX7FP
UT WOS:000384552300018
PM 27178326
ER
PT J
AU Porat-Shliom, N
Tietgens, AJ
Van Itallie, CM
Vitale-Cross, L
Jarnik, M
Harding, OJ
Anderson, JM
Gutkind, JS
Weigert, R
Arias, IM
AF Porat-Shliom, Natalie
Tietgens, Amber J.
Van Itallie, Christina M.
Vitale-Cross, Lynn
Jarnik, Michal
Harding, Olivia J.
Anderson, James M.
Gutkind, J. Silvio
Weigert, Roberto
Arias, Irwin M.
TI Liver Kinase B1 Regulates Hepatocellular Tight Junction Distribution and
Function In Vivo
SO HEPATOLOGY
LA English
DT Article
ID ACTIVATED PROTEIN-KINASE; HEPATOCYTE POLARIZATION; MITOCHONDRIAL
FISSION; CELL POLARITY; LKB1; AMPK; PERMEABILITY; CINGULIN;
PHOSPHORYLATION; BARRIER
AB Liver kinase B1 (LKB1) and its downstream effector AMP-activated protein kinase (AMPK) play critical roles in polarity establishment by regulating membrane trafficking and energy metabolism. In collagen sandwich-cultured hepatocytes, loss of LKB1 or AMPK impaired apical ABCB11 (Bsep) trafficking and bile canalicular formation. In the present study, we used liver-specific (albumin-Cre) LKB1 knockout mice (LKB1(-/-)) to investigate the role of LKB1 in the maintenance of functional tight junction (TJ) in vivo. Transmission electron microscopy examination revealed that hepatocyte apical membrane with microvilli substantially extended into the basolateral domain of LKB1(-/-) livers. Immunofluorescence studies revealed that loss of LKB1 led to longer and wider canalicular structures correlating with mislocalization of the junctional protein, cingulin. To test junctional function, we used intravital microscopy to quantify the transport kinetics of 6-carboxyfluorescein diacetate (6-CFDA), which is processed in hepatocytes into its fluorescent derivative 6-carboxyfluorescein (6-CF) and secreted into the canaliculi. In LKB1(-/-) mice, 6-CF remained largely in hepatocytes, canalicular secretion was delayed, and 6-CF appeared in the blood. To test whether 6-CF was transported through permeable TJ, we intravenously injected low molecular weight (3 kDa) dextran in combination with 6-CFDA. In wild-type mice, 3 kDa dextran remained in the vasculature, whereas it rapidly appeared in the abnormal bile canaliculi in LKB1(-/-) mice, confirming that junctional disruption resulted in paracellular exchange between the blood stream and the bile canaliculus. Conclusion: LKB1 plays a critical role in regulating the maintenance of TJ and paracellular permeability, which may explain how various drugs, chemicals, and metabolic states that inhibit the LKB1/AMPK pathway result in cholestasis.
C1 [Porat-Shliom, Natalie; Vitale-Cross, Lynn; Harding, Olivia J.; Gutkind, J. Silvio; Weigert, Roberto] Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD USA.
[Porat-Shliom, Natalie; Weigert, Roberto] NCI, Lab Cellular & Mol Biol, NIH, Bethesda, MD 20892 USA.
[Tietgens, Amber J.; Van Itallie, Christina M.; Anderson, James M.] NHLBI, Lab Tight Junct Struct & Funct, Bldg 10, Bethesda, MD 20892 USA.
[Jarnik, Michal; Arias, Irwin M.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, NIH, Bethesda, MD USA.
RP Porat-Shliom, N (reprint author), NCI, Lab Cellular & Mol Biol, Ctr Canc Res, NIH, Bldg 37,Room 2050B, Bethesda, MD 20892 USA.
EM poratshliomn@mail.nih.gov
FU Intramural Research Program of the National Institutes of Health,
National Institute of Dental and Craniofacial Research
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Dental and
Craniofacial Research.
NR 48
TC 3
Z9 3
U1 10
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
IS 4
BP 1317
EP 1329
DI 10.1002/hep.28724
PG 13
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DX7FP
UT WOS:000384552300027
PM 27396550
ER
PT J
AU Mandrekar, P
Bataller, R
Tsukamoto, H
Gao, B
AF Mandrekar, Pranoti
Bataller, Ramon
Tsukamoto, Hidekazu
Gao, Bin
TI Alcoholic Hepatitis: Translational Approaches to Develop Targeted
Therapies
SO HEPATOLOGY
LA English
DT Article
ID INDUCED LIVER-INJURY; TUMOR-NECROSIS-FACTOR; MACROPHAGE ACTIVATION;
BINGE ETHANOL; MICE; DISEASE; INFLAMMATION; STEATOSIS; CELL;
STEATOHEPATITIS
AB Alcoholic liver disease is a leading cause of liver-related mortality worldwide. In contrast to recent advances in therapeutic strategies for patients with viral hepatitis, there is a significant lack of novel therapeutic options for patients with alcoholic liver disease. In particular, there is an urgent need to focus our efforts on effective therapeutic interventions for alcoholic hepatitis (AH), the most severe form of alcoholic liver disease. AH is characterized by an abrupt development of jaundice and complications related to liver insufficiency and portal hypertension in patients with heavy alcohol intake. The mortality of patients with AH is very high (20%-50% at 3 months). Available therapies are not effective in many patients, and targeted approaches are imminently needed. The development of such therapies requires translational studies in human samples and suitable animal models that reproduce the clinical and histological features of AH. In recent years, new animal models that simulate some of the features of human AH have been developed, and translational studies using human samples have identified potential pathogenic factors and histological parameters that predict survival. Conclusion: This review summarizes the unmet needs for translational studies on the pathogenesis of AH, preclinical translational tools, and emerging drug targets to benefit the AH patient.
C1 [Mandrekar, Pranoti] Univ Massachusetts, Sch Med, Dept Med, Worcester, MA USA.
[Bataller, Ramon] Univ N Carolina, Div Gastroenterol & Hepatol, Dept Med, Chapel Hill, NC USA.
[Bataller, Ramon] Univ N Carolina, Div Gastroenterol & Hepatol, Dept Nutr, Chapel Hill, NC USA.
[Tsukamoto, Hidekazu] Univ Southern Calif, Greater Los Angeles Dept Vet Affairs Healthcare S, Southern Calif Res Ctr ALPD & Cirrhosis, Los Angeles, CA USA.
[Tsukamoto, Hidekazu] Univ Southern Calif, Greater Los Angeles Dept Vet Affairs Healthcare S, Dept Pathol, Los Angeles, CA USA.
[Gao, Bin] NIAAA, Lab Liver Dis, NIH, Bethesda, MD USA.
RP Gao, B (reprint author), NIAAA, Lab Liver Dis, NIH, Bethesda, MD USA.; Mandrekar, P (reprint author), Univ Massachusetts, Med Ctr, Gastrointestinal Div, Dept Med, LRB Rm 221 364 Plantat St, Worcester, MA 01605 USA.; Bataller, R (reprint author), Univ North Carlina, Chapel Hill, NC 27599 USA.; Tsukamoto, H (reprint author), Univ South Calif, Los Angeles, CA 90089 USA.
EM Pranoti.Mandrekar@umassmed.edu; ramon_bataller@med.unc.edu;
htsukamo@med.usc.edu; bgao@mail.nih.gov
FU Department of Defense [W81XWH-11-1-0420, W81XWH-13-1-0498]; National
Institute on Alcohol Abuse and Alcoholism [5P50AA011999, 1U01AA018663,
5R24AA012885]; Department of Veterans Affairs Merit Review award
[5I01BX001991]; National Institute on Alcohol Abuse and Alcoholism
Intramural Program; [2AA017986-01]; [1U01AA021908-01]; [1U01AA020821]
FX Supported by RO1 #2AA017986-01 and Department of Defense grants PRMRP
#W81XWH-11-1-0420 and PRMRP#W81XWH-13-1-0498 (to P.M.); grants
1U01AA021908-01 and 1U01AA020821 (to R.B.); National Institute on
Alcohol Abuse and Alcoholism grants 5P50AA011999, 1U01AA018663, and
5R24AA012885 and Department of Veterans Affairs Merit Review award
5I01BX001991 (to H.T.); and the National Institute on Alcohol Abuse and
Alcoholism Intramural Program (to B.G.).
NR 61
TC 6
Z9 6
U1 9
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
IS 4
BP 1343
EP 1355
DI 10.1002/hep.28530
PG 13
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DX7FP
UT WOS:000384552300029
PM 26940353
ER
PT J
AU Tang, DM
Heller, T
Koh, C
AF Tang, Derek M.
Heller, Theo
Koh, Christopher
TI The Many Faces of Positive Hepatitis B Surface Antigen
SO HEPATOLOGY
LA English
DT Letter
C1 [Tang, Derek M.; Koh, Christopher] NIDDK, Digest Dis Branch, NIH, Bethesda, MD 20892 USA.
[Heller, Theo; Koh, Christopher] NIDDK, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
RP Tang, DM (reprint author), NIDDK, Digest Dis Branch, NIH, Bethesda, MD 20892 USA.
FU Intramural NIH HHS [Z99 DK999999]
NR 5
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2016
VL 64
IS 4
BP 1379
EP 1381
DI 10.1002/hep.28503
PG 3
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DX7FP
UT WOS:000384552300043
PM 26890893
ER
PT J
AU Peng, GCY
AF Peng, Grace C. Y.
TI Moving Toward Model Reproducibility and Reusability
SO IEEE TRANSACTIONS ON BIOMEDICAL ENGINEERING
LA English
DT Article
DE Biological system modeling; biomedical computing; biomedical
engineering; computational biology; computational modeling; computer
simulation; reproducibility of results
AB This paper provides a brief history of the U.S. funding initiatives associated with promoting multiscale modeling of the physiome since 2003. An effort led in the United States is the Interagency Modeling and Analysis Group (IMAG) Multiscale Modeling (MSM) Consortium. Though IMAG and the MSM Consortium have generated much interest in developing MSM models of the physiome, challenges associated with model and data sharing in biomedical, biological, and behavioral systems still exist. Since 2013, the IEEE EMBS Technical Committee on Computational Biology and the Physiome (CBaP TC) has supported discussions on promoting model reproducibility through publications. This special issue on model sharing and reproducibility is a realization of the CBaP TC discussions. Though open questions remain on how we can further facilitate model reproducibility, accessibility, and reuse by the worldwide community for different biomedical domain applications, this special issue provides a unique demonstration of both the challenges and opportunities for publishing reproducible computational models.
C1 [Peng, Grace C. Y.] Natl Inst Biomed Imaging & Bioengn, NIH, Bethesda, MD 20892 USA.
RP Peng, GCY (reprint author), Natl Inst Biomed Imaging & Bioengn, NIH, Bethesda, MD 20892 USA.
EM grace.peng@nih.gov
FU Intramural NIH HHS [Z99 EB999999]
NR 8
TC 0
Z9 0
U1 3
U2 3
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA
SN 0018-9294
EI 1558-2531
J9 IEEE T BIO-MED ENG
JI IEEE Trans. Biomed. Eng.
PD OCT
PY 2016
VL 63
IS 10
BP 1997
EP 1998
DI 10.1109/TBME.2016.2603418
PG 2
WC Engineering, Biomedical
SC Engineering
GA DX7LZ
UT WOS:000384570200002
PM 27576241
ER
PT J
AU Chan, JL
Mazilu, D
Miller, JG
Hunt, T
Horvath, KA
Li, M
AF Chan, Joshua L.
Mazilu, Dumitru
Miller, Justin G.
Hunt, Timothy
Horvath, Keith A.
Li, Ming
TI Robotic-assisted real-time MRI-guided TAVR: from system deployment to in
vivo experiment in swine model
SO INTERNATIONAL JOURNAL OF COMPUTER ASSISTED RADIOLOGY AND SURGERY
LA English
DT Article
DE Robotic assistance; MRI; Magnetic resonance; TAVR; Valve replacement;
Cardiac surgery
ID AORTIC-VALVE-REPLACEMENT; IMPLANTATION; STENOSIS; SURGERY; SAFETY;
PROSTHESIS; PLACEMENT
AB Real-time magnetic resonance imaging (rtMRI) guidance provides significant advantages during transcatheter aortic valve replacement (TAVR) as it provides superior real-time visualization and accurate device delivery tracking. However, performing a TAVR within an MRI scanner remains difficult due to a constrained procedural environment. To address these concerns, a magnetic resonance (MR)-compatible robotic system to assist in TAVR deployments was developed. This study evaluates the technical design and interface considerations of an MR-compatible robotic-assisted TAVR system with the purpose of demonstrating that such a system can be developed and executed safely and precisely in a preclinical model.
An MR-compatible robotic surgical assistant system was built for TAVR deployment. This system integrates a 5-degrees of freedom (DoF) robotic arm with a 3-DoF robotic valve delivery module. A user interface system was designed for procedural planning and real-time intraoperative manipulation of the robot. The robotic device was constructed of plastic materials, pneumatic actuators, and fiber-optical encoders.
The mechanical profile and MR compatibility of the robotic system were evaluated. The system-level error based on a phantom model was 1.14 +/- 0.33 mm. A self-expanding prosthesis was successfully deployed in eight Yorkshire swine under rtMRI guidance. Post-deployment imaging and necropsy confirmed placement of the stent within 3 mm of the aortic valve annulus.
These phantom and in vivo studies demonstrate the feasibility and advantages of robotic-assisted TAVR under rtMRI guidance. This robotic system increases the precision of valve deployments, diminishes environmental constraints, and improves the overall success of TAVR.
C1 [Chan, Joshua L.; Mazilu, Dumitru; Miller, Justin G.; Hunt, Timothy; Horvath, Keith A.; Li, Ming] NHLBI, Cardiothorac Surg Res Program, NIH, Bldg 10,Room B1D47,MSC 1550,10 Ctr Dr, Bethesda, MD 20892 USA.
RP Li, M (reprint author), NHLBI, Cardiothorac Surg Res Program, NIH, Bldg 10,Room B1D47,MSC 1550,10 Ctr Dr, Bethesda, MD 20892 USA.
EM Joshua.Chan@nih.gov; horvathka@nhlbi.nih.gov; lim2@mail.nih.gov
OI Chan, Joshua/0000-0001-7220-561X
FU Intramural Research Program of the National Heart, Lung, and Blood
Institute (NHLBI), National Institutes of Health (NIH), US Department of
Health and Human Services (DHHS)
FX This research was made possible by funding from the Intramural Research
Program of the National Heart, Lung, and Blood Institute (NHLBI),
National Institutes of Health (NIH), US Department of Health and Human
Services (DHHS)
NR 39
TC 0
Z9 0
U1 2
U2 2
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1861-6410
EI 1861-6429
J9 INT J COMPUT ASS RAD
JI Int. J. Comput. Assist. Radiol. Surg.
PD OCT
PY 2016
VL 11
IS 10
BP 1905
EP 1918
DI 10.1007/s11548-016-1421-4
PG 14
WC Engineering, Biomedical; Radiology, Nuclear Medicine & Medical Imaging;
Surgery
SC Engineering; Radiology, Nuclear Medicine & Medical Imaging; Surgery
GA DX7EP
UT WOS:000384549700012
PM 27246950
ER
PT J
AU Lansford, JE
Godwin, J
Alampay, LP
Tirado, LMU
Zelli, A
Al-Hassan, SM
Bacchini, D
Bombi, AS
Bornstein, MH
Chang, L
Deater-Deckard, K
Di Giunta, L
Dodge, KA
Malone, PS
Oburu, P
Pastorelli, C
Skinner, AT
Sorbring, E
Tapanya, S
AF Lansford, Jennifer E.
Godwin, Jennifer
Pena Alampay, Liane
Uribe Tirado, Liliana Maria
Zelli, Arnaldo
Al-Hassan, Suha M.
Bacchini, Dario
Bombi, Anna Silvia
Bornstein, Marc H.
Chang, Lei
Deater-Deckard, Kirby
Di Giunta, Laura
Dodge, Kenneth A.
Malone, Patrick S.
Oburu, Paul
Pastorelli, Concetta
Skinner, Ann T.
Sorbring, Emma
Tapanya, Sombat
TI Mothers', fathers' and children's perceptions of parents' expectations
about children's family obligations in nine countries
SO INTERNATIONAL JOURNAL OF PSYCHOLOGY
LA English
DT Article
DE Culture; Family obligations; Parent-child relationships; Parental
attitudes
ID EUROPEAN BACKGROUNDS; CULTURAL-VALUES; LATIN-AMERICAN; ADOLESCENTS;
IMMIGRANT; ATTITUDES; PARENTIFICATION; ACCULTURATION; ADAPTATION;
STUDENTS
AB Children's family obligations involve assistance and respect that children are expected to provide to immediate and extended family members and reflect beliefs related to family life that may differ across cultural groups. Mothers, fathers and children (N = 1432 families) in 13 cultural groups in 9 countries (China, Colombia, Italy, Jordan, Kenya, Philippines, Sweden, Thailand and United States) reported on their expectations regarding children's family obligations and parenting attitudes and behaviours. Within families, mothers and fathers had more concordant expectations regarding children's family obligations than did parents and children. Parenting behaviours that were warmer, less neglectful and more controlling as well as parenting attitudes that were more authoritarian were related to higher expectations regarding children's family obligations between families within cultures as well as between cultures. These international findings advance understanding of children's family obligations by contextualising them both within families and across a number of diverse cultural groups in 9 countries.
C1 [Lansford, Jennifer E.; Godwin, Jennifer; Dodge, Kenneth A.; Malone, Patrick S.; Skinner, Ann T.] Duke Univ, Ctr Child & Family Policy, Box 90545, Durham, NC 27708 USA.
[Pena Alampay, Liane] Ateneo Manila Univ, Dept Psychol, Quezon City, Philippines.
[Uribe Tirado, Liliana Maria] Univ San Buenaventura, Consultorio Psicol Popular, Medellin, Colombia.
[Zelli, Arnaldo] Univ Rome Foro Italico, Dept Educ Sci, Rome, Italy.
[Al-Hassan, Suha M.] Hashemite Univ, Queen Rania Fac Childhood, Zarqa, Jordan.
[Al-Hassan, Suha M.] Emirates Coll Adv Educ, Hlth & Special Educ Div, Abu Dhabi, U Arab Emirates.
[Bacchini, Dario] Univ Naples 2, Dept Psychol, Caserta, Italy.
[Bombi, Anna Silvia; Di Giunta, Laura; Pastorelli, Concetta] Univ Roma La Sapienza, Fac Psychol, Rome, Italy.
[Bornstein, Marc H.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Child & Family Res Program Dev Neurosci, Bethesda, MD USA.
[Chang, Lei] Hong Kong Inst Educ, Dept Psychol Studies, Hong Kong, Hong Kong, Peoples R China.
[Deater-Deckard, Kirby] Virginia Polytech Inst & State Univ, Dept Psychol, Blacksburg, VA 24061 USA.
[Oburu, Paul] Maseno Univ, Dept Educ Psychol, Maseno, Kenya.
[Sorbring, Emma] Univ West, Dept Psychol, Trollhattan, Sweden.
[Tapanya, Sombat] Chiang Mai Univ, Dept Psychiat, Chiang Mai, Thailand.
RP Lansford, JE (reprint author), Duke Univ, Ctr Child & Family Policy, Box 90545, Durham, NC 27708 USA.
EM lansford@duke.edu
OI ZELLI, Arnaldo/0000-0003-4020-8159
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development [RO1-HD054805]; Fogarty International Center [RO3-TW008141];
Intramural Research Program of the NIH/NICHD
FX This research has been funded by the Eunice Kennedy Shriver National
Institute of Child Health and Human Development grant RO1-HD054805 and
Fogarty International Center grant RO3-TW008141. This research was also
supported by the Intramural Research Program of the NIH/NICHD. The
content is solely the responsibility of the authors and does not
necessarily represent the official views of the NIH or NICHD. Lansford
designed the study and drafted the Introduction and Discussion sections
of this article. Godwin conducted the statistical analyses and drafted
the Methods and Results sections. All other authors contributed to the
overall study design and data collection, provided critical feedback on
the manuscript and approved the final submitted version.
NR 25
TC 1
Z9 1
U1 5
U2 5
PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND
SN 0020-7594
EI 1464-066X
J9 INT J PSYCHOL
JI Int. J. Psychol.
PD OCT
PY 2016
VL 51
IS 5
BP 366
EP 374
DI 10.1002/ijop.12185
PG 9
WC Psychology, Multidisciplinary
SC Psychology
GA DW4NV
UT WOS:000383620900006
PM 26104262
ER
PT J
AU O'Brien, F
Gormley, M
AF O'Brien, Fearghal
Gormley, Michael
TI Risk-perception and dangerous driving among adolescents: Outcome- and
behavior-focused questions yield opposite results
SO JOURNAL OF ADOLESCENCE
LA English
DT Article
DE Dangerous driving; Adolescence; Risk taking; Risk perception; Question
focus
ID YOUNG-ADULTS; SMOKING; AGE
AB While some studies have found that those who perceive a behavior to be more risky are less likely to engage in it, others have found that those who engage in more risky behaviors see themselves as being more at-risk. Using an online questionnaire we investigated whether such conflicting findings may be due to the types of risk-questions employed in past studies. We assessed risk-perception using outcome-focused questions (e.g. the likelihood of being in an accident) and a behavior-focused question (the riskiness of speeding). Participants who reported engaging in more risky driving gave higher estimates of their chances of experiencing a negative outcome. However, those same participants gave lower estimates of the general riskiness of risky driving. Drivers may think about the risks of risky driving in different ways depending on the focus of the questions. Published by Elsevier Ltd on behalf of The Foundation for Professionals in Services for Adolescents.
C1 [O'Brien, Fearghal] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, NIH, 6100 Execut Blvd, Bethesda, MD 20892 USA.
[Gormley, Michael] Trinity Coll Dublin, Sch Psychol, Dublin 2, Ireland.
RP O'Brien, F (reprint author), NICHHD, Div Intramural Populat Hlth Res, 6100 Execut Blvd,Room 7B13L, Bethesda, MD 20892 USA.
EM obrienfk@tcd.ie
FU School of Psychology, Trinity College, Dublin; Intramural Research
Program of the Eunice Kennedy Shriver National Institute of Child Health
and Human Development
FX This research was supported by the School of Psychology, Trinity
College, Dublin and by the Intramural Research Program of the Eunice
Kennedy Shriver National Institute of Child Health and Human
Development.
NR 21
TC 0
Z9 0
U1 6
U2 6
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0140-1971
EI 1095-9254
J9 J ADOLESCENCE
JI J. Adolesc.
PD OCT
PY 2016
VL 52
BP 89
EP 94
DI 10.1016/j.adolescence.2016.07.010
PG 6
WC Psychology, Developmental
SC Psychology
GA DY0IO
UT WOS:000384780700010
PM 27518903
ER
PT J
AU Yeboah, J
Rodriguez, CJ
Qureshi, W
Liu, ST
Carr, JJ
Lima, JA
Hundley, WG
Herrington, DM
AF Yeboah, Joseph
Rodriguez, Carlos J.
Qureshi, Waqas
Liu, Songtao
Carr, J. Jeffrey
Lima, Joao A.
Hundley, W. Gregory
Herrington, David M.
TI Prognosis of Low Normal Left Ventricular Ejection Fraction in an
Asymptomatic Population-Based Adult Cohort: The Multiethnic Study of
Atherosclerosis
SO JOURNAL OF CARDIAC FAILURE
LA English
DT Article
DE Low normal left ventricular ejection fraction; congestive heart failure;
death; prognosis; prevalence
ID HEART-FAILURE; MYOCARDIAL-INFARCTION; SYSTOLIC DYSFUNCTION;
ETHNIC-MINORITIES; MANAGEMENT; TRIAL
AB Background: Reduced left ventricular systolic function predicts worse outcomes. However, the optimal threshold for "normal" left ventricular ejection fraction (LVEF) is uncertain. In general, LVEF >= 55% is considered to be "normal" by guidelines, with a low normal designation for LVEF being 50%-55%. We assessed the prognosis of participants with low normal LVEF in the Multiethnic Study of Atherosclerosis. All participants were asymptomatic and had no known clinical cardiovascular disease at baseline.
Methods and Results: A total of 4926 out of 6814 had LVEF assessed with the use of cardiac magnetic resonance imaging (MRI), had no significant valvular disease, did not have myocardial infarction during follow-up, had complete data, and were included in this analysis. A total of 83/4926 (1.7%) had LVEF <50% (low LVEF) and 101/4926 (2.1%) had low normal LVEF. Cox proportional hazard and cubic spline analyses were used to evaluate the association between LVEF category and 10 years of adjudicated incident congestive heart failure (CHF) and all-cause mortality adjusting for (model 1) age, sex, and race and (model 2) model 1 and diabetes mellitus, smoking, systolic blood pressure (BP), BP medications, body mass index, estimated glomerular filtration rate, low-density lipoprotein, family history of coronary heart disease, educational status, and LV mass. Mean age was 61 +/- 10 years, 47% were men, 35% were on BP medications, 9% had diabetes. After 10.2 years of follow-up, 109 (2.2%) had CHF and 427 (8.7%) died. Compared with normal LVEF (>= 55%), low normal LVEF and low LVEF were associated with an increased risk for incident CHF during follow-up in our multivariable Cox models: hazard ratios (HRs) 3.64 (95% CI 1.76-7.52) and 9.52 (5.63-17.52), respectively. Unlike low LVEF, low normal LVEF was not associated with increased risk of death compared with normal LVEF in our fully adjusted models: HRs 3.03 (1.94-1.73) and 1.32 (0.72-2.41), respectively. In the adjusted spline analysis HR of LVEF 55% as reference, LVEF had a U-shape association of future CHF risk and LVEF.
Conclusion: Low normal LVEF is as prevalent as low LVEF in asymptomatic community-dwelling adults. We observed a gradient-response association between the 3 categories of LVEF (low, low normal, and normal) and incident CHF but not for all-cause death.
C1 [Yeboah, Joseph; Rodriguez, Carlos J.; Qureshi, Waqas; Hundley, W. Gregory; Herrington, David M.] Wake Forest Univ, Sch Med, Heart & Vasc Ctr Excellence, Winston Salem, NC 27109 USA.
[Yeboah, Joseph; Rodriguez, Carlos J.] Wake Forest Sch Med, Epidemiol & Prevent, Winston Salem, NC USA.
[Liu, Songtao] NIH, Bldg 10, Bethesda, MD 20892 USA.
[Carr, J. Jeffrey] Vanderbilt Univ, Sch Med, Cardiol & Radiol, Nashville, TN 37212 USA.
[Lima, Joao A.] Johns Hopkins Univ, Cardiol & Radiol, Baltimore, MD USA.
RP Yeboah, J (reprint author), Wake Forest Sch Med, Heart & Vasc Ctr Excellence, Med Ctr Blvd, Winston Salem, NC 27157 USA.
EM jyeboah@wakehealth.edu
OI Carr, John/0000-0002-4398-8237
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, N01-HC-95169]; National Center
for Research Resources [UL1-TR-000040, UL1-RR-025005]
FX This research was supported by contracts 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 and N01-HC-95169 from the
National Heart, Lung, and Blood Institute and by grants UL1-TR-000040
and UL1-RR-025005 from National Center for Research Resources.
NR 18
TC 2
Z9 2
U1 0
U2 0
PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS
PI PHILADELPHIA
PA CURTIS CENTER, INDEPENDENCE SQUARE WEST, PHILADELPHIA, PA 19106-3399 USA
SN 1071-9164
EI 1532-8414
J9 J CARD FAIL
JI J. Card. Fail.
PD OCT
PY 2016
VL 22
IS 10
BP 763
EP 768
DI 10.1016/j.cardfail.2016.03.013
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA DY0JG
UT WOS:000384782500004
PM 27038640
ER
PT J
AU Lexmond, WS
Goettel, JA
Lyons, JJ
Jacobse, J
Deken, MM
Lawrence, MG
DiMaggio, TH
Kotlarz, D
Garabedian, E
Sackstein, P
Nelson, CC
Jones, N
Stone, KD
Candotti, F
Rings, EHHM
Thrasher, AJ
Milner, JD
Snapper, SB
Fiebiger, E
AF Lexmond, Willem S.
Goettel, Jeremy A.
Lyons, Jonathan J.
Jacobse, Justin
Deken, Marion M.
Lawrence, Monica G.
DiMaggio, Thomas H.
Kotlarz, Daniel
Garabedian, Elizabeth
Sackstein, Paul
Nelson, Celeste C.
Jones, Nina
Stone, Kelly D.
Candotti, Fabio
Rings, Edmond H. H. M.
Thrasher, Adrian J.
Milner, Joshua D.
Snapper, Scott B.
Fiebiger, Edda
TI FOXP3(+) Tregs require WASP to restrain Th2-mediated food allergy
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID WISKOTT-ALDRICH-SYNDROME; REGULATORY T-CELLS; SYNDROME PROTEIN WASP;
MAST-CELLS; IN-VIVO; ANTIGEN RECEPTOR; TYPE-2 IMMUNITY; NATIONAL-HEALTH;
IGE LEVELS; MICE
AB In addition to the infectious consequences of immunodeficiency, patients with Wiskott-Aldrich syndrome (WAS) often suffer from poorly understood exaggerated immune responses that result in autoimmunity and elevated levels of serum IgE. Here, we have shown that WAS patients and mice deficient in WAS protein (WASP) frequently develop IgE-mediated reactions to common food allergens. WASP-deficient animals displayed an adjuvant-free IgE-sensitization to chow antigens that was most pronounced for wheat and soy and occurred under specific pathogen-free as well as germ-free housing conditions. Conditional deletion of Was in FOXP3(+) Tregs resulted in more severe Th2-type intestinal inflammation than that observed in mice with global WASP deficiency, indicating that allergic responses to food allergens are dependent upon loss of WASP expression in this immune compartment. While WASP-deficient Tregs efficiently contained Th1- and Th17-type effector differentiation in vivo, they failed to restrain Th2 effector responses that drive allergic intestinal inflammation. Loss of WASP was phenotypically associated with increased GATA3 expression in effector memory FOXP3(+) Tregs, but not in naive like FOXP3(+) Tregs, an effect that occurred independently of increased IL-4 signaling. Our results reveal a Treg-specific role for WASP that is required for prevention of Th2 effector cell differentiation and allergic sensitization to dietary antigens.
C1 [Lexmond, Willem S.; Goettel, Jeremy A.; Jacobse, Justin; Deken, Marion M.; Kotlarz, Daniel; Snapper, Scott B.; Fiebiger, Edda] Boston Childrens Hosp, Div Gastroenterol Hepatol & Nutr, Dept Pediat, Boston, MA USA.
[Lexmond, Willem S.; Goettel, Jeremy A.; Snapper, Scott B.; Fiebiger, Edda] Harvard Med Sch, Dept Med, Boston, MA USA.
[Lyons, Jonathan J.; DiMaggio, Thomas H.; Sackstein, Paul; Nelson, Celeste C.; Milner, Joshua D.] NIAID, Genet & Pathogenesis Allergy Sect, Lab Allerg Dis, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Lawrence, Monica G.] Univ Virginia Hlth Syst, Dept Med, Div Asthma Allergy & Immunol, Charlottesville, VA USA.
[Kotlarz, Daniel] Univ Munich, Dr von Hauner Childrens Hosp, Dept Pediat, Munich, Germany.
[Garabedian, Elizabeth] NHGRI, NIH, Bethesda, MD 20892 USA.
[Jones, Nina] NCI, Clin Res Directorate, CMRP, Leidos Biomed Res Inc, Campus & Frederick, Frederick, MD 21701 USA.
[Stone, Kelly D.] NIAID, Lab Allerg Dis, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Candotti, Fabio] NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
[Rings, Edmond H. H. M.] Erasmus Univ, Erasmus Med Ctr, Dept Pediat, Rotterdam, Netherlands.
[Rings, Edmond H. H. M.] Leiden Univ, Univ Med Ctr Leiden, Leiden, Netherlands.
[Thrasher, Adrian J.] Great Ormond St Hosp NHS Trust, London, England.
[Thrasher, Adrian J.] UCL, Inst Child Hlth, London, England.
[Snapper, Scott B.] Brigham & Womens Hosp, Dept Med, Div Gastroenterol, 75 Francis St, Boston, MA 02115 USA.
RP Snapper, SB (reprint author), 300 Longwood Ave,EN670, Boston, MA 02115 USA.; Fiebiger, E (reprint author), 300 Longwood Ave,EN626, Boston, MA 02115 USA.
EM scott.snapper@childrens.harvard.edu; edda.fiebiger@childrens.harvard.edu
OI Jacobse, Justin/0000-0002-1899-0319
FU National Institutes of Health [HL59561, DK034854, AI50950, AI075037];
Crohn's and Colitis Foundation of America [CDA 352644]; Harvard
Digestive Diseases Center [P30DK034854]; Helmsley Charitable Trust;
Wolpow Family Chair in IBD Treatment and Research; Wellcome Trust;
Division of Intramural Research of the NIAID; National Cancer Institute,
National Institutes of Health [HHSN261200800001E]; Intramural Research
Program of the NIH, National Cancer Institute, Center for Cancer
Research; NHGRI, NIH
FX We thank Oliver T. Burton and all members of the Fiebiger laboratory and
Snapper laboratory for discussion and technical assistance, and Stefano
Volpi and Luigi Notarangelo at Boston Children's Hospital for providing
serum samples. The patient cohort study benefitted from technical
assistance and supply of equipment and reagents by Lisa Workman and
Thomas A. E. Platts-Mills. This work was supported by grants from the
National Institutes of Health: HL59561, DK034854, and AI50950 (to SBS),
and AI075037 (to EF). This work was further supported by a senior
research grant of the Crohn's and Colitis Foundation of America (to EF),
an unrestricted gift from the Mead Johnson Nutrition Company (to WSL and
EF), the Crohn's and Colitis Foundation of America CDA 352644 (to JAG),
and the Harvard Digestive Diseases Center grant P30DK034854. Additional
support was provided by the Helmsley Charitable Trust and the Wolpow
Family Chair in IBD Treatment and Research (to SBS), and the Wellcome
Trust (to AJT). Funding for clinical patient studies was provided in
part by the Division of Intramural Research of the NIAID and NHGRI, NIH.
This project has been funded in whole or in part with federal funds from
the National Cancer Institute, National Institutes of Health, under
Contract Number 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.
This research was supported in part by the Intramural Research Program
of the NIH, National Cancer Institute, Center for Cancer Research.
NR 63
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Z9 3
U1 3
U2 3
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD OCT
PY 2016
VL 126
IS 10
BP 4030
EP 4044
DI 10.1172/JCI85129
PG 15
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA DX9HD
UT WOS:000384703300037
PM 27643438
ER
PT J
AU Krieter, P
Chiang, N
Gyaw, S
Skolnick, P
Crystal, R
Keegan, F
Aker, J
Beck, M
Harris, J
AF Krieter, Philip
Chiang, Nora
Gyaw, Shwe
Skolnick, Phil
Crystal, Roger
Keegan, Fintan
Aker, Julie
Beck, Melissa
Harris, Jennifer
TI Pharmacokinetic Properties and Human Use Characteristics of an
FDA-Approved Intranasal Naloxone Product for the Treatment of Opioid
Overdose
SO JOURNAL OF CLINICAL PHARMACOLOGY
LA English
DT Article
DE intranasal; naloxone; opioid overdose; pharmacokinetics; Narcan (R)
Nasal Spray
ID INTRAMUSCULAR NALOXONE; HEALTHY-VOLUNTEERS; SEX-DIFFERENCES;
UNITED-STATES; NASAL; DRUG; HYDROCHLORIDE; EDUCATION; METHADONE;
PITFALLS
AB Parenteral naloxone has been approved to treat opiate overdose for over 4 decades. Intranasal naloxone, administered off label using improvised devices, has been widely used by both first responders and the lay public to treat overdose. However, these improvised devices require training for effective use, and the recommended volumes (2 to 4 mL) exceed those considered optimum for intranasal administration. The present study compared the pharmacokinetic properties of intranasal naloxone (2 to 8 mg) delivered in low volumes (0.1 to 0.2 mL) using an Aptar Unit-Dose device to an approved (0.4 mg) intramuscular dose. A parallel study assessed the ease of use of this device in a simulated overdose situation. All doses of intranasal naloxone resulted in plasma concentrations and areas under the curve greater than those observed following the intramuscular dose; the time to reach maximum plasma concentrations was not different following intranasal and intramuscular administration. Plasma concentrations of naloxone were dose proportional between 2 and 8 mg and independent of whether drug was administered to 1 or both nostrils. In a study using individuals representative of the general population, >90% were able to perform both critical tasks (inserting nozzle into a nostril and pressing plunger) needed to deliver a simulated dose of naloxone without prior training. Based on both pharmacokinetic and human use studies, a 4-mg dose delivered in a single device (0.1 mL) was selected as the final product. This product can be used by first responders and the lay public, providing an important and potentially life-saving intervention for victims of an opioid overdose.
C1 [Krieter, Philip; Chiang, Nora; Gyaw, Shwe; Skolnick, Phil] NIDA, NIH, Bethesda, MD 20892 USA.
[Crystal, Roger] Lightlake Therapeut, New York, NY USA.
[Keegan, Fintan] Adapt Pharma Ltd, Dublin, Ireland.
[Aker, Julie; Beck, Melissa; Harris, Jennifer] Concentr Res, Indianapolis, IN USA.
RP Skolnick, P (reprint author), NIDA, 6001 Execut Blvd, Bethesda, MD 20892 USA.
EM phil.skolnick@nih.gov
FU Lightlake Therapeutics; Adapt Pharma; NIDA [N01DA-12-8905,
N01DA-13-8920, N01DA-14-8914]
FX R.C. is an employee of Lightlake Therapeutics. F.K. is an employee of
Adapt Pharma, Ltd. J.A., M.B., and J.H. are employees of Concentrics
Research. P.K., N.C., S.G., and P.S. are employees of the National
Institutes of Health. The work was supported in part by Lightlake
Therapeutics, Adapt Pharma, and NIDA contracts N01DA-12-8905,
N01DA-13-8920, and N01DA-14-8914.
NR 33
TC 1
Z9 1
U1 7
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0091-2700
EI 1552-4604
J9 J CLIN PHARMACOL
JI J. Clin. Pharmacol.
PD OCT
PY 2016
VL 56
IS 10
BP 1243
EP 1253
DI 10.1002/jcph.759
PG 11
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA DX7DD
UT WOS:000384545600008
PM 27145977
ER
PT J
AU Pabayo, R
Dunn, EC
Gilman, SE
Kawachi, I
Molnar, BE
AF Pabayo, Roman
Dunn, Erin C.
Gilman, Stephen E.
Kawachi, Ichiro
Molnar, Beth E.
TI Income inequality within urban settings and depressive symptoms among
adolescents
SO JOURNAL OF EPIDEMIOLOGY AND COMMUNITY HEALTH
LA English
DT Article
DE SOCIAL EPIDEMIOLOGY; SOCIAL INEQUALITIES; DEPRESSION
ID RISK BEHAVIOR SURVEILLANCE; UNITED-STATES; MENTAL-HEALTH; NEIGHBORHOOD
CHARACTERISTICS; SOCIOECONOMIC-STATUS; MULTILEVEL ANALYSIS;
GENDER-DIFFERENCES; LEVEL; DISORDER; VIOLENCE
AB Background Although recent evidence has shown that area-level income inequality is related to increased risk for depression among adults, few studies have tested this association among adolescents.
Methods We analysed the cross-sectional data from a sample of 1878 adolescents living in 38 neighbourhoods participating in the 2008 Boston Youth Survey. Using multilevel linear regression modelling, we: (1) estimated the association between neighbourhood income inequality and depressive symptoms, (2) tested for cross-level interactions between sex and neighbourhood income inequality and (3) examined neighbourhood social cohesion as a mediator of the relationship between income inequality and depressive symptoms.
Results The association between neighbourhood income inequality and depressive symptoms varied significantly by sex, with girls in higher income inequality neighbourhood reporting higher depressive symptom scores, but not boys. Among girls, a unit increase in Gini Z-score was associated with more depressive symptoms (=0.38, 95% CI 0.28 to 0.47, p=0.01) adjusting for nativity, neighbourhood income, social cohesion, crime and social disorder. There was no evidence that the association between income inequality and depressive symptoms was due to neighbourhood-level differences in social cohesion.
Conclusions The distribution of incomes within an urban area adversely affects adolescent girls' mental health; future work is needed to understand why, as well as to examine in greater depth the potential consequences of inequality for males, which may have been difficult to detect here.
C1 [Pabayo, Roman] Univ Nevada, Sch Community Hlth Sci, 1664 North Virginia St, Reno, NV 89557 USA.
[Pabayo, Roman; Gilman, Stephen E.; Kawachi, Ichiro] Harvard TH Chan Sch Publ Hlth, Dept Social & Behav Sci, Boston, MA USA.
[Dunn, Erin C.] Massachusetts Gen Hosp, Psychiat & Neurodev Genet Unit, Boston, MA 02114 USA.
[Dunn, Erin C.] Harvard Med Sch, Dept Psychiat, Boston, MA USA.
[Dunn, Erin C.] Broad Inst Harvard & MIT, Stanley Ctr Psychiat Res, Boston, MA USA.
[Gilman, Stephen E.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Hlth Behav Branch, Div Intramural Populat Hlth Res, Rockville, MD USA.
[Molnar, Beth E.] Northeastern Univ, Bouve Coll Hlth Sci, Boston, MA 02115 USA.
RP Pabayo, R (reprint author), Univ Nevada, Sch Community Hlth Sci, 1664 North Virginia St, Reno, NV 89557 USA.
EM rpabayo@unr.edu
OI Gilman, Stephen/0000-0002-8331-6419
FU Centers for Disease Control and Prevention (CDC); National Center for
Injury Prevention and Control (NCIPC) [U49CE00740]; Canadian Institutes
of Health Research [234617]; National Institute Of Mental Health of the
National Institutes of Health [K01MH102403]; Intramural Research Program
of the Eunice Kennedy Shriver National Institute of Child Health and
Human Development
FX The Boston Youth Survey (BYS) was conducted in collaboration with the
Boston Public Health Commission (Barbara Ferrer, Executive Director),
Boston's Office of Human Services (Larry Mayes, Chief), Boston Public
Schools (Carol Johnson, Superintendent) and the Office of The Honorable
Mayor Thomas M. Menino. The survey would not have been possible without
the participation of the faculty, staff, administrators, and students of
Boston Public Schools. This work was supported by a grant from the
Centers for Disease Control and Prevention (CDC), National Center for
Injury Prevention and Control (NCIPC) (U49CE00740) to the Harvard Youth
Violence Prevention Center (David Hemenway, Principal Investigator).
During this analysis, Roman Pabayo was a Canadian Institutes of Health
Research postdoctoral fellowship recipient # 234617. Research reported
in this publication was also supported, in part, by the National
Institute Of Mental Health of the National Institutes of Health under
Award Number K01MH102403 (Dunn) and by the Intramural Research Program
of the Eunice Kennedy Shriver National Institute of Child Health and
Human Development. The content is solely the responsibility of the
authors and does not necessarily represent the official views of the
National Institutes of Health.
NR 50
TC 0
Z9 0
U1 12
U2 12
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0143-005X
EI 1470-2738
J9 J EPIDEMIOL COMMUN H
JI J. Epidemiol. Community Health
PD OCT
PY 2016
VL 70
IS 10
BP 997
EP 1003
DI 10.1136/jech-2015-206613
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA DX5RJ
UT WOS:000384439100009
PM 27103664
ER
PT J
AU Raghavan, S
Pachucki, MC
Chang, YC
Porneala, B
Fox, CS
Dupuis, J
Meigs, JB
AF Raghavan, Sridharan
Pachucki, Mark C.
Chang, Yuchiao
Porneala, Bianca
Fox, Caroline S.
Dupuis, Josee
Meigs, James B.
TI Incident Type 2 Diabetes Risk is Influenced by Obesity and Diabetes in
Social Contacts: a Social Network Analysis
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article
DE type 2 diabetes; social network; obesity; family history; epidemiology
ID PREDICTION; SELECTION; BEHAVIOR; FRIENDS; COHORT; ADULTS
AB Obesity and diabetes family history are the two strongest risk factors for type 2 diabetes (T2D). Prior work shows that an individual's obesity risk is associated with obesity in social contacts, but whether T2D risk follows similar patterns is unknown.
We aimed to estimate the relationship between obesity or diabetes in an individual's social contacts and his/her T2D risk. We hypothesized that obesity and diabetes in social contacts would increase an individual's T2D risk.
This was a retrospective analysis of the community-based Framingham Offspring Study (FOS).
FOS participants with T2D status, height and weight, and at least one social contact were eligible for this study (n = 4797 at Exam 1). Participants' interpersonal ties, cardiometabolic and demographic variables were available at eight exams from 1971 to 2008, and a T2D additive polygenic risk score was measured at the fifth exam.
Primary exposures were T2D (fasting glucose aeyen 7 mmol/L or taking diabetes medications) and obesity status (BMI aeyen 30 kg/m(2)) of social contacts at a prior exam. Primary outcome was incident T2D in participants.
Incident T2D was associated with having a social contact with diabetes (OR 1.32, p = 0.004) or with obesity (OR 1.21, p = 0.004). In stratified analyses, incident T2D was associated with diabetes in siblings (OR 1.64, p = 0.001) and obesity in spouses (OR 1.54, p = 0.0004). The associations between diabetes and obesity in social contacts and an individual's incident diabetes risk were stronger in individuals with a high diabetes genetic risk score.
T2D and obesity in social contacts, particularly siblings and spouses, were associated with an individual's risk of incident diabetes even after accounting for parental T2D history. Assessing risk factors in an individual's siblings and spouses can inform T2D risk; furthermore, social network based lifestyle interventions involving spouses and siblings might be a novel T2D prevention approach.
C1 [Raghavan, Sridharan; Chang, Yuchiao; Porneala, Bianca; Meigs, James B.] Harvard Med Sch, Dept Med, Div Gen Internal Med, Boston, MA 02115 USA.
[Raghavan, Sridharan; Chang, Yuchiao; Porneala, Bianca; Meigs, James B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Raghavan, Sridharan] Eastern Colorado Hlth Care Syst, Dept Vet Affairs Med Ctr, Denver, CO USA.
[Raghavan, Sridharan] Univ Colorado, Sch Med, Dept Med, Div Gen Internal Med, Denver, CO USA.
[Pachucki, Mark C.] Univ Massachusetts, Dept Sociol, Computat Social Sci Inst, Amherst, MA 01003 USA.
[Fox, Caroline S.] NHLBI, Lab Metab & Populat Hlth, Framingham, MA USA.
[Dupuis, Josee] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Dupuis, Josee] NHLBI, Framingham Heart Study, Framingham, MA USA.
RP Meigs, JB (reprint author), Harvard Med Sch, Dept Med, Div Gen Internal Med, Boston, MA 02115 USA.; Meigs, JB (reprint author), Massachusetts Gen Hosp, Boston, MA 02114 USA.
EM jmeigs@partners.org
FU NIH National Research Service Award [T32HP10251]; Ryoichi Sasakawa
Fellowship Fund; NIH [RO1DK78616]; National Heart, Lung and Blood
Institute's Framingham Heart Study [N01-HC-25195]; Affymetrix, Inc
[N02-HL-6-4278]; [K24 DK080140]
FX SR is supported by NIH National Research Service Award T32HP10251 and
the Ryoichi Sasakawa Fellowship Fund. JBM and JD are supported by NIH
RO1DK78616, and JBM is also supported by K24 DK080140. We gratefully
acknowledge the FHS study participants and staff for their
contributions. This work was partially supported by the National Heart,
Lung and Blood Institute's Framingham Heart Study (Contract No.
N01-HC-25195) and its contract with Affymetrix, Inc for genotyping
services (Contract No. N02-HL-6-4278).
NR 31
TC 2
Z9 2
U1 10
U2 10
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD OCT
PY 2016
VL 31
IS 10
BP 1127
EP 1133
DI 10.1007/s11606-016-3723-1
PG 7
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA DW4FF
UT WOS:000383597200006
PM 27145760
ER
PT J
AU Schapira, MM
Sprague, BL
Klabunde, CN
Tosteson, ANA
Bitton, A
Chen, JS
Beaber, EF
Onega, T
MacLean, CD
Harris, K
Howe, K
Pearson, L
Feldman, S
Brawarsky, P
Haas, JS
AF Schapira, Marilyn M.
Sprague, Brian L.
Klabunde, Carrie N.
Tosteson, Anna N. A.
Bitton, Asaf
Chen, Jane S.
Beaber, Elisabeth F.
Onega, Tracy
MacLean, Charles D.
Harris, Kimberly
Howe, Kathleen
Pearson, Loretta
Feldman, Sarah
Brawarsky, Phyllis
Haas, Jennifer S.
CA PROSPR Consortium
TI Inadequate Systems to Support Breast and Cervical Cancer Screening in
Primary Care Practice
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article; Proceedings Paper
CT Annual Research Meeting of the Academy-Health
CY JUN, 2015
CL Minneapolis, MN
SP Acad Hlth
DE breast cancer screening; cervical cancer screening; patient-centered
medical home
ID CENTERED MEDICAL HOME; QUALITY-OF-CARE; PREVENTIVE SERVICES; PHYSICIANS;
PARTICIPATION; INTERVENTIONS; METAANALYSIS; IMPROVEMENT; STRATEGIES;
CONTEXT
AB Despite substantial resources devoted to cancer screening nationally, the availability of clinical practice-based systems to support screening guidelines is not known.
To characterize the prevalence and correlates of practice-based systems to support breast and cervical cancer screening, with a focus on the patient-centered medical home (PCMH).
Web and mail survey of primary care providers conducted in 2014. The survey assessed provider (gender, training) and facility (size, specialty training, physician report of National Committee for Quality Assurance (NCQA) PCMH recognition, and practice affiliation) characteristics. A hierarchical multivariate analysis clustered by clinical practice was conducted to evaluate characteristics associated with the adoption of practice-based systems and technology to support guideline-adherent screening.
Primary care physicians in family medicine, general internal medicine, and obstetrics and gynecology, and nurse practitioners or physician assistants from four clinical care networks affiliated with PROSPR (Population-based Research Optimizing Screening through Personalized Regimens) consortium research centers.
The prevalence of routine breast cancer risk assessment, electronic health record (EHR) decision support, comparative performance reports, and panel reports of patients due for routine screening and follow-up.
There were 385 participants (57.6 % of eligible). Forty-seven percent (47.0 %) of providers reported NCQA recognition as a PCMH. Less than half reported EHR decision support for breast (48.8 %) or cervical cancer (46.2 %) screening. A minority received comparative performance reports for breast (26.2 %) or cervical (19.7 %) cancer screening, automated reports of patients overdue for breast (18.7 %) or cervical (16.4 %) cancer screening, or follow-up of abnormal breast (18.1 %) or cervical (17.6 %) cancer screening tests. In multivariate analysis, reported NCQA recognition as a PCMH was associated with greater use of comparative performance reports of guideline-adherent breast (OR 3.23, 95 % CI 1.58-6.61) or cervical (OR 2.56, 95 % CI 1.32-4.96) cancer screening and automated reports of patients overdue for breast (OR 2.19, 95 % CI 1.15-41.7) or cervical (OR. 2.56, 95 % CI 1.26-5.26) cancer screening.
Providers lack systems to support breast and cervical cancer screening. Practice transformation toward a PCMH may support the adoption of systems to achieve guideline-adherent cancer screening in primary care settings.
C1 [Schapira, Marilyn M.] Univ Penn, 1110 Blockley Hall,423 Guardian Dr, Philadelphia, PA 19104 USA.
[Schapira, Marilyn M.] Philadelphia VA Med Ctr, 1110 Blockley Hall,423 Guardian Dr, Philadelphia, PA 19104 USA.
[Sprague, Brian L.; MacLean, Charles D.; Howe, Kathleen] Univ Vermont, Burlington, VT USA.
[Klabunde, Carrie N.] NIH, Off Dis Prevent, Off Director, Bldg 10, Bethesda, MD 20892 USA.
[Tosteson, Anna N. A.; Onega, Tracy; Pearson, Loretta] Geisel Sch Med Dartmouth, Lebanon, NH USA.
[Tosteson, Anna N. A.; Onega, Tracy; Pearson, Loretta] Norris Cotton Canc Ctr, Lebanon, NH USA.
[Bitton, Asaf; Feldman, Sarah] Harvard Med Sch, Boston, MA USA.
[Bitton, Asaf; Chen, Jane S.; Harris, Kimberly; Feldman, Sarah; Brawarsky, Phyllis] Brigham & Womens Hosp, 75 Francis St, Boston, MA 02115 USA.
[Beaber, Elisabeth F.] Fred Hutchinson Canc Res Ctr, 1124 Columbia St, Seattle, WA 98104 USA.
[Haas, Jennifer S.] Brigham & Womens Hosp, Div Gen Internal Med & Primary Care, 75 Francis St, Boston, MA 02115 USA.
RP Schapira, MM (reprint author), Univ Penn, 1110 Blockley Hall,423 Guardian Dr, Philadelphia, PA 19104 USA.; Schapira, MM (reprint author), Philadelphia VA Med Ctr, 1110 Blockley Hall,423 Guardian Dr, Philadelphia, PA 19104 USA.
EM mschap@upenn.edu
FU NCI NIH HHS [U54 CA163303, P30 CA023108, U01 CA163304, U54 CA163307, U54
CA163313]
NR 39
TC 1
Z9 1
U1 8
U2 10
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD OCT
PY 2016
VL 31
IS 10
BP 1148
EP 1155
DI 10.1007/s11606-016-3726-y
PG 8
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA DW4FF
UT WOS:000383597200009
PM 27251058
ER
PT J
AU Benjamini, D
Basser, PJ
AF Benjamini, Dan
Basser, Peter J.
TI Use of marginal distributions constrained optimization (MADCO) for
accelerated 2D MRI relaxometry and diffusometry
SO JOURNAL OF MAGNETIC RESONANCE
LA English
DT Article
DE Fredholm integral; Inverse problems; Relaxometry; Diffusometry;
Reconstruction; Multidimensional; Distribution
ID MAGNETIZATION-TRANSFER; 1ST KIND; RELAXATION; T-1; INVERSION; GRADIENT;
NERVE; BRAIN
AB Measuring multidimensional (e.g., 2D) relaxation spectra in NMR and MRI clinical applications is a holy grail of the porous media and biomedical MR communities. The main bottleneck is the inversion of Fredholm integrals of the first kind, an ill-conditioned problem requiring large amounts of data to stabilize a solution. We suggest a novel experimental design and processing framework to accelerate and improve the reconstruction of such 2D spectra that uses a priori information from the 1D projections of spectra, or marginal distributions. These 1D marginal distributions provide powerful constraints when 2D spectra are reconstructed, and their estimation requires an order of magnitude less data than a conventional 2D approach. This marginal distributions constrained optimization (MADCO) methodology is demonstrated here with a polyvinylpyrrolidone-water phantom that has 3 distinct peaks in the 2D D-T1 space. The stability, sensitivity to experimental parameters, and accuracy of this new approach are compared with conventional methods by serially subsampling the full data set. While the conventional, unconstrained approach performed poorly, the new method had proven to be highly accurate and robust, only requiring a fraction of the data. Additionally, synthetic T1-T2 data are presented to explore the effects of noise on the estimations, and the performance of the proposed method with a smooth and realistic 2D spectrum. The proposed framework is quite general and can also be used with a variety of 2D MRI experiments (D-T2, T1-T2, D-D, etc.), making these potentially feasible for preclinical and even clinical applications for the first time. Published by Elsevier Inc.
C1 [Benjamini, Dan; Basser, Peter J.] NICHD, Quantitat Imaging & Tissue Sci, NIH, Bethesda, MD 20892 USA.
RP Benjamini, D (reprint author), NICHD, Quantitat Imaging & Tissue Sci, NIH, Bethesda, MD 20892 USA.
EM dan.benjamini@nih.gov
FU Intramural Research Program of The Eunice Kennedy Shriver National
Institute of Child Health and Human Development (NICHD)
FX This work was supported by funds provided by the Intramural Research
Program of The Eunice Kennedy Shriver National Institute of Child Health
and Human Development (NICHD). The authors thank Dr. Martin Lizak for
writing the IR-DWI pulse sequence, Dr. Jian Cheng for providing fruitful
discussions, and Ms. Liz Salak for editing the manuscript.
NR 19
TC 3
Z9 3
U1 0
U2 0
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1090-7807
EI 1096-0856
J9 J MAGN RESON
JI J. Magn. Reson.
PD OCT
PY 2016
VL 271
BP 40
EP 45
DI 10.1016/j.jmr.2016.08.004
PG 6
WC Biochemical Research Methods; Physics, Atomic, Molecular & Chemical;
Spectroscopy
SC Biochemistry & Molecular Biology; Physics; Spectroscopy
GA DX8JN
UT WOS:000384634000006
PM 27543810
ER
PT J
AU Riscuta, G
AF Riscuta, Gabriela
TI Nutrigenomics at the Interface of Aging, Lifespan, and Cancer Prevention
SO JOURNAL OF NUTRITION
LA English
DT Review
DE nutrigenomics; diet; aging; longevity; DNA repair; telomere; cancer;
caloric restriction; oxidative stress
ID TELOMERE LENGTH; CALORIC RESTRICTION; COLORECTAL-CANCER; OXIDATIVE
STRESS; MISMATCH REPAIR; RHESUS-MONKEYS; DNA-REPAIR; HEALTH; DISEASE;
DIET
AB The percentage of elderly people with associated age-related health deterioration, including cancer, has been increasing for decades. Among age-related diseases, the incidence of cancer has grown substantially, in part because of the overlap of some molecular pathways between cancer and aging. Studies with model organisms suggest that aging and age related conditions are manipulable processes that can be modified by both genetic and environmental factors, including dietary habits. Variations in genetic backgrounds likely lead to differential responses to dietary changes and account for some of the inconsistencies found in the literature. The intricacies of the aging process, coupled with the interrelational role of bioactive food components on gene expression, make this review a complex undertaking. Nevertheless, intriguing evidence suggests that dietary habits can manipulate the aging process and/or its consequences and potentially may have unprecedented health benefits. The present review focuses on 4 cellular events: telomerase activity, bioenergetics, DNA repair, and oxidative stress. These processes are linked to both aging and cancer risk, and their alteration in animal models by selected food components is evident.
C1 [Riscuta, Gabriela] NCI, Nutr Sci Res Grp, Canc Prevent Div, Bethesda, MD 20892 USA.
RP Riscuta, G (reprint author), NCI, Nutr Sci Res Grp, Canc Prevent Div, Bethesda, MD 20892 USA.
EM gabriela.riscuta@nih.gov
NR 79
TC 0
Z9 0
U1 19
U2 19
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-3166
EI 1541-6100
J9 J NUTR
JI J. Nutr.
PD OCT
PY 2016
VL 146
IS 10
BP 1931
EP 1939
DI 10.3945/jn.116.235119
PG 9
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA DY0KE
UT WOS:000384784900002
PM 27558581
ER
PT J
AU Tikkanen, R
Saukkonen, T
Fex, M
Bennet, H
Rautiainen, MR
Paunio, T
Koskinen, M
Panarsky, R
Bevilacqua, L
Sjoberg, RL
Tiihonen, J
Virkkunen, M
AF Tikkanen, Roope
Saukkonen, Tero
Fex, Malin
Bennet, Hedvig
Rautiainen, Marja-Riitta
Paunio, Tiina
Koskinen, Mika
Panarsky, Rony
Bevilacqua, Laura
Sjoberg, Rickard L.
Tiihonen, Jari
Virkkunen, Matti
TI The effects of a HTR2B stop codon and testosterone on energy metabolism
and beta cell function among antisocial Finnish males
SO JOURNAL OF PSYCHIATRIC RESEARCH
LA English
DT Article
DE ASPD; 5-HT2B receptor; HTR2B; Testosterone; Insulin resistance; BMI
ID VIOLENT ALCOHOLIC OFFENDERS; BROWN ADIPOSE-TISSUE; BODY-MASS INDEX;
INSULIN-SECRETION; AUTORECEPTOR GENE; SEROTONIN; OBESITY; RESISTANCE;
POLYMORPHISM; CONSUMPTION
AB Herein, we examined insulin resistance (IR), insulin sensitivity (IS), beta cell activity, and glucose metabolism in subjects with antisocial personality disorder (ASPD), and whether the serotonin 2B (5-HT2B) receptor and testosterone have a role in energy metabolism. A cohort of subjects belonging to a founder population that included 98 ASPD males, aged 25-30, was divided into groups based on the presence of a heterozygous 5-HT2B receptor loss-of-function gene mutation (HTR2B Q20*; n = 9) or not (n = 89). Serum glucose and insulin levels were measured in a 5 h oral glucose tolerance test (75 g) and indices describing IR, IS, and beta cell activity were calculated. Body mass index (BMI) was also determined. Concentrations of the serotonin metabolite 5-hydroxyindoleacetic acid were measured in cerebrospinal fluid, and testosterone levels from serum. An IR-like state comprising high IR, low IS, and high beta cell activity indices was observed among ASPD subjects without the HTR2B Q20* allele. By contrast, being an ASPD HTR2B Q20* carrier appeared to be preventive of these pathophysiologies. The HTR2B Q20* allele and testosterone predicted lower BMI independently, but an interaction between HTR2B Q20* and testosterone lead to increased insulin sensitivity among HTR2B Q20* carriers with low testosterone levels. The HTR2B Q20* allele also predicted reduced beta cell activity and enhanced glucose metabolism. Reduced 5-HT2B receptor function at low or normal testosterone levels may be protective of obesity. Results were observed among Finnish males having an antisocial personality disorder, which limits the generality. (C) 2016 Elsevier Ltd. All rights reserved.
C1 [Tikkanen, Roope; Paunio, Tiina; Virkkunen, Matti] Univ Helsinki, Helsinki Univ Cent Hosp, Dept Psychiat, Helsinki, Finland.
[Tikkanen, Roope] Rinnekoti Fdn, Res & Dev, Espoo, Finland.
[Saukkonen, Tero] Helsinki Univ Cent Hosp, Childrens Hosp, Helsinki, Finland.
[Saukkonen, Tero] Univ Helsinki, Helsinki, Finland.
[Saukkonen, Tero] Novo Nordisk Farma Oy, Espoo, Finland.
[Fex, Malin; Bennet, Hedvig] Lund Univ, Ctr Diabet, Dept Clin Sci, Scania Univ Hosp, Malmo, Sweden.
[Rautiainen, Marja-Riitta; Paunio, Tiina; Tiihonen, Jari] Natl Inst Hlth & Welf, Helsinki, Finland.
[Koskinen, Mika] Oy Aava Dev Ltd, Helsinki, Finland.
[Panarsky, Rony] NIAAA, Neurogenet Lab, Bethesda, MD USA.
[Bevilacqua, Laura] NYU, Sch Med, Dept Psychiat, New York, NY USA.
[Sjoberg, Rickard L.] Umea Univ, Dept Pharmacol & Clin Neurosci, Umea, Sweden.
[Tiihonen, Jari] Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.
[Tiihonen, Jari] Univ Eastern Finland, Niuvanniemi Hosp, Dept Forens Psychiat, Kuopio, Finland.
RP Tikkanen, R (reprint author), Univ Helsinki, Dept Psychiat, Valskarinkatu 12,POB 22, Helsinki 00260, Finland.
EM roope.tikkanen@gmail.com
FU Orion Research Foundation; Swedish Research Council [2012-1552];
Waldemar von Frenckell Foundation
FX This work was supported by the Orion Research Foundation, Swedish
Research Council (project number: 2012-1552 to M.F), and Waldemar von
Frenckell Foundation. Excellence in diabetes research (EXODIAB),
Krapperup foundation, Ake Wiberg foundation, Royal Physiographic
Society, Albert Pahlsson foundation, Crafoord foundation, Childhood
Diabetes Foundation, and the Foundation of Sigurd and Elsa Golijes
Minne.
NR 45
TC 0
Z9 0
U1 2
U2 3
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 2016
VL 81
BP 79
EP 86
DI 10.1016/j.jpsychires.2016.06.019
PG 8
WC Psychiatry
SC Psychiatry
GA DY1LB
UT WOS:000384855400011
PM 27420381
ER
PT J
AU Dember, LM
Archdeacon, P
Krishnan, M
Lacson, E
Ling, SM
Roy-Chaudhury, P
Smith, KA
Flessner, MF
AF Dember, Laura M.
Archdeacon, Patrick
Krishnan, Mahesh
Lacson, Eduardo, Jr.
Ling, Shari M.
Roy-Chaudhury, Prabir
Smith, Kimberly A.
Flessner, Michael F.
TI Pragmatic Trials in Maintenance Dialysis: Perspectives from the Kidney
Health Initiative
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Review
ID CLINICAL-TRIALS; QUALITY; CARE; NEPHROLOGY; CLINICALTRIALS.GOV;
INCREASE; CONSENT; POLICY; SAFETY; PBRN
AB Pragmatic clinical trials are conducted under the real-world conditions of clinical care delivery. As a result, these trials yield findings that are highly generalizable to the nonresearch setting, identify interventions that are readily translatable into clinical practice, and cost less than trials that require extensive research infrastructures. Maintenance dialysis is a setting especially well suited for pragmatic trials because of inherently frequent and predictable patient encounters, highly granular and uniform data collection, use of electronic data systems, and delivery of care by a small number of provider organizations to approximately 90% of patients nationally. Recognizing the potential for pragmatic trials to generate much needed evidence to guide the care of patients receiving maintenance dialysis, the Kidney Health Initiative assembled a group of individuals with relevant expertise from academia, industry, and government to provide the nephrology community with information about the design and conduct of such trials, with a specific focus on the dialysis setting. Here, we review this information, and where applicable, use experience from the ongoing Time to Reduce Mortality in End Stage Renal Disease Trial, a large cluster-randomized, pragmatic trial evaluating hemodialysis session duration, to illustrate challenges and solutions to operational, ethical, and regulatory issues.
C1 [Dember, Laura M.] Univ Penn, Renal Electrolyte & Hypertens Div, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Dember, Laura M.] Univ Penn, Dept Biostat & Epidemiol, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Archdeacon, Patrick] US FDA, Off Med Policy, Silver Spring, MD USA.
[Archdeacon, Patrick; Smith, Kimberly A.] US FDA, Ctr Drug Evaluat & Res, Silver Spring, MD USA.
[Krishnan, Mahesh] DaVita Healthcare Partners, Denver, CO USA.
[Lacson, Eduardo, Jr.] Tufts Med Ctr, Div Nephrol, Boston, MA USA.
[Lacson, Eduardo, Jr.] Tufts Univ, Sch Med, Boston, MA 02111 USA.
[Ling, Shari M.] Ctr Medicare Serv, Ctr Clin Stand & Qual, Baltimore, MD USA.
[Ling, Shari M.] Ctr Medicaid Serv, Ctr Clin Stand & Qual, Baltimore, MD USA.
[Roy-Chaudhury, Prabir] Univ Arizona, Coll Med, Div Nephrol, Tucson, AZ USA.
[Roy-Chaudhury, Prabir] Southern Arizona Vet Adm Hlth Care Syst, Tucson, AZ USA.
[Flessner, Michael F.] NIDDK, Div Kidney Urol & Hematol, Bethesda, MD 20892 USA.
RP Dember, LM (reprint author), Univ Penn, Perelman Sch Med, Blockley Hall,Room 920,423 Guardian Dr, Philadelphia, PA 19104 USA.
EM ldember@upenn.edu
FU Kidney Health Initiative (KHI); American Society of Nephrology; US Food
and Drug Administration; National Institutes of Health Office of the
Director; National Institute of Diabetes and Digestive and Kidney
Diseases [UH2-AT007797, UH3-DK102384]
FX This work was supported by the Kidney Health Initiative (KHI), a
public-private partnership between the American Society of Nephrology,
the US Food and Drug Administration, and >75 member organizations and
companies to enhance patient safety and foster innovation in kidney
disease. KHI funds were used to defray costs incurred during the conduct
of the project, including project management support which was expertly
provided by American Society of Nephrology staff members, Melissa West
and Ryan Murray. There was no honorarium or other financial support
provided to KHI workgroup members. The authors of this paper had final
review authority and are fully responsible for its content.; KHI makes
every effort to avoid actual, potential, or perceived conflicts of
interest that may arise as a result of industry relationships or
personal interests among the members of the workgroup. More information
on KHI, the workgroup, or the conflict of interest policy can be found
at www.kidneyhealthinitiative.org. The TiME Trial is funded by the
National Institutes of Health Office of the Director and the National
Institute of Diabetes and Digestive and Kidney Diseases (UH2-AT007797
and UH3-DK102384 to L.M.D.). The views and opinions expressed in this
article are those of the authors and do not necessarily reflect the
official policy or position of any agency of the US Government, DaVita
Healthcare Partners, or Fresenius Medical Care.
NR 43
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Z9 0
U1 0
U2 0
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1046-6673
EI 1533-3450
J9 J AM SOC NEPHROL
JI J. Am. Soc. Nephrol.
PD OCT
PY 2016
VL 27
IS 10
BP 2955
EP 2963
DI 10.1681/ASN.2016030340
PG 9
WC Urology & Nephrology
SC Urology & Nephrology
GA DX8HK
UT WOS:000384628500008
PM 27401689
ER
PT J
AU Bodonyi-Kovacs, G
Ma, JZ
Chang, J
Lipkowitz, MS
Kopp, JB
Winkler, CA
Le, TH
AF Bodonyi-Kovacs, Gabor
Ma, Jennie Z.
Chang, Jamison
Lipkowitz, Michael S.
Kopp, Jeffrey B.
Winkler, Cheryl Ann
Le, Thu H.
TI Combined Effects of GSTM1 Null Allele and APOL1 Renal Risk Alleles in
CKD Progression in the African American Study of Kidney Disease and
Hypertension Trial
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID GENE POLYMORPHISM; VARIANTS; NEPHROPATHY; METAANALYSIS; ASSOCIATION;
GENOTYPE; DECLINE; AASK
AB Apolipoprotein L-1 (APOL1) high risk alleles and the glutathione-S-transferase-mu 1 (GSTM1) null allele have been shown separately to associate with CKD progression in the African American Study of Kidney Disease and Hypertension (AASK) trial participants. Here, we determined combined effects of GSTM1 null and APOL1 high risk alleles on clinical outcomes in 682 AASK participants who were classified into four groups by GSTM1 null or active genotype and APOL1 high or low risk genotype. We assessed survival differences among these groups by log-rank test and Cox regression adjusted for important clinical variables for time to GFR event (change in GFR of 50% or 25-ml/min per 1.73 m(2) decline), incident ESRD, death, or composite outcomes. The groups differed significantly in event-free survival for incident ESRD and composite outcomes (P <= 0.001 by log-rank test). Compared with the reference GSTM1 active/APOL1 low risk group, other groups had these hazard ratios for the composite outcome of incident ESRD and change in GFR: GSTM1 active/APOL1 high risk hazard ratio, 2.13; 95% confidence interval, 0.76 to 5.90 (P=0.15); GSTM1 null/APOL1 low risk hazard ratio, 2.05; 95% confidence interval, 1.08 to 3.88 (P=0.03); and GSTM1 null/APOL1 high risk hazard ratio, 3.0; 95% confidence interval, 1.51 to 5.96 (P=0.002). In conclusion, GSTM1 null and APOL1 high risk alleles deleteriously affect CKD progression among blacks with hypertension, and subjects with both GSTM1 null and APOL1 high risk genotypes had highest risk of adverse renal outcomes. Larger cohorts are needed to fully explore interactions of GSTM1 and APOL1 genotypes in other subgroups.
C1 [Bodonyi-Kovacs, Gabor; Chang, Jamison; Le, Thu H.] Univ Virginia, Dept Med, Div Nephrol, Charlottesville, VA USA.
[Ma, Jennie Z.] Univ Virginia, Dept Publ Hlth Sci, Charlottesville, VA USA.
[Lipkowitz, Michael S.] Georgetown Univ, Dept Med, Div Nephrol, Washington, DC USA.
[Kopp, Jeffrey B.] NIDDK, Kidney Dis Branch, NIH, Bethesda, MD 20892 USA.
[Winkler, Cheryl Ann] NCI, Basic Res Lab, Ctr Canc Res, NIH,Leidos Biomed Inc,Frederick Natl Lab, Frederick, MD 21701 USA.
RP Le, TH (reprint author), Univ Virginia, Box 800133, Charlottesville, VA 22908 USA.
EM thl4t@virginia.edu
FU Intramural Research Program of the National Institute of Diabetes and
Digestive and Kidney Diseases, National Institutes of Health (NIH);
National Cancer Institute, NIH, Center for Cancer Research
[HHSN26120080001E]; NIH [R01DK094907-01]
FX This work was supported, in part, by the Intramural Research Program of
the National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health (NIH). This project has been funded, in
whole or in part, with federal funds from National Cancer Institute,
NIH, Center for Cancer Research contract HHSN26120080001E and in part,
by NIH extramural grant R01DK094907-01 (to T.H.L).
NR 25
TC 0
Z9 0
U1 3
U2 3
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1046-6673
EI 1533-3450
J9 J AM SOC NEPHROL
JI J. Am. Soc. Nephrol.
PD OCT
PY 2016
VL 27
IS 10
BP 3140
EP 3152
DI 10.1681/ASN.2015050487
PG 13
WC Urology & Nephrology
SC Urology & Nephrology
GA DX8HK
UT WOS:000384628500023
PM 26940095
ER
PT J
AU Lee, CP
Liu, GT
Kung, HN
Liu, PT
Liao, YT
Chow, LP
Chang, LS
Chang, YH
Chang, CW
Shu, WC
Angers, A
Farina, A
Lin, SF
Tsai, CH
Bouamr, F
Chen, MR
AF Lee, Chung-Pei
Liu, Guan-Ting
Kung, Hsiu-Ni
Liu, Po-Ting
Liao, Yen-Tzu
Chow, Lu-Ping
Chang, Ling-Shih
Chang, Yu-Hsin
Chang, Chou-Wei
Shu, Wen-Chi
Angers, Annie
Farina, Antonella
Lin, Su-Fang
Tsai, Ching-Hwa
Bouamr, Fadila
Chen, Mei-Ru
TI The Ubiquitin Ligase Itch and Ubiquitination Regulate BFRF1-Mediated
Nuclear Envelope Modification for Epstein-Barr Virus Maturation
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID PORE COMPLEX; L-DOMAIN; PROTEINS; TYPE-1; CELLS; FAMILY; EFFICIENT;
BREAKDOWN; RELEASE; ESCRTS
AB The cellular endosomal sorting complex required for transport (ESCRT) was recently found to mediate important morphogenesis processes at the nuclear envelope (NE). We previously showed that the Epstein-Barr virus (EBV) BFRF1 protein recruits the ESCRT-associated protein Alix to modulate NE structure and promote EBV nuclear egress. Here, we uncover new cellular factors and mechanisms involved in this process. BFRF1-induced NE vesicles are similar to those observed following EBV reactivation. BFRF1 is ubiquitinated, and elimination of possible ubiquitination by either lysine mutations or fusion of a deubiquitinase hampers NE-derived vesicle formation and virus maturation. While it interacts with multiple Nedd4-like ubiquitin ligases, BFRF1 preferentially binds Itch ligase. We show that Itch associates with Alix and BFRF1 and is required for BFRF1-induced NE vesicle formation. Our data demonstrate that Itch, ubiquitin, and Alix control the BFRF1-mediated modulation of the NE and EBV maturation, uncovering novel regulatory mechanisms of nuclear egress of viral nucleocapsids.
IMPORTANCE
The nuclear envelope (NE) of eukaryotic cells not only serves as a transverse scaffold for cellular processes, but also as a natural barrier for most DNA viruses that assemble their nucleocapsids in the nucleus. Previously, we showed that the cellular endosomal sorting complex required for transport (ESCRT) machinery is required for the nuclear egress of EBV. Here, we further report the molecular interplay among viral BFRF1, the ESCRT adaptor Alix, and the ubiquitin ligase Itch. We found that BFRF1-induced NE vesicles are similar to those observed following EBV reactivation. The lysine residues and the ubiquitination of BFRF1 regulate the formation of BFRF1-induced NE-derived vesicles and EBV maturation. During the process, a ubiquitin ligase, Itch, preferably associates with BFRF1 and is required for BFRF1-induced NE vesicle formation. Therefore, our data indicate that Itch, ubiquitin, and Alix control the BFRF1-mediated modulation of the NE, suggesting novel regulatory mechanisms for ESCRT-mediated NE modulation.
C1 [Lee, Chung-Pei; Liu, Guan-Ting] Natl Taipei Univ Nursing & Hlth Sci, Sch Nursing, Taipei, Taiwan.
[Liu, Guan-Ting; Liu, Po-Ting; Liao, Yen-Tzu; Chang, Ling-Shih; Chang, Yu-Hsin; Chang, Chou-Wei; Shu, Wen-Chi; Tsai, Ching-Hwa; Chen, Mei-Ru] Natl Taiwan Univ, Grad Inst, Coll Med, Taipei, Taiwan.
[Liu, Guan-Ting; Liu, Po-Ting; Liao, Yen-Tzu; Chang, Ling-Shih; Chang, Yu-Hsin; Chang, Chou-Wei; Shu, Wen-Chi; Tsai, Ching-Hwa; Chen, Mei-Ru] Natl Taiwan Univ, Dept Microbiol, Coll Med, Taipei, Taiwan.
[Kung, Hsiu-Ni] Natl Taiwan Univ, Dept Anat & Cell Biol, Coll Med, Taipei, Taiwan.
[Chow, Lu-Ping] Natl Taiwan Univ, Grad Inst Med Genom & Prote, Coll Med, Taipei, Taiwan.
[Angers, Annie] Univ Montreal, Dept Biol Sci, Montreal, PQ, Canada.
[Farina, Antonella] Sapienza Univ Rome, Dept Expt Med, Rome, Italy.
[Lin, Su-Fang] Inst Canc Res, Natl Hlth Res Inst, Taipei, Taiwan.
[Bouamr, Fadila] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
RP Chen, MR (reprint author), Natl Taiwan Univ, Grad Inst, Coll Med, Taipei, Taiwan.; Chen, MR (reprint author), Natl Taiwan Univ, Dept Microbiol, Coll Med, Taipei, Taiwan.
EM mrc@ntu.edu.tw
OI Farina, Antonella/0000-0002-8629-0971; Angers, Annie/0000-0003-0131-256X
FU National Health Research Institutes (NHRI) [NHRI-EX104-10201BI];
National Taiwan University; Ministry of Science and Technology, Taiwan
(MOST) [MOST102-2320-B-227-002, MOST103-2320-B-227-001-MY3]
FX This work, including the efforts of Mei-Ru Chen, Chou-Wei Chang, and
Wen-Chi Shu, was funded by National Health Research Institutes (NHRI)
(NHRI-EX104-10201BI). This work, including the efforts of Mei-Ru Chen,
Chou-Wei Chang, and Wen-Chi Shu, was funded by National Taiwan
University (intramural grant). This work, including the efforts of
Chung-Pei Lee, Guan-Ting Liu, Po-Ting Liu, Ling-Shih Chang, and Yu-Hsin
Chang, was funded by Ministry of Science and Technology, Taiwan (MOST)
(MOST102-2320-B-227-002 and MOST103-2320-B-227-001-MY3).
NR 40
TC 2
Z9 2
U1 3
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD OCT
PY 2016
VL 90
IS 20
BP 8994
EP 9007
DI 10.1128/JVI.01235-16
PG 14
WC Virology
SC Virology
GA DX7NO
UT WOS:000384574900017
PM 27466427
ER
PT J
AU Ajiro, M
Tang, S
Doorbar, J
Zheng, ZM
AF Ajiro, Masahiko
Tang, Shuang
Doorbar, John
Zheng, Zhi-Ming
TI Serine/Arginine-Rich Splicing Factor 3 and Heterogeneous Nuclear
Ribonucleoprotein A1 Regulate Alternative RNA Splicing and Gene
Expression of Human Papillomavirus 18 through Two Functionally
Distinguishable cis Elements
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID SPINAL MUSCULAR-ATROPHY; TRACT BINDING-PROTEIN; MESSENGER-RNA; SR
PROTEINS; FACTOR SRP20; MOUSE MODEL; HNRNP A1; CERVICAL-CANCER;
DOWN-REGULATION; EXON SEQUENCES
AB Human papillomavirus 18 (HPV18) is the second most common oncogenic HPV type associated with cervical, anogenital, and oropharyngeal cancers. Like other oncogenic HPVs, HPV18 encodes two major (one early and one late) polycistronic premRNAs that are regulated by alternative RNA splicing to produce a repertoire of viral transcripts for the expression of individual viral genes. However, RNA cis-regulatory elements and trans-acting factors contributing to HPV18 alternative RNA splicing remain unknown. In this study, an exonic splicing enhancer (ESE) in the nucleotide (nt) 3520 to 3550 region in the HPV18 genome was identified and characterized for promotion of HPV18 929 boolean AND 3434 splicing and E1 boolean AND E4 production through interaction with SRSF3, a host oncogenic splicing factor differentially expressed in epithelial cells and keratinocytes. Introduction of point mutations in the SRSF3-binding site or knockdown of SRSF3 expression in cells reduces 929 boolean AND 3434 splicing and E1 boolean AND E4 production but activates other, minor 929 boolean AND 3465 and 929 boolean AND 3506 splicing. Knockdown of SRSF3 expression also enhances the expression of E2 and L1 mRNAs. An exonic splicing silencer (ESS) in the HPV18 nt 612 to 639 region was identified as being inhibitory to the 233 boolean AND 416 splicing of HPV18 E6E7 pre-mRNAs via binding to hnRNP A1, a well-characterized, abundantly and ubiquitously expressed RNA-binding protein. Introduction of point mutations into the hnRNP A1-binding site or knockdown of hnRNP A1 expression promoted 233 boolean AND 416 splicing and reduced E6 expression. These data provide the first evidence that the alternative RNA splicing of HPV18 pre-mRNAs is subject to regulation by viral RNA cis elements and host trans-acting splicing factors.
IMPORTANCE
Expression of HPV18 genes is regulated by alternative RNA splicing of viral polycistronic pre-mRNAs to produce a repertoire of viral early and late transcripts. RNA cis elements and trans-acting factors contributing to HPV18 alternative RNA splicing have been discovered in this study for the first time. The identified ESS at the E7 open reading frame (ORF) prevents HPV18 233 boolean AND 416 splicing in the E6 ORF through interaction with a host splicing factor, hnRNP A1, and regulates E6 and E7 expression of the early E6E7 polycistronic pre-mRNA. The identified ESE at the E1 boolean AND E4 ORF promotes HPV18 929 boolean AND 3434 splicing of both viral early and late pre-mRNAs and E1 boolean AND E4 production through interaction with SRSF3. This study provides important observations on how alternative RNA splicing of HPV18 pre-mRNAs is subject to regulation by viral RNA cis elements and host splicing factors and offers potential therapeutic targets to overcome HPV-related cancer.
C1 [Ajiro, Masahiko; Tang, Shuang; Zheng, Zhi-Ming] NCI, Tumor Virus RNA Biol Sect, Gene Regulat & Chromosome Biol Lab, Ctr Canc Res,NIH, Frederick, MD 21701 USA.
[Doorbar, John] Univ Cambridge, Dept Pathol, Div Virol, Cambridge, England.
[Ajiro, Masahiko] Kyoto Univ, Grad Sch Med, Dept Anat & Dev Biol, Dept Drug Discovery Med, Kyoto, Japan.
[Tang, Shuang] US FDA, Div Viral Prod, Off Vaccines Res & Review, Ctr Biol Evaluat & Res, Silver Spring, MD USA.
RP Zheng, ZM (reprint author), NCI, Tumor Virus RNA Biol Sect, Gene Regulat & Chromosome Biol Lab, Ctr Canc Res,NIH, Frederick, MD 21701 USA.
EM zhengt@exchange.nih.gov
FU HHS \ NIH \ NIH Office of the Director (OD) [1ZIASC010357]; HHS \ NIH \
Intramural Research Program
FX This work, including the efforts of Zhi-Ming Zheng, was funded by HHS
vertical bar NIH vertical bar NIH Office of the Director (OD)
(1ZIASC010357). This work was funded by HHS vertical bar NIH vertical
bar Intramural Research Program.
NR 87
TC 1
Z9 1
U1 7
U2 7
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD OCT
PY 2016
VL 90
IS 20
BP 9138
EP 9152
DI 10.1128/JVI.00965-16
PG 15
WC Virology
SC Virology
GA DX7NO
UT WOS:000384574900002
PM 27489271
ER
PT J
AU Turnbull, ML
Wise, HM
Nicol, MQ
Smith, N
Dunfee, RL
Beard, PM
Jagger, BW
Ligertwood, Y
Hardisty, GR
Xiao, HX
Benton, DJ
Coburn, AM
Paulo, JA
Gygi, SP
McCauley, JW
Taubenberger, JK
Lycett, SJ
Weekes, MP
Dutia, BM
Digard, P
AF Turnbull, Matthew L.
Wise, Helen M.
Nicol, Marlynne Q.
Smith, Nikki
Dunfee, Rebecca L.
Beard, Philippa M.
Jagger, Brett W.
Ligertwood, Yvonne
Hardisty, Gareth R.
Xiao, Haixia
Benton, Donald J.
Coburn, Alice M.
Paulo, Joao A.
Gygi, Steven P.
McCauley, John W.
Taubenberger, Jeffery K.
Lycett, Samantha J.
Weekes, Michael P.
Dutia, Bernadette M.
Digard, Paul
TI Role of the B Allele of Influenza A Virus Segment 8 in Setting Mammalian
Host Range and Pathogenicity
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID COMPLETE GENOME SEQUENCE; NS1 PROTEIN; NUCLEAR EXPORT;
GENETIC-CHARACTERIZATION; NONSTRUCTURAL PROTEIN-1; PLASMA-MEMBRANE;
BETA-INTERFERON; SOUTHERN CHINA; MESSENGER-RNAS; AMINO-ACID
AB Two alleles of segment 8 (NS) circulate in nonchiropteran influenza A viruses. The A allele is found in avian and mammalian viruses, but the B allele is viewed as being almost exclusively found in avian viruses. This might reflect the fact that one or both of its encoded proteins (NS1 and NEP) are maladapted for replication in mammalian hosts. To test this, a number of clade A and B avian virus-derived NS segments were introduced into human H1N1 and H3N2 viruses. In no case was the peak virus titer substantially reduced following infection of various mammalian cell types. Exemplar reassortant viruses also replicated to similar titers in mice, although mice infected with viruses with the avian virus-derived segment 8s had reduced weight loss compared to that achieved in mice infected with the A/Puerto Rico/8/1934 (H1N1) parent. In vitro, the viruses coped similarly with type I interferons. Temporal proteomics analysis of cellular responses to infection showed that the avian virus-derived NS segments provoked lower levels of expression of interferon-stimulated genes in cells than wild type-derived NS segments. Thus, neither the A nor the B allele of avian virus-derived NS segments necessarily attenuates virus replication in a mammalian host, although the alleles can attenuate disease. Phylogenetic analyses identified 32 independent incursions of an avian virus-derived A allele into mammals, whereas 6 introductions of a B allele were identified. However, A-allele isolates from birds outnumbered B-allele isolates, and the relative rates of Aves-to-Mammalia transmission were not significantly different. We conclude that while the introduction of an avian virus segment 8 into mammals is a relatively rare event, the dogma of the B allele being especially restricted is misleading, with implications in the assessment of the pandemic potential of avian influenza viruses.
IMPORTANCE
Influenza A virus (IAV) can adapt to poultry and mammalian species, inflicting a great socioeconomic burden on farming and health care sectors. Host adaptation likely involves multiple viral factors. Here, we investigated the role of IAV segment 8. Segment 8 has evolved into two distinct clades: the A and B alleles. The B-allele genes have previously been suggested to be restricted to avian virus species. We introduced a selection of avian virus A-and B-allele segment 8s into human H1N1 and H3N2 virus backgrounds and found that these reassortant viruses were fully competent in mammalian host systems. We also analyzed the currently available public data on the segment 8 gene distribution and found surprisingly little evidence for specific avian host restriction of the B-clade segment. We conclude that B-allele segment 8 genes are, in fact, capable of supporting infection in mammals and that they should be considered during the assessment of the pandemic risk of zoonotic influenza A viruses.
C1 [Turnbull, Matthew L.; Wise, Helen M.; Nicol, Marlynne Q.; Smith, Nikki; Beard, Philippa M.; Ligertwood, Yvonne; Hardisty, Gareth R.; Lycett, Samantha J.; Dutia, Bernadette M.; Digard, Paul] Univ Edinburgh, Div Infect & Immun, Roslin Inst, Edinburgh, Midlothian, Scotland.
[Dunfee, Rebecca L.; Jagger, Brett W.; Taubenberger, Jeffery K.] NIAID, Viral Pathogenesis & Evolut Sect, Infect Dis Lab, Div Intramural Res, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Jagger, Brett W.] Univ Cambridge, Div Virol, Dept Pathol, Cambridge, England.
[Xiao, Haixia; Benton, Donald J.; McCauley, John W.] Francis Crick Inst, Mill Hill Lab, Mill Hill, London, England.
[Coburn, Alice M.] Univ Glasgow, Ctr Virus Res, Glasgow, Lanark, Scotland.
[Paulo, Joao A.; Gygi, Steven P.] Harvard Med Sch, Dept Cell Biol, Boston, MA USA.
[Weekes, Michael P.] Univ Cambridge, Cambridge Inst Med Res, Cambridge, England.
[Wise, Helen M.] Heriot Watt Univ, Dept Engn & Phys Sci, Edinburgh, Midlothian, Scotland.
[Xiao, Haixia] Chinese Acad Sci, Tianjin Inst Ind Biotechnol, Lab Prot Engn & Vaccines, Tianjin, Peoples R China.
RP Digard, P (reprint author), Univ Edinburgh, Div Infect & Immun, Roslin Inst, Edinburgh, Midlothian, Scotland.
EM paul.digard@roslin.ed.ac.uk
OI Lycett, Samantha/0000-0003-3159-596X
FU Wellcome Trust [108070/Z/15/Z]; Medical Research Council (MRC)
[MR/K000276/1]; Biotechnology and Biological Sciences Research Council
(BBSRC) [BB/J004324/1, BB/J01446X/1]; Division of Intramural Research,
National Institute of Allergy and Infectious Diseases (DIR, NIAID);
University Of Edinburgh
FX This work, including the efforts of Michael P. Weekes, was funded by
Wellcome Trust (108070/Z/15/Z). This work, including the efforts of Paul
Digard, was funded by Medical Research Council (MRC) (MR/K000276/1).
This work, including the efforts of Helen M. Wise, Philippa Beard,
Samantha J. Lycett, Bernadette Dutia, and Paul Digard, was funded by
Biotechnology and Biological Sciences Research Council (BBSRC)
(BB/J004324/1). This work, including the efforts of Matthew L. Turnbull,
was funded by Biotechnology and Biological Sciences Research Council
(BBSRC) (BB/J01446X/1). This work, including the efforts of Jeffery K.
Taubenberger, was funded by Division of Intramural Research, National
Institute of Allergy and Infectious Diseases (DIR, NIAID). This work,
including the efforts of Samantha J. Lycett, was funded by University Of
Edinburgh (Chancellor's Fellowship).
NR 99
TC 0
Z9 0
U1 8
U2 8
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD OCT
PY 2016
VL 90
IS 20
BP 9263
EP 9284
DI 10.1128/JVI.01205-16
PG 22
WC Virology
SC Virology
GA DX7NO
UT WOS:000384574900041
PM 27489273
ER
PT J
AU Jager, J
Mahler, A
An, D
Putnick, DL
Bornstein, MH
Lansford, JE
Dodge, KA
Skinner, AT
Deater-Deckard, K
AF Jager, Justin
Mahler, Alissa
An, Danming
Putnick, Diane L.
Bornstein, Marc H.
Lansford, Jennifer E.
Dodge, Kenneth A.
Skinner, Ann T.
Deater-Deckard, Kirby
TI Early Adolescents' Unique Perspectives of Maternal and Paternal
Rejection: Examining Their Across-Dyad Generalizability and Relations
with Adjustment 1 Year Later
SO JOURNAL OF YOUTH AND ADOLESCENCE
LA English
DT Article
DE Unique perspectives; Parental rejection; Internalizing; Externalizing;
Early adolescence
ID PARENTAL ACCEPTANCE-REJECTION; FAMILY-MEMBERS UNIQUE; INFORMANT
DISCREPANCIES; CHILD; PERCEPTIONS; PSYCHOPATHOLOGY; VALIDITY; MOTHERS;
SCORES
AB Parental rejection is linked to deep and enduring adjustment problems during adolescence. This study aims to further clarify this relation by demonstrating what has long been posited by parental acceptance/rejection theory but never validated empirically-namely that adolescents' unique or subjective experience of parental rejection independently informs their future adjustment. Among a longitudinal, multi-informant sample of 161 families (early adolescents were 47 % female and 40 % European American) this study utilized a multitrait-multimethod confirmatory factor analysis to isolate for each early adolescent-parent dyad, the adolescent's distinct view of parental rejection (i.e., the adolescent unique perspective) from the portion of his or her view that overlaps with his or her parent's view. The findings indicated that adolescents' unique perspectives of maternal rejection were not differentiated from their unique perspectives of paternal rejection. Also, consistent with parental acceptance-rejection theory, early adolescents' unique perspectives of parental rejection were associated with worse adjustment (internalizing and externalizing) 1 year later. This study further demonstrates the utility and validity of the multitrait-multimethod confirmatory factor analysis approach for identifying and examining adolescent unique perspectives. Both conceptually and analytically, this study also integrates research focused on unique perspectives with a distinct but related line of research focused on discrepancies in perspectives.
C1 [Jager, Justin; An, Danming] Arizona State Univ, T Denny Sanford Sch Social & Family Dynam, POB 873701, Tempe, AZ 85287 USA.
[Mahler, Alissa] Univ Calif Irvine, Dept Psychol & Social Behav, 5300 Social & Behav Sci Gateway, Irvine, CA 92697 USA.
[Putnick, Diane L.; Bornstein, Marc H.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Child & Family Res, 6705 Rockledge Dr, Bethesda, MD 20892 USA.
[Lansford, Jennifer E.; Dodge, Kenneth A.; Skinner, Ann T.] Duke Univ, Ctr Child & Family Policy, Box 90545, Durham, NC 27708 USA.
[Deater-Deckard, Kirby] Univ Massachusetts, Dept Psychol & Brain Sci, 441 Tobin Hall, Amherst, MA 01003 USA.
RP Jager, J (reprint author), Arizona State Univ, T Denny Sanford Sch Social & Family Dynam, POB 873701, Tempe, AZ 85287 USA.
EM justin.jager@asu.edu; amahler@uci.edu; danming.an@asu.edu;
putnickd@mail.nih.gov; Marc_H_Bornstein@nih.gov; lansford@duke.edu;
dodge@duke.edu; askinner@duke.edu; kdeaterdeck@umass.edu
OI Putnick, Diane/0000-0002-6323-749X
FU Intramural Research Program of the NIH, NICHD; Eunice Kennedy Shriver
National Institute of Child Health and Human Development [RO1-HD054805]
FX DP and MB were supported by the Intramural Research Program of the NIH,
NICHD. This research has been funded by the Eunice Kennedy Shriver
National Institute of Child Health and Human Development grant
RO1-HD054805.
NR 34
TC 1
Z9 1
U1 0
U2 0
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0047-2891
EI 1573-6601
J9 J YOUTH ADOLESCENCE
JI J. Youth Adolesc.
PD OCT
PY 2016
VL 45
IS 10
SI SI
BP 2108
EP 2124
DI 10.1007/s10964-016-0509-z
PG 17
WC Psychology, Developmental
SC Psychology
GA DX7KX
UT WOS:000384567200011
PM 27262697
ER
PT J
AU Johnson, SL
Reichenberg, R
Bradshaw, CP
Haynie, DL
Cheng, TL
AF Johnson, Sarah Lindstrom
Reichenberg, Raymond
Bradshaw, Catherine P.
Haynie, Denise L.
Cheng, Tina L.
TI Caregiver and Adolescent Discrepancies in Perceptions of Violence and
Their Associations with Early Adolescent Aggression
SO JOURNAL OF YOUTH AND ADOLESCENCE
LA English
DT Article
DE Violence; Parents; Discrepancies; Structural equation modeling
ID MIDDLE SCHOOL STUDENTS; COMMUNITY VIOLENCE; PSYCHOLOGICAL SYMPTOMS;
COLLECTIVE EFFICACY; PARENTS KNOW; EXPOSURE; CHILDREN; YOUTH; BEHAVIORS;
SUPPORT
AB This article examined the role of caregiver messages about violence and exposure to neighborhood violence on adolescent aggression in light of research regarding discrepancies between parents and their children. Drawing upon data from an urban African American sample of 144 caregiver/early adolescent dyads (M = 12.99; SD = 0.93; 58.7 % female) we examined covariates of discrepancies between caregiver and adolescent reports of perceptions of violence as well as their association with adolescent aggression. Analyses suggested that concordance in perceptions of violence was associated with children's attitudes about violence and caregivers' perceptions of family communication. Structural equation modeling indicated a unique role for individual perceptions and suggested that agreement in awareness of neighborhood violence could be protective for early adolescent involvement in aggression.
C1 [Johnson, Sarah Lindstrom; Reichenberg, Raymond] Arizona State Univ, POB 873701, Tempe, AZ 85287 USA.
[Bradshaw, Catherine P.] Univ Virginia, Bavaro Hall,112D, Charlottesville, VA 22904 USA.
[Haynie, Denise L.] Eunice Kennedy Shriver Natl Inst Child Hlth & Dev, 6100 Execut Blvd,Room 7B13P,MSC7510, Rockville, MD 20892 USA.
[Cheng, Tina L.] Johns Hopkins Univ, 200 North Wolfe St,Suite 2055, Baltimore, MD 21287 USA.
RP Johnson, SL (reprint author), Arizona State Univ, POB 873701, Tempe, AZ 85287 USA.
EM sarahlj@asu.edu
OI Haynie, Denise/0000-0002-8270-6079
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development (NICHD) [1K24HD052559]; NICHD Intramural Research Program;
DC-Baltimore Research Center on Child Health Disparities from the
National Center on Minority Health and Health Disparities [P20
MD000198]; Centers for Disease Control and Prevention [U01CE0011954]
FX This publication was supported by the Eunice Kennedy Shriver National
Institute of Child Health and Human Development (NICHD) Grant Number
1K24HD052559 (Cheng) and the NICHD Intramural Research Program (Haynie),
DC-Baltimore Research Center on Child Health Disparities Grant Number
P20 MD000198 from the National Center on Minority Health and Health
Disparities (Cheng), and Centers for Disease Control and Prevention
Grant Number U01CE0011954 (Bradshaw). Its contents are solely the
responsibility of the authors and do not necessarily represent the
official views of the funding agencies.
NR 45
TC 1
Z9 1
U1 1
U2 1
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0047-2891
EI 1573-6601
J9 J YOUTH ADOLESCENCE
JI J. Youth Adolesc.
PD OCT
PY 2016
VL 45
IS 10
SI SI
BP 2125
EP 2137
DI 10.1007/s10964-016-0505-3
PG 13
WC Psychology, Developmental
SC Psychology
GA DX7KX
UT WOS:000384567200012
ER
PT J
AU Ambikapathi, R
Kosek, MN
Lee, GO
Mahopo, C
Patil, CL
Maciel, BL
Turab, A
Islam, MM
Ulak, M
Bose, A
Olortegui, MP
Pendergast, LL
Murray-Kolb, LE
Lang, D
McCormick, BJJ
Caulfield, LE
AF Ambikapathi, Ramya
Kosek, Margaret N.
Lee, Gwenyth O.
Mahopo, Cloupas
Patil, Crystal L.
Maciel, Bruna L.
Turab, Ali
Islam, M. Munirul
Ulak, Manjeswori
Bose, Anuradha
Paredes Olortegui, Maribel
Pendergast, Laura L.
Murray-Kolb, Laura E.
Lang, Dennis
McCormick, Benjamin J. J.
Caulfield, Laura E.
TI How multiple episodes of exclusive breastfeeding impact estimates of
exclusive breastfeeding duration: report from the eight-site MAL-ED
birth cohort study
SO MATERNAL AND CHILD NUTRITION
LA English
DT Article
DE exclusive breastfeeding; duration; DHS; prevalence; metrics; MAL-ED;
Nepal; Bangladesh; Pakistan; India; Brazil; Peru; Tanzania; South Africa
ID INFANTS; HEALTH; SITE; CONSEQUENCES; PREVALENCE; BANGLADESH; BARRIERS;
MOTHERS; EXAMPLE; AFRICA
AB The duration of exclusive breastfeeding (EBF) is often defined as the time from birth to the first non-breast milk food/liquid fed (EBFLONG), or it is estimated by calculating the proportion of women at a given infant age who EBF in the previous 24h (EBFDHS). Others have measured the total days or personal prevalence of EBF (EBFPREV), recognizing that although non-EBF days may occur, EBF can be re-initiated for extended periods. We compared breastfeeding metrics in the MAL-ED study; infants' breastfeeding trajectories were characterized from enrollment (median 7days, IQR: 4, 12) to 180days at eight sites. During twice-weekly surveillance, caretakers were queried about infant feeding the prior day. Overall, 101833 visits and 356764 child days of data were collected from 1957 infants. Median duration of EBFLONG was 33days (95% CI: 32-36), compared to 49days based on the EBFDHS. Median EBFPREV was 66days (95% CI: 62-70). Differences were because of the return to EBF after a non-EBF period. The median number of returns to EBF was 2 (IQR: 1, 3). When mothers re-initiated EBF (second episode), infants gained an additional 18.8days (SD: 25.1) of EBF, and gained 13.7days (SD: 18.1) (third episode). In settings where women report short gaps in EBF, programmes should work with women to return to EBF. Interventions could positively influence the duration of these additional periods of EBF and their quantification should be considered in impact evaluation studies. (c) 2016 John Wiley & Sons Ltd
C1 [Ambikapathi, Ramya; Murray-Kolb, Laura E.; Lang, Dennis; McCormick, Benjamin J. J.] NIH, Fogarty Int Ctr, Bldg 10, Bethesda, MD 20892 USA.
[Ambikapathi, Ramya; Kosek, Margaret N.; Lee, Gwenyth O.; Murray-Kolb, Laura E.; Caulfield, Laura E.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Int Hlth, Ctr Human Nutr, 615 North Wolfe St,W2041, Baltimore, MD 21205 USA.
[Mahopo, Cloupas] Univ Venda, Sch Hlth Sci, Dept Nutr, Thohoyandou, Limpopo Provinc, South Africa.
[Patil, Crystal L.] Univ Illinois, Coll Nursing, Dept Women Children & Family Hlth Sci, Chicago, IL USA.
[Maciel, Bruna L.] Univ Estadual Ceara, Dept Nutr, Fortaleza, Ceara, Brazil.
[Turab, Ali; Pendergast, Laura L.] Aga Khan Univ, Dept Paediat & Child Hlth, Karachi, Pakistan.
[Islam, M. Munirul] Int Ctr Diarrhoeal Dis Res, Ctr Nutr & Food Secur, Dhaka, Bangladesh.
[Ulak, Manjeswori] Tribhuvan Univ, Dept Child Hlth, Kathmandu, Nepal.
[Ulak, Manjeswori] Tribhuvan Univ, Inst Med, Kathmandu, Nepal.
[Bose, Anuradha] Christian Med Coll & Hosp, Vellore, Tamil Nadu, India.
[Paredes Olortegui, Maribel] Biomed Invest Unit AB PRISMA, Iquitos, Peru.
Temple Univ, Sch Psychol Program, Philadelphia, PA 19122 USA.
Penn State Univ, Dept Nutr Sci, State Coll, PA USA.
RP Caulfield, LE (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Int Hlth, Ctr Human Nutr, 615 North Wolfe St,W2041, Baltimore, MD 21205 USA.
EM lcaulfi1@jhu.edu
FU Bill & Melinda Gates Foundation; Foundation for the NIH; National
Institutes of Health/Fogarty International Center; Integrative Graduate
Education and Research Traineeship (IGERT) [1069213]; JHU Environment,
Energy, Sustainability and Health Institute (E2SHI) fellowship; JHSPH
Center of Global Health
FX The Etiology, Risk Factors and Interactions of Enteric Infections and
Malnutrition and the Consequences for Child Health and Development
Project (MAL-ED) is carried out as a collaborative project supported by
the Bill & Melinda Gates Foundation, the Foundation for the NIH and the
National Institutes of Health/Fogarty International Center. Ramya
Ambikapathi received the Kruse Family Publications Award and is funded
by the Integrative Graduate Education and Research Traineeship (IGERT
Award 1069213), a JHU Environment, Energy, Sustainability and Health
Institute (E2SHI) fellowship and JHSPH Center of Global
Health.
NR 55
TC 1
Z9 1
U1 2
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1740-8695
EI 1740-8709
J9 MATERN CHILD NUTR
JI Matern. Child Nutr.
PD OCT
PY 2016
VL 12
IS 4
BP 740
EP 756
DI 10.1111/mcn.12352
PG 17
WC Nutrition & Dietetics; Pediatrics
SC Nutrition & Dietetics; Pediatrics
GA DX8QA
UT WOS:000384652400008
PM 27500709
ER
PT J
AU Delitala, AP
Steri, M
Pilia, MG
Dei, M
Lai, S
Delitala, G
Schlessinger, D
Cucca, F
AF Delitala, Alessandro P.
Steri, Maristella
Pilia, Maria Grazia
Dei, Mariano
Lai, Sandra
Delitala, Giuseppe
Schlessinger, David
Cucca, Francesco
TI Menopause modulates the association between thyrotropin levels and lipid
parameters: The SardiNIA study
SO MATURITAS
LA English
DT Article
DE Cholesterol; Subclinical hypothyroidism; TSH; Menopause; Estrogen
ID DENSITY-LIPOPROTEIN CHOLESTEROL; THYROID-STIMULATING HORMONE;
SUBCLINICAL HYPOTHYROIDISM; ARTERIAL STIFFNESS; HEPATIC LIPASE; DISEASE;
TSH; AGE; POPULATION; PREVALENCE
AB Objective: Thyroid hormone influences lipoprotein metabolism. The role of menopausal status in this association has not been extensively studied. The aim of the present study is to evaluate the association between lipid parameters and mild elevations of thyrotropin (TSH), and whether menopause influences this relationship.
Study design: A cross-sectional study was conducted with a sample of 2,914 women (aged 14-102 years) from the SardiNIA study.
Main outcome measures: The association of TSH with blood lipid levels was examined using regression analyses, according to menopausal status.
Results: Postmenopausal women had lower serum TSH concentrations and higher levels of total cholesterol, low-density lipoprotein cholesterol (LDLc), high-density lipoprotein cholesterol (HDLc), and triglycerides than did premenopausal women (p = 0.001 or less for all). In premenopausal women, after adjusting for the confounders age, BMI, smoking, insulin and glycaemia, TSH showed a direct relation to the levels of total cholesterol (beta = 0.046, p = 0.010), LDLc (beta = 0.044, p = 0.016) and triglycerides (beta = 0.085, p < 0.001), but no association with HDLc level. In the postmenopausal group, TSH was directly associated only with triglyceride levels (beta = 0.103, p = 0.014).
Conclusions: The association between mild elevation of TSH and lipid levels is influenced by menopausal status. Further research is needed to clarify this finding. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
C1 [Delitala, Alessandro P.] Azienda Osped Univ Sassari, Viale San Pietro 8, I-07100 Sassari, Italy.
[Steri, Maristella; Pilia, Maria Grazia; Dei, Mariano; Lai, Sandra; Cucca, Francesco] CNR, IRGB, Cittadella Univ Monserrato, Cagliari, Italy.
[Delitala, Giuseppe] Univ Sassari, Dept Clin & Expt Med, Sassari, Italy.
[Schlessinger, David] NIA, NIH, Dept Hlth & Human Serv, Baltimore, MD 21224 USA.
[Cucca, Francesco] Univ Sassari, Dept Biomed Sci, Sassari, Italy.
RP Delitala, AP (reprint author), Azienda Osped Univ Sassari, Viale San Pietro 8, I-07100 Sassari, Italy.
EM aledelitala@tiscali.it
FU NIH, National Institute on Aging [NO1-AG-1-2109]
FX This work was supported in part by Contract NO1-AG-1-2109 from the NIH,
National Institute on Aging.
NR 31
TC 1
Z9 1
U1 1
U2 1
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0378-5122
EI 1873-4111
J9 MATURITAS
JI Maturitas
PD OCT
PY 2016
VL 92
BP 30
EP 34
DI 10.1016/j.maturitas.2016.07.003
PG 5
WC Geriatrics & Gerontology; Obstetrics & Gynecology
SC Geriatrics & Gerontology; Obstetrics & Gynecology
GA DY0LG
UT WOS:000384787700006
PM 27621235
ER
PT J
AU Brosh, RM
AF Brosh, Robert M. Jrr
TI Special Methods collection on DNA helicases
SO METHODS
LA English
DT Editorial Material
AB In this special Methods collection on DNA helicases, I have solicited articles from leading experts in the field with a priority to gather a defined series of papers on highly relevant topics that encompass biological, biochemical, and biophysical aspects of helicase function. The experimental approaches described provide an opportunity for both new and more experienced scientists to use the information for the design of their own investigations. The reader will find detailed methods for single -molecule studies, novel biochemical experiments, genetic analyses, and cell biological assays in a variety of systems with an emphasis placed on state-of-the-art techniques to measure helicase function. Contributing authors were strongly encouraged to provide a carefully constructed description of the methods employed so that others might use this information in a manner that will be useful for their own particular application and helicase of interest. This special issue of Methods dedicated to DNA helicases offers readers a treasure chest of unique experimental approaches and protocols focused on rapidly developing techniques that are useful for studying both in vivo and in vitro aspects of helicase function. Published by Elsevier Inc.
C1 [Brosh, Robert M. Jrr] NIA, Lab Mol Gerontol, NIH, NIH Biomed Res Ctr, 251 Bayview Blvd, Baltimore, MD 21224 USA.
RP Brosh, RM (reprint author), NIA, Lab Mol Gerontol, NIH, NIH Biomed Res Ctr, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM broshr@mail.nih.gov
NR 16
TC 0
Z9 0
U1 3
U2 3
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 1
PY 2016
VL 108
BP 1
EP 3
DI 10.1016/j.ymeth.2016.08.009
PG 3
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA DX8IY
UT WOS:000384632500001
PM 27565743
ER
PT J
AU Lu, X
Parvathaneni, S
Li, XL
Lal, A
Sharma, S
AF Lu, Xing
Parvathaneni, Swetha
Li, Xiao Ling
Lal, Ashish
Sharma, Sudha
TI Transcriptome guided identification of novel functions of RECQ1 helicase
SO METHODS
LA English
DT Article
DE Gene expression; RecQ; Helicase; G4; Cell migration; Cell invasion
ID G-QUADRUPLEX DNA; REPLICATION STRESS; GENE-EXPRESSION; CANCER; ROLES;
RESISTANCE; PROMOTERS; GENOME; REPAIR; DAMAGE
AB Gene expression changes in the functional absence of a specific RecQ protein, and how that relates to disease outcomes including cancer predisposition and premature aging in RecQ helicase associated syndromes, are poorly understood. Here we describe detailed experimental strategy for identification of RECQ1-regulated transcriptome that led us to uncover a novel association of RECQ1 in regulation of cancer cell migration and invasion. We initiated a focused study to determine whether RECQ1, the most abundant RecQ protein in humans, alters gene expression and also investigated whether RECQ1 binds with G4 motifs predicted to form G-quadruplex structures in the target gene promoters. Rescue of mRNA expression of select RECQ1-downregulated genes harboring G4 motifs required wild-type RECQ1 helicase. However, some RECQ1-regulated genes are also regulated by BLM and WRN proteins regardless of the presence or absence of G4 motifs. The approach described here is applicable for systematic comparison of gene expression signatures of individual RecQ proteins in isogenic background, and to elucidate their participation in transcription regulation through G-quadruplex recognition and/or resolution. Such strategies might also reveal molecular pathways that drive the pathogenesis of cancer and other diseases in specific RecQ deficiency. (C) 2016 Elsevier Inc. All rights reserved.
C1 [Lu, Xing; Parvathaneni, Swetha; Sharma, Sudha] Howard Univ, Dept Biochem & Mol Biol, Coll Med, 520 W St NW, Washington, DC 20059 USA.
[Li, Xiao Ling; Lal, Ashish] NCI, Regulatory RNAs & Canc Sect, Genet Branch, NIH, Bethesda, MD 20892 USA.
RP Sharma, S (reprint author), Howard Univ, Dept Biochem & Mol Biol, Coll Med, 520 W St NW, Washington, DC 20059 USA.
EM sudha.sharma@howard.edu
OI Sharma, Sudha/0000-0003-2765-2482
FU NIGMS/NIH [5SC1GM093999-06]; Intramural Research Program of the National
Institutes of Health, National Cancer Institute, and Center for Cancer
Research; NIMHD/NIH [G12MD007597]
FX This work was funded by the NIGMS/NIH Grant 5SC1GM093999-06 to Sudha
Sharma and the Intramural Research Program of the National Institutes of
Health, National Cancer Institute, and Center for Cancer Research to
Ashish Lal. We also acknowledge infrastructure support from the
NIMHD/NIH under award number G12MD007597.
NR 36
TC 2
Z9 2
U1 2
U2 2
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 1
PY 2016
VL 108
BP 111
EP 117
DI 10.1016/j.ymeth.2016.04.018
PG 7
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA DX8IY
UT WOS:000384632500012
PM 27102625
ER
PT J
AU Banerjee, T
Aggarwal, M
Sommers, JA
Brosh, RM
AF Banerjee, Taraswi
Aggarwal, Monika
Sommers, Joshua A.
Brosh, Robert M., Jr.
TI Biochemical and cell biological assays to identify and characterize DNA
helicase inhibitors
SO METHODS
LA English
DT Article
DE Helicase; Replication; DNA repair; Small molecule; Inhibitor; Werner
syndrome; Cancer therapy
ID WERNER-SYNDROME HELICASE; FANCONI-ANEMIA PATHWAY; HOMOLOGOUS
RECOMBINATION; SYNTHETIC LETHALITY; RECENT PROGRESS; CANCER-THERAPY;
REPAIR; TELOMERES; BINDING; DISSOCIATION
AB The growing number of DNA helicases implicated in hereditary disorders and cancer indicates that this particular class of enzymes plays key roles in genomic stability and cellular homeostasis. Indeed, a large body of work has provided molecular and cellular evidence that helicases act upon a variety of nucleic acid substrates and interact with numerous proteins to enact their functions in replication, DNA repair, recombination, and transcription. Understanding how helicases operate in unique and overlapping pathways is a great challenge to researchers. In this review, we describe a series of experimental approaches and methodologies to identify and characterize DNA helicase inhibitors which collectively provide an alternative and useful strategy to explore their biological significance in cell-based systems. These procedures were used in the discovery of biologically active compounds that inhibited the DNA unwinding function catalyzed by the human WRN helicase-nuclease defective in the premature aging disorder Werner syndrome. We describe in vitro and in vivo experimental approaches to characterize helicase inhibitors with WRN as the model, anticipating that these approaches may be extrapolated to other DNA helicases, particularly those implicated in DNA repair and/or the replication stress response. Published by Elsevier Inc.
C1 [Banerjee, Taraswi; Sommers, Joshua A.; Brosh, Robert M., Jr.] NIA, Lab Mol Gerontol, NIH, NIH Biomed Res Ctr, 251 Bayview Blvd, Baltimore, MD 21224 USA.
[Aggarwal, Monika] Georgetown Univ, Lombardi Comprehens Canc Res Ctr, Med Ctr, Washington, DC 20057 USA.
RP Brosh, RM (reprint author), NIA, Lab Mol Gerontol, NIH, NIH Biomed Res Ctr, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM broshr@mail.nih.gov
FU Intramural Research Program of the NIH, National Institute on Aging
FX This research was supported in full by the Intramural Research Program
of the NIH, National Institute on Aging.
NR 39
TC 2
Z9 2
U1 8
U2 8
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 1
PY 2016
VL 108
BP 130
EP 141
DI 10.1016/j.ymeth.2016.04.007
PG 12
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA DX8IY
UT WOS:000384632500014
PM 27064001
ER
PT J
AU Denkert, C
Wienert, S
Poterie, A
Loibl, S
Budczies, J
Badve, S
Bago-Horvath, Z
Bane, A
Bedri, S
Brock, J
Chmielik, E
Christgen, M
Colpaert, C
Demaria, S
Van den Eynden, G
Floris, G
Fox, SB
Gao, D
Heppner, BI
Kim, SR
Kos, Z
Kreipe, HH
Lakhani, SR
Penault-Llorca, F
Pruneri, G
Radosevic-Robin, N
Rimm, DL
Schnitt, SJ
Sinn, BV
Sinn, P
Sirtaine, N
O'Toole, SA
Viale, G
Van de Vijver, K
de Wind, R
von Minckwitz, G
Klauschen, F
Untch, M
Fasching, PA
Reimer, T
Willard-Gallo, K
Michiels, S
Loi, S
Salgado, R
AF Denkert, Carsten
Wienert, Stephan
Poterie, Audrey
Loibl, Sibylle
Budczies, Jan
Badve, Sunil
Bago-Horvath, Zsuzsanna
Bane, Anita
Bedri, Shahinaz
Brock, Jane
Chmielik, Ewa
Christgen, Matthias
Colpaert, Cecile
Demaria, Sandra
Van den Eynden, Gert
Floris, Giuseppe
Fox, Stephen B.
Gao, Dongxia
Heppner, Barbara Ingold
Kim, S. Rim
Kos, Zuzana
Kreipe, Hans H.
Lakhani, Sunil R.
Penault-Llorca, Frederique
Pruneri, Giancarlo
Radosevic-Robin, Nina
Rimm, David L.
Schnitt, Stuart J.
Sinn, Bruno V.
Sinn, Peter
Sirtaine, Nicolas
O'Toole, Sandra A.
Viale, Giuseppe
Van de Vijver, Koen
de Wind, Roland
von Minckwitz, Gunter
Klauschen, Frederick
Untch, Michael
Fasching, Peter A.
Reimer, Toralf
Willard-Gallo, Karen
Michiels, Stefan
Loi, Sherene
Salgado, Roberto
TI Standardized evaluation of tumor-infiltrating lymphocytes in breast
cancer: results of the ring studies of the international immuno-oncology
biomarker working group
SO MODERN PATHOLOGY
LA English
DT Article
ID NEOADJUVANT CHEMOTHERAPY; CARBOPLATIN; TRIALS
AB Multiple independent studies have shown that tumor-infiltrating lymphocytes (TIL) are prognostic in breast cancer with potential relevance for response to immune-checkpoint inhibitor therapy. Although many groups are currently evaluating TIL, there is no standardized system for diagnostic applications. This study reports the results of two ring studies investigating TIL conducted by the International Working Group on Immuno-oncology Biomarkers. The study aim was to determine the intraclass correlation coefficient (ICC) for evaluation of TIL by different pathologists. A total of 120 slides were evaluated by a large group of pathologists with a web-based system in ring study 1 and a more advanced software-system in ring study 2 that included an integrated feedback with standardized reference images. The predefined aim for successful ring studies 1 and 2 was an ICC above 0.7 (lower limit of 95% confidence interval (CI)). In ring study 1 the prespecified endpoint was not reached (ICC: 0.70; 95% CI: 0.62-0.78). On the basis of an analysis of sources of variation, we developed a more advanced digital image evaluation system for ring study 2, which improved the ICC to 0.89 (95% CI: 0.85-0.92). The Fleiss' kappa value for o60 vs >= 60% TIL improved from 0.45 (ring study 1) to 0.63 in RS2 and the mean concordance improved from 88 to 92%. This large international standardization project shows that reproducible evaluation of TIL is feasible in breast cancer. This opens the way for standardized reporting of tumor immunological parameters in clinical studies and diagnostic practice. The software-guided image evaluation approach used in ring study 2 may be of value as a tool for evaluation of TIL in clinical trials and diagnostic practice. The experience gained from this approach might be applicable to the standardization of other diagnostic parameters in histopathology.
C1 [Denkert, Carsten; Wienert, Stephan; Budczies, Jan; Heppner, Barbara Ingold; Sinn, Bruno V.; Klauschen, Frederick] Charite, Inst Pathol, Charitepl 1, D-10117 Berlin, Germany.
[Denkert, Carsten; Budczies, Jan] German Canc Consortium DKTK, Partner Site Berlin, Berlin, Germany.
[Wienert, Stephan] VMscope GmbH, Berlin, Germany.
[Poterie, Audrey] Inst Gustave Roussy, Serv Biostat & Epidemiol, Villejuif, France.
[Loibl, Sibylle; von Minckwitz, Gunter] GBG, Neu Isenburg, Germany.
[Loibl, Sibylle] Sana Klinikum Offenbach, Clin Gynecol & Obstet, Offenbach, Germany.
[Badve, Sunil] Indiana Univ Sch Med, Indianapolis, IN 46202 USA.
[Bago-Horvath, Zsuzsanna] Med Univ Wien, Clin Inst Pathol, Vienna, Austria.
[Bane, Anita] McMaster Univ, Dept Pathol & Mol Med, Hamilton, ON, Canada.
[Bedri, Shahinaz] Weill Cornell Med Coll, Doha, Qatar.
[Brock, Jane] Harvard Med Sch, Boston, MA USA.
[Chmielik, Ewa] Maria Sklodowska Curie Mem Canc Ctr, Tumor Pathol Dept, Gliwice, Poland.
[Chmielik, Ewa] Inst Oncol, Gliwice Branch, Gliwice, Poland.
[Christgen, Matthias; Kreipe, Hans H.] Hannover Med Sch, Inst Pathol, Hannover, Germany.
[Colpaert, Cecile] Sint Augustinus, GZA Ziekenhuizen, Pathol, Antwerp, Belgium.
[Demaria, Sandra] Weill Cornell Med Coll, Radiat Oncol & Pathol, New York, NY USA.
[Van den Eynden, Gert; Salgado, Roberto] GZA Hosp, Dept Pathol & Cytol, Antwerp, Belgium.
[Floris, Giuseppe] Univ Hosp Leuven, Dept Pathol, Leuven, Belgium.
[Fox, Stephen B.] Peter MacCallum Canc Ctr, Dept Pathol, Melbourne, Vic, Australia.
[Gao, Dongxia] Vancouver Hosp, Anat Pathol, Vancouver, BC, Canada.
[Kim, S. Rim] NSABP, Div Pathol, Pittsburgh, PA USA.
[Kos, Zuzana] Univ Ottawa, Dept Pathol & Lab Med, Ottawa, ON, Canada.
[Lakhani, Sunil R.] Univ Queensland, Clin Res Ctr, UQ Sch Med & Pathol Queensland, Brisbane, Qld, Australia.
[Penault-Llorca, Frederique; Radosevic-Robin, Nina] Univ Auvergne, Jean Perrin Comprehens Canc Ctr, Dept Pathol, ERTICa Res Team, EA4677, Clermont Ferrand, France.
[Pruneri, Giancarlo] Univ Milan, Div Pathol & Lab Med, Milan, Italy.
[Rimm, David L.] Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06510 USA.
[Schnitt, Stuart J.] Beth Israel Deaconess Med Ctr, Dept Pathol, Boston, MA 02215 USA.
[Sinn, Bruno V.] Univ Texas MD Anderson Canc Ctr, Dept Translat Mol Pathol, Houston, TX 77030 USA.
[Sinn, Peter] Heidelberg Univ, Inst Pathol, Sekt Gynakopathol, Heidelberg, Germany.
[Sirtaine, Nicolas] Inst Jules Bordet, Anat Pathol, Brussels, Belgium.
[O'Toole, Sandra A.] Royal Prince Alfred Hosp, Dept Tissue Pathol & Diagnost Oncol, Mol Diagnost Oncol, Camperdown, NSW, Australia.
[Viale, Giuseppe] Univ Milan, European Inst Oncol, Dept Pathol, Milan, Italy.
[Van de Vijver, Koen] Netherlands Canc Inst, Dept Pathol, Amsterdam, Netherlands.
[de Wind, Roland] Inst Jules Bordet, Brussels, Belgium.
[Untch, Michael] Helios Klinikum Berlin Buch, Dept Gynecol, Berlin, Germany.
[Fasching, Peter A.] Univ Erlangen Nurnberg, Comprehens Canc Ctr Erlangen EMN, Univ Hosp Erlangen, Dept Gynecol & Obstet, Erlangen, Germany.
[Reimer, Toralf] Klinikum Sudstadt Rostock, Dept Gynecol, Rostock, Germany.
[Willard-Gallo, Karen] Inst Jules Bordet, Mol Immunol Unit, Brussels, Belgium.
[Michiels, Stefan] Univ Paris Saclay, Univ Paris 11, Serv Biostat & Epidemiol, Gustave Roussy,CESP,Inserm U1018, Villejuif, France.
[Loi, Sherene] Peter MacCallum Canc Ctr, Div Res & Clin Med, Melbourne, Vic, Australia.
[Salgado, Roberto] Inst Jules Bordet, Breast Canc Translat Res Lab, Brussels, Belgium.
RP Denkert, C (reprint author), Charite, Inst Pathol, Charitepl 1, D-10117 Berlin, Germany.
EM carsten.denkert@charite.de
RI Michiels, Stefan/L-1516-2013;
OI Michiels, Stefan/0000-0002-6963-2968; Fox, Stephen/0000-0002-7648-8896
FU European Commission [278659, BMBF-01KT1314]
FX We would like to thank all patients, clinicians, and pathologists
participating in the clinical studies and the biomaterial collection. We
are grateful for the excellent technical assistance by Britta Beyer,
Sylwia Handzik, Ines Koch, Petra Wachs as well as Peggy Wolkenstein.
Funding was given by the European Commission FP7, Grant 278659
(RESPONSIFY) and the TRANSCAN-I, Grant BMBF-01KT1314 (TRANSCAN-I UGI 1).
NR 20
TC 6
Z9 6
U1 6
U2 6
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
EI 1530-0285
J9 MODERN PATHOL
JI Mod. Pathol.
PD OCT
PY 2016
VL 29
IS 10
BP 1155
EP 1164
DI 10.1038/modpathol.2016.109
PG 10
WC Pathology
SC Pathology
GA DX7DZ
UT WOS:000384548100003
PM 27363491
ER
PT J
AU Alikhan, M
Song, JY
Sohani, AR
Moroch, J
Plonquet, A
Duffield, AS
Borowitz, MJ
Jiang, LY
Bueso-Ramos, C
Inamdar, K
Menon, MP
Gurbuxani, S
Chan, E
Smith, SM
Nicolae, A
Jaffe, ES
Gaulard, P
Venkataraman, G
AF Alikhan, Mir
Song, Joo Y.
Sohani, Aliyah R.
Moroch, Julien
Plonquet, Anne
Duffield, Amy S.
Borowitz, Michael J.
Jiang, Liuyan
Bueso-Ramos, Carlos
Inamdar, Kedar
Menon, Madhu P.
Gurbuxani, Sandeep
Chan, Ernest
Smith, Sonali M.
Nicolae, Alina
Jaffe, Elaine S.
Gaulard, Philippe
Venkataraman, Girish
TI Peripheral T-cell lymphomas of follicular helper T-cell type frequently
display an aberrant CD3(-/dim)CD(4+) population by flow cytometry: an
important clue to the diagnosis of a Hodgkin lymphoma mimic
SO MODERN PATHOLOGY
LA English
DT Article
ID IMMUNOPHENOTYPIC ANALYSIS; CONSENSUS RECOMMENDATIONS; NEOPLASTIC-CELLS;
GROWTH-PATTERN; EXPRESSION; CD10; PHENOTYPE; INVOLVEMENT; PROGRESSION;
DISEASE
AB Nodal follicular helper T-cell-derived lymphoproliferations (specifically the less common peripheral T-cell lymphomas of follicular type) exhibit a spectrum of histologic features that may mimic reactive hyperplasia or Hodgkin lymphoma. Even though angioimmunoblastic T-cell lymphoma and peripheral T-cell lymphoma of follicular type share a common biologic origin from follicular helper T-cells and their morphology has been well characterized, flow cytometry of peripheral T-cell lymphomas of follicular type has not been widely discussed as a tool for identifying this reactive hyperplasia/Hodgkin lymphoma mimic. We identified 10 peripheral T-cell lymphomas of follicular type with available flow cytometry data from five different institutions, including two cases with peripheral blood evaluation. For comparison, we examined flow cytometry data for 8 classical Hodgkin lymphomas (including 1 lymphocyte-rich classical Hodgkin lymphoma), 15 nodular lymphocyte predominant Hodgkin lymphomas, 15 angioimmunoblastic T-cell lymphomas, and 26 reactive nodes. Lymph node histology and flow cytometry data were reviewed, specifically for the presence of a CD3-/dimCD4+ aberrant T-cell population (described in angioimmunoblastic T-cell lymphomas), besides other T-cell aberrancies. Nine of 10 (90%) peripheral T-cell lymphomas of follicular type showed a CD3-/dimCD4+ T-cell population constituting 29.3% (range 7.9-62%) of all lymphocytes. Five of 10 (50%) had nodular lymphocyte predominant Hodgkin lymphoma or lymphocyte-rich classical Hodgkin lymphoma-like morphology with scattered Hodgkin-like cells that expressed CD20, CD30, CD15, and MUM1. Three cases had a nodular growth pattern and three others exhibited a perifollicular growth pattern without Hodgkin-like cells. Epstein-Barr virus was positive in 1 of 10 cases (10%). PCR analysis showed clonal T-cell receptor gamma gene rearrangement in all 10 peripheral T-cell lymphomas of follicular type. By flow cytometry, 11 of 15 (73.3%) angioimmunoblastic T-cell lymphomas showed the CD3-/dimCD4+ population (mean: 19.5%, range: 3-71.8%). Using a threshold of 3% for CD3-/dimCD4+ T cells, all 15 nodular lymphocyte predominant Hodgkin lymphoma controls and 8 classical Hodgkin lymphomas were negative (Mann-Whitney P = 0.01, F-PTCL vs Hodgkin lymphomas), as were 25 of 26 reactive lymph nodes. The high frequency of CD3-/dimCD4+ aberrant T cells is similar in angioimmunoblastic T-cell lymphomas and peripheral T-cell lymphomas of follicular type, and is a useful feature in distinguishing peripheral T-cell lymphomas of follicular type from morphologic mimics such as reactive hyperplasia or Hodgkin lymphoma.
C1 [Alikhan, Mir; Gurbuxani, Sandeep; Chan, Ernest; Venkataraman, Girish] Univ Chicago, Dept Pathol, 5841 S Maryland Ave, Chicago, IL 60637 USA.
[Song, Joo Y.] City Hope Natl Med Ctr, Med Ctr, Dept Pathol, Duarte, CA USA.
[Sohani, Aliyah R.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Moroch, Julien; Gaulard, Philippe] Univ Paris Est, Hop Henri Mondor, Dept Pathol, Creteil, France.
[Plonquet, Anne] Univ Paris Est, Hop Henri Mondor, Dept Immunol, Creteil, France.
[Duffield, Amy S.; Borowitz, Michael J.] Johns Hopkins Univ, Dept Pathol, Baltimore, MD USA.
[Jiang, Liuyan] Mayo Clin, Dept Pathol, Jacksonville, FL 32224 USA.
[Bueso-Ramos, Carlos] MD Anderson Canc Ctr, Dept Pathol, Houston, TX USA.
[Inamdar, Kedar; Menon, Madhu P.] Henry Ford Hlth Syst, Dept Pathol, Detroit, MI USA.
[Smith, Sonali M.] Univ Chicago, Dept Hematol Oncol, Chicago, IL 60637 USA.
[Nicolae, Alina; Jaffe, Elaine S.] NCI, Hematopathol Sect, NIH, Bethesda, MD 20892 USA.
RP Venkataraman, G (reprint author), Univ Chicago, Dept Pathol, Hematopathol Sect, 5841S Maryland Ave,TW055,MC0008, Chicago, IL 60637 USA.
EM Girish.Venkataraman@uchospitals.edu
NR 31
TC 1
Z9 1
U1 1
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
EI 1530-0285
J9 MODERN PATHOL
JI Mod. Pathol.
PD OCT
PY 2016
VL 29
IS 10
BP 1173
EP 1182
DI 10.1038/modpathol.2016.113
PG 10
WC Pathology
SC Pathology
GA DX7DZ
UT WOS:000384548100005
PM 27312067
ER
PT J
AU Han, JW
Lee, YH
Yoen, SI
Abramowitz, J
Birnbaumer, L
Lee, MG
Kim, JY
AF Han, Jung Woo
Lee, Young Ho
Yoen, Su-In
Abramowitz, Joel
Birnbaumer, Lutz
Lee, Min Goo
Kim, Joo Young
TI Resistance to pathologic cardiac hypertrophy and reduced expression of
Ca(V)1.2 in Trpc3-depleted mice
SO MOLECULAR AND CELLULAR BIOCHEMISTRY
LA English
DT Article
DE Transient receptor potential canonical channels 3; L-type Ca2+ channel;
Pathologic cardiac hypertrophy; Ca2+ influx
ID RECEPTOR POTENTIAL CHANNELS; TRPC CHANNELS; CA2+ CHANNELS; VENTRICULAR
DYSFUNCTION; PRESSURE-OVERLOAD; BLOOD-PRESSURE; HEART-FAILURE; MOUSE
HEART; CALCINEURIN; INHIBITION
AB Sustained elevation of intracellular Ca2+ concentration ([Ca2+](i)) reprograms cardiovascular cell fate, leading to cellular hypertrophy via Ca2+-calmodulin/calcineurin (Cn)/NFAT activation. Accumulating evidence suggests that transient receptor potential canonical (Trpc) channels play important roles in the development of pathologic cardiac hypertrophy. Here, we demonstrated that Trpc3 mediates pathologic cardiac hypertrophy in neurohumoral elevation via direct regulation of Ca(V)1.2 expressions. Elevated PE (phenylephrine) was maintained in mice by continuous infusion using an osmotic pump. Wild-type (WT) mice, but not Trpc3 (-/-) showed a sudden decrease in blood pressure (BP) or death following elevation of BP under conditions of elevated PE. Trpc3 (-/-) mesenteric artery showed decreased PE-stimulated vasoconstriction. Analysis of morphology, function, and pathologic marker expression revealed that PE elevation caused pathologic cardiac hypertrophy in WT mice, which was prevented by deletion of Trpc3. Interestingly, protection by Trpc3 deletion seemed to be a result of reduced cardiac Ca(V)1.2 expressions. Basal and PE induced increased expression of protein and mRNA of Ca(V)1.2 was decreased in Trpc3 (-/-) heart. Accordingly, altered expression of Ca(V)1.2 was observed by knockdown or stimulation of Trpc3 in cardiomyocytes. These findings suggest that Trpc3 is a mediator of pathologic cardiac hypertrophy not only through mediating part of the Ca2+ influx, but also through control of Ca(V)1.2 expressions.
C1 [Han, Jung Woo; Lee, Min Goo; Kim, Joo Young] Yonsei Univ, Coll Med, PLUS Project Med Sci 21, Dept Pharmacol & Brain Korea, 50 Yonsei Ro, Seoul 120752, South Korea.
[Lee, Young Ho; Yoen, Su-In] Yonsei Univ, Coll Med, Dept Physiol & Brain Korea, PLUS Project Med Sci 21, Seoul 120752, South Korea.
[Abramowitz, Joel; Birnbaumer, Lutz] NIEHS, Neurobiol Lab, Durham, NC 27709 USA.
RP Kim, JY (reprint author), Yonsei Univ, Coll Med, PLUS Project Med Sci 21, Dept Pharmacol & Brain Korea, 50 Yonsei Ro, Seoul 120752, South Korea.
EM ad2011@naver.com; YHLEE@yuhs.ac; YSI2012@yuhs.ac;
abramow1@niehs.nih.gov; birnbau1@gmail.com; mlee@yuhs.ac;
jooyoungkim@yuhs.ac
RI Abramowitz, Joel/A-2620-2015; Lee, Min Goo/D-5635-2012
OI Lee, Min Goo/0000-0001-7436-012X
FU National Research Foundation of Korea (NRF) - Korean government
[NRF-2011-0029459, MSIP-2013R1A3A2042197]; Intramural Research Program
of the NIH [Z01-ES101864]
FX We thank Jeungsik In in CPEC (Cardiovascular Product Evaluation Center)
at Yonsei University Health System, Jangwoo Cho in SI healthcare and
Heinmiller, Andrew in VisualSonics Inc. for helping echocardiogram
measurements and analysis. This work was supported by a National
Research Foundation of Korea (NRF) Grant funded by the Korean government
(No. NRF-2011-0029459 for JY KIM, MSIP-2013R1A3A2042197 for MG LEE) and
the Intramural Research Program of the NIH (Project Z01-ES101864 to LB).
NR 47
TC 0
Z9 0
U1 5
U2 5
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0300-8177
EI 1573-4919
J9 MOL CELL BIOCHEM
JI Mol. Cell. Biochem.
PD OCT
PY 2016
VL 421
IS 1-2
BP 55
EP 65
DI 10.1007/s11010-016-2784-0
PG 11
WC Cell Biology
SC Cell Biology
GA DW5EL
UT WOS:000383665000005
PM 27522668
ER
PT J
AU Gautam, A
Kumar, R
Dimitrov, G
Hoke, A
Hammamieh, R
Jett, M
AF Gautam, Aarti
Kumar, Raina
Dimitrov, George
Hoke, Allison
Hammamieh, Rasha
Jett, Marti
TI Identification of extracellular miRNA in archived serum samples by
next-generation sequencing from RNA extracted using multiple methods
SO MOLECULAR BIOLOGY REPORTS
LA English
DT Article
DE DoDSR; miRNA; Next-generation sequencing; Serum; Data analysis
ID CIRCULATING MICRORNA; BODY-FLUIDS; PLASMA; EXPRESSION; BIOMARKERS;
MIRBASE; MICROARRAY; CANCER; BIOGENESIS; DIAGNOSIS
AB miRNAs act as important regulators of gene expression by promoting mRNA degradation or by attenuating protein translation. Since miRNAs are stably expressed in bodily fluids, there is growing interest in profiling these miRNAs, as it is minimally invasive and cost-effective as a diagnostic matrix. A technical hurdle in studying miRNA dynamics is the ability to reliably extract miRNA as small sample volumes and low RNA abundance create challenges for extraction and downstream applications. The purpose of this study was to develop a pipeline for the recovery of miRNA using small volumes of archived serum samples. The RNA was extracted employing several widely utilized RNA isolation kits/methods with and without addition of a carrier. The small RNA library preparation was carried out using Illumina TruSeq small RNA kit and sequencing was carried out using Illumina platform. A fraction of five microliters of total RNA was used for library preparation as quantification is below the detection limit. We were able to profile miRNA levels in serum from all the methods tested. We found out that addition of nucleic acid based carrier molecules had higher numbers of processed reads but it did not enhance the mapping of any miRBase annotated sequences. However, some of the extraction procedures offer certain advantages: RNA extracted by TRIzol seemed to align to the miRBase best; extractions using TRIzol with carrier yielded higher miRNA-to-small RNA ratios. Nuclease free glycogen can be carrier of choice for miRNA sequencing. Our findings illustrate that miRNA extraction and quantification is influenced by the choice of methodologies. Addition of nucleic acid- based carrier molecules during extraction procedure is not a good choice when assaying miRNA using sequencing. The careful selection of an extraction method permits the archived serum samples to become valuable resources for high-throughput applications.
C1 [Gautam, Aarti; Hammamieh, Rasha; Jett, Marti] US Army Ctr Environm Hlth Res, 568 Doughten Dr, Ft Detrick, MD 21702 USA.
[Kumar, Raina; Dimitrov, George] Leidos Biomed Inc, Adv Biomed Comp Ctr, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
[Hoke, Allison] US Army Ctr Environm Hlth Res, Geneva Fdn, Ft Detrick, MD 21702 USA.
RP Jett, M (reprint author), US Army Ctr Environm Hlth Res, 568 Doughten Dr, Ft Detrick, MD 21702 USA.
EM marti.jett-tilton.civ@mail.mil
FU Military Operational Medicine Research Program at the United States Army
Medical Research and Materiel Command (USAMRMC) at Fort Detrick, MD
FX Work was supported by funding from the Military Operational Medicine
Research Program at the United States Army Medical Research and Materiel
Command (USAMRMC) at Fort Detrick, MD, in preparation for carrying out a
clinical trial of longitudinal assessment with Dr. Charles Marmar, New
York University Medical Center. Volunteers separately consented for
approval to use their archived samples in conjunction with their current
participation in the study. The data presented herein was obtained using
"test samples" from the DoDSR in preparation for the overarching study.
We would like to thank Dr. Julia Scheerer for her input.
NR 66
TC 0
Z9 0
U1 7
U2 7
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0301-4851
EI 1573-4978
J9 MOL BIOL REP
JI Mol. Biol. Rep.
PD OCT
PY 2016
VL 43
IS 10
BP 1165
EP 1178
DI 10.1007/s11033-016-4043-6
PG 14
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA DW3ZW
UT WOS:000383582600015
PM 27510798
ER
PT J
AU Shridhar, K
Aggarwal, A
Walia, GK
Gulati, S
Geetha, AV
Prabhakaran, D
Dhillon, PK
Rajaraman, P
AF Shridhar, Krithiga
Aggarwal, Aastha
Walia, Gagandeep Kaur
Gulati, Smriti
Geetha, A. V.
Prabhakaran, D.
Dhillon, Preet K.
Rajaraman, Preetha
TI Single nucleotide polymorphisms as markers of genetic susceptibility for
oral potentially malignant disorders risk: Review of evidence to date
SO ORAL ONCOLOGY
LA English
DT Review
DE Oral potentially malignant disorders; Susceptibility; SNP; Polymorphisms
ID SQUAMOUS-CELL CARCINOMA; GENOME-WIDE ASSOCIATION; NORTH INDIAN
POPULATION; NECROSIS-FACTOR-ALPHA; BETEL QUID CHEWERS; SUBMUCOUS
FIBROSIS; PREMALIGNANT LESIONS; DNA-REPAIR; CANCER-RISK; FUNCTIONAL
POLYMORPHISM
AB Background: Oral cancers are preceded by oral potentially malignant disorders (OPMD). Understanding genetic susceptibility for OPMD risk could provide an opportunity for risk assessment of oral cancer through early disease course. We conducted a review of single nucleotide polymorphism (SNP) studies for OPMD risk.
Methods: We identified all relevant studies examining associations of SNPs with OPMD (leukoplakia, erythroplakia and oral sub-mucous fibrosis) conducted world-wide between January, 2000 and February, 2016 using a combined keyword search on PubMed. Of these, 47 studies that presented results as odds ratios and 95% CI were considered for full review.
Results: The majority of eligible studies that explored candidate gene associations for OPMD were small (N < 200 cases), limiting their scope to provide strong inference for any SNP identified to date in any population. Commonly studied SNPs were genes of carcinogen metabolism (n = 18 studies), DNA repair (n = 11 studies), cell cycle control (n = 8 studies), extra-cellular matrix alteration (n = 8 studies) and immune-inflammatory (n = 6 studies) pathways. Based on significant associations as reported by two or more studies, suggestive markers included SNPs in GSTM1 (null), CCND1 (G870A), MMP3 (-1171; promotor region), TNF alpha (-308; rs800629), XPD (codon 751) and Gemin3 (rs197412) as well as in p53 (codon 72) in Indian populations. However, an equal or greater number of studies reported null or mixed associations for SNPs in GSTM1 (null), p53 (codon 72), XPD (codon 751), XRCC (rs25487 C/T), GSTT1 (null) and CYP1A1m1 (MspI site).
Conclusion: Candidate gene association studies have not yielded consistent data on risk loci for OPMD. High-throughput genotyping approaches for OPMD, with concurrent efforts for oral cancer, could prove useful in identifying robust risk-loci to help understand early disease course susceptibility for oral cancer. (C) 2016 The Authors. Published by Elsevier Ltd.
C1 [Shridhar, Krithiga; Aggarwal, Aastha; Walia, Gagandeep Kaur; Gulati, Smriti; Geetha, A. V.; Prabhakaran, D.; Dhillon, Preet K.] Publ Hlth Fdn India, Ctr Chron Condit & Injuries, 4th Floor,Plot 47,Sect 44, Gurgaon 122002, Haryana, India.
[Prabhakaran, D.] Ctr Chron Dis Control, Gurgaon, Haryana, India.
[Prabhakaran, D.] London Sch Hyg & Trop Med, London, England.
[Rajaraman, Preetha] NCI, Ctr Global Hlth, Bethesda, MD 20892 USA.
RP Shridhar, K (reprint author), Publ Hlth Fdn India, Ctr Chron Condit & Injuries, 4th Floor,Plot 47,Sect 44, Gurgaon 122002, Haryana, India.
EM g.krithiga@phfi.org; aastha.aggrawal@phfi.org;
gagandeep.k.walia@phfi.org; smriti5gulati@gmail.com;
geetha.nambiar@phfi.org; dprabakaran@ccdcindia.org;
preet.dhillon@phfi.org; rajarama@mail.nih.gov
OI Prabhakaran, Dorairaj/0000-0002-3172-834X
FU Wellcome Trust; consortium of UK universities [WT084754/Z/08/A]
FX This work was supported by a Wellcome Trust Capacity Strengthening
Strategic Award Extension phase to the Public Health Foundation of India
and a consortium of UK universities (WT084754/Z/08/A).
NR 68
TC 0
Z9 0
U1 6
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1368-8375
EI 1879-0593
J9 ORAL ONCOL
JI Oral Oncol.
PD OCT
PY 2016
VL 61
BP 146
EP 151
DI 10.1016/j.oraloncology.2016.08.005
PG 6
WC Oncology; Dentistry, Oral Surgery & Medicine
SC Oncology; Dentistry, Oral Surgery & Medicine
GA DX9EC
UT WOS:000384695400022
PM 27688118
ER
PT J
AU Ernst, M
Lago, T
Davis, A
Grillon, C
AF Ernst, Monique
Lago, Tiffany
Davis, Andrew
Grillon, Christian
TI The effects of methylphenidate and propranolol on the interplay between
induced-anxiety and working memory
SO PSYCHOPHARMACOLOGY
LA English
DT Article
DE Fear-potentiated startle; Stimulant; Cognition; Limited resources
theory; Dopamine; Catecholamine
ID RESPONSE-INHIBITION; STARTLE; PERFORMANCE; DISORDERS; COGNITION;
ADOLESCENTS; INVOLVEMENT; DYSFUNCTION; MODULATION; BLOCKADE
AB Research documents a reciprocal impact of anxiety on working memory (WM), although its strength and direction depend on factors like task difficulty. A better understanding of these factors may generate insights into cognitive mechanisms of action involved in anxiety, culminating into treatment implications. By blocking the physiological effects of anxiety, propranolol might also block anxiety interference on WM. Conversely, by improving task-directed attention, methylphenidate might reduce anxiety, or, alternatively, by improving cognitive efficiency and free up processing resources to compute anxiety.
To investigate the interplay between induced anxiety and WM, we pharmacologically manipulated either anxiety or cognition, using single doses of 40 mg propranolol (PRO), 20 mg methylphenidate (MPH), or placebo (PLA). In this double-blind parallel-group design study, 60 healthy volunteers (20/drug group) performed a verbal WM task under three loads, 1-, 2- and 3-back, and in two conditions, threat of shock and safety. Startle electromyography (EMG) was used to measure anxiety.
Findings were twofold: (1) MPH blocked anxiety interference only on the 3-back WM performance, while PRO or PLA had no effects on anxiety-WM interference, and (2) drugs had no effects on anxiety, but, after controlling for baseline anxiety, MPH enhanced anxiety-potentiated startle during the 3-back task.
These findings support that MPH-related improvement of cognitive efficiency permits anxiety to be processed and expressed. In conclusion, MPH may be a useful tool to investigate the mechanisms of interaction between anxiety and WM, particularly those under catecholaminergic control.
C1 [Ernst, Monique; Lago, Tiffany; Davis, Andrew; Grillon, Christian] NIMH, Neurobiol Fear & Anxiety, 15K North Dr,Bldg 15K,MSC 2670, Bethesda, MD 20892 USA.
RP Ernst, M (reprint author), NIMH, Neurobiol Fear & Anxiety, 15K North Dr,Bldg 15K,MSC 2670, Bethesda, MD 20892 USA.
EM ernstm@mail.nih.gov
FU National Institute of Mental Health [ZIAMH002798]
FX The authors report no conflicts of interest. Financial support of this
study was provided by the Intramural Research Program of the National
Institute of Mental Health, ZIAMH002798.
NR 41
TC 0
Z9 0
U1 4
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0033-3158
EI 1432-2072
J9 PSYCHOPHARMACOLOGY
JI Psychopharmacology
PD OCT
PY 2016
VL 233
IS 19-20
BP 3565
EP 3574
DI 10.1007/s00213-016-4390-y
PG 10
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA DW5GV
UT WOS:000383672500007
PM 27492789
ER
PT J
AU Meier, HCS
Haan, MN
de Leon, CFM
Simanek, AM
Dowd, JB
Aiello, AE
AF Meier, Helen C. S.
Haan, Mary N.
de Leon, Carlos F. Mendes
Simanek, Amanda M.
Dowd, Jennifer B.
Aiello, Allison E.
TI Early life socioeconomic position and immune response to persistent.
infections among elderly Latinos
SO SOCIAL SCIENCE & MEDICINE
LA English
DT Article
DE Socioeconomic position; Persistent infections; Life course epidemiology;
Latino health
ID HELICOBACTER-PYLORI INFECTION; SYSTEMIC-LUPUS-ERYTHEMATOSUS;
UNITED-STATES; CYTOMEGALOVIRUS-INFECTION; AUTOIMMUNE-DISEASES;
TOXOPLASMA-GONDII; ANTIBODY-TITERS; SEROPREVALENCE; CHILDHOOD; US
AB Persistent infections, such as cytomegalovirus (CMV), herpes simplex virus-1 (HSV-1), Helicobacter pylori (H. pylori), and Toxoplasma gondii (T. gondii), are common in the U.S. but their prevalence varies by socioeconomic status, It is unclear if early or later life socioeconomic position (SEP) is a more salient driver of disparities in immune control of these infections. Using data from the Sacramento Area Latino Study on Aging, we examined whether early or later life SEP was the strongest predictor of immune control later in life by contrasting two life course models, the critical period model and the chain of risk model. Early life SEP was measured as a latent variable, derived from parental education and occupation, and food availability. Indicators for SEP in later life included education level and occupation. Individuals were categorized by immune response to each pathogen (seronegative, low, medium and high) with increasing immune response representing poorer immune control. Cumulative immune response was estimated using a latent profile analysis with higher total immune response representing poorer immune control. Structural equation models were used to examine direct, indirect and total effects of early life SEP on each infection and cumulative immune response, controlling for age and gender. The direct effect of early life SEP on immune response was not statistically significant for the infections or cumulative immune response. Higher early life SEP was associated with lower immune response for T gondii, H. pylori and cumulative immune response through pathways mediated by later life SEP. For CMV, higher early life SEP was both directly associated and partially mediated by later life SEP. No association was found between SEP and HSV-1. Findings from this study support a chain of risk model, whereby early life SEP acts through later life SEP to affect immune response to persistent infections in older age. (C) 2016 Elsevier Ltd. All rights reserved.
C1 [Meier, Helen C. S.] Natl Inst Environm Hlth Sci, Epidemiol Branch, 171 TW Alexander Dr,POB 12233,MD A3-05, Res Triangle Pk, NC 27709 USA.
[Haan, Mary N.] Univ Calif San Francisco, Dept Epidemiol & Biostat, 550 15th St, San Francisco, CA 94158 USA.
[de Leon, Carlos F. Mendes] Univ Michigan, Sch Publ Hlth, Dept Epidemiol, Ctr Social Epidemiol & Populat Hlth, 1415 Washington Hts, Ann Arbor, MI 48109 USA.
[Simanek, Amanda M.] Univ Wisconsin, Joseph J Zilber Sch Publ Hlth, POB 413, Milwaukee, WI 53201 USA.
[Dowd, Jennifer B.] CUNY, Hunter Coll, CUNY Sch Publ Hlth, Dept Epidemiol & Biostat, 2180 Third Ave, New York, NY 10035 USA.
[Aiello, Allison E.] Univ N Carolina, Gillings Sch Global Publ Hlth, Dept Epidemiol, 135 Dauer Dr 2101B McGavran Greenberg Hall, Chapel Hill, NC 27599 USA.
RP Aiello, AE (reprint author), Univ N Carolina, Gillings Sch Global Publ Hlth, Dept Epidemiol, 135 Dauer Dr 2101B McGavran Greenberg Hall, Chapel Hill, NC 27599 USA.
EM helen.meier@nih.gov; mary.haan@ucsf.edu; cmendes@umich.edu;
simaneka@uwm.edu; jdowd@hunter.cuny.edu; aaiello@email.unc.edu
OI Meier, Helen/0000-0003-4400-0216; Dowd, Jennifer/0000-0003-2006-5656
FU National Institute on Aging, National Institutes of Health
[R01AG012975]; Intramural Research Program of the NIH, National
Institute of Environmental Health Sciences; [P60MD002249];
[R01DA022702]; [R01DK087864]
FX Funding for the SALSA study was aided by a grant from the National
Institute on Aging, National Institutes of Health: R01AG012975.
Additional support for this work from grants: P60MD002249, R01DA022702,
and R01DK087864. We thank Brisa Sanchez for her statistical consultation
and the Stanley Neurovirology Laboratory at Johns Hopkins University,
particularly Drs. Robert Yolken and Fuller Torrey, for performing the
laboratory assays. This research was supported in part by the Intramural
Research Program of the NIH, National Institute of Environmental Health
Sciences.
NR 62
TC 0
Z9 0
U1 9
U2 9
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0277-9536
J9 SOC SCI MED
JI Soc. Sci. Med.
PD OCT
PY 2016
VL 166
BP 77
EP 85
DI 10.1016/j.socscimed.2016.07.004
PG 9
WC Public, Environmental & Occupational Health; Social Sciences, Biomedical
SC Public, Environmental & Occupational Health; Biomedical Social Sciences
GA DY0LL
UT WOS:000384788200010
PM 27543684
ER
PT J
AU Stanko, JP
Kissling, GE
Chappell, VA
Fenton, SE
AF Stanko, Jason P.
Kissling, Grace E.
Chappell, Vesna A.
Fenton, Suzanne E.
TI Differences in the Rate of in Situ Mammary Gland Development and Other
Developmental Endpoints in Three Strains of Female Rat Commonly Used in
Mammary Carcinogenesis Studies: Implications for Timing of Carcinogen
Exposure
SO TOXICOLOGIC PATHOLOGY
LA English
DT Article
DE mammary gland; carcinogenesis; female reproduction; development;
epithelium; animal models; rat
ID LONG-EVANS RATS; BREAST-CANCER RISK; ESTROGEN-RECEPTOR; ENVIRONMENTAL
EXPOSURES; PERFLUOROOCTANOIC ACID; ENDOCRINE DISRUPTORS; PRENATAL
EXPOSURE; PFOA EXPOSURE; RODENT MODELS; KNOCKOUT MICE
AB The potential of chemicals to alter susceptibility to mammary tumor formation is often assessed using a carcinogen-induced study design in various rat strains. The rate of mammary gland (MG) development must be considered so that the timing of carcinogen administration is impactful. In this study, in situ MG development was assessed in females of the Harlan Sprague-Dawley (Hsd:SD), Charles River Sprague-Dawley (Crl:SD), and Charles River Long-Evans (Crl:LE) rat strains at postnatal days 25, 33, and 45. Development was evaluated by physical assessment of growth parameters, developmental scoring, and quantitative morphometric analysis. Although body weight (BW) was consistently lower and day of vaginal opening (VO) occurred latest in female Hsd:SD rats, they exhibited accelerated pre- and peripubertal MG development compared to other strains. Glands of Crl:SD and Crl:LE rats exhibited significantly more terminal end buds (TEBs) and TEB/mm than Hsd:SD rats around the time of VO. These data suggest a considerable difference in the rate of MG development across commonly used strains, which is independent of BW and timing of VO. In mammary tumor induction studies employing these strains, administration of the carcinogen should be timed appropriately, based on strain, to specifically target the peak of TEB occurrence.
C1 [Stanko, Jason P.; Chappell, Vesna A.; Fenton, Suzanne E.] NIEHS, NTPL, DNTP, 111 TW Alexander Dr,MD E1-08, Res Triangle Pk, NC 27709 USA.
[Kissling, Grace E.] NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA.
RP Fenton, SE (reprint author), NIEHS, NTPL, DNTP, 111 TW Alexander Dr,MD E1-08, Res Triangle Pk, NC 27709 USA.
EM fentonse@niehs.nih.gov
FU Intramural NIH HHS [Z99 ES999999, ZIA ES102785-02]
NR 70
TC 0
Z9 0
U1 7
U2 7
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0192-6233
EI 1533-1601
J9 TOXICOL PATHOL
JI Toxicol. Pathol.
PD OCT
PY 2016
VL 44
IS 7
BP 1021
EP 1033
DI 10.1177/0192623316655222
PG 13
WC Pathology; Toxicology
SC Pathology; Toxicology
GA DY1EL
UT WOS:000384837600011
PM 27613105
ER
PT J
AU Filgo, AJ
Foley, JF
Puvanesarajah, S
Borde, AR
Midkiff, BR
Reed, CE
Chappell, VA
Alexander, LB
Borde, PR
Troester, MA
Bouknight, SAH
Fenton, SE
AF Filgo, Adam J.
Foley, Julie F.
Puvanesarajah, Samantha
Borde, Aditi R.
Midkiff, Bentley R.
Reed, Casey E.
Chappell, Vesna A.
Alexander, Lydia B.
Borde, Pretish R.
Troester, Melissa A.
Bouknight, Schantel A. Hayes
Fenton, Suzanne E.
TI Mammary Gland Evaluation in Juvenile Toxicity Studies: Temporal
Developmental Patterns in the Male and Female Harlan Sprague-Dawley Rat
SO TOXICOLOGIC PATHOLOGY
LA English
DT Article
DE mammary gland; atlas; HSD; rat; developmental exposure; steroid
receptor; histology; whole mount
ID ENDOCRINE-DISRUPTING CHEMICALS; BREAST DEVELOPMENT; IN-UTERO;
GONADOTROPIN-SECRETION; PRENATAL EXPOSURE; ESTROGEN-RECEPTOR;
GENE-EXPRESSION; ANIMAL-MODELS; DIFFERENTIATION; MOUSE
AB There are currently no reports describing mammary gland development in the Harlan Sprague-Dawley (HSD) rat, the current strain of choice for National Toxicology Program (NTP) testing. Our goals were to empower the NTP, contract labs, and other researchers in understanding and interpreting chemical effects in this rat strain. To delineate similarities/differences between the female and male mammary gland, data were compiled starting on embryonic day 15.5 through postnatal day 70. Mammary gland whole mounts, histology sections, and immunohistochemically stained tissues for estrogen, progesterone, and androgen receptors were evaluated in both sexes; qualitative and quantitative differences are highlighted using a comprehensive visual timeline. Research on endocrine disrupting chemicals in animal models has highlighted chemically induced mammary gland anomalies that may potentially impact human health. In order to investigate these effects within the HSD strain, 2,3,7,8-tetrachlorodibenzo-p-dioxin, diethylstilbestrol, or vehicle control was gavage dosed on gestation day 15 and 18 to demonstrate delayed, accelerated, and control mammary gland growth in offspring, respectively. We provide illustrations of normal and chemically altered mammary gland development in HSD male and female rats to help inform researchers unfamiliar with the tissue and may facilitate enhanced evaluation of both male and female mammary glands in juvenile toxicity studies.
C1 [Filgo, Adam J.] Univ N Carolina, Sch Med, Curriculum Toxicol, Chapel Hill, NC USA.
[Filgo, Adam J.; Borde, Aditi R.; Reed, Casey E.; Chappell, Vesna A.; Alexander, Lydia B.; Borde, Pretish R.; Fenton, Suzanne E.] NIEHS, NTP Lab, Div NTP, NIH, 111 TW Alexander Dr,Bldg 101,MD E1-08, Res Triangle Pk, NC 27709 USA.
[Foley, Julie F.] NIEHS, Cellular & Mol Pathol Branch, Div NTP, NIH, Res Triangle Pk, NC 27709 USA.
[Puvanesarajah, Samantha; Troester, Melissa A.] UNC Lineberger Comprehens Canc Ctr, Chapel Hill, NC USA.
[Midkiff, Bentley R.] Univ N Carolina, Dept Pathol & Lab Med, Chapel Hill, NC USA.
[Troester, Melissa A.] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
[Bouknight, Schantel A. Hayes] Charles River Labs, Pathol Associates Inc, Durham, NC USA.
RP Fenton, SE (reprint author), NIEHS, NTP Lab, Div NTP, NIH, 111 TW Alexander Dr,Bldg 101,MD E1-08, Res Triangle Pk, NC 27709 USA.
EM fentonse@niehs.nih.gov
FU NIEHS Individual Research Training Award; NIEHS Summer Intern Program
FX The author(s) disclosed receipt of the following financial support for
the research, authorship, and/or publication of this article: Adam J.
Filgo was funded by a NIEHS Individual Research Training Award. Aditi R.
Borde, Lydia B. Alexander, and Pretish R. Borde were funded by the NIEHS
Summer Intern Program.
NR 73
TC 0
Z9 0
U1 4
U2 4
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0192-6233
EI 1533-1601
J9 TOXICOL PATHOL
JI Toxicol. Pathol.
PD OCT
PY 2016
VL 44
IS 7
BP 1034
EP 1058
DI 10.1177/0192623316663864
PG 25
WC Pathology; Toxicology
SC Pathology; Toxicology
GA DY1EL
UT WOS:000384837600012
PM 27613106
ER
PT J
AU Tucker, DK
Foley, JF
Hayes-Bouknight, SA
Fenton, SE
AF Tucker, Deirdre K.
Foley, Julie F.
Hayes-Bouknight, Schantel A.
Fenton, Suzanne E.
TI Preparation of High-quality Hematoxylin and Eosin-stained Sections from
Rodent Mammary Gland Whole Mounts for Histopathologic Review
SO TOXICOLOGIC PATHOLOGY
LA English
DT Article
DE mammary gland; whole mount; contralateral; development; breast;
pathology
AB Identifying environmental exposures that cause adverse mammary gland outcomes in rodents is a first step in disease prevention in humans and domestic pets. "Whole mounts" are an easy and inexpensive tissue preparation method that can elucidate typical or abnormal mammary gland morphology in rodent studies. Here, we propose procedures to facilitate the use of whole mounts for histological identification of grossly noted tissue alterations. We noted lesions in mammary whole mounts from 14-month-old CD-1 mice that were not found in the contralateral gland hematoxylin and eosin (H&E)-stained section. Whole mounts were removed from the slide and carefully processed to produce high-quality histological sections that mirrored the quality of the original H&E-stained section in order to properly diagnose the unidentified gross abnormalities. Incorporation of this method into testing protocols that focus on human relevant chemical and endocrine disruptors exposure will increase the chances of identifying lesions in the gland and reduce the risk of false negative findings. This method can be especially invaluable when lesions are not always palpable during the course of the study or visible at necropsy, or when a single cross section of the mammary gland is otherwise used for detecting lesions.
C1 [Tucker, Deirdre K.] Univ N Carolina, Curriculum Toxicol, Chapel Hill, NC USA.
[Tucker, Deirdre K.; Fenton, Suzanne E.] NIEHS, DNTP, NTP Lab, NIH, 111 TW Alexander Dr,MD E1-08, Res Triangle Pk, NC USA.
[Foley, Julie F.] NIEHS, DNTP, Cellular & Mol Pathol Branch, NIH, Res Triangle Pk, NC USA.
[Hayes-Bouknight, Schantel A.] Charles River Labs Inc, Durham, NC USA.
RP Fenton, SE (reprint author), NIEHS, DNTP, NTP Lab, NIH, 111 TW Alexander Dr,MD E1-08, Res Triangle Pk, NC USA.
EM fentonse@niehs.nih.gov
FU NIEHS Individual Research Training Award
FX The author(s) disclosed receipt of the following financial support for
the research, authorship, and/or publication of this article: Deirdre K.
Tucker was funded by a NIEHS Individual Research Training Award.
NR 10
TC 0
Z9 0
U1 3
U2 3
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0192-6233
EI 1533-1601
J9 TOXICOL PATHOL
JI Toxicol. Pathol.
PD OCT
PY 2016
VL 44
IS 7
BP 1059
EP 1064
DI 10.1177/0192623316660769
PG 6
WC Pathology; Toxicology
SC Pathology; Toxicology
GA DY1EL
UT WOS:000384837600013
PM 27474221
ER
PT J
AU Patial, S
Blackshear, PJ
AF Patial, Sonika
Blackshear, Perry J.
TI Tristetraprolin as a Therapeutic Target in Inflammatory Disease
SO TRENDS IN PHARMACOLOGICAL SCIENCES
LA English
DT Review
ID ZINC-FINGER DOMAIN; AU-RICH ELEMENT; MESSENGER-RNA; TNF-ALPHA; ANTISENSE
OLIGONUCLEOTIDES; PROTEIN TRISTETRAPROLIN; RHEUMATOID-ARTHRITIS;
DEFICIENCY SYNDROME; GLOBAL ANALYSIS; MICE
AB Members of the tristetraprolin (TTP) family of RNA-binding proteins are found in all major eukaryotic groups. TTP family members, from plants through humans, can bind adenosine-uridine rich elements in target mRNAs with high affinity. In mammalian cells, these proteins then promote deadenylation and decay of target transcripts. Four such proteins are found in mice, of which the best studied is TTP. When the gene encoding TTP is disrupted in mice, the animals develop a severe syndrome of arthritis, autoimmunity, cachexia, dermatitis, and myeloid hyperplasia. Conversely, recent overexpression studies have demonstrated protection against several experimental models of immune inflammatory disease. This endogenous anti-inflammatory protein could serve as the basis for novel approaches to therapy of similar conditions in humans.
C1 [Patial, Sonika; Blackshear, Perry J.] NIEHS, Signal Transduct Lab, POB 12233, 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.
[Patial, Sonika] Louisiana State Univ, Sch Vet Med, LADDL, Baton Rouge, LA 70803 USA.
RP Blackshear, PJ (reprint author), NIEHS, Signal Transduct Lab, POB 12233, Res Triangle Pk, NC 27709 USA.; Blackshear, PJ (reprint author), Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.; Blackshear, PJ (reprint author), Duke Univ, Med Ctr, Dept Biochem, Durham, NC 27710 USA.
EM black009@niehs.nih.gov
FU Intramural Program of the National Institute of Environmental Health
Sciences, National Institutes of Health
FX We are grateful to the members of our laboratory for many useful
discussions, and to Drs Mike Fessier and Don Cook for helpful comments
on the manuscript. This work was supported by the Intramural Program of
the National Institute of Environmental Health Sciences, National
Institutes of Health.
NR 47
TC 1
Z9 1
U1 2
U2 2
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0165-6147
J9 TRENDS PHARMACOL SCI
JI Trends Pharmacol. Sci.
PD OCT
PY 2016
VL 37
IS 10
BP 811
EP 821
DI 10.1016/j.tips.2016.07.002
PG 11
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA DY1MA
UT WOS:000384857900003
PM 27503556
ER
PT J
AU Carney, DM
Moroney, E
Machlin, L
Hahn, S
Savage, JE
Lee, M
Towbin, KA
Brotman, MA
Pine, DS
Leibenluft, E
Roberson-Nay, R
Hettema, JM
AF Carney, Dever M.
Moroney, Elizabeth
Machlin, Laura
Hahn, Shannon
Savage, Jeanne E.
Lee, Minyoung
Towbin, Kenneth A.
Brotman, Melissa A.
Pine, Daniel S.
Leibenluft, Ellen
Roberson-Nay, Roxann
Hettema, John M.
TI The Twin Study of Negative Valence Emotional Constructs
SO TWIN RESEARCH AND HUMAN GENETICS
LA English
DT Article
DE negative valence; anxiety; internalizing; twin study
ID BIPOLAR DISORDER; PANIC DISORDER; BEHAVIORAL-INHIBITION; ANXIETY
DISORDERS; NEURAL MECHANISMS; SELF-REPORT; CHILDREN; THREAT; SCALE; FEAR
AB The Twin Study of Negative Valence Emotional Constructs is a multi-site study designed to examine the relationship between a broad selection of potential measures designed to assess putative endophenotypes for negative valence systems (NVS) and early symptoms of internalizing disorders (IDs). In this article, we describe the sample characteristics, data collection protocols, and measures used. Pre-adolescent Caucasian twin pairs were recruited through the Mid-Atlantic Twin Registry; data collection began in February of 2013. Enrolled twins completed various dimensional self-report measures along with cognitive, emotional, and psychophysiological tasks designed to assess NVS function. Parents also completed surveys about their twins and themselves. In addition, a subset of the twins also participated in a neuroimaging protocols. Data collection is in the final stages, and preliminary analyses are underway. The findings will potentially expand our understanding of the mechanisms by which genetic and environmental factors contribute to individual differences in NVS phenotypes and provide new insights into underlying risk factors for IDs.
C1 [Carney, Dever M.; Hahn, Shannon; Savage, Jeanne E.; Lee, Minyoung; Roberson-Nay, Roxann; Hettema, John M.] Virginia Commonwealth Univ, Virginia Inst Psychiat & Behav Genet, Richmond, VA USA.
[Carney, Dever M.; Hahn, Shannon; Savage, Jeanne E.; Lee, Minyoung; Roberson-Nay, Roxann; Hettema, John M.] Virginia Commonwealth Univ, Dept Psychiat, POB 980126, Richmond, VA 23298 USA.
[Moroney, Elizabeth; Machlin, Laura; Towbin, Kenneth A.; Brotman, Melissa A.; Pine, Daniel S.; Leibenluft, Ellen] NIMH, Emot & Dev Branch, NIH, US Dept HHS, Bethesda, MD 20892 USA.
RP Hettema, JM (reprint author), Virginia Commonwealth Univ, Dept Psychiat, POB 980126, Richmond, VA 23298 USA.
EM john.hettema@vcuhealth.org
RI Brotman, Melissa/H-7409-2013
FU National Institutes of Health [R01MH098055, NIMH-IRP-ziamh002781]; Brain
and Behavior Research Foundation (BBRF) [21984]; NIH Center for
Advancing Translational Research [UL1TR000058]
FX This study was supported by the National Institutes of Health
(R01MH098055 to JMH and NIMH-IRP-ziamh002781 to DSP) and the Brain and
Behavior Research Foundation (BBRF Grant 21984 to JMH). REDCap and the
Mid-Atlantic Twin Registry were supported through the NIH Center for
Advancing Translational Research Grant Number UL1TR000058.
NR 51
TC 1
Z9 1
U1 6
U2 6
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 1832-4274
EI 1839-2628
J9 TWIN RES HUM GENET
JI Twin Res. Hum. Genet.
PD OCT
PY 2016
VL 19
IS 5
BP 456
EP 464
DI 10.1017/thg.2016.59
PG 9
WC Genetics & Heredity; Obstetrics & Gynecology
SC Genetics & Heredity; Obstetrics & Gynecology
GA DX5NV
UT WOS:000384428600007
PM 27457271
ER
PT J
AU Boccardo, F
Valenzano, M
Costantini, S
Casabona, F
Morotti, M
Sala, P
De Cian, F
Molinari, L
Spinaci, S
Dessalvi, S
Campisi, CC
Villa, G
Campisi, C
AF Boccardo, Francesco
Valenzano, Mario
Costantini, Sergio
Casabona, Federico
Morotti, Matteo
Sala, Paolo
De Cian, Franco
Molinari, Lidia
Spinaci, Stefano
Dessalvi, Sara
Campisi, Corrado Cesare
Villa, Giuseppe
Campisi, Corradino
TI LYMPHA Technique to Prevent Secondary Lower Limb Lymphedema
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Article
ID NODE DISSECTION; VULVAR CANCER; LYMPHATICOVENULAR ANASTOMOSIS; SURGICAL
PREVENTION; HEALING APPROACH; LEG LYMPHEDEMA; BREAST-CANCER;
RISK-FACTORS; FOLLOW-UP; MICROSURGERY
AB Inguinofemoral lymphadenectomy carries a high risk of lower limb lymphedema. This report describes the feasibility of performing multiple lymphatic-venous anastomoses (MLVA) after inguinofemoral lymph node completion (LYMPHA technique) and the possible benefit of LYMPHA for preventing lymphedema.
Between February, 2011 and October, 2014, 11 patients with vulvar cancer and 16 patients with melanoma of the trunk requiring inguinofemoral lymphadenectomy underwent lymph node dissection and the LYMPHA technique. Blue dye was injected into the thigh 10 min before surgery. Lymphatics afferent to the blue nodes were used to perform MLVA using a collateral branch of the great saphenous vein.
The mean age of patients in the vulvar cancer group was 52 years (range, 48-75 years). The melanoma group comprised seven men and nine women with a mean age of 41 years (range, 37-56 years). Of the 16 patients, 5 with vulvar cancer underwent bilateral inguinofemoral lymphadenectomy, whereas the remaining 6 patients with vulvar cancer and all 16 patients with melanoma of the trunk had unilateral node dissection. All the patients were treated by the LYMPHA technique. No lymphocele or infectious complications occurred. Transient lower-extremity edema occurred for one melanoma patient (6.25 %), which resolved after 2 months, and permanent lower-extremity edema occurred for one patient (9 %) with vulvar cancer.
The LYMPHA technique appears to be feasible, safe, and effective for the prevention of lower limb lymphedema, thereby improving the patient's quality of life and decreasing health care costs.
C1 [Boccardo, Francesco; Molinari, Lidia; Spinaci, Stefano; Dessalvi, Sara; Campisi, Corrado Cesare; Campisi, Corradino] Univ Genoa, Natl Canc Inst Canc Res, IRCCS S Martino Hosp IST, Unit Lymphat Surg,Dept Surg, Genoa, Italy.
[Valenzano, Mario; Costantini, Sergio; Casabona, Federico; Morotti, Matteo; Sala, Paolo] Univ Genoa, Natl Canc Inst, S Martino Hosp, Dept Obstet & Gynecol, Genoa, Italy.
[De Cian, Franco] Univ Genoa, Natl Canc Inst, S Martino Hosp, Unit Oncol Surg,Dept Surg, Genoa, Italy.
[Villa, Giuseppe] Univ Genoa, Natl Canc Inst, S Martino Hosp, Unit Nucl Med,Dept Surg, Genoa, Italy.
RP Boccardo, F (reprint author), Univ Genoa, Natl Canc Inst Canc Res, IRCCS S Martino Hosp IST, Unit Lymphat Surg,Dept Surg, Genoa, Italy.
EM francesco.boccardo@unige.it
NR 25
TC 0
Z9 0
U1 4
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1068-9265
EI 1534-4681
J9 ANN SURG ONCOL
JI Ann. Surg. Oncol.
PD OCT
PY 2016
VL 23
IS 11
BP 3558
EP 3563
DI 10.1245/s10434-016-5282-4
PG 6
WC Oncology; Surgery
SC Oncology; Surgery
GA DV4XV
UT WOS:000382930000023
PM 27221358
ER
PT J
AU Verma, SC
Miyashiro, T
AF Verma, Subhash C.
Miyashiro, Tim
TI Niche-Specific Impact of a Symbiotic Function on the Persistence of
Microbial Symbionts within a Natural Host
SO APPLIED AND ENVIRONMENTAL MICROBIOLOGY
LA English
DT Article
ID SQUID EUPRYMNA-SCOLOPES; VIBRIO-FISCHERI; LIGHT ORGAN; HAWAII
POPULATIONS; LUX GENES; 2 OAHU; COLONIZATION; GUT; MORPHOGENESIS;
ORGANIZATION
AB How the function of microbial symbionts is affected by their population/consortium structure within a host remains poorly understood. The symbiosis established between Euprymna scolopes and Vibrio fischeri is a well-characterized host-microbe association in which the function and structure of V. fischeri populations within the host are known: V. fischeri populations produce bioluminescence from distinct crypt spaces within a dedicated host structure called the light organ. Previous studies have revealed that luminescence is required for V. fischeri populations to persist within the light organ and that deletion of the lux gene locus, which is responsible for luminescence in V. fischeri, leads to a persistence defect. In this study, we investigated the impact of bioluminescence on V. fischeri population structure within the light organ. We report that the persistence defect is specific to crypt I, which is the most developmentally mature crypt space within the nascent light organ. This result provides insight into the structure/function relationship that will be useful for future mechanistic studies of squid-Vibrio symbiosis. In addition, our report highlights the potential impact of the host developmental program on the spatiotemporal dynamics of host-microbe interactions.
C1 [Verma, Subhash C.; Miyashiro, Tim] Penn State Univ, Dept Biochem & Mol Biol, University Pk, PA 16802 USA.
[Verma, Subhash C.] NCI, Mol Biol Lab, Ctr Canc Res, NIH, Bldg 37, Bethesda, MD 20892 USA.
RP Miyashiro, T (reprint author), Penn State Univ, Dept Biochem & Mol Biol, University Pk, PA 16802 USA.
EM tim14@psu.edu
FU HHS \ National Institutes of Health (NIH) [097032]
FX This work, including the efforts of Tim Miyashiro, was funded by HHS
vertical bar National Institutes of Health (NIH) (097032).
NR 40
TC 0
Z9 0
U1 15
U2 15
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0099-2240
EI 1098-5336
J9 APPL ENVIRON MICROB
JI Appl. Environ. Microbiol.
PD OCT
PY 2016
VL 82
IS 19
BP 5990
EP 5996
DI 10.1128/AEM.01770-16
PG 7
WC Biotechnology & Applied Microbiology; Microbiology
SC Biotechnology & Applied Microbiology; Microbiology
GA DX0JX
UT WOS:000384048700026
PM 27474717
ER
PT J
AU Adams, MJ
Lefkowitz, EJ
King, AMQ
Harrach, B
Harrison, RL
Knowles, NJ
Kropinski, AM
Krupovic, M
Kuhn, JH
Mushegian, AR
Nibert, M
Sabanadzovic, S
Sanfacon, H
Siddell, SG
Simmonds, P
Varsani, A
Zerbini, FM
Gorbalenya, AE
Davison, AJ
AF Adams, Michael J.
Lefkowitz, Elliot J.
King, Andrew M. Q.
Harrach, Balazs
Harrison, Robert L.
Knowles, Nick J.
Kropinski, Andrew M.
Krupovic, Mart
Kuhn, Jens H.
Mushegian, Arcady R.
Nibert, Max
Sabanadzovic, Sead
Sanfacon, Helene
Siddell, Stuart G.
Simmonds, Peter
Varsani, Arvind
Zerbini, Francisco Murilo
Gorbalenya, Alexander E.
Davison, Andrew J.
TI Ratification vote on taxonomic proposals to the International Committee
on Taxonomy of Viruses (2016)
SO ARCHIVES OF VIROLOGY
LA English
DT Article
AB This article lists the changes to virus taxonomy approved and ratified by the International Committee on Taxonomy of Viruses (ICTV) in April 2016.
Changes to virus taxonomy (the Universal Scheme of Virus Classification of the International Committee on Taxonomy of Viruses [ICTV]) now take place annually and are the result of a multi-stage process. In accordance with the ICTV Statutes http://www.ictvonline.org/statutes.asp), proposals submitted to the ICTV Executive Committee (EC) undergo a review process that involves input from the ICTV Study Groups (SGs) and Subcommittees (SCs), other interested virologists, and the EC. After final approval by the EC, proposals are then presented for ratification to the full ICTV membership by publication on an ICTV web site (http://www.ictvonline.org/) followed by an electronic vote. The latest set of proposals approved by the EC was made available on the ICTV website by January 2016 (https://talk.ictvonline.org/files/proposals/). A list of these proposals was then emailed on 28 March 2016 to the 148 members of ICTV, namely the EC Members, Life Members, ICTV Subcommittee Members (including the SG chairs) and ICTV National Representatives. Members were then requested to vote on whether to ratify the taxonomic proposals (voting closed on 29 April 2016).
C1 [Adams, Michael J.] 24 Woodland Way, Stevenage SG2 8BT, Herts, England.
[Lefkowitz, Elliot J.] UAB, Dept Microbiol, BBRB 276,845 19th ST South, Birmingham, AL 35294 USA.
[King, Andrew M. Q.] Sunfield, Dawney Hill, Woking GU24 0JB, Surrey, England.
[Harrach, Balazs] Hungarian Acad Sci, Vet Med Res Inst, Hungaria Krt 21, H-1143 Budapest, Hungary.
[Harrison, Robert L.] USDA, Invas Insect Biocontrol & Behav Lab, 10300 Baltimore Ave,Bldg 007 Barc West, Beltsville, MD 20705 USA.
[Knowles, Nick J.] Pirbright Inst, Ash Rd, Pirbright GU24 0NF, Surrey, England.
[Kropinski, Andrew M.] Univ Guelph, Dept Food Sci, Guelph, ON N1G 2W1, Canada.
[Kropinski, Andrew M.] Univ Guelph, Dept Mol & Cellular Biol, Guelph, ON N1G 2W1, Canada.
[Kropinski, Andrew M.] Univ Guelph, Dept Pathobiol, Guelph, ON N1G 2W1, Canada.
[Krupovic, Mart] Inst Pasteur, Dept Microbiol, 25 Rue Dr Roux, F-75015 Paris, France.
[Kuhn, Jens H.] NIAID, NIH, DCR Integrated Res Facil, Ft Detrick IRF Frederick, B-8200 Res Plaza, Frederick, MD 21702 USA.
[Mushegian, Arcady R.] Natl Sci Fdn, Div Mol & Cellular Biosci, 4201 Wilson Blvd, Arlington, VA 22230 USA.
[Nibert, Max] Harvard Med Sch, Dept Microbiol & Immunobiol, 77 Ave Louis Pasteur, Boston, MA 02115 USA.
[Sabanadzovic, Sead] Mississippi State Univ, Dept Biochem Mol Biol Entomol & Plant Pathol, 100 Old Hwy 12 Mail Stop 9775, Mississippi State, MS 39762 USA.
[Sanfacon, Helene] Agr & Agri Food Canada, Summerland Res & Dev Ctr, 4200 Highway 97, Summerland, BC V0H 1Z0, Canada.
[Siddell, Stuart G.] Univ Bristol, Dept Cellular & Mol Med, Fac Biomed Sci, Univ Walk, Bristol BS8 1TD, Avon, England.
[Simmonds, Peter] Univ Oxford, Nuffield Dept Expt Med, Peter Medawar Bldg,South Pk Rd, Oxford OX1 3PS, England.
[Varsani, Arvind] Univ Canterbury, Sch Biol Sci, Private Bag 4800, Christchurch 8140, New Zealand.
[Varsani, Arvind] Univ Canterbury, Biomol Interact Ctr, Private Bag 4800, Christchurch 8140, New Zealand.
[Zerbini, Francisco Murilo] Univ Fed Vicosa, Dept Fitopatol, BIOAGRO, BR-36570900 Vicosa, MG, Brazil.
[Gorbalenya, Alexander E.] Leiden Univ, Dept Med Microbiol, Med Ctr, POB 9600,E4-P,Rm E4-72, NL-2300 RC Leiden, Netherlands.
[Davison, Andrew J.] Univ Glasgow, Ctr Virus Res, MRC, Sir Michael Stoker Bldg,464 Bearsden Rd, Glasgow G61 1QH, Lanark, Scotland.
RP Adams, MJ (reprint author), 24 Woodland Way, Stevenage SG2 8BT, Herts, England.
EM mike.adams.ictv@gmail.com; elliotl@uab.edu; amqking@gmail.com;
harrach@vmri.hu; robert.l.harrison@ars.usda.gov;
nick.knowles@pirbright.ac.uk; Phage.Canada@gmail.com;
mart.krupovic@pasteur.fr; kuhnjens@mail.nih.gov; mushegian2@gmail.com;
mnibert@hms.harvard.edu; ssabanadzovic@entomology.msstate.edu;
helene.sanfacon@agr.gc.ca; stuart.siddell@bristol.ac.uk;
peter.simmonds@ndm.ox.ac.uk; Arvind.varsani@canterbury.ac.nz;
zerbini@ufv.br; a.e.gorbalenya@lumc.nl; andrew.davison@glasgow.ac.uk
RI Harrach, Balazs/A-3680-2008; Institute, Pirbright/K-4476-2014; Krupovic,
Mart/I-4209-2012; Gorbalenya, Alexander/J-4818-2012; Zerbini, Francisco
Murilo/N-7359-2013;
OI Harrach, Balazs/0000-0002-1410-6469; Krupovic, Mart/0000-0001-5486-0098;
Gorbalenya, Alexander/0000-0002-4967-7341; Zerbini, Francisco
Murilo/0000-0001-8617-0200; Siddell, Stuart/0000-0002-8702-7868;
Sabanadzovic, Sead/0000-0002-2995-2633
FU Medical Research Council [MC_UU_12014/3]
NR 69
TC 9
Z9 9
U1 10
U2 10
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 2016
VL 161
IS 10
BP 2921
EP 2949
DI 10.1007/s00705-016-2977-6
PG 29
WC Virology
SC Virology
GA DV1LE
UT WOS:000382681800036
PM 27424026
ER
PT J
AU Aggarwal, M
Saxena, R
Sinclair, E
Fu, Y
Jacobs, A
Dyba, M
Wang, X
Cruz, I
Berry, D
Kallakury, B
Mueller, SC
Agostino, SD
Blandino, G
Avantaggiati, ML
Chung, FL
AF Aggarwal, M.
Saxena, R.
Sinclair, E.
Fu, Y.
Jacobs, A.
Dyba, M.
Wang, X.
Cruz, I.
Berry, D.
Kallakury, B.
Mueller, S. C.
Agostino, S. D.
Blandino, G.
Avantaggiati, M. L.
Chung, F-L
TI Reactivation of mutant p53 by a dietary-related compound phenethyl
isothiocyanate inhibits tumor growth
SO CELL DEATH AND DIFFERENTIATION
LA English
DT Article
ID HUMAN PROSTATE-CANCER; BETA-PHENYLETHYL ISOTHIOCYANATE; INDUCED
APOPTOSIS; IN-VIVO; CELLS; SUPPRESSOR; MUTATIONS; MICE; SULFORAPHANE;
DEGRADATION
AB Mutations in the p53 tumor-suppressor gene are prevalent in human cancers. The majority of p53 mutations are missense, which can be classified into contact mutations (that directly disrupts the DNA-binding activity of p53) and structural mutations (that disrupts the conformation of p53). Both of the mutations can disable the normal wild-type (WT) p53 activities. Nevertheless, it has been amply documented that small molecules can rescue activity from mutant p53 by restoring WT tumor-suppressive functions. These compounds hold promise for cancer therapy and have now entered clinical trials. In this study, we show that cruciferousvegetable- derived phenethyl isothiocyanate (PEITC) can reactivate p53 mutant under in vitro and in vivo conditions, revealing a new mechanism of action for a dietary-related compound. PEITC exhibits growth-inhibitory activity in cells expressing p53 mutants with preferential activity toward p53(R175), one of the most frequent 'hotspot' mutations within the p53 sequence. Mechanistic studies revealed that PEITC induces apoptosis in a p53(R175) mutant-dependent manner by restoring p53 WT conformation and transactivation functions. Accordingly, in PEITC-treated cells the reactivated p53(R175) mutant induces apoptosis by activating canonical WT p53 targets, inducing a delay in S and G2/M phase, and by phosphorylating ATM/CHK2. Interestingly, the growth-inhibitory effects of PEITC depend on the redox state of the cell. Further, PEITC treatments render the p53(R175) mutant sensitive to degradation by the proteasome and autophagy in a concentration-dependent manner. PEITC-induced reactivation of p53(R175) and its subsequent sensitivity to the degradation pathways likely contribute to its anticancer activities. We further show that dietary supplementation of PEITC is able to reactivate WT activity in vivo as well, inhibiting tumor growth in xenograft mouse model. These findings provide the first example of mutant p53 reactivation by a dietary compound and have important implications for cancer prevention and therapy.
C1 [Aggarwal, M.; Sinclair, E.; Fu, Y.; Jacobs, A.; Dyba, M.; Cruz, I.; Berry, D.; Kallakury, B.; Mueller, S. C.; Avantaggiati, M. L.; Chung, F-L] Georgetown Univ, Dept Oncol, Lombardi Comprehens Canc Ctr, Washington, DC 20007 USA.
[Saxena, R.] Georgetown Univ, Dept Biochem & Mol & Cellular Biol, Washington, DC 20007 USA.
[Wang, X.] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Agostino, S. D.; Blandino, G.] Italian Natl Canc Inst Regina Elena, Translat Oncogen Unit, Rome, Italy.
RP Avantaggiati, ML; Chung, FL (reprint author), Georgetown Univ, Dept Oncol, Lombardi Comprehens Canc Ctr, Washington, DC 20007 USA.
EM ma1274@georgetown.edu; flc6@georgetown.edu
OI Di Agostino, Silvia/0000-0003-3730-1125; Dyba,
Marcin/0000-0001-6311-6877
FU National Cancer Institute at National Institutes of Health [CA100853];
National Cancer Institute at National Institutes of Health (Lombardi
Cancer Center Support Grant) [P30 CA51008]
FX We thank Dr. Shivendra V Singh (University of Pittsburgh, Pennsylvania,
USA) for the ATG5 siRNA and ATG5 antibody; Dr. Darren R Carpizo (The
Cancer Institute of New Jersy, New Brunswick, NJ, USA) for the (10)3 MEF
transfectants; Dr. Thomas TY Wang, Dr. Michael Johnson and Dr. Priscilla
Furth for comments and discussions; and Angela Bai for the proofreading.
We thank Peter Johnson and Karen Creswell for imaging and Flow Cytometry
and Supti Sen and Anna Coffey for Histology and Tissue Shared Resources
at Georgetown University. This work is supported by the National Cancer
Institute at National Institutes of Health (CA100853 and Lombardi Cancer
Center Support Grant P30 CA51008).
NR 44
TC 3
Z9 3
U1 14
U2 14
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1350-9047
EI 1476-5403
J9 CELL DEATH DIFFER
JI Cell Death Differ.
PD OCT
PY 2016
VL 23
IS 10
BP 1615
EP 1627
DI 10.1038/cdd.2016.48
PG 13
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA DX1QO
UT WOS:000384142300005
PM 27258787
ER
PT J
AU Shah, P
Kerns, E
Nguyen, DT
Obach, RS
Wang, AQ
Zakharov, A
McKew, J
Simeonov, A
Hop, CECA
Xu, X
AF Shah, Pranav
Kerns, Edward
Dac-Trung Nguyen
Obach, R. Scott
Wang, Amy Q.
Zakharov, Alexey
McKew, John
Simeonov, Anton
Hop, Cornelis E. C. A.
Xu, Xin
TI An Automated High-Throughput Metabolic Stability Assay Using an
Integrated High-Resolution Accurate Mass Method and Automated Data
Analysis Software
SO DRUG METABOLISM AND DISPOSITION
LA English
DT Article
ID DRUG-METABOLISM; QUANTITATIVE-ANALYSIS; MICROSOMAL STABILITY;
SPECTROMETRY; CANDIDATES; CLEARANCE; OPTIMIZATION; HEPATOCYTES; MODELS;
PLASMA
AB Advancement of in silico tools would be enabled by the availability of data for metabolic reaction rates and intrinsic clearance (CLint) of a diverse compound structure data set by specific metabolic enzymes. Our goal is to measure CLint for a large set of compounds with each major human cytochrome P450 (P450) isozyme. To achieve our goal, it is of utmost importance to develop an automated, robust, sensitive, high-throughput metabolic stability assay that can efficiently handle a large volume of compound sets. The substrate depletion method [in vitro half-life (t(1/2)) method] was chosen to determine CLint. The assay (384-well format) consisted of three parts: 1) a robotic system for incubation and sample cleanup; 2) two different integrated, ultraperformance liquid chromatography/mass spectrometry (UPLC/MS) platforms to determine the percent remaining of parent compound, and 3) an automated data analysis system. The CYP3A4 assay was evaluated using two long t(1/2) compounds, carbamazepine and antipyrine (t(1/2) > 30 minutes); one moderate t(1/2) compound, ketoconazole (10 < t(1/2) < 30 minutes); and two short t(1/2) compounds, loperamide and buspirone (t(1/2) < 10 minutes). Interday and intraday precision and accuracy of the assay were within acceptable range (similar to 12%) for the linear range observed. Using this assay, CYP3A4 CLint and t(1/2) values for more than 3000 compounds were measured. This high-throughput, automated, and robust assay allows for rapid metabolic stability screening of large compound sets and enables advanced computational modeling for individual human P450 isozymes.
C1 [Shah, Pranav; Kerns, Edward; Dac-Trung Nguyen; Wang, Amy Q.; Zakharov, Alexey; McKew, John; Simeonov, Anton; Xu, Xin] Natl Ctr Adv Translat Sci, Div Preclin Innovat, 9800 Med Ctr Dr, Rockville, MD 20850 USA.
[Obach, R. Scott] Pfizer, Dept Pharmacokinet Dynam & Metab, Groton, CT USA.
[Hop, Cornelis E. C. A.] Genentech Inc, Dept Drug Metab & Pharmacokinet, San Francisco, CA 94080 USA.
RP Xu, X (reprint author), Natl Ctr Adv Translat Sci, Div Preclin Innovat, 9800 Med Ctr Dr, Rockville, MD 20850 USA.
EM xin.xu3@nih.gov
FU Intramural Research Program of the National Center for Advancing
Translational Sciences/National Institutes of Health
FX This work was supported by the Intramural Research Program of the
National Center for Advancing Translational Sciences/National Institutes
of Health.
NR 22
TC 0
Z9 0
U1 3
U2 3
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0090-9556
EI 1521-009X
J9 DRUG METAB DISPOS
JI Drug Metab. Dispos.
PD OCT
PY 2016
VL 44
IS 10
BP 1653
EP 1661
DI 10.1124/dmd.116.072017
PG 9
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA DX0WY
UT WOS:000384088300014
PM 27417180
ER
PT J
AU Noble, JA
Nelson, RG
Fufaa, GD
Kang, P
Shafir, SC
Galgiani, JN
AF Noble, Jason A.
Nelson, Robert G.
Fufaa, Gudeta D.
Kang, Paul
Shafir, Shira Chani
Galgiani, John N.
TI Effect of Geography on the Analysis of Coccidioidomycosis-Associated
Deaths, United states
SO EMERGING INFECTIOUS DISEASES
LA English
DT Article
ID PIMA-INDIANS; CALIFORNIA; ARIZONA; IMPACT
AB Because coccidioidomycosis death rates vary by region, we reanalyzed coccidioidomycosis-associated mortality in the United States by race/ethnicity, then limited analysis to Arizona and California. Coccidioidomycosis-associated deaths were shown to increase among African-Americans but decrease among Native Americans and Hispanics. Separately, in a Native American cohort, diabetes co-varied with coccidioidomycosis-associated death.
C1 [Noble, Jason A.; Kang, Paul] Univ Arizona, Coll Med, Phoenix, AZ USA.
[Nelson, Robert G.; Fufaa, Gudeta D.] NIH, Bldg 10, Bethesda, MD 20892 USA.
[Shafir, Shira Chani] Univ Calif Los Angeles, Los Angeles, CA USA.
[Galgiani, John N.] Univ Arizona, Coll Med, Tucson, AZ USA.
RP Galgiani, JN (reprint author), Univ Arizona, Coll Med, Valley Fever Ctr Excellence, 1656 East Mabel St, Tucson, AZ 85712 USA.
EM spherule@u.arizona.edu
NR 12
TC 1
Z9 1
U1 2
U2 2
PU CENTERS DISEASE CONTROL
PI ATLANTA
PA 1600 CLIFTON RD, ATLANTA, GA 30333 USA
SN 1080-6040
EI 1080-6059
J9 EMERG INFECT DIS
JI Emerg. Infect. Dis
PD OCT
PY 2016
VL 22
IS 10
BP 1821
EP 1823
DI 10.3201/eid2210.160696
PG 3
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA DX4YQ
UT WOS:000384387400021
PM 27649029
ER
PT J
AU Dennis, KK
Auerbach, SS
Balshaw, DM
Cui, YX
Fallin, MD
Smith, M
Spira, A
Sumner, S
Miller, GW
AF Dennis, Kristine K.
Auerbach, Scott S.
Balshaw, David M.
Cui, Yuxia
Fallin, Margaret Daniele
Smith, MartynT.
Spira, Avrum
Sumner, Susan
Miller, Gary W.
TI The Importance of the Biological Impact of Exposure to the Concept of
the Exposome
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article
ID HUMAN METABOLOME DATABASE; TELOMERE LENGTH; ENVIRONMENTAL-HEALTH;
GENE-EXPRESSION; LIFE-STYLE; DISEASE; GENOME; CANCER; RISKS;
TECHNOLOGIES
AB BACKGROUND: The term "exposome" was originally coined in 2005 and defined as the totality of exposures throughout the lifetime. The exposome provides an excellent scientific framework for studying human health and disease. Recently, it has been suggested that how exposures affect our biology and how our bodies respond to such exposures should be part of the exposome.
OBJECTIVES: The authors describe the biological impact of the exposome and outline many of the targets and processes that can be assessed as part of a comprehensive analysis of the exposome.
DISCUSSION: The processes that occur downstream from the initial interactions with exogenous and endogenous compounds determine the biological impact of exposures. If the effects are not considered in the same context as the exposures, it will be difficult to determine cause and effect. The exposome and biology are interactive-changes in biology due to the environment change one's vulnerability to subsequent exposures. Additionally, highly resilient individuals are able to withstand environmental exposures with minimal effects to their health. We expect that the vast majority of exposures are transient, and chemicals underlying exposures that occurred weeks, months, or years ago are long gone from the body. However, these past chemical exposures often leave molecular fingerprints that may be able to provide information on these past exposures.
CONCLUSIONS: Through linking exposures to specific biological responses, exposome research could serve to improve understanding of the mechanistic connections between exposures and health to help mitigate adverse health outcomes across the lifespan.
C1 [Dennis, Kristine K.; Miller, Gary W.] Emory Univ, Rollins Sch Publ Hlth, Dept Environm Hlth, 1518 Clifton Rd NE,Mailstop 1518-002-8BB, Atlanta, GA 30322 USA.
[Auerbach, Scott S.] NIEHS, Biomol Screening Branch, Div Natl Toxicol Program, NIH,Dept Hlth & Human Resources, POB 12233, Res Triangle Pk, NC 27709 USA.
[Balshaw, David M.; Cui, Yuxia] NIEHS, Exposure Response & Technol Branch, Div Extramural Res & Training, NIH,Dept Hlth & Human Resources, POB 12233, Res Triangle Pk, NC 27709 USA.
[Fallin, Margaret Daniele] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Mental Hlth, Baltimore, MD USA.
[Smith, MartynT.] Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, Berkeley, CA 94720 USA.
[Spira, Avrum] Boston Univ, Sch Med, Div Computat Biomed, Boston, MA 02118 USA.
[Sumner, Susan] RTI Int, Discovery Sci, Res Triangle Pk, NC USA.
RP Miller, GW (reprint author), Emory Univ, Rollins Sch Publ Hlth, Dept Environm Hlth, 1518 Clifton Rd NE,Mailstop 1518-002-8BB, Atlanta, GA 30322 USA.
EM gary.miller@emory.edu
FU National Institute of Environmental Health Sciences, National Exposure
Assessment Laboratory Network [1U2CES026560, 1U2CES026544]
FX G.W.M. receives royalties from his book The Exposome: A Primer. G.W.M.
and S.S. received CHEAR (Children's Health Exposure Analysis Resource)
awards from the National Institute of Environmental Health Sciences as
part of the National Exposure Assessment Laboratory Network to provide
targeted and untargeted environmental exposure and biological response
analyses in human samples (1U2CES026560 and 1U2CES026544). A.S. is the
founder of AllegroDx, Inc., Maynard, MA and a consultant to Veracyte,
Inc., South San Francisco, CA. S.S. is employed by Discovery Sciences,
RTI International, Research Triangle Park, NC.
NR 42
TC 8
Z9 8
U1 8
U2 8
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
EI 1552-9924
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD OCT
PY 2016
VL 124
IS 10
BP 1504
EP 1510
DI 10.1289/EHP140
PG 7
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA DX4EQ
UT WOS:000384334400012
PM 27258438
ER
PT J
AU Le, NT
Michels, FAS
Song, MY
Zhang, XH
Bernstein, AM
Giovannucci, EL
Fuchs, CS
Ogino, S
Chan, AT
Sinha, R
Willett, WC
Wu, KN
AF Ngoan Tran Le
Michels, Fernanda Alessandra Silva
Song, Mingyang
Zhang, Xuehong
Bernstein, Adam M.
Giovannucci, Edward L.
Fuchs, Charles S.
Ogino, Shuji
Chan, Andrew T.
Sinha, Rashmi
Willett, Walter C.
Wu, Kana
TI A Prospective Analysis of Meat Mutagens and Colorectal Cancer in the
Nurses' Health Study and Health Professionals Follow-up Study
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article
ID FOOD FREQUENCY QUESTIONNAIRE; DIETARY HETEROCYCLIC AMINES; NATIONAL
DEATH INDEX; COLON-CANCER; MULTIETHNIC COHORT; RED MEAT; COOKING
METHODS; RISK FINDINGS; HEME IRON; CONSUMPTION
AB BACKGROUND: Heterocyclic amines (HCAs) in cooked meats may play a role in colorectal cancer (CRC) development.
OBJECTIVES: We aimed to prospectively examine the association between estimated intakes of HCAs and meat-derived mutagenicity (MDM) in two cohorts of health professionals, the Health Professionals Follow-up Study (HPFS) and the Nurses' Health Study (NHS).
METHODS: In 29,615 men and 65,875 women, intake of the HCAs 2-amino-3,8-dimethylimidazo(4,5-j) quinoxaline (MeIQx), 2-amino-1-methyl-6-phenylimidazo(4,5-b) pyridine (PhIP), 2-amino-3,4,8-trimethylimidazo(4,5-f) quinoxaline (DiMeIQx), and MDM was estimated using a 1996 cooking questionnaire, the 1994 food frequency questionnaire, and an online database. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) and to adjust for potential confounders. Estimates for both cohorts were pooled using random-effects meta-analysis.
RESULTS: Between 1996 and 2010, 418 male and 790 female CRC cases were identified. Meat mutagen intake was not statistically significantly associated with risk of CRC [highest vs. lowest quintile, pooled HR (95% CI) for MeIQx: 1.12 (0.93, 1.34), p for trend 0.23; PhIP: 1.10 (0.90, 1.33), p for trend 0.35; MDM: 1.03 (0.86, 1.24), p for trend 0.75] or subtypes of CRC defined by tumor location (proximal or distal colon, or rectum). When analyzed by source of meat, PhIP from red but not from white meat was nonsignificantly positively associated with CRC and significantly positively associated with proximal cancers [HR (95% CI) per standard deviation increase of log-transformed intake: PhIP red meat: CRC: 1.06 (0.99, 1.12), proximal: 1.11 (1.02, 1.21); PhIP white meat: CRC: 0.99 (0.94, 1.04), proximal: 1.00 (0.93, 1.09)].
CONCLUSIONS: Estimated intakes of meat mutagens were not significantly associated with CRC risk over 14 years of follow-up in the NHS and HPFS cohorts. Results for PhIP from red but not from white meat warrant further investigation.
C1 [Ngoan Tran Le] Hanoi Med Univ, Dept Occupat Hlth, Hanoi, Vietnam.
[Ngoan Tran Le; Michels, Fernanda Alessandra Silva; Song, Mingyang; Giovannucci, Edward L.; Willett, Walter C.; Wu, Kana] Harvard TH Chan Sch Publ Hlth, Dept Nutr, 665 Huntington Ave, Boston, MA 02115 USA.
[Song, Mingyang; Chan, Andrew T.] Massachusetts Gen Hosp, Clin & Translat Epidemiol Unit, Boston, MA 02114 USA.
[Song, Mingyang; Chan, Andrew T.] Massachusetts Gen Hosp, Div Gastroenterol, Boston, MA 02114 USA.
[Song, Mingyang; Zhang, Xuehong; Giovannucci, Edward L.; Fuchs, Charles S.; Ogino, Shuji; Chan, Andrew T.; Willett, Walter C.] Harvard Med Sch, Boston, MA USA.
[Song, Mingyang; Giovannucci, Edward L.; Ogino, Shuji; Willett, Walter C.] Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
[Zhang, Xuehong; Giovannucci, Edward L.; Ogino, Shuji; Chan, Andrew T.; Willett, Walter C.] Brigham & Womens Hosp, Dept Med, Channing Div Network Med, 75 Francis St, Boston, MA 02115 USA.
[Bernstein, Adam M.] Rally Hlth, San Francisco, CA USA.
[Fuchs, Charles S.; Ogino, Shuji] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Ogino, Shuji] Brigham & Womens Hosp, Dept Pathol, Div Mol Pathol Epidemiol, 75 Francis St, Boston, MA 02115 USA.
[Sinha, Rashmi] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
RP Le, NT (reprint author), Harvard TH Chan Sch Publ Hlth, Dept Nutr, 665 Huntington Ave, Boston, MA 02115 USA.
EM letngoan@hmu.edu.vn
FU National Institutes of Health [UM1 CA167552, UM1 CA186107, P50 CA127003,
R35 CA197735, P01 CA87969, P01 CA 55075]; Union for International Cancer
Control (UICC) American Cancer Society Beginning Investigators
Fellowship - American Cancer Society; UICC Yamagiwa-Yoshida Memorial
International Cancer Study Grant
FX This work was supported by federal grants (National Institutes of
Health): UM1 CA167552, UM1 CA186107, P50 CA127003, R35 CA197735, P01
CA87969, and P01 CA 55075. This work has also been supported by a Union
for International Cancer Control (UICC) American Cancer Society
Beginning Investigators Fellowship funded by the American Cancer Society
and by a UICC Yamagiwa-Yoshida Memorial International Cancer Study Grant
to N.T.L.
NR 64
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Z9 2
U1 9
U2 9
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 2016
VL 124
IS 10
BP 1529
EP 1536
DI 10.1289/EHP238
PG 8
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA DX4EQ
UT WOS:000384334400015
PM 27105317
ER
PT J
AU Nagrani, R
Mhatre, S
Rajaraman, P
Soerjomataram, I
Boffetta, P
Gupta, S
Parmar, V
Badwe, R
Dikshit, R
AF Nagrani, R.
Mhatre, S.
Rajaraman, P.
Soerjomataram, I.
Boffetta, P.
Gupta, S.
Parmar, V.
Badwe, R.
Dikshit, R.
TI Central obesity increases risk of breast cancer irrespective of
menopausal and hormonal receptor status in women of South Asian
Ethnicity
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Article
DE Breast cancer; Central obesity; Menopausal status; Hormone receptor
status; South Asian
ID BODY-MASS INDEX; ABDOMINAL ADIPOSITY; INSULIN-RESISTANCE; FAT
DISTRIBUTION; SIZE; PROFILE; ANTHROPOMETRY; METAANALYSIS; ASSOCIATION;
CAUCASIANS
AB Background: Current evidence suggests that the relationship between obesity and breast cancer (BC) risk may vary between ethnic groups.
Methods: A total of 1633 BC cases and 1504 controls were enrolled in hospital-based case econtrol study in Mumbai, India, from 2009 to 2013. Along with detailed questionnaire, we collected anthropometric measurements on all participants. We used unconditional logistic regression models to estimate odds ratios (ORs) and 95% confidence interval (CI) for BC risk associated with anthropometry measurements, stratified on tumour subtype and menopausal status.
Results: Waist-to-hip ratio (WHR) of >= 0.95 was strongly associated with risk of BC compared to WHR <= 0.84 in both premenopausal (OR = 4.3; 95% CI: 2.9-6.3) and postmenopausal women (OR = 3.4; 95% CI: 2.4-4.8) after adjustment for body mass index (BMI). Premenopausal women with a BMI >= 30 were at lower risk compared to women with normal BMI (OR = 0.5; 95% CI: 0.4-0.8). A similar protective effect was observed in women who were postmenopausal for <10 years (OR = 0.6; 95% CI: 0.4-0.9) but not in women who were postmenopausal for >= 10 years (OR = 1.8; 95% CI: 1.1-3.3). Overweight and obese women (BMI: 25-29.9 and >= 30 kg/m(2), respectively) were at increased BC risk irrespective of menopausal status if their WHR >= 0.95. Central obesity (measured in terms of WC and WHR) increased the risk of both premenopausal and postmenopausal BCs irrespective of hormone receptor (HR) status.
Conclusions: Central obesity appears to be a key risk factor for BC irrespective of menopausal or HR status in Indian women with no history of hormone replacement therapy. (C) 2016 The Authors. Published by Elsevier Ltd.
C1 [Nagrani, R.; Mhatre, S.; Dikshit, R.] Tata Mem Hosp, Ctr Canc Epidemiol, E Borges Rd, Bombay 400012, Maharashtra, India.
[Rajaraman, P.] US Natl Canc Inst, Ctr Global Hlth, 9609 Med Ctr Dr, Rockville, MD 20892 USA.
[Soerjomataram, I.] Int Agcy Res Canc, Sect Canc Surveillance, 150 Cours Albert Thomas, F-69372 Lyon, France.
[Boffetta, P.] Mt Sinai Hosp, Inst Translat Epidemiol, 1 Gustave L Levy Pl, New York, NY 10029 USA.
[Gupta, S.] Adv Ctr Treatment Res & Educ Canc, Navi Mumbai 400012, Maharashtra, India.
[Parmar, V.; Badwe, R.] Tata Mem Hosp, Dept Surg Oncol, Bombay 400012, Maharashtra, India.
RP Dikshit, R (reprint author), Tata Mem Hosp, Ctr Canc Epidemiol, E Borges Rd, Bombay 400012, Maharashtra, India.
EM dixr24@hotmail.com
OI nagrani, rajini/0000-0002-1708-2319
FU Department of Biotechnology, India [102/IFD/SAN/2935/2012-2013];
International Agency for research on Cancer, France [GEE/08/02-Extension
1]
FX The authors would like to thank the funding agencies viz. Department of
Biotechnology, India (102/IFD/SAN/2935/2012-2013); International Agency
for research on Cancer, France (GEE/08/02-Extension 1).
NR 35
TC 0
Z9 0
U1 9
U2 9
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0959-8049
EI 1879-0852
J9 EUR J CANCER
JI Eur. J. Cancer
PD OCT
PY 2016
VL 66
BP 153
EP 161
DI 10.1016/j.ejca.2016.07.022
PG 9
WC Oncology
SC Oncology
GA DX0YB
UT WOS:000384091400019
PM 27573429
ER
PT J
AU Maddipati, KR
Romero, R
Chaiworapongsa, T
Chaemsaithong, P
Zhou, SL
Xu, ZH
Tarca, AL
Kusanovic, JP
Gomez, R
Chaiyasit, N
Honn, KV
AF Maddipati, Krishna Rao
Romero, Roberto
Chaiworapongsa, Tinnakorn
Chaemsaithong, Piya
Zhou, Sen-Lin
Xu, Zhonghui
Tarca, Adi L.
Kusanovic, Juan Pedro
Gomez, Ricardo
Chaiyasit, Noppadol
Honn, Kenneth V.
TI Lipidomic analysis of patients with microbial invasion of the amniotic
cavity reveals up-regulation of leukotriene B-4
SO FASEB JOURNAL
LA English
DT Article
DE infection; inflammation; clinical chorioamnionitis; amniotic fluid;
5-lipoxygenase
ID PRETERM PREMATURE RUPTURE; PRO-RESOLVING MEDIATORS;
TUMOR-NECROSIS-FACTOR; INTRAAMNIOTIC INFECTION; SPONTANEOUS LABOR;
CLINICAL CHORIOAMNIONITIS; HUMAN PARTURITION; FLUID INTERLEUKIN-6;
INTACT MEMBRANES; CONCENTRATIONS INCREASE
AB Bioactive lipids derived from the metabolism of polyunsaturated fatty acids are important mediators of the inflammatory response. Labor per se is considered a sterile inflammatory process. Intra-amniotic inflammation (IAI) due to microorganisms (i.e., intra-amniotic infection) or danger signals (i.e., sterile IAI) has been implicated in the pathogenesis of preterm labor and clinical chorioamnionitis at term. Early and accurate diagnosis of microbial invasion of the amniotic cavity (MIAC) requires analysis of amniotic fluid (AF). It is possible that IAI caused by microorganisms is associated with a stereotypic lipidomic profile, and that analysis of AF may help in the identification of patients with this condition. To test this hypothesis, we analyzed the fatty acyl lipidome of AF by liquid chromatography-mass spectrometry from patients in spontaneous labor at term and preterm gestations. We report that the AF concentrations of proinflammatory lipid mediators of the 5-lipoxygenase pathway are significantly higher in MIAC than in cases of sterile IAI. These results suggest that the concentrations of 5-lipoxygenase metabolites of arachidonic acid, 5-hydroxyeicosatetraenoic acid, and leukotriene B-4 in particular could serve as potential biomarkers of MIAC. This finding could have important implications for the rapid identification of patients who may benefit from anti-microbial treatment.-Maddipati, K. R., Romero, R., Chaiworapongsa ,T., Chaemsaithong, P., Zhou, S.-L., Xu, Z., Tarca, A. L., Kusanovic, J. P., Gomez, R., Chaiyasit, N., Honn, K. V. Lipidomic analysis of patients with microbial invasion of the amniotic cavity reveals up-regulation of leukotriene B-4.
C1 [Maddipati, Krishna Rao; Zhou, Sen-Lin; Honn, Kenneth V.] Wayne State Univ, Sch Med, Dept Pathol, Detroit, MI 48201 USA.
[Maddipati, Krishna Rao; Zhou, Sen-Lin] Wayne State Univ, Sch Med, Lipid Core Facil, Detroit, MI USA.
[Chaiworapongsa, Tinnakorn; Chaemsaithong, Piya; Tarca, Adi L.; Chaiyasit, Noppadol] Wayne State Univ, Sch Med, Dept Obstet & Gynecol, Detroit, MI 48201 USA.
[Romero, Roberto; Chaiworapongsa, Tinnakorn; Chaemsaithong, Piya; Xu, Zhonghui; Tarca, Adi L.; Kusanovic, Juan Pedro; Chaiyasit, Noppadol] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, Div Intramural Res, Natl Inst Hlth,Dept Hlth & Human Serv, Bethesda, MD USA.
[Romero, Roberto] Univ Michigan, Dept Obstet & Gynecol, Ann Arbor, MI 48109 USA.
[Romero, Roberto] Wayne State Univ, Ctr Mol Med & Genet, Detroit, MI USA.
[Tarca, Adi L.] Wayne State Univ, Dept Comp Sci, Detroit, MI 48202 USA.
[Romero, Roberto] Michigan State Univ, Dept Epidemiol & Biostat, E Lansing, MI 48824 USA.
[Kusanovic, Juan Pedro] Hosp Dr Sotero del Rio, Dept Obstet & Gynecol, Ctr Res & Innovat Maternal Fetal Med CIMAF, Santiago, Chile.
[Kusanovic, Juan Pedro; Gomez, Ricardo] Pontificia Univ Catolica Chile, Div Obstet & Gynecol, Santiago, Chile.
[Gomez, Ricardo] Hosp Clin La Florida, Res & Acad Innovat, Ctr Perinatal Diag CEDIP, Santiago, Chile.
RP Maddipati, KR (reprint author), Wayne State Univ, Dept Pathol, 435 Chem Bldg,410 W Warren Ave, Detroit, MI 48202 USA.
EM maddipati@wayne.edu
FU Perinatology Research Branch, Division of Intramural Research Branch of
the Eunice Kennedy Shriver National Institute of Child Health and Human
Development, U.S. National Institutes of Health, U.S. Department of
Health and Human Services (NICHD/NIH/DHHS); NICHD/NIH/DHHS
[HHSN275201300006C]; National Center for Research Resources
[S10RR027926]; Wayne State University
FX This research was supported, in part, by the Perinatology Research
Branch, Division of Intramural Research Branch of the Eunice Kennedy
Shriver National Institute of Child Health and Human Development, U.S.
National Institutes of Health, U.S. Department of Health and Human
Services (NICHD/NIH/DHHS); and, in part, with Federal funds from
NICHD/NIH/DHHS Contract No. HHSN275201300006C; and, in part, by the
National Center for Research Resources Grant S10RR027926 and the
Perinatal Virtual Discovery Grant from Wayne State University (to
K.R.M.). The authors declare no conflicts of interest.
NR 91
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U1 3
U2 3
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
EI 1530-6860
J9 FASEB J
JI Faseb J.
PD OCT
PY 2016
VL 30
IS 10
BP 3296
EP 3307
DI 10.1096/fj.201600583R
PG 12
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA DX4DD
UT WOS:000384329800004
PM 27312808
ER
PT J
AU Hu, N
Wang, ZM
Song, X
Wei, LX
Kim, BS
Freedman, ND
Baek, J
Burdette, L
Chang, J
Chung, C
Dawsey, SM
Ding, T
Gao, YT
Giffen, C
Han, YL
Hong, M
Huang, J
Kim, HS
Koh, WP
Liao, LDM
Mao, YM
Qiao, YL
Shu, XO
Tan, W
Wang, CY
Wu, C
Wu, MJ
Xiang, YB
Yeager, M
Yook, JH
Yuan, JM
Zhang, P
Zhao, XK
Zheng, W
Song, K
Wang, LD
Lin, DX
Chanock, SJ
Goldstein, AM
Taylor, PR
Abnet, CC
AF Hu, Nan
Wang, Zhaoming
Song, Xin
Wei, Lixuan
Kim, Byung Sik
Freedman, Neal D.
Baek, Jiwon
Burdette, Laurie
Chang, Jiang
Chung, Charles
Dawsey, Sanford M.
Ding, Ti
Gao, Yu-Tang
Giffen, Carol
Han, Yaling
Hong, Myunghee
Huang, Jia
Kim, Hee Sung
Koh, Woon-Puay
Liao, Linda M.
Mao, Yi Min
Qiao, You-Lin
Shu, Xiao-Ou
Tan, Wen
Wang, Chaoyu
Wu, Chen
Wu, Min-Jie
Xiang, Yong-Bing
Yeager, Meredith
Yook, Jeong Hwan
Yuan, Jian-Min
Zhang, Peng
Zhao, Xue-Ke
Zheng, Wei
Song, Kyuyoung
Wang, Li-Dong
Lin, Dongxin
Chanock, Stephen J.
Goldstein, Alisa M.
Taylor, Philip R.
Abnet, Christian C.
TI Genome-wide association study of gastric adenocarcinoma in Asia: a
comparison of associations between cardia and non-cardia tumours
SO GUT
LA English
DT Article
ID SQUAMOUS-CELL CARCINOMA; HELICOBACTER-PYLORI; SUSCEPTIBILITY LOCI;
KOREAN POPULATION; CANCER; ESOPHAGEAL; CHINESE; DIFFUSE; RISK
AB Objective Genome-wide association studies (GWAS) of gastric cancer have reported differences in single-nucleotide polymorphism (SNP) associations for tumour subtypes, particularly when divided by location into the gastric cardia versus the non-cardia.
Design Here we present results for a GWAS using 2350 East Asian gastric cancer cases divided as 1189 gastric cardia and 1027 gastric non-cardia cases and 2708 controls. We also included up to 3042 cardia cases, 4359 non-cardia cases and 7548 controls for replication from two Chinese studies and one Korean study. From the GWAS, we selected 12 top SNPs for each gastric cancer subtype, 4 top SNPs for total gastric cancer and 1 SNP in MUC1 for replication testing.
Results We observed genome-wide significant associations for rs10074991 in PRKAA1 at 5p13.1 for cardia (p=7.36x10(-12)) and non-cardia cancers (p=2.42x10(-23)) with per allele OR (95% CI) for the combined endpoint of 0.80 (0.77 to 0.83). At 6p21.1, rs2294693 near UNC5CL was significantly associated with gastric non-cardia cancer risk (p=2.50x10(-8)), with OR (95% CI) of 1.18 (1.12 to 1.26), but there was only a nominal association for cardia cancer (p=1.47x10(-2)). We also confirmed a previously reported association for rs4072037 in MUC1 with p=6.59x10(-8) for total gastric cancer and similar estimates for cardia and non-cardia cancers. Three SNPs in PSCA previously reported to be associated with gastric non-cardia cancer showed no apparent association for cardia cancer.
Conclusions Our results suggest that associations for SNPs with gastric cancer show some different results by tumour location in the stomach.
C1 [Hu, Nan; Wang, Zhaoming; Freedman, Neal D.; Burdette, Laurie; Chung, Charles; Dawsey, Sanford M.; Liao, Linda M.; Wang, Chaoyu; Yeager, Meredith; Chanock, Stephen J.; Goldstein, Alisa M.; Taylor, Philip R.; Abnet, Christian C.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Song, Xin; Huang, Jia; Mao, Yi Min; Zhang, Peng; Zhao, Xue-Ke; Wang, Li-Dong] Zhengzhou Univ, Affiliated Hosp 1, Henan Key Lab Esophageal Canc Res, Zhengzhou, Henan, Peoples R China.
[Wei, Lixuan; Chang, Jiang; Han, Yaling; Tan, Wen; Wu, Chen; Lin, Dongxin] Chinese Acad Med Sci, Canc Inst & Hosp, Dept Etiol & Carcinogenesis, Beijing, Peoples R China.
[Wei, Lixuan; Chang, Jiang; Han, Yaling; Tan, Wen; Wu, Chen; Lin, Dongxin] Peking Union Med Coll, Beijing, Peoples R China.
[Kim, Byung Sik; Kim, Hee Sung; Yook, Jeong Hwan] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Surg, Seoul, South Korea.
[Baek, Jiwon; Hong, Myunghee; Song, Kyuyoung] Univ Ulsan, Coll Med, Dept Biochem & Mol Biol, Seoul, South Korea.
[Burdette, Laurie; Chung, Charles; Yeager, Meredith] NCI, Canc Genome Res Lab, Div Canc Epidemiol & Genet, Adv Technol Program,SAIC Frederick Inc, Frederick, MD 21701 USA.
[Ding, Ti] Shanxi Canc Hosp, Taiyuan, Shanxi, Peoples R China.
[Gao, Yu-Tang; Xiang, Yong-Bing] Shanghai Canc Inst, Shanghai, Peoples R China.
[Giffen, Carol] Informat Management Serv Inc, Silver Spring, MD USA.
[Koh, Woon-Puay] Duke NUS Grad Med Sch Singapore, Singapore, Singapore.
[Qiao, You-Lin] Chinese Acad Med Sci, Canc Inst & Hosp, Dept Epidemiol, Beijing, Peoples R China.
[Shu, Xiao-Ou; Zheng, Wei] Vanderbilt Univ, Dept Med, Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
[Wu, Min-Jie] Xinxiang Med Univ, Canc Res Ctr, Xinxiang, Henan, Peoples R China.
[Yuan, Jian-Min] Univ Pittsburgh, Inst Canc, Pittsburgh, PA USA.
RP Abnet, CC (reprint author), NCI, Div Canc Epidemiol & Genet, Nutr Epidemiol Branch, 9609 Med Ctr Dr,Rm 6e430,MSC 9768, Bethesda, MD 20892 USA.
EM abnet@nih.gov
RI Zheng, Wei/O-3351-2013; Abnet, Christian/C-4111-2015
OI Zheng, Wei/0000-0003-1226-070X; Abnet, Christian/0000-0002-3008-7843
FU National Cancer Institute [R01CA80205, R01CA144034, R37: CA070867, R01:
CA082729, UM: CA173640]; National Natural Science Foundation of China
[81472323]; Top Talent Support Project of Zhengzhou University
[ZDGD13001]; Innovation Scientists and Technicians Troop Construction
Projects of Henan Province [3047]; Mid-career Researcher Program grant
through National Research Foundation from the Ministry of Science,
Information and Communication Technology (ICT) and Future Planning,
Republic of Korea [2014R1A2A1A09005824]
FX This work was supported by the intramural research programme of the
National Institutes of Health, National Cancer Institute. The Singapore
Chinese Health Study was supported by National Cancer Institute grants
R01CA80205 and R01CA144034. The Shanghai Women's Health Study was
supported by National Cancer Institute grants R37: CA070867 and the
Shanghai Men's Health Study was supported by National Cancer Institute
grants R01: CA082729 and UM: CA173640. The Henan province study was
supported by the National Natural Science Foundation of China, grant
number 81472323; the Top Talent Support Project of Zhengzhou University,
grant number ZDGD13001; and the Innovation Scientists and Technicians
Troop Construction Projects of Henan Province, grant number 3047 to LDW.
KS was supported by a Mid-career Researcher Program grant
(2014R1A2A1A09005824) through National Research Foundation from the
Ministry of Science, Information and Communication Technology (ICT) and
Future Planning, Republic of Korea.
NR 16
TC 4
Z9 4
U1 5
U2 5
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0017-5749
EI 1468-3288
J9 GUT
JI Gut
PD OCT
PY 2016
VL 65
IS 10
BP 1611
EP 1618
DI 10.1136/gutjnl-2015-309340
PG 8
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DX5XR
UT WOS:000384456500008
PM 26129866
ER
PT J
AU Scarzello, AJ
Jiang, Q
Back, T
Dang, H
Hodge, D
Hanson, C
Subleski, J
Weiss, JM
Stauffer, JK
Chaisaingmongkol, J
Rabibhadana, S
Ruchirawat, M
Ortaldo, J
Wang, XW
Norris, PS
Ware, CF
Wiltrout, RH
AF Scarzello, Anthony J.
Jiang, Qun
Back, Timothy
Dang, Hien
Hodge, Deborah
Hanson, Charlotte
Subleski, Jeffrey
Weiss, Jonathan M.
Stauffer, Jimmy K.
Chaisaingmongkol, Jitti
Rabibhadana, Siritida
Ruchirawat, Mathuros
Ortaldo, John
Wang, Xin Wei
Norris, Paula S.
Ware, Carl F.
Wiltrout, Robert H.
TI LT beta R signalling preferentially accelerates oncogenic AKT-initiated
liver tumours
SO GUT
LA English
DT Article
ID NF-KAPPA-B; INTRAHEPATIC CHOLANGIOCARCINOMA; HEPATOCELLULAR-CARCINOMA;
LYMPHOTOXIN-BETA; HYDRODYNAMIC INJECTION; NEXT-GENERATION; CYCLIN D1;
T-CELLS; CANCER; ACTIVATION
AB Objectives The relative contributions of inflammatory signalling and sequential oncogenic dysregulation driving liver cancer pathogenesis remain incompletely understood. Lymphotoxin-beta receptor (LT beta R) signalling is critically involved in hepatitis and liver tumorigenesis. Therefore, we explored the interdependence of inflammatory lymphotoxin signalling and specific oncogenic pathways in the progression of hepatic cancer.
Design Pathologically distinct liver tumours were initiated by hydrodynamic transfection of oncogenic V-Akt Murine Thymoma Viral Oncogene Homolog 1 (AKT)/beta-catenin or AKT/Notch expressing plasmids. To investigate the relationship of LT beta R signalling and specific oncogenic pathways, LT beta R antagonist (LT beta R-Fc) or agonist (anti-LT beta R) were administered post oncogene transfection. Initiated livers/tumours were investigated for changes in oncogene expression, tumour proliferation, progression, latency and pathology. Moreover, specific LT beta R-mediated molecular events were investigated in human liver cancer cell lines and through transcriptional analyses of samples from patients with intrahepatic cholangiocarcinoma (ICC).
Results AKT/beta-catenin-transfected livers displayed increased expression of LT beta and LT beta R, with antagonism of LT beta R signalling reducing tumour progression and enhancing survival. Conversely, enforced LT beta R-activation of AKT/beta-catenin-initiated tumours induced robust increases in proliferation and progression of hepatic tumour phenotypes in an AKT-dependent manner. LT beta R-activation also rapidly accelerated ICC progression initiated by AKT/Notch, but not Notch alone. Moreover, LT beta R-accelerated development coincides with increases of Notch, Hes1, c-MYC, pAKT and beta-catenin. We further demonstrate LT beta R signalling in human liver cancer cell lines to be a regulator of Notch, pAKTser473 and beta-catenin. Transcriptome analysis of samples from patients with ICC links increased LT beta R network expression with poor patient survival, increased Notch1 expression and Notch and AKT/PI3K signalling.
Conclusions Our findings link LT beta R and oncogenic AKT signalling in the development of ICC.
C1 [Scarzello, Anthony J.; Jiang, Qun; Back, Timothy; Hodge, Deborah; Hanson, Charlotte; Subleski, Jeffrey; Weiss, Jonathan M.; Stauffer, Jimmy K.; Ortaldo, John; Wiltrout, Robert H.] NCI, Canc & Inflamat Program, Ctr Canc Res, Frederick, MD 21701 USA.
[Dang, Hien; Wang, Xin Wei] NCI, Human Carcinogenesis Lab, Ctr Canc Res, Bldg 37, Bethesda, MD 20892 USA.
[Norris, Paula S.; Ware, Carl F.] Sanford Burnham Med Res Inst, Infect & Inflammatory Dis Res Ctr, La Jolla, CA USA.
[Chaisaingmongkol, Jitti; Rabibhadana, Siritida; Ruchirawat, Mathuros] Chulabhorn Res Inst, Bangkok, Thailand.
RP Wiltrout, RH (reprint author), NCI, Expt Therapeut Sect, Canc & Inflammat Program, Ctr Canc Res,NIH, Frederick, MD 21702 USA.
EM wiltrour@mail.nih.gov
RI Wang, Xin/B-6162-2009
FU Intramural Research Program of the National Cancer Institute, National
Institutes of Health (NCI/NIH); NIH [R01CA164679, P01CA177322,
R37AI33068]
FX This research was supported by the Intramural Research Program of the
National Cancer Institute, National Institutes of Health (NCI/NIH) and
NIH grants R01CA164679, P01CA177322 and R37AI33068 (CFW).
NR 50
TC 2
Z9 2
U1 4
U2 4
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0017-5749
EI 1468-3288
J9 GUT
JI Gut
PD OCT
PY 2016
VL 65
IS 10
BP 1765
EP U203
DI 10.1136/gutjnl-2014-308810
PG 11
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA DX5XR
UT WOS:000384456500022
PM 26206664
ER
PT J
AU Yu, KR
Natanson, H
Dunbar, CE
AF Yu, Kyung-Rok
Natanson, Hannah
Dunbar, Cynthia E.
TI Gene Editing of Human Hematopoietic Stem and Progenitor Cells: Promise
and Potential Hurdles
SO HUMAN GENE THERAPY
LA English
DT Review
ID ZINC-FINGER NUCLEASES; RNA-GUIDED ENDONUCLEASE; SEVERE COMBINED
IMMUNODEFICIENCY; GENOME-WIDE ANALYSIS; CRISPR-CAS SYSTEM;
STEM/PROGENITOR CELLS; IN-VIVO; TRANSCRIPTION FACTOR; LENTIVIRAL
VECTORS; THERAPY
AB Hematopoietic stem and progenitor cells (HSPCs) have great therapeutic potential because of their ability to both self-renew and differentiate. It has been proposed that, given their unique properties, a small number of genetically modified HSPCs could accomplish lifelong, corrective reconstitution of the entire hematopoietic system in patients with various hematologic disorders. Scientists have demonstrated that gene addition therapies-targeted to HSPCs and using integrating retroviral vectors-possess clear clinical benefits in multiple diseases, among them immunodeficiencies, storage disorders, and hemoglobinopathies. Scientists attempting to develop clinically relevant gene therapy protocols have, however, encountered a number of unexpected hurdles because of their incomplete knowledge of target cells, genomic control, and gene transfer technologies. Targeted gene-editing technologies using engineered nucleases such as ZFN, TALEN, and/or CRISPR/Cas9 RGEN show great clinical promise, allowing for the site-specific correction of disease-causing mutations-a process with important applications in autosomal dominant or dominant-negative genetic disorders. The relative simplicity of the CRISPR/Cas9 system, in particular, has sparked an exponential increase in the scientific community's interest in and use of these gene-editing technologies. In this minireview, we discuss the specific applications of gene-editing technologies in human HSPCs, as informed by prior experience with gene addition strategies. HSPCs are desirable but challenging targets; the specific mechanisms these cells evolved to protect themselves from DNA damage render them potentially more susceptible to oncogenesis, especially given their ability to self-renew and their long-term proliferative potential. We further review scientists' experience with gene-editing technologies to date, focusing on strategies to move these techniques toward implementation in safe and effective clinical trials.
C1 [Yu, Kyung-Rok; Natanson, Hannah; Dunbar, Cynthia E.] NHLBI, Hematol Branch, NIH, Room 4E-5132,CRC Bldg 10,9000 Rockville Pike, Bethesda, MD 20892 USA.
RP Dunbar, CE (reprint author), NHLBI, Hematol Branch, NIH, Room 4E-5132,CRC Bldg 10,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM dunbarc@nhlbi.nih.gov
FU National Heart, Lung, and Blood Institute
FX The authors are supported by funding through the intramural research
program of the National Heart, Lung, and Blood Institute.
NR 72
TC 0
Z9 0
U1 29
U2 29
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1043-0342
EI 1557-7422
J9 HUM GENE THER
JI Hum. Gene Ther.
PD OCT
PY 2016
VL 27
IS 10
BP 729
EP 740
DI 10.1089/hum.2016.107
PG 12
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA DX5ZY
UT WOS:000384462600002
ER
PT J
AU Li, YC
Fariss, RN
Qian, JW
Cohen, ED
Qian, HH
AF Li, Yichao
Fariss, Robert N.
Qian, Jennifer W.
Cohen, Ethan D.
Qian, Haohua
TI Light-Induced Thickening of Photoreceptor Outer Segment Layer Detected
by Ultra-High Resolution OCT Imaging
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
DE optical coherence tomography; subretinal space; light/dark adaptation;
outer segments; retinal pigment epithelium
ID OPTICAL COHERENCE TOMOGRAPHY; SPACE SURROUNDING PHOTORECEPTORS; RAT
RETINA; IN-VIVO; INTERPHOTORECEPTOR MATRIX; DEPENDENT HYDRATION;
POSTERIOR SEGMENT; PHAGOCYTOSIS; PHOTOSTASIS; BANDS
AB PURPOSE. We examined if light induces changes in the retinal structure that can be observed using optical coherence tomography (OCT).
METHODS. Normal C57BL/6J mice ( age 3-6 months) adapted to either room light (15 minutes to similar to 5 hours, 50-500 lux) or darkness (overnight) were imaged using a Bioptigen UHR-OCT system. Confocal histologic images were obtained from mice killed under light- or dark-adapted conditions.
RESULTS. The OCT image of eyes adapted to room light exhibited significant increases (6.1 +/- 0.8 mu m, n = 13) in total retina thickness compared to the same eyes after overnight dark adaptation. These light- adapted retinal thickness changes occurred mainly in the outer retina, with the development of a hyporeflective band between the RPE and photoreceptor-tip layers. Histologic analysis revealed a light- evoked elongation between the outer limiting membrane and Bruch's membrane from 45.8 +/- 1.7 mu m in the dark (n = 5) to 52.1 +/- 3.7 mu m (n = 5) in the light. Light-adapted retinas showed an increase of actin staining in RPE apical microvilli at the same location as the hyporeflective band observed in OCT images. Elongation of the outer retina could be detected even with brief light exposures, increasing 2.1 +/- 0.3 mu m after 15 minutes (n = 9), and 4.1 +/- 1.0 mu m after 2 hours (n = 6). Conversely, dark-adaptation caused outer retinal shortening of 1.4 +/- 0.4 mu m (n = 7) and 3.0 +/- 0.5 mu m (n = 8) after 15 minutes and 2 hours, respectively.
CONCLUSIONS. Light-adaption induces an increase in the thickness of the outer retina and the appearance of a hyporeflective band in the OCT image. This is consistent with previous reports of light-induced fluid accumulation in the subretinal space.
C1 [Li, Yichao; Qian, Haohua] NEI, Visual Funct Core, NIH, Bethesda, MD 20892 USA.
[Fariss, Robert N.] NEI, Biol Imaging Core, NIH, Bethesda, MD 20892 USA.
[Qian, Jennifer W.] Univ Virginia, Coll Arts & Sci, Charlottesville, VA USA.
[Cohen, Ethan D.] US FDA, Div Biomed Phys, Off Sci & Engn Labs, Ctr Devices & Radiol Hlth, Silver Spring, MD USA.
RP Qian, HH (reprint author), NEI, Visual Funct Core, NIH, Bethesda, MD 20892 USA.
EM Haohua.qian@nih.gov
FU intramural program of the National Eye Institute (Bethesda, MD, USA)
FX Supported by the intramural program of the National Eye Institute
(Bethesda, MD, USA). The mention of commercial products, their sources,
or their use in connection with material reported herein is not to be
construed as either an actual or implied endorsement of such products by
the Department of Health and Human Services.
NR 30
TC 0
Z9 0
U1 3
U2 3
PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC
PI ROCKVILLE
PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA
SN 0146-0404
EI 1552-5783
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD JUL
PY 2016
VL 57
IS 9
BP OCT105
EP OCT111
DI 10.1167/iovs.15-18539
PG 7
WC Ophthalmology
SC Ophthalmology
GA DW9MY
UT WOS:000383985400002
PM 27409460
ER
PT J
AU Zeng, Y
Petralia, RS
Vijayasarathy, C
Wu, ZJ
Hiriyanna, S
Song, HM
Wang, YX
Sieving, PA
Bush, RA
AF Zeng, Yong
Petralia, Ronald S.
Vijayasarathy, Camasamudram
Wu, Zhijian
Hiriyanna, Suja
Song, Hongman
Wang, Ya-Xian
Sieving, Paul A.
Bush, Ronald A.
TI Retinal Structure and Gene Therapy Outcome in Retinoschisin-Deficient
Mice Assessed by Spectral-Domain Optical Coherence Tomography
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
DE optical coherence tomography; X-linked retinoschisis; outer nuclear
layer; outer retina reflective band; AAV gene therapy
ID X-LINKED RETINOSCHISIS; JUVENILE RETINOSCHISIS; MOUSE MODEL; DISEASE
PROGRESSION; ADAPTIVE OPTICS; DEGENERATION; CELLS; PHOTORECEPTOR;
EXPRESSION; MECHANISMS
AB PURPOSE. Spectral-domain optical coherence tomography (SD-OCT) was used to characterize the retinal phenotype, natural history, and treatment responses in a mouse model of X-linked retinoschisis (Rs1-KO) and to identify new structural markers of AAV8-mediated gene therapy outcome.
METHODS. Optical coherence tomography scans were performed on wild-type and Rs1-KO mouse retinas between 1 and 12 months of age and on Rs1-KO mice after intravitreal injection of AAV8-scRS/IRBPhRS (AAV8-RS1). Cavities and photoreceptor outer nuclear layer (ONL) thickness were measured, and outer retina reflective band (ORRB) morphology was examined with age and after AAV8-RS1 treatment. Outer retina reflective band morphology was compared to immunohistochemical staining of the outer limiting membrane (OLM) and photoreceptor inner segment (IS) mitochondria and to electron microscopy (EM) images of IS.
RESULTS. Retinal cavity size in Rs1-KO mice increased between 1 and 4 months and decreased thereafter, while ONL thickness declined steadily, comparable to previous histologic studies. Wild-type retina had four ORRBs. In Rs1-KO, ORRB1was fragmented from 1 month, but was normal after 8 months; ORRB2 and ORRB3 were merged at all ages. Outer retina reflective band morphology returned to normal after AAV-RS1 therapy, paralleling the recovery of the OLM and IS mitochondria as indicated by anti-beta-catenin and anti-COX4 labeling, respectively, and EM.
CONCLUSIONS. Spectral-domain OCT is a sensitive, noninvasive tool to monitor subtle changes in retinal morphology, disease progression, and effects of therapies in mouse models. The ORRBs may be useful to assess the outcome of gene therapy in the treatment of X-linked retinoschisis patients.
C1 [Zeng, Yong; Vijayasarathy, Camasamudram; Song, Hongman; Sieving, Paul A.; Bush, Ronald A.] NIDCD, Sect Translat Res Retinal & Macular Degenerat, NIH, Bethesda, MD USA.
[Petralia, Ronald S.; Wang, Ya-Xian] NIDCD, Adv Imaging Core, NIH, Bethesda, MD USA.
[Wu, Zhijian; Hiriyanna, Suja] NEI, Ocular Gene Therapy Core, NIH, Bethesda, MD 20892 USA.
[Sieving, Paul A.] NEI, NIH, Bethesda, MD 20892 USA.
RP Bush, RA (reprint author), NIDCD, NIH, 50 South Dr,Room 4339,MSC 8021, Bethesda, MD 20892 USA.
EM bushr@nidcd.nih.gov
FU Intramural Research Program of the National Institutes of Health,
National Institute on Deafness and other Communication Disorders (ZIC)
[DC000065-14, DC000081-03]; National Eye Institute
FX Supported by the Intramural Research Program of the National Institutes
of Health, National Institute on Deafness and other Communication
Disorders (ZIC, DC000065-14, DC000081-03), and the National Eye
Institute.
NR 50
TC 0
Z9 0
U1 1
U2 1
PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC
PI ROCKVILLE
PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA
SN 0146-0404
EI 1552-5783
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD JUL
PY 2016
VL 57
IS 9
BP OCT277
EP OCT287
DI 10.1167/iovs.15-18920
PG 11
WC Ophthalmology
SC Ophthalmology
GA DW9MY
UT WOS:000383985400026
PM 27409484
ER
PT J
AU Marks, G
Patel, U
Stirratt, MJ
Mugavero, MJ
Mathews, WC
Giordano, TP
Crepaz, N
Gardner, LI
Grossman, C
Davila, J
Sullivan, M
Rose, CE
O'Daniels, C
Rodriguez, A
Wawrzyniak, AJ
Golden, MR
Dhanireddy, S
Ellison, J
Drainoni, ML
Metsch, LR
Cachay, ER
AF Marks, Gary
Patel, Unnati
Stirratt, Michael J.
Mugavero, Michael J.
Mathews, William C.
Giordano, Thomas P.
Crepaz, Nicole
Gardner, Lytt I.
Grossman, Cynthia
Davila, Jessica
Sullivan, Meg
Rose, Charles E.
O'Daniels, Christine
Rodriguez, Allan
Wawrzyniak, Andrew J.
Golden, Matthew R.
Dhanireddy, Shireesha
Ellison, Jacqueline
Drainoni, Mari-Lynn
Metsch, Lisa R.
Cachay, Edward R.
TI Single Viral Load Measurements Overestimate Stable Viral Suppression
Among HIV Patients in Care: Clinical and Public Health Implications
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE HIV; viral suppression; viral load; care
ID UNITED-STATES; RETENTION; PREVENTION; ATTENDANCE; CONTINUUM; COUNTS;
TRENDS
AB Background: The HIV continuum of care paradigm uses a single viral load test per patient to estimate the prevalence of viral suppression. We compared this single-value approach with approaches that used multiple viral load tests to examine the stability of suppression.
Methods: The retrospective analysis included HIV patients who had at least 2 viral load tests during a 12-month observation period. We assessed the (1) percent with suppressed viral load (<200 copies/mL) based on a single test during observation, (2) percent with suppressed viral loads on all tests during observation, (3) percent who maintained viral suppression among patients whose first observed viral load was suppressed, and (4) change in viral suppression status comparing first with last measurement occasions. Prevalence ratios compared demographic and clinical subgroups.
Results: Of 10,942 patients, 78.5% had a suppressed viral load based on a single test, whereas 65.9% were virally suppressed on all tests during observation. Of patients whose first observed viral load was suppressed, 87.5% were suppressed on all subsequent tests in the next 12 months. More patients exhibited improving status (13.3% went from unsuppressed to suppressed) than worsening status (5.6% went from suppressed to unsuppressed). Stable suppression was less likely among women, younger patients, black patients, those recently diagnosed with HIV, and those who missed >= 1 scheduled clinic visits.
Conclusions: Using single viral load measurements overestimated the percent of HIV patients with stable suppressed viral load by 16% (relative difference). Targeted clinical interventions are needed to increase the percent of patients with stable suppression.
C1 [Marks, Gary; Crepaz, Nicole; Gardner, Lytt I.; Rose, Charles E.] Ctr Dis Control & Prevent, Div HIV AIDS Prevent, 1600 Clifton Ave,MS E-45, Atlanta, GA 30333 USA.
[Patel, Unnati] ICF Int, Atlanta, GA USA.
[Stirratt, Michael J.; Grossman, Cynthia] NIMH, Div AIDS Res, Bethesda, MD 20892 USA.
[Mugavero, Michael J.] Univ Alabama Birmingham, HIV AIDS Clin 1917, Birmingham, AL USA.
[Mugavero, Michael J.] Univ Alabama Birmingham, Dept Med, Birmingham, AL 35294 USA.
[Mathews, William C.; Cachay, Edward R.] Univ Calif San Diego, Dept Med, San Diego, CA 92103 USA.
[Giordano, Thomas P.; Davila, Jessica] Baylor Coll Med, Dept Med, Houston, TX 77030 USA.
[Giordano, Thomas P.; Davila, Jessica] Michael E DeBakey VA Med Ctr, Ctr Innovat Qual Effectiveness & Safety, Houston, TX USA.
[Sullivan, Meg] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
[O'Daniels, Christine] Carter Consulting Inc, Atlanta, GA USA.
[Rodriguez, Allan] Univ Miami, Miller Sch Med, Div Infect Dis, Coral Gables, FL 33124 USA.
[Wawrzyniak, Andrew J.] Univ Miami, Miller Sch Med, Psychiat & Behav Sci, Miami, FL 33136 USA.
[Golden, Matthew R.] Univ Washington, Ctr AIDS & STD & Publ Health Seattle & King Cty, Seattle, WA 98195 USA.
[Dhanireddy, Shireesha] Univ Washington, Dept Med, Seattle, WA USA.
[Ellison, Jacqueline; Drainoni, Mari-Lynn] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[Metsch, Lisa R.] Columbia Univ, Mailman Sch Publ Hlth, New York, NY USA.
RP Marks, G (reprint author), Ctr Dis Control & Prevent, Div HIV AIDS Prevent, 1600 Clifton Ave,MS E-45, Atlanta, GA 30333 USA.
EM gmarks@cdc.gov
FU NIAID NIH HHS [P30 AI073961]
NR 14
TC 0
Z9 0
U1 4
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1525-4135
EI 1077-9450
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD OCT 1
PY 2016
VL 73
IS 2
BP 205
EP 212
PG 8
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA DX1EW
UT WOS:000384109800017
PM 27105049
ER
PT J
AU Guha, R
Griner, LAM
Keller, JM
Zhang, XH
Fitzgerald, D
Antignani, A
Pastan, I
Thomas, CJ
Ferrer, M
AF Guha, Rajarshi
Griner, Lesley A. Mathews
Keller, Jonathan M.
Zhang, Xiaohu
Fitzgerald, David
Antignani, Antonella
Pastan, Ira
Thomas, Craig J.
Ferrer, Marc
TI Ranking Differential Drug Activities from Dose-Response Synthetic
Lethality Screens
SO JOURNAL OF BIOMOLECULAR SCREENING
LA English
DT Article
DE qHTS; immunotoxin; synthetic lethal screen; ranking
ID RECOMBINANT IMMUNOTOXIN; CANCER; DISCOVERY; LEUKEMIA; THERAPY; CELLS;
HA22
AB Synthetic lethal screens are used to discover new combination treatments for cancer. In traditional high-throughput synthetic lethal screens, compounds are tested at a single dose, and hit selection is based on threshold activity values from the variance of the efficacy of the compounds tested. The limitation of the single-dose screening for synthetic lethal screens is that it does not allow for the robust detection of differential activities from compound collections with a broad range of potencies and efficacies. There is therefore a need to develop screening approaches that enable the identification of compounds with synthetic lethal effects based on changes in both potency and efficacy. Here we describe the implementation of a dose response-based synthetic lethal screen to find drugs that enhance or mitigate the cytotoxic effect of an immunotoxin protein (HA22). We developed a data analysis framework for the selection of compounds with enhancing or mitigating cytotoxic activities based on the use of dose-response parameters. The data analysis framework includes an ensemble ranking approach that allows the use of multiple dose-response parameters in a nonparametric fashion. Quantitative high-throughput screening (HTS) enables the identification of compounds with synthetic lethal activity not identified by single-dose HTS.
C1 [Guha, Rajarshi; Griner, Lesley A. Mathews; Keller, Jonathan M.; Zhang, Xiaohu; Thomas, Craig J.; Ferrer, Marc] NIH, Div Preclin Innovat, Natl Ctr Adv Translat Sci, Rockville, MD USA.
[Fitzgerald, David; Antignani, Antonella; Pastan, Ira] NCI, Mol Biol Lab, Ctr Canc Res, NIH, Bldg 37, Bethesda, MD 20892 USA.
RP Guha, R; Ferrer, M (reprint author), NCATS, 9800 Med Ctr Dr,Bldg B,Room 3005, Rockville, MD 20850 USA.
EM guhar@mail.nih.gov; ferrerm@mail.nih.gov
FU National Cancer Institute; National Center for Advancing Translational
Sciences
FX The authors disclosed receipt of the following financial support for the
research, authorship, and/or publication of this article: This work was
funded by the intramural programs of the National Cancer Institute and
the National Center for Advancing Translational Sciences.
NR 26
TC 0
Z9 0
U1 1
U2 1
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1087-0571
EI 1552-454X
J9 J BIOMOL SCREEN
JI J. Biomol. Screen
PD OCT
PY 2016
VL 21
IS 9
BP 942
EP 955
DI 10.1177/1087057116644890
PG 14
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Chemistry, Analytical
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Chemistry
GA DX6CD
UT WOS:000384469400007
PM 27112173
ER
PT J
AU Grabb, MC
Cross, AJ
Potter, WZ
McCracken, JT
AF Grabb, Margaret C.
Cross, Alan J.
Potter, William Z.
McCracken, James T.
TI Derisking Psychiatric Drug Development The NIMH's Fast Fail Program, A
Novel Precompetitive Model
SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY
LA English
DT Editorial Material
ID NERVOUS-SYSTEM; AUTISM; PHARMACOLOGY; DISORDERS
C1 [Grabb, Margaret C.; Potter, William Z.] NIMH, NIH, 6001 Execut Blvd,Room 7203,MSC 9645, Rockville, MD 20852 USA.
[Cross, Alan J.] AstraZeneca Neurosci Innovat Med Unit, Cambridge, MA USA.
[McCracken, James T.] UCLA Semel Inst Neurosci, Los Angeles, CA USA.
RP Grabb, MC (reprint author), NIMH, NIH, 6001 Execut Blvd,Room 7203,MSC 9645, Rockville, MD 20852 USA.
EM mgrabb@mail.nih.gov
FU NIMH NIH HHS [HHSN271201200005I]
NR 21
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0271-0749
EI 1533-712X
J9 J CLIN PSYCHOPHARM
JI J. Clin. Psychopharmacol.
PD OCT
PY 2016
VL 36
IS 5
BP 419
EP 421
DI 10.1097/JCP.0000000000000536
PG 3
WC Pharmacology & Pharmacy; Psychiatry
SC Pharmacology & Pharmacy; Psychiatry
GA DX2KD
UT WOS:000384197000004
PM 27404513
ER
PT J
AU Gowans, LJJ
Adeyemo, WL
Eshete, M
Mossey, PA
Busch, T
Aregbesola, B
Donkor, P
Arthur, FKN
Bello, SA
Martinez, A
Li, M
Augustine-Akpan, EA
Deressa, W
Twumasi, P
Olutayo, J
Deribew, M
Agbenorku, P
Oti, AA
Braimah, R
Plange-Rhule, G
Gesses, M
Obiri-Yeboah, S
Oseni, GO
Olaitan, PB
Abdur-Rahman, L
Abate, F
Hailu, T
Gravem, P
Ogunlewe, MO
Buxo, CJ
Marazita, ML
Adeyemo, AA
Murray, JC
Butali, A
AF Gowans, L. J. J.
Adeyemo, W. L.
Eshete, M.
Mossey, P. A.
Busch, T.
Aregbesola, B.
Donkor, P.
Arthur, F. K. N.
Bello, S. A.
Martinez, A.
Li, M.
Augustine-Akpan, E. A.
Deressa, W.
Twumasi, P.
Olutayo, J.
Deribew, M.
Agbenorku, P.
Oti, A. A.
Braimah, R.
Plange-Rhule, G.
Gesses, M.
Obiri-Yeboah, S.
Oseni, G. O.
Olaitan, P. B.
Abdur-Rahman, L.
Abate, F.
Hailu, T.
Gravem, P.
Ogunlewe, M. O.
Buxo, C. J.
Marazita, M. L.
Adeyemo, A. A.
Murray, J. C.
Butali, A.
TI Association Studies and Direct DNA Sequencing Implicate Genetic
Susceptibility Loci in the Etiology of Nonsyndromic Orofacial Clefts in
Sub-Saharan African Populations
SO JOURNAL OF DENTAL RESEARCH
LA English
DT Article
DE genetic heterogeneity; rare variants; genome-wide association studies
(GWAS); candidate genes; craniofacial genetics; population genetics
ID GENOME-WIDE ASSOCIATION; IDENTIFIED CANDIDATE GENES; FUNCTIONAL
VARIANTS; ORAL CLEFTS; LIP; PALATE; RISK; POLYMORPHISMS; LIP/PALATE;
IRF6
AB Orofacial clefts (OFCs) are congenital dysmorphologies of the human face and oral cavity, with a global incidence of 1 per 700 live births. These anomalies exhibit a multifactorial pattern of inheritance, with genetic and environmental factors both playing crucial roles. Many loci have been implicated in the etiology of nonsyndromic cleft lip with or without cleft palate (NSCL/P) in populations of Asian and European ancestries, through genome-wide association studies and candidate gene studies. However, few populations of African descent have been studied to date. Here, the authors show evidence of an association of some loci with NSCL/P and nonsyndromic cleft palate only (NSCPO) in cohorts from Africa (Ghana, Ethiopia, and Nigeria). The authors genotyped 48 single-nucleotide polymorphisms that were selected from previous genome-wide association studies and candidate gene studies. These markers were successfully genotyped on 701 NSCL/P and 163 NSCPO cases, 1,070 unaffected relatives, and 1,078 unrelated controls. The authors also directly sequenced 7 genes in 184 nonsyndromic OFC (NSOFC) cases and 96 controls from Ghana. Population-specific associations were observed in the case-control analyses of the subpopulations, with West African subpopulations (Ghana and Nigeria) showing a similar pattern of associations. In meta-analyses of the case-control cohort, PAX7 (rs742071, P = 5.10 x 10(-3)), 8q24 (rs987525, P = 1.22 x 10(-3)), and VAX1 (rs7078160, P = 0.04) were nominally associated with NSCL/P, and MSX1 (rs115200552, P = 0.01), TULP4 (rs651333, P = 0.04), CRISPLD2 (rs4783099, P = 0.02), and NOG1 (rs17760296, P = 0.04) were nominally associated with NSCPO. Moreover, 7 loci exhibited evidence of threshold overtransmission in NSOFC cases through the transmission disequilibrium test and through analyses of the family-based association for disease traits. Through DNA sequencing, the authors also identified 2 novel, rare, potentially pathogenic variants (p.Asn323Asp and p.Lys426IlefsTer6) in ARHGAP29. In conclusion, the authors have shown evidence for the association of many loci with NSCL/P and NSCPO. To the best of this knowledge, this study is the first to demonstrate any of these association signals in any African population.
C1 [Gowans, L. J. J.; Arthur, F. K. N.; Twumasi, P.] Kwame Nkrumah Univ Sci & Technol, Dept Biochem & Biotechnol, Kumasi, Ghana.
[Gowans, L. J. J.; Donkor, P.; Agbenorku, P.; Oti, A. A.; Plange-Rhule, G.; Obiri-Yeboah, S.] Komfo Anokye Teaching Hosp, Cleft Clin, Kumasi, Ghana.
[Gowans, L. J. J.; Murray, J. C.] Univ Iowa, Dept Pediat, Iowa City, IA 52242 USA.
[Gowans, L. J. J.; Busch, T.; Martinez, A.; Li, M.; Augustine-Akpan, E. A.; Butali, A.] Univ Iowa, Dept Oral Pathol Radiol & Med, Iowa City, IA USA.
[Adeyemo, W. L.; Olutayo, J.] Univ Lagos, Coll Med, Lagos, Nigeria.
[Eshete, M.; Deressa, W.; Deribew, M.] Univ Addis Ababa, Addis Ababa, Ethiopia.
[Mossey, P. A.] Univ Dundee, Dept Orthodont, Dundee, Scotland.
[Aregbesola, B.; Braimah, R.] Obafemi Awolowo Univ Teaching Hosp, Ife, Nigeria.
[Donkor, P.; Agbenorku, P.; Oti, A. A.; Obiri-Yeboah, S.] Kwame Nkrumah Univ Sci & Technol, Sch Med Sci, Dept Surg, Kumasi, Ghana.
[Bello, S. A.] State House Hosp, Dept Oral & Maxillofacial Surg, Abuja, Nigeria.
[Gesses, M.; Abate, F.; Hailu, T.] Yekatit 12 Hosp, Coll Med, Addis Ababa, Ethiopia.
[Oseni, G. O.; Olaitan, P. B.; Ogunlewe, M. O.] Ladoke Akintola Univ Technol, Dept Burns & Plast Surg, Teaching Hosp, Osogbo, Nigeria.
[Abdur-Rahman, L.] Univ Ilorin, Dept Surg, Div Pediat Surg, Ilorin, Nigeria.
[Gravem, P.] Haukeland Univ Hosp Bergen, Bergen, Norway.
[Buxo, C. J.] Univ Puerto Rico Med Sci Campus, Sch Dent Med, San Juan, PR USA.
[Marazita, M. L.] Univ Pittsburgh, Dept Oral Biol, Pittsburgh, PA USA.
[Adeyemo, A. A.] NHGRI, Ctr Res Genom & Global Hlth, NIH, Bethesda, MD 20892 USA.
RP Butali, A (reprint author), Univ Iowa, Dows Inst Dent Res, Dept Oral Pathol Radiol & Med, Coll Dent,Butali Lab, ML2198,500 Newton Rd, Iowa City, IA 52242 USA.
EM azeez-butali@uiowa.edu
FU National Institute of Dental and Craniofacial Research [R00 DE022378,
R01-DE009886, R01-DE012472, K99-DE024571]; Robert Wood Johnson
Foundation [72429]; National Institutes of Health [R37 DE-08559,
DE-016148]; Ghana Cleft Foundation; National Institute of Minority
Health and Disparities [U54-MD007587, R25-MD007607]
FX The authors are grateful to all families that participated in this
research. We also appreciate all the doctors and nurses at the various
teaching hospitals where sample collections were carried out: Komfo
Anokye Teaching Hospital (Ghana), University of Lagos Teaching Hospital
(Nigeria), Obafemi Awolowo University Teaching Hospital (Nigeria),
Ladoke Akintola University of Technology Teaching Hospital (Nigeria),
and Yekatit 12 Hospital Medical college (Ethiopia). Contributions of
members of the Murray and Butali laboratories, University of Iowa, are
acknowledged. This work was supported by the National Institute of
Dental and Craniofacial Research (R00 DE022378) and the Robert Wood
Johnson Foundation (72429; A.B.); the National Institutes of Health (R37
DE-08559 and DE-016148; J.C.M.); the Ghana Cleft Foundation (L.J.J.G.);
the National Institute of Dental and Craniofacial Research (R01-DE009886
and R01-DE012472; M.L.M.); and the National Institute of Minority Health
and Disparities (U54-MD007587, R25-MD007607; C.J.B.) and the National
Institute of Dental and Craniofacial Research (K99-DE024571; C.J.B.).
The authors declare no potential conflicts of interest with respect to
the authorship and/or publication of this article.
NR 38
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U1 4
U2 4
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0022-0345
EI 1544-0591
J9 J DENT RES
JI J. Dent. Res.
PD OCT
PY 2016
VL 95
IS 11
BP 1245
EP 1256
DI 10.1177/0022034516657003
PG 12
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA DX5XU
UT WOS:000384456800007
PM 27369588
ER
PT J
AU Chu, EY
Tamasas, B
Fong, H
Foster, BL
LaCourse, MR
Tran, AB
Martin, JF
Schutte, BC
Somerman, MJ
Cox, TC
AF Chu, E. Y.
Tamasas, B.
Fong, H.
Foster, B. L.
LaCourse, M. R.
Tran, A. B.
Martin, J. F.
Schutte, B. C.
Somerman, M. J.
Cox, T. C.
TI Full Spectrum of Postnatal Tooth Phenotypes in a Novel Irf6 Cleft Lip
Model
SO JOURNAL OF DENTAL RESEARCH
LA English
DT Article
DE amelogenesis; hypodontia; supernumerary teeth; van der Woude; cleft lip;
palate; taurodontism
ID DER-WOUDE-SYNDROME; REGULATORY FACTOR 6; ENAMEL DEFECTS; DENTAL
ANOMALIES; CAUSE VAN; PALATE; CHILDREN; GENE; MORPHOGENESIS; EXPRESSION
AB Clefting of the lip, with or without palatal involvement (CLP), is associated with a higher incidence of developmental tooth abnormalities, including hypodontia and supernumerary teeth, aberrant crown and root morphologies, and enamel defects, although the underlying mechanistic link is poorly understood. As most CLP genes are expressed throughout the oral epithelium, the authors hypothesized that the expression of CLP genes may persist in the dental epithelium and thus, in addition to their earlier role in labiopalatine development, may play an important functional role in subsequent tooth patterning and amelogenesis. To address this, the authors generated a unique conditional knockout model involving the major CLP gene, Irf6, that overcomes the previously reported perinatal lethality to enable assessment of any posteruption dental phenotypes. A dental epithelium-specific Irf6 conditional knockout (Irf6-cKO) mouse was generated via a Pitx2-Cre driver line. Dental development was analyzed by microcomputed tomography, scanning electron microscopy, histology, immunohistochemistry, and quantitative polymerase chain reaction. Irf6-cKO mice displayed variable hypodontia, occasional supernumerary incisors and molars, as well as crown and root patterning anomalies, including peg-shaped first molars and taurodontic and C-shaped mandibular second molars. Enamel density was reduced in preeruption Irf6-cKO mice, and some shearing of enamel rods was noted in posteruption incisors. There was also rapid attrition of Irf6-cKO molars following eruption. Histologically, Irf6-cKO ameloblasts exhibited disturbances in adhesion and polarity, and delayed enamel formation was confirmed immunohistochemically. Altered structure of Hertwig's epithelial root sheath was also observed. These data support a role for IRF6 in tooth number, crown and root morphology and amelogenesis that is likely due to a functional role of Irf6 in organization and polarity of epithelial cell types. This data reinforce the notion that various isolated tooth defects could be considered part of the CLP spectrum in relatives of an affected individual.
C1 [Chu, E. Y.; Tamasas, B.] Univ Washington, Dept Oral Hlth Sci, Seattle, WA 98195 USA.
[Chu, E. Y.; Tamasas, B.; LaCourse, M. R.; Cox, T. C.] Seattle Childrens Res Inst, Ctr Dev Biol & Regenerat Med, Seattle, WA USA.
[Chu, E. Y.; Tran, A. B.; Somerman, M. J.] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Fong, H.] Univ Washington, Dept Mat Sci & Engn, Seattle, WA 98195 USA.
[Foster, B. L.] Ohio State Univ, Coll Dent, Biosci Div, Columbus, OH 43210 USA.
[Martin, J. F.] Baylor Coll Med, Dept Mol Physiol & Biophys, Houston, TX 77030 USA.
[Martin, J. F.] Texas Heart Inst, Houston, TX 77025 USA.
[Schutte, B. C.] Michigan State Univ, Dept Microbiol & Mol Genet, E Lansing, MI 48824 USA.
[Cox, T. C.] Univ Washington, Dept Pediat, Div Craniofacial Med, Seattle, WA 98195 USA.
[Cox, T. C.] Monash Univ, Dept Anat & Dev Biol, Clayton, Vic, Australia.
RP Cox, TC (reprint author), Seattle Childrens Res Inst, Ctr Dev Biol & Regenerat Med, M-S C9S-5,1900 Ninth Ave, Seattle, WA 98101 USA.
EM tccox@uw.edu
FU Laurel Foundation Endowment for Craniofacial Research; University of
Washington National Institute of Dental and Craniofacial Research T32
Institutional Trainee Award [DE007132]; National Institute of Diabetes
and Digestive and Kidney Diseases Ruth L. Kirschstein F30 fellowship
[DK100280]; National Institutes of Health [DE023177]; Cleft Palate
Foundation Junior Investigator Research Grant; Libyan Government
scholarship; Internal Research Program of the National Institute of
Arthritis and Musculoskeletal and Skin Diseases of the National
Institutes of Health
FX This research was supported in part by the Laurel Foundation Endowment
for Craniofacial Research (T.C.C.), a University of Washington National
Institute of Dental and Craniofacial Research T32 Institutional Trainee
Award (DE007132; E.Y.C.), an National Institute of Diabetes and
Digestive and Kidney Diseases Ruth L. Kirschstein F30 fellowship
(DK100280; E.Y.C.), National Institutes of Health DE023177 (J.F.M.), a
Cleft Palate Foundation Junior Investigator Research Grant (E.Y.C.), a
Libyan Government scholarship (B.T.), and the Internal Research Program
of the National Institute of Arthritis and Musculoskeletal and Skin
Diseases of the National Institutes of Health (M.J.S.). The authors
declare no potential conflicts of interest with respect to the
authorship and/or publication of this article. The authors thank members
of the Somerman and Cox laboratories for their support and Thuy Tien
Tran (Baylor College of Medicine) and Youssef Kousa (Michigan State
University) for providing assistance with genotyping. Additionally, the
authors thank the Light Imaging Core Facility (National Institute of
Arthritis and Musculoskeletal and Skin Diseases / National Institutes of
Health), James Schmitz (University of Texas Health Sciences Center at
San Antonio), Dr. Yong-Hee Chun (University of Texas Health Science
Center at San Antonio), and Drs. Daniel Chan, Michael Cunningham, Tracy
Popowics, and Avina Paranjpe (University of Washington) for their
support and advice.
NR 40
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U1 5
U2 5
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0022-0345
EI 1544-0591
J9 J DENT RES
JI J. Dent. Res.
PD OCT
PY 2016
VL 95
IS 11
BP 1265
EP 1273
DI 10.1177/0022034516656787
PG 9
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA DX5XU
UT WOS:000384456800009
PM 27369589
ER
PT J
AU Doyle, DL
Awwad, RI
Austin, JC
Baty, BJ
Bergner, AL
Brewster, SJ
Erby, LAH
Franklin, CR
Greb, AE
Grubs, RE
Hooker, GW
Noblin, SJ
Ormond, KE
Palmer, CG
Petty, EM
Singletary, CN
Thomas, MJ
Toriello, H
Walton, CS
Uhlmann, WR
AF Doyle, Debra Lochner
Awwad, Rawan I.
Austin, Jehannine C.
Baty, Bonnie J.
Bergner, Amanda L.
Brewster, Stephanie J.
Erby, Lori A. H.
Franklin, Cathi Rubin
Greb, Anne E.
Grubs, Robin E.
Hooker, Gillian W.
Noblin, Sarah Jane
Ormond, Kelly E.
Palmer, Christina G.
Petty, Elizabeth M.
Singletary, Claire N.
Thomas, Matthew J.
Toriello, Helga
Walton, Carol S.
Uhlmann, Wendy R.
TI 2013 Review and Update of the Genetic Counseling Practice Based
Competencies by a Task Force of the Accreditation Council for Genetic
Counseling
SO JOURNAL OF GENETIC COUNSELING
LA English
DT Review
DE Genetic counseling; Practice based competencies (PBCs); Graduate program
accreditation; Genetic counselors; Training; Curriculum
AB The first practice based competencies (PBCs) for the field of genetic counseling were adopted by the American Board of Genetic Counseling (ABGC), 1996. Since that time, there has been significant growth in established and new work settings (clinical and non-clinical) and changes in service delivery models and the roles of genetic counselors. These changes prompted the ABGC to appoint a PBC Task Force in 2011 to review the PBCs with respect to their current relevance and to revise and update them as necessary. There are four domains in the revised PBCs: (I) Genetics Expertise and Analysis (II) Interpersonal, Psychosocial and Counseling Skills (III) Education and (IV) Professional Development and Practice. There are 22 competencies, each clarified with learning objectives or samples of activities and skills; a glossary is included. New competencies were added that address genomics, genetic testing and genetic counselors' roles in risk assessment, education, supervision, conducting research and presenting research options to patients. With PBCs serving as the pre-defined abilities or outcomes of training, graduating genetic counselors will be well prepared to enter the field with a minimum level of skills and abilities. A description of the Task Force's work, key changes and the 2013 PBCs are presented herein.
C1 [Doyle, Debra Lochner] Washington State Dept Hlth, Screening & Genet Unit, 20425 72nd Ave S,Suite 310, Kent, WA 98032 USA.
[Awwad, Rawan I.] Counsyl Inc, San Francisco, CA USA.
[Austin, Jehannine C.] Univ British Columbia, Dept Med Genet, Vancouver, BC, Canada.
[Austin, Jehannine C.] Univ British Columbia, Dept Psychiat, Vancouver, BC, Canada.
[Baty, Bonnie J.] Univ Utah, Dept Pediat, Salt Lake City, UT USA.
[Bergner, Amanda L.] Johns Hopkins Univ, Dept Neurol, Baltimore, MD USA.
[Brewster, Stephanie J.] Boston Childrens Hosp, Translat Neurosci Ctr, Boston, MA USA.
[Erby, Lori A. H.] Johns Hopkins Bloomberg Sch Publ Hlth, Hlth Behav & Soc, Baltimore, MD USA.
[Erby, Lori A. H.] NHGRI, Social & Behav Res Branch, Bethesda, MD 20892 USA.
[Franklin, Cathi Rubin] Quest Diagnost Inc, Valencia, CA USA.
[Greb, Anne E.] Sarah Lawrence Coll, Joan H Marks Grad Program Human Genet, Bronxville, NY 10708 USA.
[Grubs, Robin E.] Univ Pittsburgh, Dept Human Genet, Pittsburgh, PA USA.
[Hooker, Gillian W.] NextGxDx Inc, Franklin, TN USA.
[Noblin, Sarah Jane] Univ Texas Hlth Sci Ctr Houston, Dept Obstet Gynecol & Reprod Serv, Houston, TX 77030 USA.
[Noblin, Sarah Jane] Univ Texas Hlth Sci Ctr Houston, Dept Pediat, Houston, TX 77030 USA.
[Ormond, Kelly E.] Stanford Univ, Sch Med, Dept Genet, Stanford, CA USA.
[Palmer, Christina G.] Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA.
[Petty, Elizabeth M.] Univ Wisconsin, Sch Med & Publ Hlth, Dept Pediat, Madison, WI USA.
[Singletary, Claire N.] Univ Texas Hlth Sci Ctr Houston, Dept Pediat & Obstet Gynecol & Reprod Serv, Houston, TX 77030 USA.
[Thomas, Matthew J.] Univ Virginia Hlth Syst, Dept Pediat, Charlottesville, VA USA.
[Toriello, Helga] Spectrum Hlth, Grand Rapids, MI USA.
[Walton, Carol S.] Univ Colorado, Sch Med, Dept Pediat, Aurora, CO USA.
[Uhlmann, Wendy R.] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA.
[Uhlmann, Wendy R.] Univ Michigan, Dept Human Genet, Ann Arbor, MI 48109 USA.
RP Doyle, DL (reprint author), Washington State Dept Hlth, Screening & Genet Unit, 20425 72nd Ave S,Suite 310, Kent, WA 98032 USA.
EM debra.lochnerdoyle@doh.wa.gov
FU ABGC
FX While all PBCTF members volunteered their time, funds to support their
travel were provided by the ABGC. In addition, the authors would like to
offer their heartfelt appreciation to Morry Fiddler, PhD for his
thoughtful review of our article and sharing his expertise in describing
the processes used to develop competencies. We also wish to thank the
AGCPD for their thoughtful review of comments offered regarding draft
versions of the PBCs, and express our gratitude to the ACGC Executive
Director, Sheila O'Neal, for her support in developing the final PBC
document and posting it to the ACGC website at:
http://gceducation.org/Documents/ACGC%20Core%20Competencies%20Brochure_1
4_Web_FINAL.pdf
NR 12
TC 0
Z9 1
U1 1
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1059-7700
EI 1573-3599
J9 J GENET COUNS
JI J. Genet. Couns.
PD OCT
PY 2016
VL 25
IS 5
BP 868
EP 879
DI 10.1007/s10897-016-9984-3
PG 12
WC Genetics & Heredity
SC Genetics & Heredity
GA DX4EB
UT WOS:000384332900003
PM 27333894
ER
PT J
AU Nakamura, T
Campbell, JR
Moore, AR
Otsu, S
Aikawa, H
Tamamura, H
Mitsuya, H
AF Nakamura, Tomofumi
Campbell, Joseph R.
Moore, Amber R.
Otsu, Sachiko
Aikawa, Haruo
Tamamura, Hirokazu
Mitsuya, Hiroaki
TI Development and validation of a cell-based assay system to assess human
immunodeficiency virus type 1 integrase multimerization
SO JOURNAL OF VIROLOGICAL METHODS
LA English
DT Article
DE HIV-1; HIV-1 integrase multimerization; BiFC; NCINIs
ID THROUGHPUT SCREENING ASSAYS; SMALL-MOLECULE INHIBITORS; DNA STRAND
TRANSFER; HIV-1 INTEGRASE; VIRAL-DNA; IN-VIVO; FLUORESCENCE
COMPLEMENTATION; BINDING-SITE; PROTEIN; EXPRESSION
AB Multimerization of HIV-1 integrase (IN) subunits is required for the concerted integration of HIV-1 proviral DNA into the host genome. Thus, the disruption of IN multimerization represents a new avenue for intervening HIV-1 infection. Here, we generated a cell-based assay system to assess IN multimerization using a newly constructed bimolecular fluorescence complementation (BiFC-IN) system. BiFC-IN proteins were efficient in emitting fluorescence, and amino acid (AA) substitutions associated with IN multimerization attenuated fluorescence, suggesting that the BiFC-IN system may be useful for evaluating the profile of IN multimerization. A recently reported non-catalytic site IN inhibitor (NCINI), which allosterically induces IN over-multimerization/aggregation, significantly increased fluorescence in the BiFC-IN system. An IN's substitution, A128T, associated with viral resistance to NCINIs, decreased the NCINI-induced increase of fluorescence, suggesting that A128T reduces the potential for IN over-multimerization. Moreover, E11K and F181T substitutions known to inhibit IN tetramerization also reduced the NCINI-induced fluorescence increase, suggesting that NCINI-induced IN over-multimerization was more likely to occur from tetramer subunits than from dimer subunits. The present study demonstrates that our cell-based BiFC-IN system may be useful in elucidating the profile of IN multimerization, and also help evaluate and identify novel compounds that disrupt IN multimerization in living cells. (C) 2016 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license.
C1 [Nakamura, Tomofumi; Campbell, Joseph R.; Moore, Amber R.; Otsu, Sachiko; Mitsuya, Hiroaki] Kumamoto Univ, Grad Sch Med Sci, Dept Infect Dis, Kumamoto 8608556, Japan.
[Nakamura, Tomofumi; Campbell, Joseph R.; Moore, Amber R.; Otsu, Sachiko; Mitsuya, Hiroaki] Kumamoto Univ, Grad Sch Med Sci, Dept Hematol, Kumamoto 8608556, Japan.
[Aikawa, Haruo; Tamamura, Hirokazu] Tokyo Med & Dent Univ, Inst Biomat & Bioengn, Chiyoda Ku, Tokyo 1010062, Japan.
[Mitsuya, Hiroaki] Natl Ctr Global Hlth & Med Res Inst, Expt Retrovirol Sect, Shinjuku Ku, Tokyo 1628655, Japan.
[Mitsuya, Hiroaki] NCI, HIV & AIDS Malignancy Branch, NIH, Bethesda, MD 20892 USA.
RP Mitsuya, H (reprint author), Kumamoto Univ, Grad Sch Med Sci, Dept Infect Dis, Kumamoto 8608556, Japan.; Mitsuya, H (reprint author), Kumamoto Univ, Grad Sch Med Sci, Dept Hematol, Kumamoto 8608556, Japan.; Mitsuya, H (reprint author), Natl Ctr Global Hlth & Med Res Inst, Expt Retrovirol Sect, Shinjuku Ku, Tokyo 1628655, Japan.; Mitsuya, H (reprint author), NCI, HIV & AIDS Malignancy Branch, NIH, Bethesda, MD 20892 USA.
EM mitsuyah@helix.nih.gov
FU Japan Agency for Medical Research and Development (AMED); Grant for
global education and research center aiming at the control of AIDS
(Global Center of Excellence - Monbu-Kagakusho); Promotion of AIDS
Research from the Ministry of Health, Welfare, and Labor of Japan;
Kumamoto University [78]; Monbu-Kagakusho [21790527]; Intramural
Research Program of Center for Cancer Research, National Cancer
Institute, National Institutes of Health
FX We thank Gene Technology, Center Institute of Resource Development and
Analysis, Kumamoto University for providing technical supports of FCM
and confocal lazer scanning microscope. We also thank Toshikazu
Miyagawa, Masayuki Amano, and Hironori Hayashi for helpful discussion,
and Miho Matsumoto for technical assistance. This work was supported in
part by a Grant for Development of Novel Drugs for Treating HIV-1
Infection and AIDS from Japan Agency for Medical Research and
Development (AMED), by a Grant for global education and research center
aiming at the control of AIDS (Global Center of Excellence supported by
Monbu-Kagakusho), a Promotion of AIDS Research from the Ministry of
Health, Welfare, and Labor of Japan, a Grant to the Cooperative Research
Project on Clinical and Epidemiological Studies of Emerging and
Re-emerging Infectious Diseases (Renkei Jigyo: No. 78, Kumamoto
University) of Monbu-Kagakusho, and a Grant-in-Aid for Young Scientists
(B) (21790527) of Monbu-Kagakusho, and in part by the Intramural
Research Program of Center for Cancer Research, National Cancer
Institute, National Institutes of Health.
NR 60
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U1 1
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-0934
EI 1879-0984
J9 J VIROL METHODS
JI J. Virol. Methods
PD OCT
PY 2016
VL 236
BP 196
EP 206
DI 10.1016/j.jviromet.2016.07.023
PG 11
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Virology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Virology
GA DW8YR
UT WOS:000383941900029
PM 27474494
ER
PT J
AU Limou, S
Parsa, A
AF Limou, Sophie
Parsa, Afshin
TI Diving into the abyss of undiscovered kidney function-related factors
SO KIDNEY INTERNATIONAL
LA English
DT Editorial Material
ID LOCI
AB Meta-analyses and reintroduction of biological knowledge are 2 classic strategies to increase genomewide association study statistical power and overcome the burden of multiple testing. These strategies have empowered the nephrology community to discover new signals associated with kidney function and nephropathies: Here we discuss the current genomewide association study limitations and strategies to dive further into the abyss of yet-to-be discovered kidney function-related factors.
C1 [Limou, Sophie] NCI, Mol Genet Epidemiol Sect, Basic Res Lab, Basic Sci Program,Leidos Biomed Res Inc,Frederick, Frederick, MD 21701 USA.
[Parsa, Afshin] Univ Maryland, Sch Med, Div Nephrol, Baltimore, MD 21201 USA.
[Parsa, Afshin] Baltimore VA Med Ctr, Dept Med, Baltimore, MD USA.
RP Parsa, A (reprint author), Univ Maryland, Sch Med, 685 W Baltimore St,MSTF 357, Baltimore, MD 21201 USA.
EM aparsa@medicine.umaryland.edu
NR 9
TC 1
Z9 1
U1 2
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0085-2538
EI 1523-1755
J9 KIDNEY INT
JI Kidney Int.
PD OCT
PY 2016
VL 90
IS 4
BP 724
EP 726
DI 10.1016/j.kint.2016.05.034
PG 3
WC Urology & Nephrology
SC Urology & Nephrology
GA DX4ZE
UT WOS:000384388800003
PM 27633863
ER
PT J
AU Jing, JJ
Pattaro, C
Hoppmann, A
Okada, Y
Fox, CS
Kottgen, A
AF Jing, Jiaojiao
Pattaro, Cristian
Hoppmann, Anselm
Okada, Yukinori
Fox, Caroline S.
Koettgen, Anna
CA CKDGen Consortium
TI Combination of mouse models and genomewide association studies
highlights novel genes associated with human kidney function
SO KIDNEY INTERNATIONAL
LA English
DT Article
DE chronic kidney disease; genomewide association studies; kidney
development
ID GLOMERULAR-FILTRATION-RATE; WIDE ASSOCIATION; COLLABORATIVE
METAANALYSIS; POPULATION COHORTS; RETINOIC ACID; HIGHER ALBUMINURIA;
EMBRYONIC KIDNEY; HUMAN BIOLOGY; DISEASE; BONE
AB Genomewide association studies have identified numerous chronic kidney disease-associated genetic variants, but often do not pinpoint causal genes. This limitation was addressed by combining Mouse Genome Informatics with human genomewide association studies of kidney function. Genes for which mouse models showed abnormal renal physiology, morphology, glomerular filtration rate (GFR), or urinary albumin-to-creatinine ratio were identified from Mouse Genome Informatics. The corresponding human orthologs were then evaluated for GFR-associated single-nucleotide polymorphisms in 133,814 individuals and urinary albumin-to-creatinine ratio-associated SNPs in 54,451 individuals in genome-wide association studies meta-analysis of the CKDGen Consortium. After multiple testing corrections, significant associations with estimated GFR in humans were identified for single-nucleotide polymorphisms in 2, 7, and 17 genes causing abnormal GFR, abnormal physiology, and abnormal morphology in mice, respectively. Genes identified for abnormal kidney morphology showed significant enrichment for estimated GFR-associated single-nucleotide polymorphisms. In total, 19 genes contained variants associated with estimated GFR or the urinary albumin-to-creatinine ratio of which 16 mapped into previously reported genomewide significant loci. CYP26A1 and BMP4 emerged as novel signals subsequently validated in a large, independent study. An additional gene, CYP24A1, was discovered after conditioning on a published nearby association signal. Thus, our novel approach to combine comprehensive mouse phenotype information with human genomewide association studies data resulted in the identification of candidate genes for kidney disease pathogenesis.
C1 [Jing, Jiaojiao; Hoppmann, Anselm; Koettgen, Anna] Univ Freiburg, Div Genet Epidemiol, Med Ctr, Freiburg, Germany.
[Jing, Jiaojiao; Hoppmann, Anselm] Univ Freiburg, Genet & Expt Bioinformat, Fac Biol, Freiburg, Germany.
[Jing, Jiaojiao; Koettgen, Anna] Univ Freiburg, Div Renal, Med Ctr, Freiburg, Germany.
[Pattaro, Cristian] European Acad Bolzano Bozen EURAC, Ctr Biomed, Bolzano, Italy.
[Okada, Yukinori] Tokyo Med & Dent Univ, Grad Sch Med & Dent Sci, Dept Human Genet & Dis Divers, Tokyo, Japan.
[Okada, Yukinori] RIKEN, Lab Stat Anal, Ctr Integrat Med Sci, Yokohama, Kanagawa, Japan.
[Fox, Caroline S.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Fox, Caroline S.] NHLBI, Ctr Populat Studies, Framingham, MA USA.
[Fox, Caroline S.] Brigham & Womens Hosp, Div Endocrinol Metab & Hypertens, 75 Francis St, Boston, MA 02115 USA.
[Fox, Caroline S.] Harvard Med Sch, Boston, MA USA.
[Koettgen, Anna] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
RP Kottgen, A (reprint author), Univ Freiburg, Med Ctr, Berliner Allee 29, D-79110 Freiburg, Germany.
EM anna.koettgen@uniklinik-freiburg.de
FU Emmy Noether Programme; Heisenberg Programme; German Research Foundation
[CRC 1140]; Chinese Scholarship Council; Wellcome Trust [076113, 085475]
FX The work of AK was funded by the Emmy Noether Programme, the Heisenberg
Programme, and CRC 1140 of the German Research Foundation. JJ was funded
by the Chinese Scholarship Council. This study makes use of data
generated by the Wellcome Trust Case Control Consortium. A full list of
the investigators who contributed to the generation of the data is
available at www.wtccc.org.uk. Funding for the project was provided by
the Wellcome Trust under award 076113 and 085475. We thank Vladan
Mijatovic for helpful discussions.
NR 54
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U1 1
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PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0085-2538
EI 1523-1755
J9 KIDNEY INT
JI Kidney Int.
PD OCT
PY 2016
VL 90
IS 4
BP 764
EP 773
DI 10.1016/j.kint.2016.04.004
PG 10
WC Urology & Nephrology
SC Urology & Nephrology
GA DX4ZE
UT WOS:000384388800012
PM 27263491
ER
PT J
AU Kasiske, BL
Kumar, R
Kimmel, PL
Pesavento, TE
Kalil, RS
Kraus, ES
Rabb, H
Posselt, AM
Anderson-Haag, TL
Steffes, MW
Israni, AK
Snyder, JJ
Singh, RJ
Weir, MR
AF Kasiske, Bertram L.
Kumar, Rajiv
Kimmel, Paul L.
Pesavento, Todd E.
Kalil, Roberto S.
Kraus, Edward S.
Rabb, Hamid
Posselt, Andrew M.
Anderson-Haag, Teresa L.
Steffes, Michael W.
Israni, Ajay K.
Snyder, Jon J.
Singh, Ravinder J.
Weir, Matthew R.
TI Abnormalities in biomarkers of mineral and bone metabolism in kidney
donors
SO KIDNEY INTERNATIONAL
LA English
DT Article
DE FGF23; hyperparathyroidism; mineral metabolism; parathyroid hormone
ID FIBROBLAST GROWTH FACTOR-23; UNILATERAL NEPHRECTOMY; FOLLOW-UP;
CARDIOVASCULAR-DISEASE; PARATHYROID-HORMONE; PHOSPHATE-TRANSPORT;
MATCHED COHORT; VITAMIN-D; DONATION; FGF-23
AB Previous studies have suggested that kidney donors may have abnormalities of mineral and bone metabolism typically seen in chronic kidney disease. This may have important implications for the skeletal health of living kidney donors and for our understanding of the pathogenesis of long-term mineral and bone disorders in chronic kidney disease. In this prospective study, 182 of 203 kidney donors' and 173 of 201 paired normal controls had markers of mineral and bone metabolism measured before and at 6 and 36 months after donation (ALTOLD Study). Donors had significantly higher serum concentrations of intact parathyroid hormone (24.6% and 19.5%) and fibroblast growth factor-23 (9.5% and 8.4%) at 6 and 36 months, respectively, as compared to healthy controls, and significantly reduced tubular phosphate reabsorption (-7.0% and -5.0%) and serum phosphate concentrations (-6.4% and -2.3%). Serum 1,25-dihydroxyvitamin D-3 concentrations were significantly lower (-17.1% and -12.6%), while 25-hydroxyvitamin D (21.4% and 19.4%) concentrations were significantly higher in donors compared to controls. Moreover, significantly higher concentrations of the bone resorption markers, carboxyterminal cross-linking telopeptide of bone collagen (30.1% and 13.8%) and aminoterminal cross-linking telopeptide of bone collagen (14.2% and 13.0%), and the bone formation markers, osteocalcin (26.3% and 2.7%) and procollagen type I N-terminal propeptide (24.3% and 8.9%), were observed in donors. Thus, kidney donation alters serum markers of bone metabolism that could reflect impaired bone health. Additional long-term studies that include assessment of skeletal architecture and integrity are warranted in kidney donors.
C1 [Kasiske, Bertram L.; Anderson-Haag, Teresa L.; Israni, Ajay K.] Hennepin Cty Med Ctr, Dept Med, 701 Pk Ave, Minneapolis, MN 55415 USA.
[Kumar, Rajiv] Mayo Clin, Dept Med, Rochester, MN USA.
[Kimmel, Paul L.] NIDDK, Div Kidney Urol & Hematol Dis, NIH, Bethesda, MD 20892 USA.
[Pesavento, Todd E.] Ohio State Univ, Dept Med, Columbus, OH 43210 USA.
[Kalil, Roberto S.] Univ Iowa, Dept Med, Iowa City, IA 52242 USA.
[Kraus, Edward S.; Rabb, Hamid] Johns Hopkins Univ, Dept Med, Baltimore, MD USA.
[Posselt, Andrew M.] Univ Calif San Francisco, Dept Surg, San Francisco, CA USA.
[Steffes, Michael W.] Univ Minnesota, Dept Lab Med & Pathol, Minneapolis, MN 55455 USA.
[Israni, Ajay K.; Snyder, Jon J.] Minneapolis Med Res Fdn Inc, Minneapolis, MN USA.
[Singh, Ravinder J.] Mayo Clin, Dept Lab Med & Pathol, Rochester, MN USA.
[Weir, Matthew R.] Univ Maryland, Dept Med, Baltimore, MD 21201 USA.
RP Kasiske, BL (reprint author), Hennepin Cty Med Ctr, Dept Med, 701 Pk Ave, Minneapolis, MN 55415 USA.; Kumar, R (reprint author), Mayo Clin, MS 1-120,200 First St SW, Rochester, MN 55905 USA.
EM bkasiske@cdrg.org; rkumar@mayo.edu
FU National Institutes of Health [U01-DK066013]
FX This study was funded by the National Institutes of Health under the
cooperative agreement U01-DK066013. The National Institutes of Health
participated in the interpretation of data, the writing of the report,
and the decision to submit the report for publication. The opinions
expressed herein do not necessarily reflect those of the National
Institute of Diabetes and Digestive and Kidney Diseases, the National
Institutes of Health, the Department of Health and Human Services, or
the government of the United States.
NR 33
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0085-2538
EI 1523-1755
J9 KIDNEY INT
JI Kidney Int.
PD OCT
PY 2016
VL 90
IS 4
BP 861
EP 868
DI 10.1016/j.kint.2016.05.012
PG 8
WC Urology & Nephrology
SC Urology & Nephrology
GA DX4ZE
UT WOS:000384388800022
ER
PT J
AU Fallah, MP
Skrip, LA
Dahn, BT
Nyenswah, TG
Flumo, H
Glayweon, M
Lorseh, TL
Kaler, SG
Higgs, ES
Galvani, AP
AF Fallah, Mosoka P.
Skrip, Laura A.
Dahn, Bernice T.
Nyenswah, Tolbert G.
Flumo, Hilary
Glayweon, Meekie
Lorseh, Tee L.
Kaler, Stephen G.
Higgs, Elizabeth S.
Galvani, Alison P.
TI Pregnancy outcomes in Liberian women who conceived after recovery from
Ebola virus disease
SO LANCET GLOBAL HEALTH
LA English
DT Editorial Material
C1 [Fallah, Mosoka P.; Dahn, Bernice T.; Nyenswah, Tolbert G.; Glayweon, Meekie; Lorseh, Tee L.] Minist Hlth, Monrovia, Liberia.
[Fallah, Mosoka P.; Galvani, Alison P.] Univ Liberia, AM Dogliotti Coll Med, Monrovia, Liberia.
[Fallah, Mosoka P.; Flumo, Hilary] PREVAIL III Study, US Natl Inst Allergy & Infect Dis, Monrovia, Liberia.
[Skrip, Laura A.; Galvani, Alison P.] Yale Sch Publ Hlth, Ctr Infect Dis Modeling & Anal, New Haven, CT 06510 USA.
[Kaler, Stephen G.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Translat Neurosci, Mol Med Branch, NIH, Bethesda, MD USA.
[Higgs, Elizabeth S.] NIAID, US Natl Inst Hlth, 9000 Rockville Pike, Bethesda, MD 20892 USA.
RP Galvani, AP (reprint author), Univ Liberia, AM Dogliotti Coll Med, Monrovia, Liberia.; Galvani, AP (reprint author), Yale Sch Publ Hlth, Ctr Infect Dis Modeling & Anal, New Haven, CT 06510 USA.
EM alison.galvani@yale.edu
NR 10
TC 0
Z9 0
U1 3
U2 3
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 2214-109X
J9 LANCET GLOB HEALTH
JI Lancet Glob. Health
PD OCT
PY 2016
VL 4
IS 10
BP E678
EP E679
PG 2
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA DW7RE
UT WOS:000383848000009
PM 27633422
ER
PT J
AU Mokdad, AH
Forouzanfar, MH
Daoud, F
El Bcheraoui, C
Moradi-Lakeh, M
Khalil, I
Afshin, A
Tuffaha, M
Charara, R
Barber, RM
Wagner, J
Cercy, K
Kravitz, H
Coates, MM
Robinson, M
Estep, K
Steiner, C
Jaber, S
Mokdad, AA
O'Rourke, KF
Chew, A
Kim, P
El Razek, MMA
Abdalla, S
Abd-Allah, F
Abraham, JP
Abu-Raddad, LJ
Abu-Rmeileh, NME
Al-Nehmi, AA
Akanda, AS
Al Ahmadi, H
Al Khabouri, MJ
Al Lami, FH
Al Rayess, ZA
Alasfoor, D
AlBuhairan, FS
Aldhahri, SF
Alghnam, S
Alhabib, S
Al-Hamad, N
Ali, R
Ali, SD
Alkhateeb, M
AlMazroa, MA
Alomari, MA
Al-Raddadi, R
Alsharif, U
Al-Sheyab, N
Alsowaidi, S
Al-Thani, M
Altirkawi, KA
Amare, AT
Amini, H
Ammar, W
Anwari, P
Asayesh, H
Asghar, R
Assabri, AM
Assadi, R
Bacha, U
Badawi, A
Bakfalouni, T
Basulaiman, MO
Bazargan-Hejazi, S
Bedi, N
Bhakta, AR
Bhutta, ZA
Bin Abdulhak, AA
Boufous, S
Bourne, RRA
Danawi, H
Das, J
Deribew, A
Ding, EL
Durrani, AM
Elshrek, Y
Ibrahim, ME
Eshrati, B
Esteghamati, A
Faghmous, IAD
Farzadfar, F
Feigl, AB
Fereshtehnejad, SM
Filip, I
Fischer, F
Gankpe, FG
Ginawi, I
Gishu, MD
Gupta, R
Habash, RM
Hafezi-Nejad, N
Hamadeh, RR
Hamdouni, H
Hamidi, S
Harb, HL
Hassanvand, MS
Hedayati, MT
Heydarpour, P
Hsairi, M
Husseini, A
Jahanmehr, N
Jha, V
Jonas, JB
Karam, NE
Kasaeian, A
Kassa, NA
Kaul, A
Khader, Y
Khalifa, SEA
Khan, EA
Khan, G
Khoja, TK
Khosravi, A
Kinfu, Y
Defo, BK
Balaji, AL
Lunevicius, R
Obermeyer, CM
Malekzadeh, R
Mansourian, M
Marcenes, W
Farid, HM
Mehari, A
Memish, ZA
Mehio-Sibai, A
Memish, ZA
Mensah, GA
Mohammad, KA
Nahas, Z
Nasher, JT
Nawaz, H
Nejjari, C
Nisar, MI
Omer, SB
Parsaeian, M
Peprah, EK
Pervaiz, A
Pourmalek, F
Qato, DM
Qorbani, M
Radfar, A
Rafay, A
Rahimi, K
Rahimi-Movaghar, V
Rahman, SU
Rai, RK
Rana, SM
Rao, SR
Refaat, AH
Resnikoff, S
Roshandel, G
Saade, G
Saeedi, MY
Sahraian, MA
Saleh, S
Sanchez-Riera, L
Satpathy, M
Sepanlou, SG
Setegn, T
Shaheen, A
Shahraz, S
Sheikhbahaei, S
Shishani, K
Sliwa, K
Tavakkoli, M
Terkawi, AS
Uthman, OA
Westerman, R
Younis, MZ
Zaki, MES
Zannad, F
Roth, GA
Wang, HD
Naghavi, M
Vos, T
Al Rabeeah, AA
Lopez, AD
Murray, CJL
AF Mokdad, Ali H.
Forouzanfar, Mohammad Hossein
Daoud, Farah
El Bcheraoui, Charbel
Moradi-Lakeh, Maziar
Khalil, Ibrahim
Afshin, Ashkan
Tuffaha, Marwa
Charara, Raghid
Barber, Ryan M.
Wagner, Joseph
Cercy, Kelly
Kravitz, Hannah
Coates, Matthew M.
Robinson, Margaret
Estep, Kara
Steiner, Caitlyn
Jaber, Sara
Mokdad, Ali A.
O'Rourke, Kevin F.
Chew, Adrienne
Kim, Pauline
El Razek, Mohamed Magdy Abd
Abdalla, Safa
Abd-Allah, Foad
Abraham, Jerry P.
Abu-Raddad, Laith J.
Abu-Rmeileh, Niveen M. E.
Al-Nehmi, Abdulwahab A.
Akanda, Ali S.
Al Ahmadi, Hanan
Al Khabouri, Mazin J.
Al Lami, Faris H.
Al Rayess, Zulfa A.
Alasfoor, Deena
AlBuhairan, Fadia S.
Aldhahri, Saleh F.
Alghnam, Suliman
Alhabib, Samia
Al-Hamad, Nawal
Ali, Raghib
Ali, Syed Danish
Alkhateeb, Mohammad
AlMazroa, Mohammad A.
Alomari, Mahmoud A.
Al-Raddadi, Rajaa
Alsharif, Ubai
Al-Sheyab, Nihaya
Alsowaidi, Shirina
Al-Thani, Mohamed
Altirkawi, Khalid A.
Amare, Azmeraw T.
Amini, Heresh
Ammar, Walid
Anwari, Palwasha
Asayesh, Hamid
Asghar, Rana
Assabri, Ali M.
Assadi, Reza
Bacha, Umar
Badawi, Alaa
Bakfalouni, Talal
Basulaiman, Mohammed O.
Bazargan-Hejazi, Shahrzad
Bedi, Neeraj
Bhakta, Amit R.
Bhutta, Zulfiqar A.
Bin Abdulhak, Aref A.
Boufous, Soufiane
Bourne, Rupert R. A.
Danawi, Hadi
Das, Jai
Deribew, Amare
Ding, Eric L.
Durrani, Adnan M.
Elshrek, Yousef
Ibrahim, Mohamed E.
Eshrati, Babak
Esteghamati, Alireza
Faghmous, Imad A. D.
Farzadfar, Farshad
Feigl, Andrea B.
Fereshtehnejad, Seyed-Mohammad
Filip, Irina
Fischer, Florian
Gankpe, Fortune G.
Ginawi, Ibrahim
Gishu, Melkamu Dedefo
Gupta, Rahul
Habash, Rami M.
Hafezi-Nejad, Nima
Hamadeh, Randah R.
Hamdouni, Hayet
Hamidi, Samer
Harb, Hilda L.
Hassanvand, Mohammad Sadegh
Hedayati, Mohammad T.
Heydarpour, Pouria
Hsairi, Mohamed
Husseini, Abdullatif
Jahanmehr, Nader
Jha, Vivekanand
Jonas, Jost B.
Karam, Nadim E.
Kasaeian, Amir
Kassa, Nega Assefa
Kaul, Anil
Khader, Yousef
Khalifa, Shams Eldin A.
Khan, Ejaz A.
Khan, Gulfaraz
Khoja, Tawfi K.
Khosravi, Ardeshir
Kinfu, Yohannes
Defo, Barthelemy Kuate
Balaji, Arjun Lakshmana
Lunevicius, Raimundas
Obermeyer, Carla Makhlouf
Malekzadeh, Reza
Mansourian, Morteza
Marcenes, Wagner
Farid, Habibolah Masoudi
Mehari, Alem
Memish, Ziad A.
Mehio-Sibai, Abla
Memish, Ziad A.
Mensah, George A.
Mohammad, Karzan A.
Nahas, Ziad
Nasher, Jamal T.
Nawaz, Haseeb
Nejjari, Chakib
Nisar, Muhammad Imran
Omer, Saad B.
Parsaeian, Mahboubeh
Peprah, Emmanuel K.
Pervaiz, Aslam
Pourmalek, Farshad
Qato, Dima M.
Qorbani, Mostafa
Radfar, Amir
Rafay, Anwar
Rahimi, Kazem
Rahimi-Movaghar, Vafa
Rahman, Sajjad Ur
Rai, Rajesh K.
Rana, Saleem M.
Rao, Sowmya R.
Refaat, Amany H.
Resnikoff, Serge
Roshandel, Gholamreza
Saade, Georges
Saeedi, Mohammad Y.
Sahraian, Mohammad Ali
Saleh, Shadi
Sanchez-Riera, Lidia
Satpathy, Maheswar
Sepanlou, Sadaf G.
Setegn, Tesfaye
Shaheen, Amira
Shahraz, Saeid
Sheikhbahaei, Sara
Shishani, Kawkab
Sliwa, Karen
Tavakkoli, Mohammad
Terkawi, Abdullah S.
Uthman, Olalekan A.
Westerman, Ronny
Younis, Mustafa Z.
Zaki, Maysaa El Sayed
Zannad, Faiez
Roth, Gregory A.
Wang, Haidong
Naghavi, Mohsen
Vos, Theo
Al Rabeeah, Abdullah A.
Lopez, Alan D.
Murray, Christopher J. L.
TI Health in times of uncertainty in the eastern Mediterranean region,
1990-2013: a systematic analysis for the Global Burden of Disease Study
2013
SO LANCET GLOBAL HEALTH
LA English
DT Article
ID 188 COUNTRIES; INJURIES; DISABILITY; MORTALITY
AB Background The eastern Mediterranean region is comprised of 22 countries: Afghanistan, Bahrain, Djibouti, Egypt, Iran, Iraq, Jordan, Kuwait, Lebanon, Libya, Morocco, Oman, Pakistan, Palestine, Qatar, Saudi Arabia, Somalia, Sudan, Syria, Tunisia, the United Arab Emirates, and Yemen. Since our Global Burden of Disease Study 2010 (GBD 2010), the region has faced unrest as a result of revolutions, wars, and the so-called Arab uprisings. The objective of this study was to present the burden of diseases, injuries, and risk factors in the eastern Mediterranean region as of 2013.
Methods GBD 2013 includes an annual assessment covering 188 countries from 1990 to 2013. The study covers 306 diseases and injuries, 1233 sequelae, and 79 risk factors. Our GBD 2013 analyses included the addition of new data through updated systematic reviews and through the contribution of unpublished data sources from collaborators, an updated version of modelling software, and several improvements in our methods. In this systematic analysis, we use data from GBD 2013 to analyse the burden of disease and injuries in the eastern Mediterranean region specifically.
Findings The leading cause of death in the region in 2013 was ischaemic heart disease (90.3 deaths per 100 000 people), which increased by 17.2% since 1990. However, diarrhoeal diseases were the leading cause of death in Somalia (186.7 deaths per 100 000 people) in 2013, which decreased by 26 . 9% since 1990. The leading cause of disability-adjusted life-years (DALYs) was ischaemic heart disease for males and lower respiratory infection for females. High blood pressure was the leading risk factor for DALYs in 2013, with an increase of 83 . 3% since 1990. Risk factors for DALYs varied by country. In low-income countries, childhood wasting was the leading cause of DALYs in Afghanistan, Somalia, and Yemen, whereas unsafe sex was the leading cause in Djibouti. Non-communicable risk factors were the leading cause of DALYs in high-income and middle-income countries in the region. DALY risk factors varied by age, with child and maternal malnutrition affecting the younger age groups (aged 28 days to 4 years), whereas high bodyweight and systolic blood pressure affected older people (aged 60-80 years). The proportion of DALYs attributed to high body-mass index increased from 3.7% to 7.5% between 1990 and 2013. Burden of mental health problems and drug use increased. Most increases in DALYs, especially from non-communicable diseases, were due to population growth. The crises in Egypt, Yemen, Libya, and Syria have resulted in a reduction in life expectancy; life expectancy in Syria would have been 5 years higher than that recorded for females and 6 years higher for males had the crisis not occurred.
Interpretation Our study shows that the eastern Mediterranean region is going through a crucial health phase. The Arab uprisings and the wars that followed, coupled with ageing and population growth, will have a major impact on the region's health and resources. The region has historically seen improvements in life expectancy and other health indicators, even under stress. However, the current situation will cause deteriorating health conditions for many countries and for many years and will have an impact on the region and the rest of the world. Based on our findings, we call for increased investment in health in the region in addition to reducing the conflicts. Copyright (C) The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY license.
C1 [Mokdad, Ali H.; Forouzanfar, Mohammad Hossein; Daoud, Farah; El Bcheraoui, Charbel; Moradi-Lakeh, Maziar; Khalil, Ibrahim; Afshin, Ashkan; Tuffaha, Marwa; Charara, Raghid; Barber, Ryan M.; Wagner, Joseph; Cercy, Kelly; Kravitz, Hannah; Coates, Matthew M.; Robinson, Margaret; Estep, Kara; Steiner, Caitlyn; Jaber, Sara; Mokdad, Ali A.; O'Rourke, Kevin F.; Roth, Gregory A.; Wang, Haidong; Naghavi, Mohsen; Vos, Theo; Lopez, Alan D.] Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA USA.
[Moradi-Lakeh, Maziar] Iran Univ Med Sci, Dept Community Med Prevent Med, Tehran, Iran.
[Moradi-Lakeh, Maziar] Iran Univ Med Sci, Publ Hlth Res Ctr, Tehran, Iran.
[Mansourian, Morteza] Iran Univ Med Sci, Dept Hlth Educ & Promot, Sch Hlth, Tehran, Iran.
[Mokdad, Ali A.] Univ Texas Southwestern Med Ctr, Div Surg Oncol, Dept Surg, Dallas, TX USA.
[El Razek, Mohamed Magdy Abd] Aswan Univ Hosp, Aswan Fac Med, Aswan, Egypt.
[Abdalla, Safa] Sudanese Publ Hlth Consultancy Grp, Solihull, W Midlands, England.
[Abd-Allah, Foad] Cairo Univ, Dept Neurol, Cairo, Egypt.
[Abraham, Jerry P.] Univ So Calif, Family Med Residency Program, Calif Hosp, Los Angeles, CA USA.
[Abraham, Jerry P.] Harvard Univ, Inst Global Hlth, Boston, MA USA.
[Feigl, Andrea B.] Harvard Univ, Dept Global Hlth & Populat, Boston, MA USA.
[Ding, Eric L.] Harvard Univ, Harvard T H Chan Sch Publ Hlth, Boston, MA USA.
[Abu-Raddad, Laith J.] Weill Cornell Med Coll Qatar, Infect Dis Epidemiol Grp, Doha, Qatar.
[Abu-Rmeileh, Niveen M. E.] Birzeit Univ Ramallah, Inst Commun & Publ Hlth, Birzeit, Israel.
[Al-Nehmi, Abdulwahab A.] Minist Hlth Sanaa Yemen, Kingston, RI USA.
[Akanda, Ali S.] Univ Rhode Isl, Kingston, RI USA.
[Al Ahmadi, Hanan] Majlis Al Shura, Riyadh, Saudi Arabia.
[Al Khabouri, Mazin J.; Alasfoor, Deena] Minist Hlth, Muscat, Oman.
[Al Lami, Faris H.] Univ Baghdad, Coll Med, Baghdad, Iraq.
[Al Rayess, Zulfa A.] Kingdom Saudi Arabia Minist Hlth, Saudi Ctr Evidence Based Healthcare, Riyadh, Saudi Arabia.
[Ibrahim, Mohamed E.] Kingdom Saudi Arabia Minist Hlth, Cardiovasc Dis Control & Prevent Program, Riyadh, Saudi Arabia.
[AlMazroa, Mohammad A.; Al-Raddadi, Rajaa; Basulaiman, Mohammed O.; Habash, Rami M.; Memish, Ziad A.; Saeedi, Mohammad Y.; Al Rabeeah, Abdullah A.] Kingdom Saudi Arabia Minist Hlth, Riyadh, Saudi Arabia.
[AlBuhairan, Fadia S.] King Saud bin Abdulaziz Univ Hlth Sci, King Abdullah Specialized Childrens Hosp, Riyadh, Saudi Arabia.
[AlBuhairan, Fadia S.; Alghnam, Suliman] King Abdullah Int Med Res Ctr, Riyadh, Saudi Arabia.
[Alkhateeb, Mohammad] King Khalid Univ Hosp, Dept Pediat, Riyadh, Saudi Arabia.
[Aldhahri, Saleh F.; Altirkawi, Khalid A.] King Saud Univ, Riyadh, Saudi Arabia.
[Terkawi, Abdullah S.] King Fahad Med City, Dept Anesthesiol, Riyadh, Saudi Arabia.
[Aldhahri, Saleh F.] King Fahad Med City, Riyadh, Saudi Arabia.
[Alghnam, Suliman] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Hlth Policy & Management, Baltimore, MD USA.
[Alhabib, Samia] King Abdullah Bin Abdulaziz Univ Hosp, Riyadh, Saudi Arabia.
[Al-Hamad, Nawal] Publ Author Food & Nutr, Kuwait, Kuwait.
[Deribew, Amare] Univ Oxford, Nuffield Dept Med, Oxford, England.
[Ali, Raghib; Rahimi, Kazem] Univ Oxford, Oxford, England.
[Ali, Syed Danish] Univ London, London, England.
[Ali, Syed Danish] Inst & Fac Actuaries, Oxford, England.
[Alomari, Mahmoud A.] Jordan Univ Sci & Technol, Div Phys Therapy, Dept Rehabil Sci, Irbid, Jordan.
[Al-Sheyab, Nihaya] Jordan Univ Sci & Technol, Maternal & Child Hlth Dept, Irbid, Jordan.
[Khader, Yousef] Jordan Univ Sci & Technol, Irbid, Jordan.
[Alsharif, Ubai] Charite, Berlin, Germany.
[Alsowaidi, Shirina] Univ Al Ain, Dept Internal Med, Al Ain, U Arab Emirates.
[Khan, Gulfaraz] Coll Med & Hlth Sci, Dept Microbiol & Immunol, Al Ain, U Arab Emirates.
[Al-Thani, Mohamed; Khalifa, Shams Eldin A.] Supreme Council Hlth, Doha, Qatar.
[Amare, Azmeraw T.] Univ Adelaide, Discipline Psychiat, Sch Med, Adelaide, SA, Australia.
[Amare, Azmeraw T.] Bahir Dar Univ, Coll Med & Hlth Sci, Bahir Dar, Ethiopia.
[Setegn, Tesfaye] Bahir Dar Univ, Bahir Dar, Ethiopia.
[Amini, Heresh] Kurdistan Univ Med Sci, Environm Hlth Res Ctr, Sanandaj, Iran.
[Amini, Heresh] Swiss Trop & Publ Hlth Inst, Dept Epidemiol & Publ Hlth, Basel, Switzerland.
[Amini, Heresh] Univ Basel, Basel, Switzerland.
[Ammar, Walid; Harb, Hilda L.] Minist Publ Hlth, Beirut, Lebanon.
[Anwari, Palwasha] Minist Publ Hlth, Kabul, Afghanistan.
[Asayesh, Hamid] Qom Univ Med Sci, Sch Paramed, Dept Emergency Med, Qom, Iran.
[Asghar, Rana] South Asian Publ Hlth Forum, Islamabad, Pakistan.
[Assabri, Ali M.] Sanaa Univ, Fac Med & Hlth Sci, Sanaa, Yemen.
[Assadi, Reza] Mashhad Univ Med Sci, Mashhad, Iran.
[Bacha, Umar] Univ Management & Technol, Sch Hlth Sci, Lahore, Pakistan.
[Badawi, Alaa] Publ Hlth Agcy Canada, Toronto, ON, Canada.
[Bakfalouni, Talal] Minist Hlth, Damascus, Syria.
[Bazargan-Hejazi, Shahrzad] Charles R Drew Univ Med & Sci, Los Angeles, CA USA.
[Bedi, Neeraj] Coll Publ Hlth & Trop Med, Jazan, Saudi Arabia.
[Bhakta, Amit R.] Natl Inst Mental Hlth, Montgomery, MD USA.
[Durrani, Adnan M.] NHLBI, Ctr Translat Res & Implementat Sci, Montgomery, MD USA.
[Bhutta, Zulfiqar A.] Aga Khan Univ, Ctr Excellence Women & Child Hlth, Karachi, Pakistan.
[Das, Jai] Aga Khan Univ, Dept Paediat & Child Hlth, Karachi, Pakistan.
[Nisar, Muhammad Imran] Aga Khan Univ, Karachi, Pakistan.
[Bhutta, Zulfiqar A.] Hosp Sick Children, Ctr Global Child Hlth, Toronto, ON, Canada.
[Bin Abdulhak, Aref A.] Univ Iowa, Hosp & Clin, Iowa City, IA USA.
[Boufous, Soufiane] Univ New South Wales, Transport & Rd Safety TARS Res, Sydney, NSW, Australia.
[Resnikoff, Serge] Univ New South Wales, Brien Holden Vision Inst, Sydney, NSW, Australia.
[Bourne, Rupert R. A.] Anglia Ruskin Univ, Vision Eye Res Unit, Cambridge, England.
[Danawi, Hadi; Refaat, Amany H.] Walden Univ, Minneapolis, MN USA.
[Deribew, Amare] KEMRI Wellcome Trust Res Programme, Kilifi, Kenya.
[Elshrek, Yousef] Univ Tripoli, Fac Agr, Dept Food Sci, Tripoli, Libya.
[Eshrati, Babak] Minist Hlth & Med Educ, Tehran, Iran.
[Eshrati, Babak] Arak Univ Med Sci, Arak, Iran.
[Esteghamati, Alireza; Hafezi-Nejad, Nima; Sheikhbahaei, Sara] Univ Tehran Med Sci, Endocrinol & Metab Res Ctr, Tehran, Iran.
[Farzadfar, Farshad; Kasaeian, Amir; Khosravi, Ardeshir; Parsaeian, Mahboubeh] Univ Tehran Med Sci, Endocrinol & Metab Res Ctr, Non Communicable Dis Res Ctr, Tehran, Iran.
[Hassanvand, Mohammad Sadegh] Univ Tehran Med Sci, Ctr Air Pollut Res, Inst Environm Res, Tehran, Iran.
[Heydarpour, Pouria; Sahraian, Mohammad Ali] Univ Tehran Med Sci, Neurosci Inst, Multiple Sclerosis Res Ctr, Tehran, Iran.
[Kasaeian, Amir] Univ Tehran Med Sci, Hematol Oncol & Stem Cell Transplantat Res Ctr, Tehran, Iran.
[Malekzadeh, Reza; Roshandel, Gholamreza; Sepanlou, Sadaf G.] Univ Tehran Med Sci, Digest Dis Res Inst, Tehran, Iran.
[Parsaeian, Mahboubeh] Univ Tehran Med Sci, Dept Epidemiol Biostat, Sch Publ Hlth, Tehran, Iran.
[Rahimi-Movaghar, Vafa] Univ Tehran Med Sci, Sina Trauma & Surg Res Ctr, Tehran, Iran.
[Faghmous, Imad A. D.] London Sch Hyg & Trop Med, London, England.
[Zannad, Faiez] Univ Lorraine, INSERM, Clin Invest Ctr, Vandoeuvre Les Nancy, France.
[Zannad, Faiez] CHU Nancy, Vandoeuvre Les Nancy, France.
[Fereshtehnejad, Seyed-Mohammad] Karolinska Inst, Dept Neurobiol Care Sci & Soc, Stockholm, Sweden.
[Filip, Irina] Kaiser Permanente Psychiat Residency Program, Fontana, CA USA.
[Fischer, Florian] Univ Bielefeld, Bielefeld, Germany.
[Gankpe, Fortune G.] Leras Afrique, Cotonou, Benin.
[Gankpe, Fortune G.] CHU Hassan II, Fes, Morocco.
[Ginawi, Ibrahim] Univ Hail, Coll Med, Hail, Saudi Arabia.
[Gishu, Melkamu Dedefo] Haramaya Univ, Dira Dawa, Ethiopia.
[Gishu, Melkamu Dedefo] Kersa Hlth & Demog Surveillance Syst, Harar, Ethiopia.
[Gupta, Rahul] West Virginia Bur Publ Hlth, Charleston, WV USA.
[Hamadeh, Randah R.] Arabian Gulf Univ, Manama, Bahrain.
[Hamdouni, Hayet] Minist Hlth, Direct Soins Sante Base, Tunis, Tunisia.
[Hamidi, Samer] Hamdan Bin Mohammed Smart Univ, Dubai, U Arab Emirates.
[Hedayati, Mohammad T.] Mazndaran Univ Med Sci, Sch Med, Dept Med Mycol & Parasitol, Sari, Iran.
[Hsairi, Mohamed] Salah Azaiz Inst, Tunis, Tunisia.
[Husseini, Abdullatif] Qatar Univ, Doha, Qatar.
[Jahanmehr, Nader] Shahid Beheshti Univ Med Sci, Sch Publ Hlth, Tehran, Iran.
[Jha, Vivekanand] Univ Oxford, George Inst Global Hlth India, New Delhi, India.
[Jonas, Jost B.] Heidelberg Univ, Dept Ophthalmol, Med Fac Mannheim, Mannheim, Germany.
[Karam, Nadim E.] Univ Balamand, Beirut, Lebanon.
[Kassa, Nega Assefa] Haramaya Univ, Harari, Ethiopia.
[Kaul, Anil] Oklahoma State Univ, Ctr Hlth Sci, Tulsa, OK USA.
[Khan, Ejaz A.] Hlth Serv Acad, Islamabad, Pakistan.
[Khoja, Tawfi K.] Hlth Ministers Council Cooperat Council States, Riyadh, Saudi Arabia.
[Khosravi, Ardeshir] Iranian Minist Hlth & Med Educ, Tehran, Iran.
[Kinfu, Yohannes] Univ Canberra, Fac Hlth, Ctr Res & Action Publ Hlth, Canberra, ACT, Australia.
[Defo, Barthelemy Kuate] Univ Montreal, Dept Demog, Montreal, PQ, Canada.
[Defo, Barthelemy Kuate] Univ Montreal, Publ Hlth Res Inst, Montreal, PQ, Canada.
[Defo, Barthelemy Kuate] Univ Montreal, Dept Social & Prevent Med, Sch Publ Hlth, Montreal, PQ, Canada.
[Balaji, Arjun Lakshmana] Indegene, Bangalore, Karnataka, India.
[Lopez, Alan D.] Univ Melbourne, Melbourne Sch Populat & Global Hlth, Melbourne, Vic, Australia.
[Lunevicius, Raimundas] Aintree Univ Hosp NHS Fdn Trust, Natl Hlth Serv Fdn, Liverpool, Merseyside, England.
[Lunevicius, Raimundas] Univ Liverpool, Sch Med, Liverpool, Merseyside, England.
[Obermeyer, Carla Makhlouf] Amer Univ Beirut, Ctr Res Populat & Hlth, Fac Hlth Sci, Beirut, Lebanon.
[Mehio-Sibai, Abla] Amer Univ Beirut, Dept Epidemiol & Populat Hlth, Fac Hlth Sci, Beirut, Lebanon.
[Nahas, Ziad] Amer Univ Beirut, Med Ctr, Beirut, Lebanon.
[Saleh, Shadi] Amer Univ Beirut, Dept Hlth Management & Policy, Beirut, Lebanon.
[Marcenes, Wagner] Univ London, London, England.
[Farid, Habibolah Masoudi] State Welf Org, Tehran, Iran.
[Mehari, Alem] Howard Univ, Coll Med, Washington, DC USA.
[Memish, Ziad A.] Alfaisal Univ, Coll Med, Riyadh, Saudi Arabia.
[Mohammad, Karzan A.] Univ Salahaddin, Erbil, Iraq.
[Nasher, Jamal T.] Minist Publ Hlth & Populat, Sanaa, Yemen.
[Nawaz, Haseeb] Southern Illinois Univ, Springfield, IL USA.
[Nejjari, Chakib] Fac Med, Fes, Morocco.
[Omer, Saad B.] Emory Univ, Atlanta, GA USA.
[Peprah, Emmanuel K.] NHLBI, Bldg 10, Bethesda, MD 20892 USA.
[Pervaiz, Aslam] Postgrad Med Inst, Lahore, Pakistan.
[Pourmalek, Farshad] Univ British Columbia, Vancouver, BC, Canada.
[Qato, Dima M.] Univ Illinois, Coll Pharm, Chicago, IL USA.
[Qorbani, Mostafa] Alborz Univ Med, Sch Med, Dept Commun Med, Karaj, Iran.
[Radfar, Amir] AT Still Univ Hlth Sci, Kirksville, MO USA.
[Rafay, Anwar; Rana, Saleem M.] Contech Int Hlth Consultants, Lahore, Pakistan.
[Rahman, Sajjad Ur] Hamad Med Corp, Doha, Qatar.
[Rai, Rajesh K.] Soc Hlth & Demog Surveillance, Suri, India.
[Rana, Saleem M.] Contech Sch Publ Hlth, Lahore, Pakistan.
[Rao, Sowmya R.] Boston Univ, Sch Med, Dept Surg, Boston, MA USA.
[Refaat, Amany H.] Suez Canal Univ, Ismailia, Egypt.
[Resnikoff, Serge] Int Hlth & Dev, Geneva, Switzerland.
[Roshandel, Gholamreza] Golestan Univ Med Sci, Golestan Res Ctr Gastroenterol & Hepatol, Gorgan, Iran.
[Saade, Georges] Lebanese Univ, Beirut, Lebanon.
[Saade, Georges] Bellevue Med Ctr, Mansourieh El Metn, Lebanon.
[Sanchez-Riera, Lidia] Hosp Llobregat, IDIBELL, Barcelona, Spain.
[Satpathy, Maheswar] All India Inst Med Sci, New Delhi, India.
[Shaheen, Amira] An Najah Univ, Dept Publ Hlth, Nablus, Israel.
[Shahraz, Saeid] Tufts Med Ctr, Boston, MA USA.
[Shishani, Kawkab] Washington State Univ, Spokane, WA USA.
[Sliwa, Karen] Univ Cape Town, Fac Hlth Sci, Hatter Inst Cardiovascular Res Afr, Cape Town, South Africa.
[Tavakkoli, Mohammad] Westchester Med Ctr, Valhalla, NY USA.
[Terkawi, Abdullah S.] Univ Virginia, Dept Anesthesiol, Charlottesville, VA USA.
[Uthman, Olalekan A.] Univ Warwick, Warwick Med Sch, Warwick, England.
[Westerman, Ronny] Fed Inst Populat Res, Wiesbaden, Germany.
[Westerman, Ronny] German Natl Cohort Consortium, Heidelberg, Germany.
[Younis, Mustafa Z.] Jackson State Univ, Jackson, MS USA.
[Zaki, Maysaa El Sayed] Mansoura Univ, Fac Med, Mansoura, Egypt.
RP Mokdad, AH (reprint author), Inst Hlth Metr & Evaluat, Seattle, WA 98121 USA.
EM mokdaa@uw.edu
RI Gishu, Melkamu Dedefo/C-3747-2017; Alsharif, Ubai/C-6527-2017; Amini,
Heresh/B-3076-2010; Altirkawi, Khalid/D-7302-2017; Hedayati, Mohammad
T./E-2304-2017;
OI Gishu, Melkamu Dedefo/0000-0002-3466-1232; Alsharif,
Ubai/0000-0002-4024-3950; Amini, Heresh/0000-0002-4825-1322; Altirkawi,
Khalid/0000-0002-7331-4196; Hedayati, Mohammad T./0000-0001-6415-4648;
assadi, reza/0000-0002-5016-2994; Heydarpour,
Pouria/0000-0001-5644-7555; Husseini, Abdullatif/0000-0001-8767-5956;
Uthman, Olalekan/0000-0002-8567-3081
FU Bill & Melinda Gates Foundation
FX Funding Bill & Melinda Gates Foundation.
NR 20
TC 4
Z9 4
U1 21
U2 21
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 2214-109X
J9 LANCET GLOB HEALTH
JI Lancet Glob. Health
PD OCT
PY 2016
VL 4
IS 10
BP E704
EP E713
DI 10.1016/S2214-109X(16)30168-1
PG 10
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA DW7RE
UT WOS:000383848000021
PM 27568068
ER
PT J
AU Bauss, F
Lechmann, M
Krippendorff, BF
Staack, R
Herting, F
Festag, M
Imhof-Jung, S
Hesse, F
Pompiati, M
Kollmorgen, G
Seidl, RDM
Bossenmaier, B
Lau, W
Schantz, C
Stracke, JO
Brinkmann, U
Onda, M
Pastan, I
Bosslet, K
Niederfellner, G
AF Bauss, Frieder
Lechmann, Martin
Krippendorff, Ben-Fillippo
Staack, Roland
Herting, Frank
Festag, Matthias
Imhof-Jung, Sabine
Hesse, Friederike
Pompiati, Marc
Kollmorgen, Gwendlyn
Seidl, Rita da Silva Mateus
Bossenmaier, Birgit
Lau, Wilma
Schantz, Christian
Stracke, Jan O.
Brinkmann, Ulrich
Onda, Masanori
Pastan, Ira
Bosslet, Klaus
Niederfellner, Gerhard
TI Characterization of a re-engineered, mesothelin-targeted Pseudomonas
exotoxin fusion protein for lung cancer therapy
SO MOLECULAR ONCOLOGY
LA English
DT Article
DE Immunotoxin; De-immunization; Pharmacokinetics; Lung cancer;
Patient-derived xenografts; Targeted therapy
ID VASCULAR LEAK SYNDROME; B-CELL EPITOPES; RECOMBINANT IMMUNOTOXIN;
AERUGINOSA EXOTOXIN; PANCREATIC-CANCER; TUMOR XENOGRAFTS; KUPFFER CELLS;
IN-VITRO; PHASE-I; MICE
AB Mesothelin overexpression in lung adenocarcinomas correlates with the presence of activating KRAS mutations and poor prognosis. Hence SS1P, a mesothelin-targeted immunotoxin, could offer valuable treatment options for these patients, but its use in solid tumor therapy is hampered by high immunogenicity and non-specific toxicity. To overcome both obstacles we developed RG7787, a de-immunized cytotoxic fusion protein comprising a humanized SS1 Fab fragment and a truncated, B-cell epitope silenced, 24 kD fragment of Pseudomonas exotoxin A (PE24). Reactivity of RG7787 with sera from immunotoxin-treated patients was >1000 fold reduced. In vitro RG7787 inhibited cell viability of lung cancer cell lines with picomolar potency. The pharmacokinetic properties of RG7787 in rodents were comparable to SS1P, yet it was tolerated up to 10 fold better without causing severe vascular leak syndrome or hepatotoxicity. A pharmacokinetic/pharmacodynamic model developed based on NCI-H596 xenograft studies showed that for RG7787 and SS1P, their in vitro and in vivo potencies closely correlate. At optimal doses of 2-3 mg/kg RG7787 is more efficacious than SS1P. Even large, well established tumors (600 mm(3)) underwent remission during three treatment cycles with RG7787. Also in two patient-derived lung cancer xenograft models, Lu7336 and Lu7187, RG7787 showed antitumor efficacy. In monotherapy two treatment cycles were moderately efficacious in the Lu7336 model but showed good anti-tumor activity in the KRAS mutant Lu7187 model (26% and 80% tumor growth inhibition, respectively). Combination of RG7787 with standard chemotherapies further enhanced efficacy in both models achieving near complete eradication of Lu7187 tumors. (C) 2016 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
C1 [Bauss, Frieder; Herting, Frank; Kollmorgen, Gwendlyn; Seidl, Rita da Silva Mateus; Bossenmaier, Birgit; Bosslet, Klaus; Niederfellner, Gerhard] Roche Diagnost GmbH Penzberg, Innovat Ctr Munich, Roche Pharma Res & Early Dev pRED, Discovery Oncol, Nonnenwald 2, D-82377 Penzberg, Germany.
[Lechmann, Martin; Staack, Roland] Roche Diagnost GmbH Penzberg, Innovat Ctr Munich, Roche Pharma Res & Early Dev pRED, Pharmaceut Sci, Nonnenwald 2, D-82377 Penzberg, Germany.
[Imhof-Jung, Sabine; Hesse, Friederike; Pompiati, Marc; Lau, Wilma; Schantz, Christian; Stracke, Jan O.; Brinkmann, Ulrich] Roche Diagnost GmbH Penzberg, Innovat Ctr Munich, Roche Pharma Res & Early Dev pRED, Large Mol Res, Nonnenwald 2, D-82377 Penzberg, Germany.
[Krippendorff, Ben-Fillippo; Festag, Matthias] F Hoffmann La Roche & Cie AG, Pharmaceut Sci, Roche pRED Innovat Ctr Basel, Grenzacherstr 124, CH-4070 Basel, Switzerland.
[Onda, Masanori; Pastan, Ira] NCI, Mol Biol Lab, Ctr Canc Res, Bldg 37, Bethesda, MD 20892 USA.
[Stracke, Jan O.] F Hoffmann La Roche Ltd, Pharmaceut Dev & Supplies, Pharma Tech Dev Biol Europe, Basel, Switzerland.
RP Niederfellner, G (reprint author), Roche Diagnost GmbH Penzberg, Nonnenwald 2, D-82377 Penzberg, Germany.
EM gerhard.niederfellner@roche.com
FU Center for Cancer Research of the National Cancer Institute; Roche
Pharmaceuticals
FX This research was supported by the Center for Cancer Research of the
National Cancer Institute and by a Cooperative Research and Development
Agreement with Roche Pharmaceuticals for the development of Pseudomonas
exotoxin-derived entities in targeted cancer therapy.
NR 47
TC 1
Z9 1
U1 7
U2 7
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1574-7891
EI 1878-0261
J9 MOL ONCOL
JI Mol. Oncol.
PD OCT
PY 2016
VL 10
IS 8
BP 1317
EP 1329
DI 10.1016/j.molonc.2016.07.003
PG 13
WC Oncology
SC Oncology
GA DX5AJ
UT WOS:000384391900015
PM 27507537
ER
PT J
AU Surendran, P
Drenos, F
Young, R
Warren, H
Cook, JP
Manning, AK
Grarup, N
Sim, X
Barnes, DR
Witkowska, K
Staley, JR
Tragante, V
Tukiainen, T
Yaghootkar, H
Masca, N
Freitag, DF
Ferreira, T
Giannakopoulou, O
Tinker, A
Harakalova, M
Mihailov, E
Liu, C
Kraja, AT
Nielsen, SF
Rasheed, A
Samue, M
Zhao, W
Bonnycastle, LL
Jackson, AU
Narisu, N
Swift, AJ
Southam, L
Marten, J
Huyghe, JR
Stancakova, A
Fava, C
Ohlsson, T
Matchan, A
Stirrups, KE
Bork-Jensen, J
Gjesing, AP
Kontto, J
Perola, M
Shaw-Hawkins, S
Havulinna, AS
Zhang, H
Donnelly, LA
Groves, CJ
Rayner, NW
Neville, MJ
Robertson, NR
Yiorkas, AM
Herzig, KH
Kajantie, E
Zhang, W
Willems, SM
Lannfelt, L
Malerba, G
Soranzo, N
Trabetti, E
Verweij, N
Evangelou, E
Moayyeri, A
Vergnaud, AC
Nelson, CP
Poveda, A
Varga, TV
Caslake, M
de Craen, AJM
Trompet, S
Luan, J
Scott, RA
Harris, SE
Liewald, DCM
Marioni, R
Menni, C
Farmaki, AE
Hallmans, G
Renstrom, F
Huffman, JE
Hassinen, M
Burgess, S
Vasan, RS
Felix, JF
Uria-Nickelsen, M
Malarstign, A
Reilly, DF
Hoek, M
Vogt, TF
Lin, HH
Lieb, W
Traylor, M
Markus, HS
Highland, HM
Justice, AE
Marouli, E
Lindstrom, J
Uusitupa, M
Komulainen, P
Lakka, TA
Rauramaa, R
Polasek, O
Rudan, I
Rolandsson, O
Franks, PW
Dedoussis, G
Spector, TD
Jousilahti, P
Mannisto, S
Deary, IJ
Starr, JM
Langenberg, C
Wareham, NJ
Brown, MJ
Dominiczak, AF
Connell, JM
Jukema, JW
Sattar, N
Ford, I
Packard, CJ
Esko, T
Magi, R
Metspalu, A
de Boer, RA
van der Meer, P
van der Harst, P
Gambaro, G
Ingelsson, E
Lind, L
de Bakker, PIW
Numans, ME
Brandslund, I
Christensen, C
Petersen, ERB
Korpi-Hyovalti, E
Oksa, H
Chambers, JC
Kooner, JS
Blakemore, AIF
Franks, S
Jarvelin, MR
Husemoen, LL
Linneberg, A
Skaaby, T
Thuesen, B
Karpe, F
Tuomilehto, J
Doney, ASF
Morris, AD
Palmer, CNA
Holmen, OL
Hveem, K
Willer, CJ
Tuomi, T
Groop, L
Karajamaki, A
Palotie, A
Ripatti, S
Salomaa, V
Alam, DS
Majmnder, AAS
Di Angelantonio, E
Chowdhury, R
McCarthy, MI
Poulter, N
Stanton, AV
Sever, P
Amouyel, P
Arveiler, D
Blankenberg, S
Ferrieres, J
Kee, F
Kuulasmaa, K
Muller-Nurasyid, M
Veronesi, G
Virtamo, J
Deloukas, P
Elliott, P
Zeggini, E
Kathiresan, S
Melander, O
Kuusisto, J
Laakso, M
Padmanabhan, S
Porteous, DJ
Hayward, C
Scotland, G
Collins, FS
Mohlke, KL
Hansen, T
Pedersen, O
Boehnke, M
Stringham, HM
Frossard, P
Newton-Cheh, C
Tobin, MD
Nordestgaard, BG
Caulfield, MJ
Mahajan, A
Morris, AP
Tomaszewski, M
Samani, NJ
Saleheen, D
Asselbergs, FW
Lindgren, CM
Danesh, J
Wain, LV
Butterworth, AS
Howson, JMM
Munroe, PB
AF Surendran, Praveen
Drenos, Fotios
Young, Robin
Warren, Helen
Cook, James P.
Manning, Alisa K.
Grarup, Niels
Sim, Xueling
Barnes, Daniel R.
Witkowska, Kate
Staley, James R.
Tragante, Vinicius
Tukiainen, Taru
Yaghootkar, Hanieh
Masca, Nicholas
Freitag, Daniel F.
Ferreira, Teresa
Giannakopoulou, Olga
Tinker, Andrew
Harakalova, Magdalena
Mihailov, Evelin
Liu, Chunyu
Kraja, Aldi T.
Nielsen, Sune Fallgaard
Rasheed, Asif
Samue, Maria
Zhao, Wei
Bonnycastle, Lori L.
Jackson, Anne U.
Narisu, Narisu
Swift, Amy J.
Southam, Lorraine
Marten, Jonathan
Huyghe, Jeroen R.
Stancakova, Alena
Fava, Cristiano
Ohlsson, Therese
Matchan, Angela
Stirrups, Kathleen E.
Bork-Jensen, Jette
Gjesing, Anette P.
Kontto, Jukka
Perola, Markus
Shaw-Hawkins, Susan
Havulinna, Aki S.
Zhang, He
Donnelly, Louise A.
Groves, Christopher J.
Rayner, N. William
Neville, Matt J.
Robertson, Neil R.
Yiorkas, Andrianos M.
Herzig, Karl-Heinz
Kajantie, Eero
Zhang, Weihua
Willems, Sara M.
Lannfelt, Lars
Malerba, Giovanni
Soranzo, Nicole
Trabetti, Elisabetta
Verweij, Niek
Evangelou, Evangelos
Moayyeri, Alireza
Vergnaud, Anne-Claire
Nelson, Christopher P.
Poveda, Alaitz
Varga, Tibor V.
Caslake, Muriel
de Craen, Anton J. M.
Trompet, Stella
Luan, Jian'an
Scott, Robert A.
Harris, Sarah E.
Liewald, David C. M.
Marioni, Riccardo
Menni, Cristina
Farmaki, Aliki-Eleni
Hallmans, Goran
Renstrom, Frida
Huffman, Jennifer E.
Hassinen, Maija
Burgess, Stephen
Vasan, Ramachandran S.
Felix, Janine F.
Uria-Nickelsen, Maria
Malarstign, Anders
Reilly, Dermot F.
Hoek, Maarten
Vogt, Thomas F.
Lin, Honghuang
Lieb, Wolfgang
Traylor, Matthew
Markus, Hugh S.
Highland, Heather M.
Justice, Anne E.
Marouli, Eirini
Lindstrom, Jaana
Uusitupa, Matti
Komulainen, Pirjo
Lakka, Timo A.
Rauramaa, Rainer
Polasek, Ozren
Rudan, Igor
Rolandsson, Olov
Franks, Paul W.
Dedoussis, George
Spector, Timothy D.
Jousilahti, Pekka
Mannisto, Satu
Deary, Ian J.
Starr, John M.
Langenberg, Claudia
Wareham, Nick J.
Brown, Morris J.
Dominiczak, Anna F.
Connell, John M.
Jukema, J. Wouter
Sattar, Naveed
Ford, Ian
Packard, Chris J.
Esko, Tonu
Magi, Reedik
Metspalu, Andres
de Boer, Rudolf A.
van der Meer, Peter
van der Harst, Pim
Gambaro, Giovanni
Ingelsson, Erik
Lind, Lars
de Bakker, Paul I. W.
Numans, Mattijs E.
Brandslund, Ivan
Christensen, Cramer
Petersen, Eva R. B.
Korpi-Hyovalti, Eeva
Oksa, Heikki
Chambers, John C.
Kooner, Jaspal S.
Blakemore, Alexandra I. F.
Franks, Steve
Jarvelin, Marjo-Riitta
Husemoen, Lise L.
Linneberg, Allan
Skaaby, Tea
Thuesen, Betina
Karpe, Fredrik
Tuomilehto, Jaakko
Doney, Alex S. F.
Morris, Andrew D.
Palmer, Colin N. A.
Holmen, Oddgeir Lingaas
Hveem, Kristian
Willer, Cristen J.
Tuomi, Tiinamaija
Groop, Leif
Karajamaki, AnneMari
Palotie, Aarno
Ripatti, Samuli
Salomaa, Veikko
Alam, Dewan S.
Majmnder, Abdulla Al Shafi
Di Angelantonio, Emanuele
Chowdhury, Rajiv
McCarthy, Mark I.
Poulter, Neil
Stanton, Alice V.
Sever, Peter
Amouyel, Philippe
Arveiler, Dominique
Blankenberg, Stefan
Ferrieres, Jean
Kee, Frank
Kuulasmaa, Kari
Muller-Nurasyid, Martina
Veronesi, Giovanni
Virtamo, Jarmo
Deloukas, Panos
Elliott, Paul
Zeggini, Eleftheria
Kathiresan, Sekar
Melander, Olle
Kuusisto, Johanna
Laakso, Markku
Padmanabhan, Sandosh
Porteous, David J.
Hayward, Caroline
Scotland, Generation
Collins, Francis S.
Mohlke, Karen L.
Hansen, Torben
Pedersen, Oluf
Boehnke, Michael
Stringham, Heather M.
Frossard, Philippe
Newton-Cheh, Christopher
Tobin, Martin D.
Nordestgaard, Borge Gronne
Caulfield, Mark J.
Mahajan, Anubha
Morris, Andrew P.
Tomaszewski, Maciej
Samani, Nilesh J.
Saleheen, Danish
Asselbergs, Folkert W.
Lindgren, Cecilia M.
Danesh, John
Wain, Louise V.
Butterworth, Adam S.
Howson, Joanna M. M.
Munroe, Patricia B.
CA CHARGE Heart Failure Consortiumm
EchoGen Consortiumm
Metastroke Consortiumm
Giant Consortiumm
EPIC-InterAct Consortium
Lifelines Cohort Study
Wellcome Trust Case Control Consor
Understanding Soc Sci Grp
EPIC-CVD Consortium
CHARGE Exome Chip Blood Pressure C
T2D-GENES Consortium
GoT2DGenes Consortium
ExomeBP Consortium
CHD Exome Consortium
TI Trans-ancestry meta-analyses identify rare and common variants
associated with blood pressure and hypertension
SO NATURE GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; GENE-CENTRIC ARRAY; CARDIOVASCULAR-DISEASE;
AGING RESEARCH; PLASMA-LEVELS; RISK-FACTORS; LOCI; CHARGE; HEART;
IDENTIFICATION
AB High blood pressure is a major risk factor for cardiovascular disease and premature death. However, there is limited knowledge on specific causal genes and pathways. To better understand the genetics of blood pressure, we genotyped 242,296 rare, low frequency and common genetic variants in up to 192,763 individuals and used similar to 155,063 samples for independent replication. We identified 30 new blood pressure- or hypertension-associated genetic regions in the general population, including 3 rare missense variants in RBM47, COL21A1 and RRAS with larger effects (>1.5 mm Hg/allele) than common variants. Multiple rare nonsense and missense variant associations were found in A2ML1, and a low-frequency nonsense variant in ENPEP was identified. Our data extend the spectrum of allelic variation underlying blood pressure traits and hypertension, provide new insights into the pathophysiology of hypertension and indicate new targets for clinical intervention.
C1 [Surendran, Praveen; Young, Robin; Barnes, Daniel R.; Staley, James R.; Freitag, Daniel F.; Burgess, Stephen; Di Angelantonio, Emanuele; Chowdhury, Rajiv; Saleheen, Danish; Danesh, John; Butterworth, Adam S.; Howson, Joanna M. M.] Univ Cambridge, Dept Publ Hlth & Primary Care, MRC BHF Cardiovasc Epidemiol Unit, Cambridge, England.
[Drenos, Fotios] Univ Bristol, Sch Social & Community Med, Med Res Council Integrat Epidemiol Unit, Oakfield House, Bristol, Avon, England.
[Drenos, Fotios] UCL, Inst Cardiovasc Sci, Ctr Cardiovasc Genet, London, England.
[Warren, Helen; Witkowska, Kate; Shaw-Hawkins, Susan; Brown, Morris J.; Caulfield, Mark J.; Munroe, Patricia B.] Queen Mary Univ London, William Harvey Res Inst, Clin Pharmacol, London, England.
[Warren, Helen; Witkowska, Kate; Tinker, Andrew; Caulfield, Mark J.; Munroe, Patricia B.] Queen Mary Univ London, Natl Inst Hlth Res, Barts Cardiovasc Biomed Res Unit, London, England.
[Cook, James P.; Tobin, Martin D.; Wain, Louise V.] Univ Leicester, Dept Hlth Sci, Leicester, Leics, England.
[Cook, James P.; Morris, Andrew P.] Univ Liverpool, Dept Biostat, Liverpool, Merseyside, England.
[Manning, Alisa K.; Tukiainen, Taru; Esko, Tonu] Harvard Med Sch, Dept Genet, Boston, MA USA.
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[Manning, Alisa K.] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
[Grarup, Niels; Bork-Jensen, Jette; Gjesing, Anette P.; Hansen, Torben; Pedersen, Oluf] Univ Copenhagen, Fac Hlth & Med Sci, Novo Nordisk Fdn Ctr Basic Metab Res, Copenhagen, Denmark.
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[Sim, Xueling] Natl Univ Singapore, Natl Univ Hlth Syst, Saw Swee Hock Sch Publ Hlth, Singapore, Singapore.
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[Amouyel, Philippe] INSERM, Lille, France.
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[Arveiler, Dominique] Univ Strasbourg, Dept Epidemiol & Publ Hlth, EA 3430, Strasbourg, France.
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[Ferrieres, Jean] Toulouse Univ, Dept Epidemiol, UMR 1027, INSERM,CHU Toulouse, Toulouse, France.
[Kee, Frank] Queens Univ, UKCRC Ctr Excellence Publ Hlth, Belfast, Antrim, North Ireland.
[Muller-Nurasyid, Martina] Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Genet Epidemiol, Neuherberg, Germany.
[Muller-Nurasyid, Martina] Univ Munich, Dept Med 1, Univ Hosp Grosshadern, Munich, Germany.
[Muller-Nurasyid, Martina] DZHK German Ctr Cardiovasc Res, Partner Site Munich Heart Alliance, Munich, Germany.
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[Kathiresan, Sekar] Harvard Med Sch, Dept Med, Boston, MA USA.
[Scotland, Generation] Collaborat Univ Med Sch & NHS, Aberdeen, Scotland.
[Scotland, Generation] Collaborat Univ Med Sch & NHS, Dundee, Scotland.
[Scotland, Generation] Collaborat Univ Med Sch & NHS, Edinburgh, Midlothian, Scotland.
[Scotland, Generation] Collaborat Univ Med Sch & NHS, Glasgow, Lanark, Scotland.
[Mohlke, Karen L.] Univ N Carolina, Dept Genet, Chapel Hill, NC USA.
[Tomaszewski, Maciej] Univ Manchester, Div Cardiovasc Sci, Manchester, Lancs, England.
[Asselbergs, Folkert W.] UCL, Inst Cardiovasc Sci, Fac Populat Hlth Sci, London, England.
[Lindgren, Cecilia M.] Univ Oxford, Big Data Inst, Li Ka Shing Ctr Hlth Informat & Discovery, Oxford, England.
[Danesh, John; Munroe, Patricia B.] Wellcome Trust Sanger Inst, Hinxton, England.
RP Howson, JMM (reprint author), Univ Cambridge, Dept Publ Hlth & Primary Care, MRC BHF Cardiovasc Epidemiol Unit, Cambridge, England.; Howson, JMM (reprint author), Queen Mary Univ London, William Harvey Res Inst, Clin Pharmacol, London, England.; Howson, JMM (reprint author), Queen Mary Univ London, Natl Inst Hlth Res, Barts Cardiovasc Biomed Res Unit, London, England.; Howson, JMM; Munroe, PB (reprint author), Wellcome Trust Sanger Inst, Hinxton, England.
EM jmmh2@medschl.cam.ac.uk; p.b.munroe@qmul.ac.uk
RI Palmer, Colin/C-7053-2008; Deloukas, Panos/B-2922-2013; Padmanabhan,
Sandosh/S-3963-2016; Verweij, Niek/A-4499-2017; Grarup,
Niels/K-2807-2015; Lieb, Wolfgang/C-1990-2012; Polasek,
Ozren/B-6002-2011;
OI Palmer, Colin/0000-0002-6415-6560; Deloukas, Panos/0000-0001-9251-070X;
Grarup, Niels/0000-0001-5526-1070; Polasek, Ozren/0000-0002-5765-1862;
Traylor, Matthew/0000-0001-6624-8621; Kuulasmaa,
Kari/0000-0003-2165-1411; Jarvelin, Marjo-Riitta/0000-0002-2149-0630;
Tuomi, Tiinamaija/0000-0002-8306-6202; Varga, Tibor/0000-0002-2383-699X;
Evangelou, Evangelos/0000-0002-5488-2999; Kontto,
Jukka/0000-0003-3899-9852; Burgess, Stephen/0000-0001-5365-8760;
Linneberg, Allan/0000-0002-0994-0184; Wain, Louise/0000-0003-4951-1867;
Skaaby, Tea/0000-0003-0031-5726
FU British Heart Foundation [RG/14/5/30893, RG/15/15/31742]; Chief
Scientist Office [CZD/16/6/4]; Medical Research Council [G0600237,
G0601966, G0700931, MC_PC_U127561128, MC_UU_12013/5, MC_UU_12015/1,
MR/K006584/1, MR/K026992/1, MR/L01341X/1]; NHLBI NIH HHS [R01 HL127564];
NIDDK NIH HHS [U01 DK062370, P30 DK020595]
NR 43
TC 8
Z9 8
U1 25
U2 25
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 2016
VL 48
IS 10
BP 1151
EP 1161
DI 10.1038/ng.3654
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA DX5AG
UT WOS:000384391600010
PM 27618447
ER
PT J
AU Liu, CY
Kraja, AT
Smith, JA
Brody, JA
Franceschini, N
Bis, JC
Rice, K
Morrison, AC
Lu, YC
Weiss, S
Guo, XQ
Palmas, W
Martin, LW
Chen, YDI
Surendran, P
Drenos, F
Cook, JP
Auer, PL
Chu, AY
Giri, A
Zhao, W
Jakobsdottir, J
Lin, LA
Stafford, JM
Amin, N
Mei, H
Yao, J
Voorman, A
Larson, MG
Grove, ML
Smith, AV
Hwang, SJ
Chen, H
Huan, T
Kosova, G
Stitziel, NO
Kathiresan, S
Samani, N
Schunkert, H
Deloukas, P
Li, M
Fuchsberger, C
Pattaro, C
Gorski, M
Kooperberg, C
Papanicolaou, GJ
Rossouw, JE
Paul, JD
Kardia, SLR
Bouchard, C
Raffe, LF
Uitterlinden, AG
Franco, OH
Vasan, RS
O'Donnell, CJ
Taylor, KD
Liu, K
Bottinger, EP
Gottesman, O
Daw, EW
Giulianini, F
Ganesh, S
Salfati, E
Harris, TB
Launer, LJ
Dorr, M
Felix, SB
Rettig, R
Volzke, H
Kim, E
Lee, WJ
Lee, IT
Sheu, WHH
Tsosie, KS
Edwards, DRV
Liu, YM
Correa, A
Weir, DR
Volker, U
Ridker, PM
Boerwinkle, E
Gudnason, V
Reiner, AP
van Duijn, CM
Boreckill, IB
Edwards, TL
Chakravarti, A
Rotter, JI
Psaty, BM
Loos, RJF
Fornage, M
Ehret, GB
Newton-Cheh, C
Levy, D
Chasman, DI
AF Liu, Chunyu
Kraja, Aldi T.
Smith, Jennifer A.
Brody, Jennifer A.
Franceschini, Nora
Bis, Joshua C.
Rice, Kenneth
Morrison, Alanna C.
Lu, Yingchang
Weiss, Stefan
Guo, Xiuqing
Palmas, Walter
Martin, Lisa W.
Chen, Yii-Der Ida
Surendran, Praveen
Drenos, Fotios
Cook, James P.
Auer, Paul L.
Chu, Audrey Y.
Giri, Ayush
Zhao, Wei
Jakobsdottir, Johanna
Lin, Li-An
Stafford, Jeanette M.
Amin, Najaf
Mei, Hao
Yao, Jie
Voorman, Arend
Larson, Martin G.
Grove, Megan L.
Smith, Albert V.
Hwang, Shih-Jen
Chen, Han
Huan, Tiamdao
Kosova, Gulum
Stitziel, Nathan O.
Kathiresan, Sekar
Samani, Nilesh
Schunkert, Heribert
Deloukas, Panos
Li, Man
Fuchsberger, Christian
Pattaro, Cristian
Gorski, Mathias
Kooperberg, Charles
Papanicolaou, George J.
Rossouw, Jacques E.
Paul, Jessica D.
Kardia, Sharon L. R.
Bouchard, Claude
Raffe, Leslie F.
Uitterlinden, Andre G.
Franco, Oscar H.
Vasan, Ramachandran S.
O'Donnell, Christopher J.
Taylor, Kent D.
Liu, Kiang
Bottinger, Erwin P.
Gottesman, Omri
Daw, E. Warwick
Giulianini, Franco
Ganesh, Santhi
Salfati, Elias
Harris, Tamara B.
Launer, Lenore J.
Dorr, Marcus
Felix, Stephan B.
Rettig, Rainer
Volzke, Henry
Kim, Eric
Lee, Wen-Jane
Lee, I-Te
Sheu, Wayne H-H
Tsosie, Krystal S.
Edwards, Digna R. Velez
Liu, Yongmei
Correa, Adolfo
Weir, David R.
Volker, Uwe
Ridker, Paul M.
Boerwinkle, Eric
Gudnason, Vilmundur
Reiner, Alexander P.
van Duijn, Cornelia M.
Boreckill, Ingrid B.
Edwards, Todd L.
Chakravarti, Aravinda
Rotter, Jerome I.
Psaty, Bruce M.
Loos, Ruth J. F.
Fornage, Myriam
Ehret, Georg B.
Newton-Cheh, Christopher
Levy, Daniel
Chasman, Daniel I.
CA CHD Exome Consortium
ExomeBP Consortium
GOT2Dgenes Consortium
T2D-Genes Consortium
Myocardial Infarction Genetics CAR
CKDGen Consortium
TI Meta-analysis identifies common and rare variants influencing blood
pressure and overlapping with metabolic trait loci
SO NATURE GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; LIPOPROTEIN-LIPASE GENE; NATRIURETIC PEPTIDE
RECEPTOR; SUSCEPTIBILITY LOCI; MONOGENIC FORMS; CENTRIC ARRAY;
HYPERTENSION; DISEASE; EXPRESSION; RISK
AB Meta-analyses of association results for blood pressure using exome-centric single-variant and gene-based tests identified 31 new loci in a discovery stage among 146,562 individuals, with follow-up and meta-analysis in 180,726 additional individuals (total n = 327,288). These blood pressure-associated loci are enriched for known variants for cardiometabolic traits. Associations were also observed for the aggregation of rare and low-frequency missense variants in three genes, NPR1, DBH, and PTPMT1. In addition, blood pressure associations at 39 previously reported loci were confirmed. The identified variants implicate biological pathways related to cardiometabolic traits, vascular function, and development. Several new variants are inferred to have roles in transcription or as hubs in protein-protein interaction networks. Genetic risk scores constructed from the identified variants were strongly associated with coronary disease and myocardial infarction. This large collection of blood pressure-associated loci suggests new therapeutic strategies for hypertension, emphasizing a link with cardiometabolic risk.
C1 [Liu, Chunyu; Chu, Audrey Y.; Larson, Martin G.; Hwang, Shih-Jen; Huan, Tiamdao; Vasan, Ramachandran S.; O'Donnell, Christopher J.; Levy, Daniel] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Liu, Chunyu; Larson, Martin G.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Liu, Chunyu; Chu, Audrey Y.; Hwang, Shih-Jen; Huan, Tiamdao; Levy, Daniel] NHLBI, Populat Sci Branch, Bldg 10, Bethesda, MD 20892 USA.
[Kraja, Aldi T.; Daw, E. Warwick; Boreckill, Ingrid B.] Washington Univ, Sch Med, Div Stat Genom, St Louis, MO USA.
[Kraja, Aldi T.; Daw, E. Warwick; Boreckill, Ingrid B.] Washington Univ, Sch Med, Ctr Genome Sci & Syst Biol, St Louis, MO USA.
[Smith, Jennifer A.; Zhao, Wei; Kardia, Sharon L. R.] Univ Michigan, Sch Publ Hlth, Dept Epidemiol, Ann Arbor, MI 48109 USA.
[Brody, Jennifer A.; Bis, Joshua C.; Psaty, Bruce M.] Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA USA.
[Franceschini, Nora] Univ N Carolina, Gillings Sch Global Publ Hlth, Chapel Hill, NC USA.
[Rice, Kenneth] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Morrison, Alanna C.; Grove, Megan L.; Boerwinkle, Eric] Univ Texas Hlth Sci Ctr Houston, Ctr Human Genet, Sch Publ Hlth, Houston, TX 77030 USA.
[Lu, Yingchang; Bottinger, Erwin P.; Gottesman, Omri; Loos, Ruth J. F.] Icahn Sch Med Mt Sinai, Charles Bronfman Inst Personalized Med, New York, NY 10029 USA.
[Weiss, Stefan; Dorr, Marcus; Felix, Stephan B.; Rettig, Rainer; Volzke, Henry; Volker, Uwe] DZHK German Ctr Cardiovasc Res, Partner Site Greifswald, Greifswald, Germany.
[Weiss, Stefan; Volker, Uwe] Univ Med, Interfac Inst Genet & Funct Genom, Greifswald, Germany.
[Weiss, Stefan; Correa, Adolfo; Volker, Uwe] Ernst Moritz Arndt Univ Greifswald, Greifswald, Germany.
[Guo, Xiuqing; Chen, Yii-Der Ida; Yao, Jie; Taylor, Kent D.; Kim, Eric; Rotter, Jerome I.] Harbor UCLA Med Ctr, Los Angeles Biomed Res Inst, Inst Translat Genom & Populat Sci, Torrance, CA 90509 USA.
[Guo, Xiuqing; Chen, Yii-Der Ida; Yao, Jie; Taylor, Kent D.; Kim, Eric; Rotter, Jerome I.] Harbor UCLA Med Ctr, Dept Pediat, Torrance, CA 90509 USA.
[Palmas, Walter] Columbia Univ, Med Ctr, Div Gen Med, New York, NY USA.
[Martin, Lisa W.] George Washington Univ, Sch Med & Hlth Sci, Washington, DC 20052 USA.
[Surendran, Praveen] Univ Cambridge, Dept Publ Hlth & Primary Care, Cardiovasc Epidemiol Unit, Cambridge, England.
[Drenos, Fotios] UCL, Inst Cardiovasc Sci, Ctr Cardiovasc Genet, London, England.
[Drenos, Fotios] Univ Bristol, Sch Social & Community Med, MRC Integrat Epidemiol Unit, Oakfield House, Bristol, Avon, England.
[Cook, James P.] Univ Liverpool, Dept Biostat, Liverpool, Merseyside, England.
[Cook, James P.] Univ Leicester, Dept Hlth Sci, Leicester, Leics, England.
[Auer, Paul L.] Univ Wisconsin, Joseph J Zilber Sch Publ Hlth, Milwaukee, WI 53201 USA.
[Chu, Audrey Y.; Giulianini, Franco; Ridker, Paul M.; Levy, Daniel] Brigham & Womens Hosp, Div Prevent Med, 75 Francis St, Boston, MA 02115 USA.
[Giri, Ayush; Tsosie, Krystal S.; Edwards, Digna R. Velez; Edwards, Todd L.] Vanderbilt Univ, Vanderbilt Genet Inst, Inst Med & Publ Hlth, Vanderbilt Epidemiol Ctr,Med Ctr, Nashville, TN USA.
[Jakobsdottir, Johanna; Smith, Albert V.; Gudnason, Vilmundur] Iceland Heart Assoc, Kopavogur, Iceland.
[Lin, Li-An; Fornage, Myriam] Univ Texas Hlth Sci Ctr Houston, Inst Mol Med, Houston, TX 77030 USA.
[Stafford, Jeanette M.] Wake Forest Sch Med, Dept Biostat Sci, Div Publ Hlth Sci, Winston Salem, NC USA.
[Amin, Najaf; van Duijn, Cornelia M.] Erasmus MC, Dept Epidemiol, Genet Epidemiol Unit, Rotterdam, Netherlands.
[Mei, Hao] Univ Mississippi, Med Ctr, Dept Data Sci, Sch Populat Hlth, Jackson, MS 39216 USA.
[Voorman, Arend] Bill & Melinda Gates Fdn, Seattle, WA USA.
[Larson, Martin G.] Boston Univ, Dept Math & Stat, Boston, MA 02215 USA.
[Smith, Albert V.] Univ Iceland, Fac Med, Reykjavik, Iceland.
[Chen, Han] Harvard TH Chan Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Kosova, Gulum] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Kosova, Gulum; Kathiresan, Sekar; Newton-Cheh, Christopher] Broad Inst MIT & Harvard, Program Med & Populat Genet, Boston, MA USA.
[Stitziel, Nathan O.] Washington Univ, Dept Med, Sch Med, Div Cardiol, St Louis, MO USA.
[Stitziel, Nathan O.] Washington Univ, Dept Genet, Sch Med, St Louis, MO USA.
[Samani, Nilesh] Univ Leicester, Dept Cardiovasc Sci, Leicester, Leics, England.
[Samani, Nilesh] Glenfield Hosp, NIHR Leicester Cardiovasc Biomed Res Unit, Leicester, Leics, England.
[Schunkert, Heribert] Tech Univ Munich, Deutsch Herzzentrum Munchen, Munich, Germany.
[Schunkert, Heribert] DZHK German Ctr Cardiovasc Res, Munich Heart Alliance, Munich, Germany.
[Deloukas, Panos] King Abdulaziz Univ, Princess Al Jawhara Al Brahim Ctr Excellence Res, Jeddah, Saudi Arabia.
[Deloukas, Panos] Queen Mary Univ London, Barts & London Sch Med & Dent, William Harvey Res Inst, London, England.
[Li, Man] Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD USA.
[Fuchsberger, Christian; Pattaro, Cristian] European Acad Bozen Bolzano EURAC, Ctr Biomed, Bolzano, Italy.
[Fuchsberger, Christian; Pattaro, Cristian] Univ Lubeck, Lubeck, Germany.
[Gorski, Mathias] Univ Regensburg, Inst Epidemiol & Prevent Med, Dept Genet Epidemiol, Regensburg, Germany.
[Kooperberg, Charles] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, 1124 Columbia St, Seattle, WA 98104 USA.
[Papanicolaou, George J.; Rossouw, Jacques E.] NHLBI, Div Cardiovasc Sci, Bldg 10, Bethesda, MD 20892 USA.
[Paul, Jessica D.] Univ Michigan, Inst Social Res, Survey Res Ctr, Ann Arbor, MI USA.
[Bouchard, Claude] Louisiana State Univ Syst, Pennington Biomed Res Ctr, Baton Rouge, LA USA.
[Raffe, Leslie F.] Cedars Sinai Med Ctr, Inst Med Genet, Los Angeles, CA 90048 USA.
[Uitterlinden, Andre G.; Franco, Oscar H.] Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
[Uitterlinden, Andre G.] Erasmus MC, Dept Internal Med, Rotterdam, Netherlands.
[Vasan, Ramachandran S.] Boston Univ, Sch Med, Dept Prevent Med, Boston, MA 02215 USA.
[O'Donnell, Christopher J.] Boston Vet Adm Healthcare, Cardiol Sect, Dept Med, Boston, MA USA.
[O'Donnell, Christopher J.] Brigham & Womens Hosp, Cardiovasc Div, 75 Francis St, Boston, MA 02115 USA.
[O'Donnell, Christopher J.] Harvard Med Sch, Dept Med, Boston, MA USA.
[Liu, Kiang] Northwestern Univ, Sch Med, Chicago, IL 60611 USA.
[Ganesh, Santhi] Univ Michigan, Dept Human Genet, Ann Arbor, MI 48109 USA.
[Ganesh, Santhi] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA.
[Salfati, Elias] Johns Hopkins Univ, Sch Med, Ctr Complex Dis Genom, McKusick Nathans Inst Genet Med, Baltimore, MD USA.
[Harris, Tamara B.; Chakravarti, Aravinda; Ehret, Georg B.] NIA, Lab Epidemiol Demog & Biometry, US Natl Inst Hlth, Bethesda, MD 20892 USA.
[Launer, Lenore J.] NIA, Neuroepidemiol Sect, US Natl Inst Hlth, Bethesda, MD 20892 USA.
[Dorr, Marcus] Univ Med Greifswald, Dept Internal Med B, Greifswald, Germany.
[Rettig, Rainer] Ernst Moritz Arndt Univ Greifswald, Inst Physiol, Greifswald, Germany.
[Volzke, Henry] DZD German Ctr Diabet Res, Site Greifswald, Greifswald, Germany.
[Volzke, Henry] Univ Med Greifswald, Inst Community Med, Greifswald, Germany.
[Lee, Wen-Jane] Taichung Vet Gen Hosp, Dept Med Res, Taichung, Taiwan.
[Lee, I-Te; Sheu, Wayne H-H] Taichung Vet Gen Hosp, Dept Internal Med, Div Endocrinol & Metab, Taichung, Taiwan.
[Sheu, Wayne H-H] Natl Yang Ming Univ, Sch Med, Taipei, Taiwan.
[Lee, I-Te] Chung Shan Med Univ, Sch Med, Taichung, Taiwan.
[Sheu, Wayne H-H] Natl Chung Hsing Univ, Inst Med Technol, Taichung, Taiwan.
[Sheu, Wayne H-H] Natl Def Med Ctr, Sch Med, Taipei, Taiwan.
[Edwards, Digna R. Velez] Vanderbilt Univ, Med Ctr, Dept Obstet & Gynecol, 221 Kirkland Hall, Nashville, TN 37235 USA.
[Liu, Yongmei] Wake Forest Baptist Med Ctr, Epidemiol & Prevent Ctr Genom & Personalized Med, Winston Salem, NC USA.
[Correa, Adolfo] Univ Mississippi, Med Ctr, Dept Med, Jackson, MS 39216 USA.
[Ridker, Paul M.; Chasman, Daniel I.] Harvard Med Sch, Boston, MA USA.
[Reiner, Alexander P.; Psaty, Bruce M.; Chasman, Daniel I.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Edwards, Todd L.] Vanderbilt Univ, Med Ctr, Dept Med, 221 Kirkland Hall, Nashville, TN 37235 USA.
[Rotter, Jerome I.] Harbor UCLA Med Ctr, Inst Translat Genom & Populat Sci, Los Angeles Biomed Res Inst, Torrance, CA 90509 USA.
[Rotter, Jerome I.] Harbor UCLA Med Ctr, Dept Med, Torrance, CA 90509 USA.
[Psaty, Bruce M.] Univ Washington, Dept Hlth Serv, Seattle, WA 98195 USA.
[Psaty, Bruce M.] Grp Hlth Cooperat Puget Sound, Grp Hlth Res Inst, Seattle, WA USA.
[Loos, Ruth J. F.] Icahn Sch Med Mt Sinai, Mindich Child Hlth & Dev Inst, New York, NY 10029 USA.
[Ehret, Georg B.] Univ Hosp Geneva, Cardiol, Geneva, Switzerland.
[Newton-Cheh, Christopher] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
RP Liu, C; Levy, D (reprint author), NHLBI, Framingham Heart Study, Framingham, MA USA.; Liu, C (reprint author), Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.; Liu, C; Levy, D (reprint author), NHLBI, Populat Sci Branch, Bldg 10, Bethesda, MD 20892 USA.; Chasman, DI (reprint author), Brigham & Womens Hosp, Div Prevent Med, 75 Francis St, Boston, MA 02115 USA.; Chasman, DI (reprint author), Harvard Med Sch, Boston, MA USA.
EM chunyu.liu@nih.gov; levyd@nhlbi.nih.gov;
dchasman@research.bwh.harvard.edu
RI Deloukas, Panos/B-2922-2013; Lin, LiAn/C-5819-2017; Bouchard,
Claude/A-7637-2009;
OI Deloukas, Panos/0000-0001-9251-070X; Lin, LiAn/0000-0003-2731-1346;
Chen, Han/0000-0002-9510-4923; Smith, Jennifer/0000-0002-3575-5468
FU British Heart Foundation [RG/14/5/30893]; Medical Research Council
[MC_UU_12013/5]; NHGRI NIH HHS [U01 HG004603, U01 HG004729]; NHLBI NIH
HHS [R01 HL120393, HHSN268200800007C, HHSN268200900041C,
HHSN268201100005C, HHSN268201100006C, HHSN268201100007C,
HHSN268201100008C, HHSN268201100009C, HHSN268201100010C,
HHSN268201100011C, HHSN268201100012C, HHSN268201200036C,
HHSN268201300025C, HHSN268201300026C, HHSN268201300027C,
HHSN268201300028C, HHSN268201300029C, HHSN268201300046C, N01 HC025195,
N01 HC085079, N01 HC095159, N01HC55222, N01HC85080, N01HC85081,
N01HC85082, N01HC85083, N01HC85086, R01 HL068986, R01 HL080295, R01
HL084099, R01 HL087652, R01 HL093029, R01 HL103612, R01 HL105756, R01
HL117078, R21 HL121429, RC2 HL102419, T32 HL007208, U01 HL130114]; NIA
NIH HHS [HHSN271201200022C, N01AG12100, R01 AG023629]; NIGMS NIH HHS
[RC2 GM092618]; NIH HHS [S10 OD020069]
NR 74
TC 6
Z9 6
U1 7
U2 7
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 2016
VL 48
IS 10
BP 1162
EP 1170
DI 10.1038/ng.3660
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA DX5AG
UT WOS:000384391600011
PM 27618448
ER
PT J
AU Ehret, GB
Ferreira, T
Chasman, DI
Jackson, AU
Schmidt, EM
Johnson, T
Thorleifsson, G
Luan, J
Donnelly, LA
Kanoni, S
Petersen, AK
Pihurl, V
Strawbridge, RJ
Shungin, D
Hughes, MF
Meirelles, O
Kaakinen, M
Bouatia-Naji, N
Kristiansson, K
Shah, S
Kleber, ME
Guo, XQ
Lyytikainen, LP
Fava, C
Eriksson, N
Nolte, IM
Magnusson, PK
Salfati, EL
Rallidis, LS
Theusch, E
Smith, AJP
Folkersen, L
Witkowska, K
Pers, TH
Joehanes, R
Kim, SK
Lataniotis, L
Jansen, R
Johnson, AD
Warren, H
Kim, YJ
Zhao, W
Wu, Y
Tayo, BO
Bochud, M
Absher, D
Adair, LS
Amin, N
Arkingl, DE
Axelsson, T
Baldassarre, D
Balkau, B
Bandinelli, S
Barnes, MR
Barroso, I
Bevan, S
Bis, JC
Bjornsdottir, G
Boehnke, M
Boerwinkle, E
Bonnycastle, LL
Boomsma, DI
Bornstein, SR
Brown, MJ
Burnier, M
Cabrera, CP
Chambers, JC
Chang, IS
Cheng, CY
Chines, PS
Chung, RH
Collins, FS
Connell, JM
Doring, A
Dallongeville, J
Danesh, J
de Faire, U
Delgado, G
Dominiczak, AF
Doney, ASF
Drenos, F
Edkins, S
Eicher, JD
Elosua, R
Enroth, S
Erdmann, J
Eriksson, P
Esko, T
Evangelou, E
Evans, A
Fai, T
Farra, M
Felixl, JF
Ferrieres, J
Ferrucci, L
Fornage, M
Forrester, T
Franceschinil, N
Franco, OH
Franco-Cereceda, A
Fraser, RM
Ganesh, SK
Gao, H
Gertow, K
Gianfagna, F
Gigante, B
Giulianini, F
Goe, A
Goodall, AH
Goodarzi, M
Gorski, M
Grassler, J
Groves, CJ
Gudnason, V
Gyllensten, U
Hallmans, G
Hartikainen, AL
Hassinen, M
Havulinna, AS
Hayward, C
Hercberg, S
Herzig, KH
Hicks, AA
Hingorani, AD
Hirschhorn, JN
Hofmanl, A
Holmen, J
Holmen, OL
Hottenga, JJ
Howard, P
Hsiung, CA
Hunt, SC
Ikram, MA
Illig, T
Iribarren, C
Jensen, RA
Kahonen, M
Kang, HM
Kathiresan, S
Keating, BJ
Khaw, KT
Kim, YK
Kim, E
Kivimaki, M
Klopp, N
Kolovou, G
Komulainen, P
Kooner, JS
Kosova, G
Krauss, RM
Kuh, D
Kutalik, Z
Kuusisto, J
Kvaloy, K
Lakka, TA
Lee, NR
Lee, IT
Lee, WJ
Levy, D
Li, X
Liang, KW
Lin, H
Lin, L
Lindstrom, J
Lobbens, S
Mannisto, S
Muller, G
Muller-Nurasyid, M
Mach, F
Markus, HS
Marouli, E
McCarthy, MI
McKenzie, CA
Meneton, P
Menni, C
Metspalu, A
Mijatovic, V
Moilanen, L
Montasser, ME
Morris, AD
Morrison, AC
Mulas, A
Nagaraja, R
Narisu, N
Nikus, K
O'Donnell, CJ
O'Reilly, PF
Ong, KK
Paccaud, F
Palmer, CD
Parsa, A
Pedersen, NL
Penninx, BW
Perola, M
Peters, A
Poulter, N
Pramstaller, PP
Psaty, BM
Quertermous, T
Rao, DC
Rasheed, A
Rayner, NW
Renstrom, F
Rettig, R
Rice, KM
Roberts, R
Rose, LM
Rossouw, J
Samani, NJ
Sanna, S
Saramies, J
Schunkert, H
Sebert, S
Sheu, WHH
Shin, YA
Sim, X
Smit, JH
Smith, AV
Sosa, MX
Spector, TD
Stancakova, A
Stanton, AV
Stirrups, KE
Stringham, HM
Sundstrom, J
Swift, AJ
Syvanen, AC
Tai, ES
Tanaka, T
Tarasov, KV
Teumer, A
Thorsteinsdottir, U
Tobin, MD
Tremoli, E
Uitterlinden, AG
Uusitupa, M
Vaez, A
Vaidya, D
van Duijn, CM
van Iperen, EPA
Vasan, RS
Verwoert, GC
Virtamo, J
Vitart, V
Voight, BF
Vollenweider, P
Wagner, A
Wain, LV
Wareham, NJ
Watldns, H
Weder, AB
Westra, HJ
Wilks, R
Wilsgaard, T
Wilson, JF
Wong, TY
Yang, TP
Yao, J
Yengo, L
Zhang, W
Zhao, JH
Zhu, X
Bovet, P
Cooper, RS
Mohlke, KL
Saleheen, D
Lee, JY
Elliott, P
Gierman, HJ
Willer, CJ
Franke, L
Hovingh, GK
Taylor, KD
Dedoussis, G
Sever, P
Wong, A
Lind, L
Assimes, TL
Njolstad, I
Schwarz, PEH
Langenberg, C
Snieder, H
Caulfield, MJ
Melander, E
Laakso, M
Saltevo, J
Rauramaa, R
Tuomilehto, J
Ingelsson, E
Lehtimaki, T
Hveem, K
Palmas, W
Marz, W
Kumar, M
Salomaa, V
Chen, YDI
Rotter, JI
Froguel, P
Jarvelin, MR
Lakatta, EG
Kuulasmaa, K
Franks, PW
Hamsten, A
Wichmann, HE
Palmer, CNA
Stefansson, K
Ridker, PM
Loos, RJF
Chalcravarti, A
Deloukas, P
Morris, AP
Newton-Cheh, C
Munroe, PB
AF Ehret, Georg B.
Ferreira, Teresa
Chasman, Daniel I.
Jackson, Anne U.
Schmidt, Ellen M.
Johnson, Toby
Thorleifsson, Gudmar
Luan, Jian'an
Donnelly, Louise A.
Kanoni, Stavroula
Petersen, Ann -Kristin
Pihurl, Vasyl
Strawbridge, Rona J.
Shungin, Dmitry
Hughes, Maria F.
Meirelles, Osorio
Kaakinen, Marika
Bouatia-Naji, Nabila
Kristiansson, Kati
Shah, Sonia
Kleber, Marcus E.
Guo, Xiuqing
Lyytikainen, Leo-Pekka
Fava, Cristiano
Eriksson, Nidas
Nolte, Ilja M.
Magnusson, Patrik K.
Salfati, Elias L.
Rallidis, Loukianos S.
Theusch, Elizabeth
Smith, Andrew J. P.
Folkersen, Lasse
Witkowska, Kate
Pers, Tune H.
Joehanes, Roby
Kim, Stuart K.
Lataniotis, Lazaros
Jansen, Rick
Johnson, Andrew D.
Warren, Helen
Kim, Young Jin
Zhao, Wei
Wu, Ying
Tayo, Bamidele O.
Bochud, Murielle
Absher, Devin
Adair, Linda S.
Amin, Najaf
Arkingl, Dan E.
Axelsson, Tomas
Baldassarre, Damian
Balkau, Beverley
Bandinelli, Stefania
Barnes, Michael R.
Barroso, Ines
Bevan, Stephen
Bis, Joshua C.
Bjornsdottir, Gyda
Boehnke, Michael
Boerwinkle, Eric
Bonnycastle, Lori L.
Boomsma, Dorret I.
Bornstein, Stefan R.
Brown, Morris J.
Burnier, Michel
Cabrera, Claudia P.
Chambers, John C.
Chang, I-Shou
Cheng, Ching-Yu
Chines, Peter S.
Chung, Ren-Hua
Collins, Francis S.
Connell, John M.
Doring, Angela
Dallongeville, Jean
Danesh, John
de Faire, Ulf
Delgado, Graciela
Dominiczak, Anna F.
Doney, Alex S. F.
Drenos, Fotios
Edkins, Sarah
Eicher, John D.
Elosua, Roberto
Enroth, Stefan
Erdmann, Jeanette
Eriksson, Per
Esko, Tonu
Evangelou, Evangelos
Evans, Alun
Fai, Tove
Farra, Martin
Felixl, Janine F.
Ferrieres, Jean
Ferrucci, Luigi
Fornage, Myriam
Forrester, Terrence
Franceschinil, Nora
Franco, Oscar H.
Franco-Cereceda, Anders
Fraser, Ross M.
Ganesh, Santhi K.
Gao, He
Gertow, Karl
Gianfagna, Francesco
Gigante, Bruna
Giulianini, Franco
Goe, Anuj
Goodall, Alison H.
Goodarzi, Mark
Gorski, Mathias
Grassler, Jurgen
Groves, Christopher J.
Gudnason, Vilmundur
Gyllensten, Ulf
Hallmans, Goran
Hartikainen, Anna-Liisa
Hassinen, Maija
Havulinna, Aki S.
Hayward, Caroline
Hercberg, Serge
Herzig, Karl-Heinz
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Yao, Jie
Yengo, Loic
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Zhao, Jing Hua
Zhu, Xiaofeng
Bovet, Pascal
Cooper, Richard S.
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Saleheen, Danish
Lee, Jong-Young
Elliott, Paul
Gierman, Hinco J.
Willer, Cristen J.
Franke, Lude
Hovingh, G. Kees
Taylor, Kent D.
Dedoussis, George
Sever, Peter
Wong, Andrew
Lind, Lars
Assimes, Themistocles L.
Njolstad, Inger
Schwarz, Peter E. H.
Langenberg, Claudia
Snieder, Harold
Caulfield, Mark J.
Melander, E.
Laakso, Markku
Saltevo, Juha
Rauramaa, Rainer
Tuomilehto, Jaakko
Ingelsson, Erik
Lehtimaki, Terho
Hveem, Kristian
Palmas, Walter
Marz, Winfried
Kumar, Meena
Salomaa, Veikko
Chen, Yii-Der I.
Rotter, Jerome I.
Froguel, Philippe
Jarvelin, Marjo-Riitta
Lakatta, Edward G.
Kuulasmaa, Kari
Franks, Paul W.
Hamsten, Anders
Wichmann, H-Erich
Palmer, Colin N. A.
Stefansson, Kari
Ridker, Paul M.
Loos, Ruth J. F.
Chalcravarti, Aravinda
Deloukas, Panos
Morris, Andrew P.
Newton-Cheh, Christopher
Munroe, Patricia B.
CA CHARGE-EchoGen Consortium
CHARGE-HF Consortium
Wellcome Trust Case Control Consor
TI The genetics of blood pressure regulation and its target organs from
association studies in 342,415 individuals
SO NATURE GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; ARTERIAL-HYPERTENSION; COMMON VARIANTS;
CELL-TYPES; LOCI; TRAITS; CHROMATIN; SUSCEPTIBILITY; METAANALYSIS;
BIOLOGY
AB To dissect the genetic architecture of blood pressure and assess effects on target organ damage, we analyzed 128,272 SNPs from targeted and genome-wide arrays in 201,529 individuals of European ancestry, and genotypes from an additional 140,886 individuals were used for validation. We identified 66 blood pressure-associated loci, of which 17 were new; 15 harbored multiple distinct association signals. The 66 index SNPs were enriched for cis-regulatory elements, particularly in vascular endothelial cells, consistent with a primary role in blood pressure control through modulation of vascular tone across multiple tissues. The 66 index SNPs combined in a risk score showed comparable effects in 64,421 individuals of non-European descent. The 66-SNP blood pressure risk score was significantly associated with target organ damage in multiple tissues but with minor effects in the kidney. Our findings expand current knowledge of blood pressure-related pathways and highlight tissues beyond the classical renal system in blood pressure regulation.
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[Kutalik, Zoltan] Kuopio Univ Hosp, Kuopio, Finland.
[Kutalik, Zoltan] Univ Eastern Finland, Inst Biomed Physiol, Kuopio, Finland.
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[Lakka, Timo A.] Off Populat Studies Fdn Inc, Cebu, Philippines.
[Lakka, Timo A.; Sebert, Sylvain; Rauramaa, Rainer] Univ San Carlos, Dept Anthropol Sociol & Hist, Cebu, Philippines.
[Lee, Nanette R.] Taichung Vet Gen Hosp, Dept Internal Med, Div Endocrine & Metab, Taichung, Taiwan.
[Lee, Nanette R.] Natl Yang Ming Univ, Sch Med, Taipei, Taiwan.
[Lee, I-Te; Sheu, Wayne H-H] Taichung Vet Gen Hosp, Dept Med Res, Taichung, Taiwan.
[Lee, I-Te; Sheu, Wayne H-H] NHLBI, Populat Sci Branch, US Natl Inst Hlth, Bldg 10, Bethesda, MD 20892 USA.
[Lee, Wen-Jane] Taichung Vet Gen Hosp, Cardiovasc Ctr, Taichung, Taiwan.
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[Liang, Kae-Woei] EGID, Lille, France.
[Lin, Honghuang] Lille Pasteur Inst, CNRS UMR 8199, Lille, France.
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[Lobbens, Stephane; Yengo, Loic; Froguel, Philippe] Univ Dresden, Med Fac Carl Gustav Carus, Ctr Evidence Based Healthcare, Dresden, Germany.
[Lobbens, Stephane; Yengo, Loic; Froguel, Philippe] Univ Munich, Univ Hosp Grosshadern, Dept Med 1, Munich, Germany.
[Muller, Gabriele] Univ Munich, Inst Med Informat Biometry & Epidemiol, Munich, Germany.
[Muller-Nurasyid, Martina] Univ Cambridge, Neurol Unit, Biomed Campus, Cambridge, England.
[Muller-Nurasyid, Martina; Wichmann, H-Erich] Harokopio Univ, Dept Dietet Nutr, Athens, Greece.
[Markus, Hugh S.] Univ Paris 13, Univ Paris 06, Sorbonne Univ, INSERM U1142,LIMICS,UMRS 1142, Paris, France.
[Marouli, Eirini; Dedoussis, George] Kings Coll London, Dept Twin Res & Genet Epidemiol, London, England.
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[Morrison, Alanna C.] Tampere Univ Hosp, Ctr Heart, Dept Cardiol, Tampere, Finland.
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[Nikus, Kjell] Kings Coll London, Inst Psychiat Psychol & Neurosci, London, England.
[O'Donnell, Christopher J.; Rossouw, Jacques] Childrens Hosp Boston, Genet & Program Genom, Boston, MA USA.
[O'Reilly, Paul F.] Vrije Univ Amsterdam, Dept Psychiat, EMGO Inst, Med Ctr, Neurosci Campus, Amsterdam, Netherlands.
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[Poulter, Neil; Sever, Peter] Univ Lubeck, Dept Neurol, Lubeck, Germany.
[Pramstaller, Peter P.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
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[Psaty, Bruce M.; Sheu, Wayne H-H] Grp Hlth Res Inst, Grp Hlth Cooperat, Seattle, WA USA.
[Psaty, Bruce M.] Washington Univ, Sch Med, Div Biostat, St Louis, MO USA.
[Psaty, Bruce M.] Ctr Noncommunicable Dis, Karachi, Pakistan.
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[Rasheed, Asif; Saleheen, Danish] Univ Med Greifswald, Inst Physiol, Greifswald, Germany.
[Renstrom, Frida] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
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[Roberts, Robert] South Karelia Cent Hosp, Lappeenranta, Finland.
[Roberts, Robert] Deutsch Herzzentrum Munich, Munich, Germany.
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[Schunkert, Heribert] Munich Heart Alliance, Munich, Germany.
[Schunkert, Heribert] Univ Oulu, Ctr Lifecourse Hlth Res, Oulu, Finland.
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[Stancakova, Alena] Royal Coll Surgeons Ireland, Mol & Cellular Therapeut, Dublin, Ireland.
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[Stirrups, Kathleen E.] Natl Univ Hlth Syst, Singapore, Singapore.
[Tai, E-Shyong] NIA, Intramural Res Program, Lab Cardiovasc Sci, US Natl Inst Hlth, Baltimore, MD 21224 USA.
[Tarasov, Kirill V.; Lakatta, Edward G.] Univ Med Greifswald, Inst Community Med, Greifswald, Germany.
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[Tobin, Martin D.; Wain, Louise V.] Erasmus MC, Dept Internal Med, Rotterdam, Netherlands.
[Uitterlinden, Andre G.] Univ Eastern Finland, Dept Publ Hlth & Clin Nutr, Kuopio, Finland.
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[Uusitupa, Matti] Isfahan Univ Med Sci, Res Inst Primordial Prevent Noncommunicable Dis, Esfahan, Iran.
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[van Iperen, Erik P. A.] Boston Univ, Dept Med, Sect Prevent Med, Sch Med, Boston, MA USA.
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[Saltevo, Juha] Cent Finland Hlth Care Dist, Dept Med, Jyvaskyla, Finland.
[Tuomilehto, Jaakko] Dasman Diabet Inst, Dasman, Kuwait.
[Tuomilehto, Jaakko] King Abdulaziz Univ, Saudi Diabet Res Grp, Jeddah, Saudi Arabia.
[Tuomilehto, Jaakko] Danube Univ Krems, Ctr Vasc Prevent, Krems, Austria.
[Palmas, Walter] Columbia Univ, Dept Med, New York, NY USA.
[Marz, Winfried] Synlab Acad, Synlab Serv, Mannheim, Germany.
[Marz, Winfried] Med Univ Graz, Clin Inst Med & Chem Lab Diagnost, Graz, Austria.
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[Franks, Paul W.] Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA.
[Wichmann, H-Erich] Tech Univ Munich, Inst Med Stat & Epidemiol, Munich, Germany.
[Loos, Ruth J. F.] Icahn Sch Med Mt Sinai, Charles Bronfman Inst Personalized Med, New York, NY 10029 USA.
[Loos, Ruth J. F.] Icahn Sch Med Mt Sinai, Mindich Child Hlth Dev Inst, New York, NY 10029 USA.
[Deloukas, Panos] King Abdulaziz Univ, Princess Al Jawhara Al Brahim Ctr Excellence Res, Jeddah, Saudi Arabia.
[Morris, Andrew P.] Univ Liverpool, Dept Biostat, Liverpool, Merseyside, England.
RP Munroe, PB (reprint author), Queen Mary Univ London, William Harvey Res Inst, Clin Pharmacol, London, England.; Munroe, PB (reprint author), Queen Mary Univ London, NIHR Barts Cardiovasc Biomed Res Unit, London, England.; Newton-Cheh, C (reprint author), Broad Inst MIT & Harvard, Program Med & Populat Genet, Cambridge, MA USA.; Newton-Cheh, C (reprint author), Broad Inst MIT & Harvard, Cambridge, MA USA.; Newton-Cheh, C (reprint author), Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
EM cnewtoncheh@mgh.harvard.edu; p.b.munroe@qmul.ac.uk
RI Magnusson, Patrik/C-4458-2017; Yengo, Loic/D-2692-2017; Hicks,
Andrew/E-9518-2017; BOUATIA-NAJI, NABILA/D-5863-2013; Assimes,
Themistocles/D-9696-2015; Johnson, Andrew/G-6520-2013; Franke,
Lude/P-7036-2016; Wong, Andrew/M-8899-2016; Shah, Sonia/N-7547-2013;
Bovet, Pascal/F-4477-2011; Palmer, Colin/C-7053-2008; Peters,
Annette/A-6117-2011; Vollenweider, Peter/Q-4603-2016; Deloukas,
Panos/B-2922-2013; Colaus, PsyColaus/K-6607-2013
OI Evangelou, Evangelos/0000-0002-5488-2999; Vaidya,
Dhananjay/0000-0002-7164-1601; Folkersen, Lasse/0000-0003-0708-9530;
Tai, E Shyong/0000-0003-2929-8966; Smith, Andrew/0000-0003-1141-2978;
Peters, Annette/0000-0001-6645-0985; Wain, Louise/0000-0003-4951-1867;
Yengo, Loic/0000-0002-4272-9305; Hicks, Andrew/0000-0001-6320-0411;
Gianfagna, Francesco/0000-0003-4615-0816; Enroth,
Stefan/0000-0002-5056-9137; Bevan, Steve/0000-0003-0490-6830; Kumari,
Meena/0000-0001-9716-1035; Kuulasmaa, Kari/0000-0003-2165-1411;
Jarvelin, Marjo-Riitta/0000-0002-2149-0630; Assimes,
Themistocles/0000-0003-2349-0009; Franke, Lude/0000-0002-5159-8802;
Wong, Andrew/0000-0003-2079-4779; Shah, Sonia/0000-0001-5860-4526;
Bovet, Pascal/0000-0002-0242-4259; Palmer, Colin/0000-0002-6415-6560;
Vollenweider, Peter/0000-0002-0765-896X; Deloukas,
Panos/0000-0001-9251-070X;
FU British Heart Foundation [RG/10/12/28456, RG/13/2/30098, RG/14/5/30893];
Medical Research Council [G0401527, G0600237, G0601261, G1000143,
MC_PC_U127561128, MC_UU_12013/5, MC_UU_12015/1, MC_UU_12019/1,
MR/K006584/1, MR/K013351/1, MR/L01341X/1]; NCATS NIH HHS [UL1 TR000124];
NHLBI NIH HHS [R01 HL086694, R01 HL113933, R01 HL122684, T32 HL007208,
T32 HL098049]; NIA NIH HHS [R01 AG025941]; NICHD NIH HHS [P2C HD050924];
NIDDK NIH HHS [P30 DK063491, U01 DK062370]
NR 40
TC 9
Z9 9
U1 30
U2 30
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 2016
VL 48
IS 10
BP 1171
EP 1184
DI 10.1038/ng.3667
PG 14
WC Genetics & Heredity
SC Genetics & Heredity
GA DX5AG
UT WOS:000384391600012
PM 27618452
ER
PT J
AU McCarthy, S
Das, S
Kretzschmar, W
Delaneau, O
Wood, AR
Teumer, A
Kang, HM
Fuchsberger, C
Danecek, P
Sharp, K
Luo, Y
Sidorel, C
Kwong, A
Timpson, N
Koskinen, S
Vrieze, S
Scott, LJ
Zhang, H
Mahajan, A
Veldink, J
Peters, U
Pato, C
van Duijn, CM
Gillies, CE
Gandin, I
Mezzavilla, M
Gilly, A
Cocca, M
Traglia, M
Angius, A
Barrett, JC
Boomsma, D
Branham, K
Breen, G
Brummett, CM
Busonero, F
Campbell, H
Chan, A
Che, S
Chew, E
Collins, FS
Corbin, LJ
Smith, GD
Dedoussis, G
Dorr, M
Farmaki, AE
Ferrucci, L
Forer, L
Fraser, RM
Gabriel, S
Levy, S
Groop, L
Harrison, T
Hattersley, A
Holmen, OL
Hveem, K
Kretzler, M
Lee, JC
McGue, M
Meitinger, T
Melzer, D
Min, JL
Mohlke, KL
Vincent, JB
Nauck, M
Nickerson, D
Palotie, A
Pato, M
Pirastu, N
McInnis, M
Richards, JB
Sala, C
Salomaa, V
Schlessinger, D
Schoenherr, S
Slagboom, PE
Small, K
Spector, T
Stambolian, D
Tuke, M
Tuomilehto, J
van den Berg, LH
Van Rheenen, W
Volker, U
Wijmenga, C
Toniolo, D
Zeggini, E
Gasparini, P
Sampson, MG
Wilson, JF
Frayling, T
de Bakker, PIW
Swertz, MA
McCarroll, S
Kooperberg, C
Dekker, A
Altshuler, D
Willer, C
Iacono, W
Ripatti, S
Soranzo, N
Walter, K
Swaroop, A
Cucca, F
Anderson, CA
Myers, RM
Boehnke, M
McCarthy, MI
Durbin, R
Abecasis, G
Marchini, J
AF McCarthy, Shane
Das, Sayantan
Kretzschmar, Warren
Delaneau, Olivier
Wood, Andrew R.
Teumer, Alexander
Kang, Hyun Min
Fuchsberger, Christian
Danecek, Petr
Sharp, Kevin
Luo, Yang
Sidorel, Carlo
Kwong, Alan
Timpson, Nicholas
Koskinen, Seppo
Vrieze, Scott
Scott, Laura J.
Zhang, He
Mahajan, Anubha
Veldink, Jan
Peters, Ulrike
Pato, Carlos
van Duijn, Cornelia M.
Gillies, Christopher E.
Gandin, Ilaria
Mezzavilla, Massimo
Gilly, Arthur
Cocca, Massimiliano
Traglia, Michela
Angius, Andrea
Barrett, Jeffrey C.
Boomsma, Dorrett
Branham, Kari
Breen, Gerome
Brummett, Chad M.
Busonero, Fabio
Campbell, Harry
Chan, Andrew
Che, Sai
Chew, Emily
Collins, Francis S.
Corbin, Laura J.
Smith, George Davey
Dedoussis, George
Dorr, Marcus
Farmaki, Aliki-Eleni
Ferrucci, Luigi
Forer, Lukas
Fraser, Ross M.
Gabriel, Stacey
Levy, Shawn
Groop, Leif
Harrison, Tabitha
Hattersley, Andrew
Holmen, Oddgeir L.
Hveem, Kristian
Kretzler, Matthias
Lee, James C.
McGue, Matt
Meitinger, Thomas
Melzer, David
Min, Josine L.
Mohlke, Karen L.
Vincent, John B.
Nauck, Matthias
Nickerson, Deborah
Palotie, Aarno
Pato, Michele
Pirastu, Nicola
McInnis, Melvin
Richards, J. Brent
Sala, Cinzia
Salomaa, Veikko
Schlessinger, David
Schoenherr, Sebastian
Slagboom, P. Eline
Small, Kerrin
Spector, Timothy
Stambolian, Dwight
Tuke, Marcus
Tuomilehto, Jaakko
van den Berg, Leonard H.
Van Rheenen, Wouter
Volker, Uwe
Wijmenga, Cisca
Toniolo, Daniela
Zeggini, Eleftheria
Gasparini, Paolo
Sampson, Matthew G.
Wilson, James F.
Frayling, Timothy
de Bakker, Paul I. W.
Swertz, Morris A.
McCarroll, Steven
Kooperberg, Charles
Dekker, Annelot
Altshuler, David
Willer, Cristen
Iacono, William
Ripatti, Samuli
Soranzo, Nicole
Walter, Klaudia
Swaroop, Anand
Cucca, Francesco
Anderson, Carl A.
Myers, Richard M.
Boehnke, Michael
McCarthy, Mark I.
Durbin, Richard
Abecasis, Goncalo
Marchini, Jonathan
CA Haplotype Reference Consortium
TI A reference panel of 64,976 haplotypes for genotype imputation
SO NATURE GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; RARE VARIANTS; POPULATION; SEQUENCE
AB We describe a reference panel of 64,976 human haplotypes at 39,235,157 SNPs constructed using whole-genome sequence data from 20 studies of predominantly European ancestry. Using this resource leads to accurate genotype imputation at minor allele frequencies as low as 0.1% and a large increase in the number of SNPs tested in association studies, and it can help to discover and refine causal loci. We describe remote server resources that allow researchers to carry out imputation and phasing consistently and efficiently.
C1 [McCarthy, Shane; Luo, Yang; Gilly, Arthur; Barrett, Jeffrey C.; Zeggini, Eleftheria; Soranzo, Nicole; Walter, Klaudia; Anderson, Carl A.; Durbin, Richard] Wellcome Trust Sanger Inst, Human Genet, Hinxton, England.
[Das, Sayantan; Kang, Hyun Min; Fuchsberger, Christian; Kwong, Alan; Scott, Laura J.; Che, Sai; Boehnke, Michael; Abecasis, Goncalo] Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.
[Das, Sayantan; Kang, Hyun Min; Fuchsberger, Christian; Kwong, Alan; Scott, Laura J.; Che, Sai; Abecasis, Goncalo] Univ Michigan, Ctr Stat Genet, Ann Arbor, MI 48109 USA.
[Kretzschmar, Warren; Mahajan, Anubha; McCarthy, Mark I.; Marchini, Jonathan] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England.
[Delaneau, Olivier] Univ Geneva, Genet & Dev, Geneva, Switzerland.
[Wood, Andrew R.; Tuke, Marcus; Frayling, Timothy] Univ Exeter, Sch Med, Inst Biomed Sci, Genet Complex Traits, Exeter, Devon, England.
[Teumer, Alexander] Univ Med Greifswald, Inst Community Med, Greifswald, Germany.
[Teumer, Alexander; Nauck, Matthias] DZHK German Ctr Cardiovasc Res, Greifswald, Germany.
[Danecek, Petr] Wellcome Trust Sanger Inst, Vertebrate Resequencing Informat, Hinxton, England.
[Sharp, Kevin; Marchini, Jonathan] Univ Oxford, Dept Stat, Oxford, MS USA.
[Sidorel, Carlo; Angius, Andrea; Busonero, Fabio; Cucca, Francesco] CNR, IRGB, Sardinia, Italy.
[Timpson, Nicholas; Corbin, Laura J.; Smith, George Davey; Min, Josine L.] Univ Bristol, MRC, Integrat Epidemiol Unit, Oakfield Grove, England.
[Koskinen, Seppo; Salomaa, Veikko] THL, Helsinki, Finland.
[Vrieze, Scott] Univ Colorado, Inst Behav Genet, Boulder, CO 80309 USA.
[Vrieze, Scott] Univ Colorado, Dept Psychol & Neurosurg, Boulder, CO 80309 USA.
[Zhang, He; Willer, Cristen] Univ Michigan, Dept Internal Med, Div Cardiovasc Med, Ann Arbor, MI 48109 USA.
[Veldink, Jan; van den Berg, Leonard H.; Van Rheenen, Wouter; Dekker, Annelot] Brain Ctr Rudolf Magnus, Dept Neurol & Neurosurg, Utrecht, Netherlands.
[Peters, Ulrike; Harrison, Tabitha; Kooperberg, Charles] Fred Hutchinson Canc Res Ctr, Publ Hlth Sci Div, 1124 Columbia St, Seattle, WA 98104 USA.
[Peters, Ulrike] Univ Washington, Sch Publ Hlth, Dept Epidemiol, Seattle, WA 98195 USA.
[Pato, Carlos; Pato, Michele] SUNY Downstate, Dept Psychiat, Brooklyn, NY USA.
[van Duijn, Cornelia M.] Erasmus MC, Dept Epidemiol, Genet Epidemiol Unit, Rotterdam, Netherlands.
[Gillies, Christopher E.; Sampson, Matthew G.] Univ Michigan, Sch Med, Dept Pediat Nephrol, Ann Arbor, MI USA.
[Gandin, Ilaria; Cocca, Massimiliano; Pirastu, Nicola; Gasparini, Paolo] Univ Trieste, Dept Med Surg & Hlth Sci, Trieste, Italy.
[Mezzavilla, Massimo] IRCCS Burlo Garofolo, Genet Med, Trieste, Italy.
[Mezzavilla, Massimo; Gasparini, Paolo] Dept Expt Genet, Doha, Qatar.
[Traglia, Michela; Sala, Cinzia; Toniolo, Daniela] San Raffaele Res Inst, Genet & Cell Biol, Milan, Italy.
[Boomsma, Dorrett] Vrije Univ Amsterdam, Dept Biol Psychol, Netherlands Twin Register, Amsterdam, Netherlands.
[Branham, Kari] Univ Michigan, Dept Ophthalmol & Visual Sci, Ann Arbor, MI 48109 USA.
[Breen, Gerome] Kings Coll London, Inst Psychiat Psychol & Neurosci, MRC, Social Genet & Dev Psychiat Ctr, London, England.
[Breen, Gerome] Kings Coll London, Inst Psychiat Psychol & Neurosci, NIHR Biomed Res Ctr Mental Hlth, London, England.
[Breen, Gerome] South London Maudsley Hosp, London, ON, Canada.
[Brummett, Chad M.; Fraser, Ross M.] Univ Michigan, Dept Anesthesiol, Ann Arbor, MI 48109 USA.
[Campbell, Harry; Wilson, James F.] Univ Edinburgh, Usher Inst Populat Hlth Sci & Informat, Edinburgh, Midlothian, Scotland.
[Chan, Andrew; Boehnke, Michael] Massachusetts Gen Hosp, Div Gastroenterol, Boston, MA 02114 USA.
[Chan, Andrew; Boehnke, Michael] Harvard Med Sch, Boston, MA USA.
[Chan, Andrew] Brigham & Womens Hosp, Channing Div Network Med, 75 Francis St, Boston, MA 02115 USA.
[Che, Sai; Kretzler, Matthias; Willer, Cristen] Univ Michigan, Dept Computat Med, Ann Arbor, MI USA.
[Che, Sai; Kretzler, Matthias; Willer, Cristen] Univ Michigan, Dept Bioinformat, Ann Arbor, MI 48109 USA.
[Chew, Emily] NEI, Div Epidemiol & Clin Applicat, Bethesda, MD 20892 USA.
[Collins, Francis S.] US Natl Inst Hlth, Med Genom & Metab Genet Branch, NHGRI, Bethesda, MD USA.
[Dedoussis, George; Farmaki, Aliki-Eleni] Harokopio Univ, Sch Hlth Sci & Educ, Dept Nutr & Dietet, Athens, Greece.
[Dorr, Marcus] Univ Med Greifswald, Dept Internal Med B, Greifswald, Germany.
[Dorr, Marcus; Nauck, Matthias; Volker, Uwe] Univ Med Greifswald, Inst Clin Chem & Lab Med, Greifswald, Germany.
[Ferrucci, Luigi] NIA, Longitudinal Studies Sect, Clin Res Branch, Gerontol Res Ctr, Baltimore, MD 21224 USA.
[Ferrucci, Luigi] Med Univ Innsbruck, Dept Med Genet Mol & Clin Pharmacol, Div Genet Epidemiol, Innsbruck, Austria.
[Gabriel, Stacey; Palotie, Aarno; Altshuler, David] Broad Inst MIT & Harvard, Program Med & Populat Genet, Cambridge, MA USA.
[Levy, Shawn; Myers, Richard M.] HudsonAlpha Inst Biotechnol, Huntsville, AL USA.
[Groop, Leif] Lund Univ, Dept Clin Sci Diabet & Endocrinol, Malmo, Sweden.
[Groop, Leif] Univ Helsinki, Finnish Inst Mol Med, Helsinki, Finland.
[Groop, Leif] Univ Helsinki, Res Programs Unit, Diabet & Obes, Helsinki, Finland.
[Hattersley, Andrew] Univ Exeter, Sch Med, Inst Biomed & Clin Res, Exeter, Devon, England.
[Holmen, Oddgeir L.; Hveem, Kristian] Norwegian Univ Sci & Technol, Dept Publ Hlth & Gen Practice, Hunt Res Ctr, Levanger, Norway.
[Kretzler, Matthias] Univ Michigan, Sch Med, Dept Internal Med, Ann Arbor, MI 48109 USA.
[Lee, James C.] Univ Cambridge, Cambridge Inst Med Res, Cambridge, England.
[Lee, James C.] Univ Cambridge, Addenbrookes Hosp, Sch Clin Med, Dept Med, Cambridge, England.
[McGue, Matt; Iacono, William] Univ Minnesota, Dept Psychol, Minneapolis, MN USA.
[Meitinger, Thomas] Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Human Genet, Neuherberg, Germany.
[Meitinger, Thomas] Tech Univ Munich, Inst Human Genet, Munich, Germany.
[Meitinger, Thomas] Partner Site Munich Heart Alliance, DZHK German Ctr Cardiovasc Res, Munich, Germany.
[Melzer, David] Univ Exeter, Sch Med, Inst Biomed & Clin Sci, Epidemiol & Publ Hlth, Exeter, Devon, England.
[Mohlke, Karen L.] Univ N Carolina, Dept Genet, Chapel Hill, NC USA.
[Vincent, John B.] Ctr Addict & Mental Hlth, Mol Neuropsychiat & Dev Lab, Toronto, ON, Canada.
[Vincent, John B.] Univ Toronto, Dept Psychiat, Toronto, ON, Canada.
[Vincent, John B.] Univ Toronto, Inst Med Sci, Toronto, ON, Canada.
[Nickerson, Deborah] Univ Washington, Dept Genome Sci, Seattle, WA 98195 USA.
[Palotie, Aarno] FIMM, Inst Mol Med, Helsinki, Finland.
[Palotie, Aarno] Massachusetts Gen Hosp, Dept Med, Analyt & Translat Genet Unit, Boston, MA 02114 USA.
[Palotie, Aarno; Altshuler, David] Broad Inst MIT & Harvard, Stanley Ctr Psychiat Res, Cambridge, MA USA.
[Palotie, Aarno] Massachusetts Gen Hosp, Dept Psychiat, Psychiat & Neurodev Genet Unit, Boston, MA 02114 USA.
[Palotie, Aarno] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[McInnis, Melvin] Univ Michigan, Dept Psychiat, Ann Arbor, MI 48109 USA.
[Richards, J. Brent] McGill Univ, Dept Med, Montreal, PQ, Canada.
[Richards, J. Brent] McGill Univ, Dept Human Genet, Montreal, PQ, Canada.
[Richards, J. Brent; Small, Kerrin; Spector, Timothy] Kings Coll London, Dept Twin Res & Genet Epidemiol, London, England.
[Schlessinger, David] US Natl Inst Hlth, Natl Inst Aging, Baltimore, MD USA.
[Slagboom, P. Eline] Leiden Univ, Med Ctr, Dept Med Stat & Bioinformat, Mol Epidemiol Sect, Leiden, Netherlands.
[Stambolian, Dwight] Univ Penn, Dept Ophthalmol, Philadelphia, PA 19104 USA.
[Tuomilehto, Jaakko] Natl Inst Hlth & Welf, Chron Dis Prevent Unit, Helsinki, Finland.
[Tuomilehto, Jaakko] Dasman Diabet Inst, Dasman, Kuwait.
[Tuomilehto, Jaakko] Danube Univ Krems, Ctr Vasc Prevent, Krems, Austria.
[Tuomilehto, Jaakko] King Abdulaziz Univ, Diabet Res Grp, Jeddah, Saudi Arabia.
[Volker, Uwe] Univ Med Greifswald, Interfac Inst Genet & Funct Genom, Greifswald, Germany.
[Wijmenga, Cisca; Swertz, Morris A.] Univ Groningen, Univ Med Ctr Groningen, Dept Genet, Groningen, Netherlands.
[Wilson, James F.] Univ Edinburgh, Western Gen Hosp, MRC, Human Genet Unit,Inst Genet & Mol Med, Edinburgh, Midlothian, Scotland.
[de Bakker, Paul I. W.] Univ Med Ctr Utrecht, Med Genet, Utrecht, Netherlands.
[de Bakker, Paul I. W.] Univ Med Ctr Utrecht, Ctr Mol Med, Dept Genet, Utrecht, Netherlands.
[Swertz, Morris A.] Univ Groningen, Univ Med Ctr Groningen, Genom Coordinat Ctr, Groningen, Netherlands.
[McCarroll, Steven] Harvard Med Sch, Dept Genet, Boston, MA USA.
[McCarroll, Steven] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
[Altshuler, David] Massachusetts Gen Hosp, Dept Med, Diabet Unit, Diabet Res Ctr, Boston, MA 02114 USA.
[Altshuler, David] Harvard Med Sch, Dept Med, Boston, MA USA.
[Altshuler, David] MIT, Dept Biol, Cambridge, MA USA.
[Altshuler, David] Vertex Pharmaceut, Boston, MA USA.
[Ripatti, Samuli] Univ Helsinki, Dept Publ Hlth, Helsinki, Finland.
[Soranzo, Nicole] Univ Cambridge, Dept Hematol, Cambridge, England.
[Soranzo, Nicole] Univ Cambridge, NIHR Blood & Transplant Unit BTRU Donor Hlth Geno, Cambridge, England.
[Swaroop, Anand] US Natl Inst Hlth, Neurobiol Neurodegenerat & Repair Lab, NEI, Bethesda, MD USA.
[McCarthy, Mark I.] Univ Oxford, Radcliffe Dept Med, Oxford Ctr Diabet Endocrinol & Metab, Oxford, MS USA.
[McCarthy, Mark I.] Churchill Hosp, Oxford NIHR Biomed Res Ctr, Oxford, England.
RP Abecasis, G (reprint author), Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.; Abecasis, G (reprint author), Univ Michigan, Ctr Stat Genet, Ann Arbor, MI 48109 USA.; Marchini, J (reprint author), Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England.; Marchini, J (reprint author), Univ Oxford, Dept Stat, Oxford, MS USA.
EM rd@sanger.ac.uk; marchini@stats.ox.ac.uk
RI Wijmenga, Cisca/D-2173-2009; Fox, Laura /C-6249-2016; Slagboom, P.
Eline/R-4790-2016; Davey Smith, George/A-7407-2013;
OI Slagboom, P. Eline/0000-0002-2875-4723; Davey Smith,
George/0000-0002-1407-8314; Hattersley, Andrew/0000-0001-5620-473X;
Brummett, Chad/0000-0003-0974-7242; Swaroop, Anand/0000-0002-1975-1141;
McCarthy, Shane/0000-0002-2715-4187; Small, Kerrin/0000-0003-4566-0005;
Timpson, Nicholas/0000-0002-7141-9189
FU ERC [617306]; Wellcome Trust [WT097307, WT090851]
FX We are grateful to all participants of all the studies that have
contributed data to the HRC. J.M. acknowledges support from the ERC
(grant 617306). W.K. acknowledges support from the Wellcome Trust (grant
WT097307). S. McCarthy and R.D. acknowledge support from Wellcome Trust
grant WT090851. A full list of acknowledgments for the cohorts is given
in the Supplementary Note.
NR 21
TC 11
Z9 11
U1 10
U2 10
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 2016
VL 48
IS 10
BP 1279
EP 1283
DI 10.1038/ng.3643
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA DX5AG
UT WOS:000384391600025
PM 27548312
ER
PT J
AU Das, S
Forer, L
Schonherr, S
Sidore, C
Locke, AE
Kwong, A
Vrieze, SI
Chew, EY
Levy, S
McGue, M
Schlessinger, D
Stambolian, D
Loh, PR
Iacono, WG
Swaroop, A
Scott, LJ
Cucca, F
Kronenberg, F
Boehnke, M
Abecasis, GR
Fuchsberger, C
AF Das, Sayantan
Forer, Lukas
Schoenherr, Sebastian
Sidore, Carlo
Locke, Adam E.
Kwong, Alan
Vrieze, Scott I.
Chew, Emily Y.
Levy, Shawn
McGue, Matt
Schlessinger, David
Stambolian, Dwight
Loh, Po-Ru
Iacono, William G.
Swaroop, Anand
Scott, Laura J.
Cucca, Francesco
Kronenberg, Florian
Boehnke, Michael
Abecasis, Goncalo R.
Fuchsberger, Christian
TI Next-generation genotype imputation service and methods
SO NATURE GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; CORONARY-HEART-DISEASE; GENETIC-VARIATION;
POPULATION; PROTECTION; MAPREDUCE; THOUSANDS
AB Genotype imputation is a key component of genetic association studies, where it increases power, facilitates meta-analysis, and aids interpretation of signals. Genotype imputation is computationally demanding and, with current tools, typically requires access to a high-performance computing cluster and to a reference panel of sequenced genomes. Here we describe improvements to imputation machinery that reduce computational requirements by more than an order of magnitude with no loss of accuracy in comparison to standard imputation tools. We also describe a new web-based service for imputation that facilitates access to new reference panels and greatly improves user experience and productivity.
C1 [Das, Sayantan; Sidore, Carlo; Locke, Adam E.; Kwong, Alan; Scott, Laura J.; Boehnke, Michael; Abecasis, Goncalo R.; Fuchsberger, Christian] Univ Michigan, Ctr Stat Genet, Dept Biostat, Ann Arbor, MI 48109 USA.
[Forer, Lukas; Schoenherr, Sebastian; Kronenberg, Florian; Fuchsberger, Christian] Med Univ Innsbruck, Dept Med Genet Mol & Clin Pharmacol, Div Genet Epidemiol, Innsbruck, Austria.
[Sidore, Carlo; Cucca, Francesco] CNR, Ist Ric Genet & Biomed, Cagliari, Italy.
[Sidore, Carlo; Cucca, Francesco] Univ Sassari, Dipartimento Sci Biomed, Sassari, Italy.
[Vrieze, Scott I.] Univ Colorado, Inst Behav Sci, Boulder, CO 80309 USA.
[Chew, Emily Y.] NEI, Clin Trials Branch, Div Epidemiol & Clin Applicat, US Natl Inst Hlth, Bethesda, MD 20892 USA.
[Levy, Shawn] HudsonAlpha Inst Biotechnol, Huntsville, AL USA.
[McGue, Matt; Iacono, William G.] Univ Minnesota, Dept Psychol, Minneapolis, MN USA.
[Schlessinger, David] NIA, Genet Lab, US Natl Inst Hlth, Baltimore, MD 21224 USA.
[Stambolian, Dwight] Univ Penn, Dept Genet, Philadelphia, PA USA.
[Loh, Po-Ru] Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
[Loh, Po-Ru] Broad Inst Harvard & MIT, Program Med & Populat Genet, Cambridge, MA USA.
[Swaroop, Anand] NEI, Neurobiol Neurodegenerat & Repair Lab, US Natl Inst Hlth, Bethesda, MD 20892 USA.
[Fuchsberger, Christian] Univ Lubeck, European Acad Bolzano Bozen EURAC, Ctr Biomed, Bolzano, Italy.
RP Abecasis, GR; Fuchsberger, C (reprint author), Univ Michigan, Ctr Stat Genet, Dept Biostat, Ann Arbor, MI 48109 USA.; Fuchsberger, C (reprint author), Med Univ Innsbruck, Dept Med Genet Mol & Clin Pharmacol, Div Genet Epidemiol, Innsbruck, Austria.; Fuchsberger, C (reprint author), Univ Lubeck, European Acad Bolzano Bozen EURAC, Ctr Biomed, Bolzano, Italy.
EM goncalo@umich.edu; christian.fuchsberger@eurac.edu
RI Kronenberg, Florian/B-1736-2008;
OI Kronenberg, Florian/0000-0003-2229-1120; Locke,
Adam/0000-0001-6227-198X; Swaroop, Anand/0000-0002-1975-1141
FU National Institutes of Health [HG007022, HL117626, HG000376,
R01DA037904]; Austrian Science Fund (FWF) [J-3401]; European Community
[602133]; Intramural Research Program of the National Institute on
Aging, National Institutes of Health
FX The authors gratefully acknowledge D. Hinds for assistance with minimac3
code optimizations and A.L. Williams for providing HAPI-UR. We
acknowledge support from National Institutes of Health grants HG007022
and HL117626 (G.R.A.), HG000376 (M.B.), and R01DA037904 (S.I.V.),
Austrian Science Fund (FWF) grant J-3401 (C.F.), and the European
Community's Seventh Framework Programme (FP7/2007-2013) under grant
agreement 602133 (L.F. and S.S.). This work was also supported in part
by the Intramural Research Program of the National Institute on Aging,
National Institutes of Health (D. Schlessinger).
NR 27
TC 5
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U1 12
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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 2016
VL 48
IS 10
BP 1284
EP 1287
DI 10.1038/ng.3656
PG 4
WC Genetics & Heredity
SC Genetics & Heredity
GA DX5AG
UT WOS:000384391600026
PM 27571263
ER
PT J
AU Leong, YA
Chen, YP
Ong, HS
Wu, D
Man, KV
Deleage, C
Minnich, M
Meckiff, BJ
Wei, YB
Hou, ZH
Zotos, D
Fenix, KA
Atnerkar, A
Preston, S
Chipman, JG
Beilman, GJ
Allison, CC
Sun, L
Wang, P
Xu, JW
Toe, JG
Lu, HK
Tao, Y
Palendira, U
Dent, AL
Landay, AL
Pellegrini, M
Comerford, I
McColl, SR
Schacker, TW
Long, HM
Estes, JD
Busslinger, M
Belz, GT
Lewin, SR
Kallies, A
Yu, D
AF Leong, Yew Ann
Chen, Yaping
Ong, Hong Sheng
Wu, Di
Man, Kevin
Deleage, Claire
Minnich, Martina
Meckiff, Benjamin J.
Wei, Yunbo
Hou, Zhaohua
Zotos, Dimitra
Fenix, Kevin A.
Atnerkar, Anurag
Preston, Simon
Chipman, Jeffrey G.
Beilman, Greg J.
Allison, Cody C.
Sun, Lei
Wang, Peng
Xu, Jiawei
Toe, Jesse G.
Lu, Hao K.
Tao, Yong
Palendira, Umaimainthan
Dent, Alexander L.
Landay, Alan L.
Pellegrini, Marc
Comerford, Iain
McColl, Shaun R.
Schacker, Timothy W.
Long, Heather M.
Estes, Jacob D.
Busslinger, Meinrad
Belz, Gabrielle T.
Lewin, Sharon R.
Kallies, Axel
Yu, Di
TI CXCR5(+) follicular cytotoxic T cells control viral infection in B cell
follicles
SO NATURE IMMUNOLOGY
LA English
DT Article
ID HELPER-CELLS; VIRUS-INFECTION; HIV-INFECTION; DIFFERENTIATION;
TRANSCRIPTION; BLIMP-1; EXPRESSION; EFFECTOR; TCF-1; BCL6
AB During unresolved infections, some viruses escape immunological control and establish a persistant reservoir in certain cell types, such as human immunodeficiency virus (HIV), which persists in follicular helper T cells (T-FH cells), and Epstein-Barr virus (EBV), which persists in B cells. Here we identified a specialized group of cytotoxic T cells (T-C cells) that expressed the chemokine receptor CXCR5, selectively entered B cell follicles and eradicated infected TFH cells and B cells. The differentiation of these cells, which we have called 'follicular cytotoxic T cells' (T-FC cells), required the transcription factors Bcl6, E2A and TCF-1 but was inhibited by the transcriptional regulators Blimp1, Id2 and Id3. Blimp1 and E2A directly regulated Cxcr5 expression and, together with Bcl6 and TCF-1, formed a transcriptional circuit that guided T-FC cell development. The identification of T-FC cells has far-reaching implications for the development of strategies to control infections that target B cells and T-FH cells and to treat B cell-derived malignancies.
C1 [Leong, Yew Ann; Chen, Yaping; Ong, Hong Sheng; Atnerkar, Anurag; Yu, Di] Monash Univ, Monash Biomed Discovery Inst, Infect & Immun Program, Clayton, Vic, Australia.
[Leong, Yew Ann; Chen, Yaping; Ong, Hong Sheng; Atnerkar, Anurag; Yu, Di] Monash Univ, Dept Biochem & Mol Biol, Clayton, Vic, Australia.
[Wu, Di] Univ North Carolina Chapel Hill, Sch Dent, Chapel Hill, NC USA.
[Man, Kevin; Zotos, Dimitra; Preston, Simon; Allison, Cody C.; Toe, Jesse G.; Pellegrini, Marc; Belz, Gabrielle T.; Kallies, Axel] Walter & Eliza Hall Inst Med Res, Parkville, Vic, Australia.
[Man, Kevin; Zotos, Dimitra; Preston, Simon; Allison, Cody C.; Toe, Jesse G.; Pellegrini, Marc; Belz, Gabrielle T.; Kallies, Axel] Univ Melbourne, Dept Med Biol, Parkville, Vic, Australia.
[Deleage, Claire; Estes, Jacob D.] Frederick Natl Lab Canc Res, Leidos Biomed Res, AIDS & Canc Virus Program, Frederick, MD USA.
[Minnich, Martina; Busslinger, Meinrad] Vienna Bioctr, Res Inst Mol Pathol, Vienna, Austria.
[Meckiff, Benjamin J.; Long, Heather M.] Univ Birmingham, Ctr Human Virol, Inst Immunol & Immunotherapy, Birmingham B15 2TT, W Midlands, England.
[Meckiff, Benjamin J.; Long, Heather M.] Univ Birmingham, Canc Immunol & Immunotherapy Ctr, Birmingham B15 2TT, W Midlands, England.
[Wei, Yunbo; Hou, Zhaohua; Yu, Di] Shandong Acad Sci, Shandong Anal & Test Ctr, Jinan, Peoples R China.
[Fenix, Kevin A.; Comerford, Iain; McColl, Shaun R.] Univ Adelaide, Sch Biol Sci, Dept Mol & Cellular Biol, Adelaide, SA, Australia.
[Chipman, Jeffrey G.; Beilman, Greg J.] Univ Minnesota, Dept Surg, Box 242 UMHC, Minneapolis, MN 55455 USA.
[Sun, Lei; Wang, Peng] Capital Med Univ, Beijing Ditan Hosp, Dept Pathol, Beijing, Peoples R China.
[Xu, Jiawei] Univ N Carolina, Gillings Sch Global Publ Hlth, Dept Biostat, Chapel Hill, NC USA.
[Lu, Hao K.; Lewin, Sharon R.] Univ Melbourne, Peter Doherty Inst Infect & Immun, Melbourne, Vic, Australia.
[Lu, Hao K.; Lewin, Sharon R.] Royal Melbourne Hosp, Melbourne, Vic, Australia.
[Tao, Yong] Capital Med Univ, Beijing Chaoyang Hosp, Dept Ophthalmol, Beijing, Peoples R China.
[Palendira, Umaimainthan] Centenary Inst, Newtown, Tas, Australia.
[Dent, Alexander L.] Indiana Univ Sch Med, Dept Microbiol & Immunol, Indianapolis, IN 46202 USA.
[Landay, Alan L.] Rush Univ, Med Ctr, Dept Immunol Microbiol, Chicago, IL 60612 USA.
[Schacker, Timothy W.] Univ Minnesota, Dept Med, Box 736 UMHC, Minneapolis, MN 55455 USA.
[Lewin, Sharon R.] Monash Univ, Alfred Hosp, Dept Infect Dis, Melbourne, Vic, Australia.
[Yu, Di] Monash Univ, Sch Clin Sci, Ctr Inflammatory Dis, Clayton, Vic, Australia.
RP Yu, D (reprint author), Monash Univ, Monash Biomed Discovery Inst, Infect & Immun Program, Clayton, Vic, Australia.; Yu, D (reprint author), Monash Univ, Dept Biochem & Mol Biol, Clayton, Vic, Australia.; Kallies, A (reprint author), Walter & Eliza Hall Inst Med Res, Parkville, Vic, Australia.; Kallies, A (reprint author), Univ Melbourne, Dept Med Biol, Parkville, Vic, Australia.; Yu, D (reprint author), Shandong Acad Sci, Shandong Anal & Test Ctr, Jinan, Peoples R China.; Yu, D (reprint author), Monash Univ, Sch Clin Sci, Ctr Inflammatory Dis, Clayton, Vic, Australia.
EM kallies@wehi.edu.au; di.yu@monash.edu
RI Yu, Di/C-2163-2009;
OI Yu, Di/0000-0003-1721-8922; Hou, Zhaohua/0000-0003-3093-0279;
Busslinger, Meinrad/0000-0002-9111-9351
FU Birmingham Science City - Experimental Medicine Network of Excellence
project; National Health and Medical Research Council of Australia
[GNT1085509, GNT1085151]; Monash University; amfAR Research Consortium
on HIV Eradication [109327-59-RGRL]; Creative and Novel Ideas in HIV
Research Program of The International AIDS Society; Australian Centre
for HIV and Hepatitis Virology Research [2015-69]; Priority Research
Program of Shandong Academy of Sciences; Shandong Province Taishan
Scholar Program; Sylvia and Charles Viertel Foundation; Delaney AIDS
Research Enterprise; Martin Delaney Collaboratories; National Institute
for Allergy and Infectious Diseases of the US National Institutes of
Health [U19 AI096109]; Bloodwise, UK [15021]; National Cancer Institute
of the US National Institutes of Health [HHSN261200800001E]; Victorian
State Government Operational Infrastructure Support and Australian
Government NHMRC Independent Research Institute Infrastructure Support
scheme
FX We acknowledge the facilities, scientific and technical assistance of
Flowcore, Monash Micro Imaging, and Monash Bioinformatics Platform (S.
Archer and K. Tsyganov) at Monash University, and University of
Birmingham's Human Biomaterials Resource Centre (supported through
Birmingham Science City - Experimental Medicine Network of Excellence
project). We thank L. Ye (Third Military Medical University) for Thy1.1
reporter constructs; C. Vinuesa (Australian National University) and S.
Nutt (Walter and Eliza Hall Institute of Medical Research) for mice; R.
Gloury and L. Mackiewicz for technical support; C. Dong for the list of
Bcl6-bound genes; and H. Xue for the list of TCF-1-bound genes.
Supported by the National Health and Medical Research Council of
Australia (Y.A.L. and S.R.L.; GNT1085509 to D.Y.; and GNT1085151 to
A.K.), Monash University (D.Y.), the amfAR Research Consortium on HIV
Eradication (109327-59-RGRL, D.Y., S. R. L. and A. L. L.), The Creative
and Novel Ideas in HIV Research Program of The International AIDS
Society (D.Y.), Australian Centre for HIV and Hepatitis Virology
Research (2015-69 to D.Y.), The Priority Research Program of Shandong
Academy of Sciences (D.Y.), Shandong Province Taishan Scholar Program
(D.Y.), the Sylvia and Charles Viertel Foundation (A.K.), the Delaney
AIDS Research Enterprise to find a cure, Martin Delaney Collaboratories,
the National Institute for Allergy and Infectious Diseases of the US
National Institutes of Health (U19 AI096109 to S.R.L., T.W.S. and
J.D.E.), Bloodwise, UK (15021 to H.M.L. and B.J.M.), the National Cancer
Institute of the US National Institutes of Health (HHSN261200800001E),
and the Victorian State Government Operational Infrastructure Support
and Australian Government NHMRC Independent Research Institute
Infrastructure Support scheme. The content of this publication does not
necessarily reflect the views or policies of the Department of Health
and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the US Government.
NR 62
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U1 6
U2 6
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1529-2908
EI 1529-2916
J9 NAT IMMUNOL
JI Nat. Immunol.
PD OCT
PY 2016
VL 17
IS 10
BP 1187
EP +
DI 10.1038/ni.3543
PG 13
WC Immunology
SC Immunology
GA DX3VD
UT WOS:000384302900010
PM 27487330
ER
PT J
AU Garcia-Cossio, E
Witkowski, M
Robinson, SE
Cohen, LG
Birbaumer, N
Soekadar, SR
AF Garcia-Cossio, Eliana
Witkowski, Matthias
Robinson, Stephen E.
Cohen, Leonardo G.
Birbaumer, Niels
Soekadar, Surjo R.
TI Simultaneous transcranial direct current stimulation (tDCS) and
whole-head magnetoencephalography (MEG): assessing the impact of tDCS on
slow cortical magnetic fields
SO NEUROIMAGE
LA English
DT Article
DE Transcranial direct current stimulation; Magnetoencephalography; Slow
cortical fields; Source-reconstruction
ID NONINVASIVE BRAIN-STIMULATION; CONTINGENT NEGATIVE-VARIATION; MOTOR
CORTEX; NEURONAL-ACTIVITY; NETWORK DYNAMICS; EEG FLUCTUATIONS; HUMANS;
EXCITABILITY; FMRI; POTENTIALS
AB Transcranial direct current stimulation (tDCS) can influence cognitive, affective or motor brain functions. Whereas previous imaging studies demonstrated widespread tDCS effects on brain metabolism, direct impact of tDCS on electric or magnetic source activity in task-related brain areas could not be confirmed due to the difficulty to record such activity simultaneously during tDCS. The aim of this proof-of-principal study was to demonstrate the feasibility of whole-head source localization and reconstruction of neuromagnetic brain activity during tDCS and to confirm the direct effect of tDCS on ongoing neuromagnetic activity in task-related brain areas. Here we show for the first time that tDCS has an immediate impact on slow cortical magnetic fields (SCF, 0-4 Hz) of task-related areas that are identical with brain regions previously described in metabolic neuroimaging studies. 14 healthy volunteers performed a choice reaction time (RT) task while whole-head magnetoencephalography (MEG) was recorded. Task-related source-activity of SCFs was calculated using synthetic aperture magnetometry (SAM) in absence of stimulation and while anodal, cathodal or sham tDCS was delivered over the right primary motor cortex (M1). Source reconstruction revealed task-related SCF modulations in brain regions that precisely matched prior metabolic neuroimaging studies. Anodal and cathodal tDCS had a polarity-dependent impact on RT and SCF in primary sensorimotor and medial centro-parietal cortices. Combining tDCS and whole-head MEG is a powerful approach to investigate the direct effects of transcranial electric currents on ongoing neuromagnetic source activity, brain function and behavior. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Garcia-Cossio, Eliana; Witkowski, Matthias; Birbaumer, Niels; Soekadar, Surjo R.] Univ Tubingen, Inst Med Psychol & Behav Neurobiol, D-72076 Tubingen, Germany.
[Garcia-Cossio, Eliana; Witkowski, Matthias; Birbaumer, Niels; Soekadar, Surjo R.] Univ Tubingen, MEG Ctr, D-72076 Tubingen, Germany.
[Garcia-Cossio, Eliana; Witkowski, Matthias; Soekadar, Surjo R.] Univ Tubingen, Dept Psychiat & Psychotherapy, Appl Neurotechnol Lab, D-72076 Tubingen, Germany.
[Garcia-Cossio, Eliana] Radboud Univ Nijmegen, Dept Artificial Intelligence, Donders Ctr Brain Cognit & Behav, Nijmegen, Netherlands.
[Robinson, Stephen E.] NIMH, NIH, MEG Core Facil, Bethesda, MD 20892 USA.
[Cohen, Leonardo G.] NINDS, NIH, Human Cort Physiol & Stroke Neurorehabil Sect, Bethesda, MD 20892 USA.
[Birbaumer, Niels] Osped San Camillo, Ist Ricovero & Cura Carattere Sci, I-30126 Venice, Italy.
RP Soekadar, SR (reprint author), Univ Tubingen, Calwerstr 14, D-72076 Tubingen, Germany.
EM surjo.soekadar@uni-tuebingen.de
FU Intramural Research Program (IRP) of the National Institute of
Neurological Disorders and Stroke (NINDS); National Institute of Mental
Health (NIMH), Bethesda, Maryland, USA; German Federal Ministry of
Education and Research (BMBF, Foderzeichen) [01GQ0831, 16SV5840];
Deutsche Forschungsgemeinschaft (DFG) [SO932-2]; European Union
[FP7-ICT-2011-288551, AIDE 645322]; DAAD (Deutscher Akademischer
Austauschdienst); fortune Program of the University of Tubingen's
Medical Faculty [2216-0-0/ F-No. 1331418]; Brain Products GmbH;
Volkswagenstiftung
FX This work was supported by the Intramural Research Program (IRP) of the
National Institute of Neurological Disorders and Stroke (NINDS) and
National Institute of Mental Health (NIMH), Bethesda, Maryland, USA, the
German Federal Ministry of Education and Research (BMBF, Foderzeichen
01GQ0831, 16SV5840), the Deutsche Forschungsgemeinschaft (DFG SO932-2),
the European Union (FP7-ICT-2011-288551, Horizon 2020: AIDE 645322) and
DAAD (Deutscher Akademischer Austauschdienst), fortune Program of the
University of Tubingen's (No. 2216-0-0/ F-No. 1331418) Medical Faculty,
the Brain Products GmbH and Volkswagenstiftung. All authors reported no
financial interests or potential conflicts of interest.
NR 59
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U1 12
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PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
EI 1095-9572
J9 NEUROIMAGE
JI Neuroimage
PD OCT
PY 2016
VL 140
BP 33
EP 40
DI 10.1016/j.neuroimage.2015.09.068
PG 8
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA DX0RK
UT WOS:000384071900004
PM 26455796
ER
PT J
AU Witkowski, M
Garcia-Cossio, E
Chander, BS
Braun, C
Birbaumer, N
Robinson, SE
Soekadar, SR
AF Witkowski, Matthias
Garcia-Cossio, Eliana
Chander, Bankim S.
Braun, Christoph
Birbaumer, Niels
Robinson, Stephen E.
Soekadar, Surjo R.
TI Mapping entrained brain oscillations during transcranial alternating
current stimulation (tACS)
SO NEUROIMAGE
LA English
DT Article
DE Neuromagnetic brain oscillations; Entrainment; Transcranial alternating
current stimulation; Whole-head magnetoencephalography
ID ELECTRICAL-STIMULATION; IN-VIVO; CORTEX; PERFORMANCE; RESPONSES;
STIMULUS; NEURONS; RECORDINGS; PLASTICITY; RESONANCE
AB Transcranial alternating current stimulation (tACS), a non-invasive and well-tolerated form of electric brain stimulation, can influence perception, memory, as well as motor and cognitive function. While the exact underlying neurophysiological mechanisms are unknown, the effects of tACS are mainly attributed to frequency-specific entrainment of endogenous brain oscillations in brain areas close to the stimulation electrodes, and modulation of spike timing dependent plasticity reflected in gamma band oscillatory responses. tACS-related electromagnetic stimulator artifacts, however, impede investigation of these neurophysiological mechanisms. Here we introduce a novel approach combining amplitude-modulated tACS during whole-head magnetoencephalography (MEG) allowing for artifact-free source reconstruction and precise mapping of entrained brain oscillations underneath the stimulator electrodes. Using this approach, we show that reliable reconstruction of neuromagnetic low and high-frequency oscillations including high gamma band activity in stimulated cortical areas is feasible opening a new window to unveil the mechanisms underlying the effects of stimulation protocols that entrain brain oscillatory activity. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Witkowski, Matthias; Garcia-Cossio, Eliana; Chander, Bankim S.; Soekadar, Surjo R.] Univ Tubingen Hosp, Dept Psychiat & Psychotherapy, Appl Neurotechnol Lab, Calwerstr 14, D-72076 Tubingen, Germany.
[Garcia-Cossio, Eliana; Birbaumer, Niels; Soekadar, Surjo R.] Univ Tubingen, Inst Med Psychol & Behav Neurobiol, Tubingen, Germany.
[Garcia-Cossio, Eliana] Radboud Univ Nijmegen, Dept Artificial Intelligence, Donders Ctr Brain Cognit & Behav, Nijmegen, Netherlands.
[Braun, Christoph] Univ Tubingen, MEG Ctr, Tubingen, Germany.
[Braun, Christoph] Univ Trento, Ctr Mind Brain Sci, CIMeC, Trento, Italy.
[Robinson, Stephen E.] NIMH, MEG Core Facil, Bethesda, MD 20892 USA.
RP Soekadar, SR (reprint author), Univ Tubingen Hosp, Dept Psychiat & Psychotherapy, Appl Neurotechnol Lab, Calwerstr 14, D-72076 Tubingen, Germany.
EM surjo.soekadar@uni-tuebingen.de
NR 54
TC 7
Z9 7
U1 14
U2 14
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
EI 1095-9572
J9 NEUROIMAGE
JI Neuroimage
PD OCT
PY 2016
VL 140
BP 89
EP 98
DI 10.1016/j.neuroimage.2015.10.024
PG 10
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA DX0RK
UT WOS:000384071900011
PM 26481671
ER
PT J
AU Forthun, I
Wilcox, AJ
Strandberg-Larsen, K
Moster, D
Nohr, EA
Lie, RT
Suren, P
Tollanes, MC
AF Forthun, Ingeborg
Wilcox, Allen J.
Strandberg-Larsen, Katrine
Moster, Dag
Nohr, Ellen A.
Lie, Rolv Terje
Suren, Pal
Tollanes, Mette C.
TI Maternal Prepregnancy BMI and Risk of Cerebral Palsy in Offspring
SO PEDIATRICS
LA English
DT Article
ID AUTISM SPECTRUM DISORDERS; MEDICAL BIRTH REGISTRY; FOLIC-ACID
SUPPLEMENTS; OBESITY; COHORT; CHILDREN; SURVEILLANCE; INFLAMMATION;
METAANALYSIS; PREVALENCE
AB OBJECTIVES: To investigate the association between maternal pre-pregnancy BMI and risk of cerebral palsy (CP) in offspring.
METHODS: The study population consisted of 188 788 children in the Mothers and Babies in Norway and Denmark CP study, using data from 2 population-based, prospective birth cohorts: the Norwegian Mother and Child Cohort Study and the Danish National Birth Cohort. Prepregnancy BMI was classified as underweight (BMI <18.5), lower normal weight (BMI 18.5-22.9), upper normal weight (BMI 23.0-24.9), overweight (BMI 25.0-29.9), and obese (BMI >= 30). CP diagnoses were obtained from the national CP registries. Associations between maternal prepregnancy BMI and CP in offspring were investigated by using log-binomial regression models.
RESULTS: The 2 cohorts had 390 eligible cases of CP (2.1 per 1000 live-born children). Compared with mothers in the lower normal weight group, mothers in the upper normal group had a 40% excess risk of having a child with CP (relative risk [RR], 1.35; 95% confidence interval [CI], 1.03-1.78). Excess risk was 60% (RR, 1.56; 95% CI, 1.21-2.01) for overweight mothers and 60% (RR, 1.55; 95% CI 1.11-2.18) for obese mothers. The risk of CP increased similar to 4% for each unit increase in BMI (RR, 1.04; 95% CI, 1.02-1.06). Estimates changed little with adjustment for mother's occupational status, age, and smoking habits.
CONCLUSIONS: Higher prepregnancy maternal BMI was associated with increased risk of CP in offspring.
C1 [Forthun, Ingeborg; Moster, Dag; Lie, Rolv Terje; Tollanes, Mette C.] Univ Bergen, Dept Global Publ Hlth & Primary Care, PB 7804, N-5020 Bergen, Norway.
[Forthun, Ingeborg; Moster, Dag] Haukeland Hosp, Dept Pediat, Bergen, Norway.
[Wilcox, Allen J.] Natl Inst Environm Hlth Sci, Epidemiol Branch, NIH, Durham, NC USA.
[Strandberg-Larsen, Katrine] Univ Copenhagen, Dept Publ Hlth, Sect Social Med, Copenhagen, Denmark.
[Moster, Dag; Suren, Pal; Tollanes, Mette C.] Norwegian Inst Publ Hlth, Oslo, Norway.
[Nohr, Ellen A.] Univ Southern Denmark, Inst Clin Res, Res Unit Gynaecol & Obstet, Odense, Denmark.
RP Forthun, I (reprint author), Univ Bergen, Dept Global Publ Hlth & Primary Care, PB 7804, N-5020 Bergen, Norway.
EM ingeborg.forthun@uib.no
OI Wilcox, Allen/0000-0002-3376-1311
FU Norwegian Ministry of Health; Norwegian Ministry of Education and
Research; National Institutes of Health (NIH)/National Institute of
Environmental Health Sciences [N01-ES-75558]; NIH/National Institute of
Neurological Disorders and Stroke [U01 NS 047537-01, U01 NS
047537-06A1]; Pharmacy Foundation; Egmont Foundation; March of Dimes
Birth Defects Foundation; Augustinus Foundation; Health Foundation;
Western Norwegian Regional Health Authority; Intramural Research Program
at the National Institute of Environmental Health Sciences, NIH;
Norwegian Institute of Public Health; University of Copenhagen; Aarhus
University; National Institutes of Health (NIH)
FX The Norwegian Mother and Child Cohort Study is supported by the
Norwegian Ministry of Health and the Ministry of Education and Research,
the National Institutes of Health (NIH)/National Institute of
Environmental Health Sciences (contract N01-ES-75558), NIH/National
Institute of Neurological Disorders and Stroke (grants U01 NS 047537-01
and U01 NS 047537-06A1). The Danish National Research Foundation has
established the Danish Epidemiology Science Centre that initiated and
created the Danish National Birth Cohort. The cohort is furthermore a
result of a major grant from this foundation. Additional support for the
Danish National Birth Cohort is obtained from the Pharmacy Foundation,
the Egmont Foundation, the March of Dimes Birth Defects Foundation, the
Augustinus Foundation, and the Health Foundation. The analyses presented
in this article were funded by the Western Norwegian Regional Health
Authority and by the Intramural Research Program at the National
Institute of Environmental Health Sciences, NIH. In addition, the
Norwegian Institute of Public Health, the University of Copenhagen, and
Aarhus University contributed to the funding by paying for data files
and linkage to registries, and providing administrative support. Funded
by the National Institutes of Health (NIH).
NR 35
TC 1
Z9 1
U1 7
U2 7
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
EI 1098-4275
J9 PEDIATRICS
JI Pediatrics
PD OCT
PY 2016
VL 138
IS 4
AR e20160874
DI 10.1542/peds.2016-0874
PG 9
WC Pediatrics
SC Pediatrics
GA DX3ZT
UT WOS:000384317700031
ER
PT J
AU Li, KG
Haynie, D
Lipsky, L
Iannotti, RJ
Pratt, C
Simons-Morton, B
AF Li, Kaigang
Haynie, Denise
Lipsky, Leah
Iannotti, Ronald J.
Pratt, Charlotte
Simons-Morton, Bruce
TI Changes in Moderate-to-Vigorous Physical Activity Among Older
Adolescents
SO PEDIATRICS
LA English
DT Article
ID SEDENTARY BEHAVIOR; UNITED-STATES; PATTERNS; TRANSITION; OVERWEIGHT;
ADULTHOOD; CHILDREN; WEIGHT; YOUTH; GIRLS
AB OBJECTIVES: Examined patterns and determinants of objectively measured moderate-to-vigorous physical activity (MVPA) over 4 years in US emerging adults.
METHODS: Waves 1 through 4 (W1 [10th grade] to W4 data of a national cohort starting in 2010 (N = 561; 16.19 +/- 0.51 years) were used. MVPA was assessed annually from accelerometers; BMI calculated from measured height/weight; and surveys ascertained self-reported physical activity (PA) planning, peer PA, family support, W1 sociodemographics, W4 school status, W4 residence, and W4 employment. Latent growth modeling estimated trajectories in log-transformed duration (minutes/day) of MVPA and associations with covariates.
RESULTS: Less than 9% of participants met the recommended 60+ minutes/day MVPA across W1 through W4. W1 MVPA was greater in males versus females (B = 0.46, P < .001) and Hispanic versus White (B = 0.34, P < .001) participants. Increased BMI change (W1 to W4 slope) was associated with decreased MVPA. MVPA was positively associated with PA planning (W1-W3: B = 0.10, B = 0.06, B = 0.08, Ps < .05), but not with peer PA or family support. Participants attending 4-year college versus not-attending school (B = 0.52, P < .001), and college students living on campus versus at home (B = 0.37, P < .001) were more likely to engage in MVPA at W4. Weekend MVPA remained relatively constant from W1 through W4.
CONCLUSIONS: High-school students engaged in little MVPA and maintained this low level through the transition to adulthood. Emerging adults' MVPA engagement may vary according to social contexts. Those with high BMI may benefit most from interventions to promote MVPA.
C1 [Li, Kaigang] Colorado State Univ, Dept Hlth & Exercise Sci, B 215E Moby Complex, Ft Collins, CO 80523 USA.
[Haynie, Denise; Lipsky, Leah; Simons-Morton, Bruce] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Intramural Populat Hlth Res, Bethesda, MD USA.
[Iannotti, Ronald J.] CDM Grp Inc, Bethesda, MD USA.
[Pratt, Charlotte] NHLBI, Div Cardiovasc Sci, Bldg 10, Bethesda, MD 20892 USA.
RP Li, KG (reprint author), Colorado State Univ, Dept Hlth & Exercise Sci, B 215E Moby Complex, Ft Collins, CO 80523 USA.
EM kaigang.li@colostate.edu
RI Dey, Kamalesh/E-6568-2017;
OI Simons-Morton, Bruce/0000-0003-1099-6617; Haynie,
Denise/0000-0002-8270-6079; Lipsky, Leah/0000-0003-2645-4388
FU Intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development [HHSN275201200001I];
National Heart, Lung, and Blood Institute; National Institute on Alcohol
Abuse and Alcoholism; National Institute on Drug Abuse; Maternal and
Child Health Bureau of the Health Resources and Services Administration;
National Institutes of Health (NIH)
FX This project (contract HHSN275201200001I) was supported in part by the
Intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development; the National Heart,
Lung, and Blood Institute; the National Institute on Alcohol Abuse and
Alcoholism; the National Institute on Drug Abuse; and the Maternal and
Child Health Bureau of the Health Resources and Services Administration.
Funded by the National Institutes of Health (NIH).
NR 36
TC 0
Z9 0
U1 9
U2 9
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
EI 1098-4275
J9 PEDIATRICS
JI Pediatrics
PD OCT
PY 2016
VL 138
IS 4
AR e20161372
DI 10.1542/peds.2016-1372
PG 10
WC Pediatrics
SC Pediatrics
GA DX3ZT
UT WOS:000384317700042
ER
PT J
AU Sheftall, AH
Asti, L
Horowitz, LM
Felts, A
Fontanella, CA
Campo, JV
Bridge, JA
AF Sheftall, Arielle H.
Asti, Lindsey
Horowitz, Lisa M.
Felts, Adrienne
Fontanella, Cynthia A.
Campo, John V.
Bridge, Jeffrey A.
TI Suicide in Elementary School-Aged Children and Early Adolescents
SO PEDIATRICS
LA English
DT Article
ID DEATH REPORTING SYSTEM; PREVENTION PROGRAM; COMPLETED SUICIDE;
PRIMARY-CARE; YOUTH SUICIDE; RISK-FACTORS; 16 STATES; BEHAVIOR;
CHILDHOOD; INTERVENTIONS
AB BACKGROUND AND OBJECTIVES: Suicide in elementary school-aged children is not well studied, despite a recent increase in the suicide rate among US black children. The objectives of this study were to describe characteristics and precipitating circumstances of suicide in elementary school-aged children relative to early adolescent decedents and identify potential within-group racial differences.
METHODS: We analyzed National Violent Death Reporting System (NVDRS) surveillance data capturing suicide deaths from 2003 to 2012 for 17 US states. Participants included all suicide decedents aged 5 to 14 years (N = 693). Age group comparisons (5-11 years and 12-14 years) were conducted by using the chi(2) test or Fisher's exact test, as appropriate.
RESULTS: Compared with early adolescents who died by suicide, children who died by suicide were more commonly male, black, died by hanging/strangulation/suffocation, and died at home. Children who died by suicide more often experienced relationship problems with family members/friends (60.3% vs 46.0%; P = .02) and less often experienced boyfriend/girlfriend problems (0% vs 16.0%; P < .001) or left a suicide note (7.7% vs 30.2%; P < .001). Among suicide decedents with known mental health problems (n = 210), childhood decedents more often experienced attention-deficit disorder with or without hyperactivity (59.3% vs 29.0%; P = .002) and less often experienced depression/dysthymia (33.3% vs 65.6%; P = .001) compared with early adolescent decedents.
CONCLUSIONS: These findings raise questions about impulsive responding to psychosocial adversity in younger suicide decedents, and they suggest a need for both common and developmentally-specific suicide prevention strategies during the elementary school-aged and early adolescent years. Further research should investigate factors associated with the recent increase in suicide rates among black children.
C1 [Sheftall, Arielle H.; Felts, Adrienne; Bridge, Jeffrey A.] Ohio State Univ, Coll Med, Res Inst, Nationwide Childrens Hosp, Columbus, OH 43210 USA.
[Fontanella, Cynthia A.; Campo, John V.] Ohio State Univ, Coll Med, Dept Psychiat, Columbus, OH 43210 USA.
[Bridge, Jeffrey A.] Ohio State Univ, Coll Med, Dept Pediat, Columbus, OH 43210 USA.
[Asti, Lindsey] Johns Hopkins Univ, Sch Publ Hlth, Dept Int Hlth, Baltimore, MD USA.
[Horowitz, Lisa M.] NIMH, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
RP Bridge, JA (reprint author), Nationwide Childrens Hosp, Res Inst, Ctr Innovat Pediat Practice, 700 Childrens Dr, Columbus, OH 43205 USA.
EM jeff.bridge@nationwidechildrens.org
FU National Institute of Mental Health, National Institutes of Health
[R01-MH093552]; Centers for Disease Control and Prevention
[R01-CE002129]; National Institutes of Health (NIH)
FX All phases of the study were supported by grant R01-MH093552 from the
National Institute of Mental Health, National Institutes of Health, and
grant R01-CE002129 from the Centers for Disease Control and Prevention.
Supported by the National Institutes of Health (NIH).
NR 55
TC 0
Z9 0
U1 14
U2 14
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
EI 1098-4275
J9 PEDIATRICS
JI Pediatrics
PD OCT
PY 2016
VL 138
IS 4
AR e20160436
DI 10.1542/peds.2016-0436
PG 10
WC Pediatrics
SC Pediatrics
GA DX3ZT
UT WOS:000384317700021
ER
PT J
AU Calogero, JP
Frecker, MI
Hasnain, Z
Hubbard, JE
AF Calogero, J. P.
Frecker, M. I.
Hasnain, Z.
Hubbard, J. E., Jr.
TI A dynamic spar numerical model for passive shape change
SO SMART MATERIALS AND STRUCTURES
LA English
DT Article
DE contact-aided compliant mechanism; passive shape change; flapping wing
morphing; constraint dynamics
ID COMPLIANT MECHANISMS; WINGS; DESIGN
AB A three-dimensional constraint-driven dynamic rigid-link numerical model of a flapping wing structure with compliant joints (CJs) called the dynamic spar numerical model is introduced and implemented. CJs are modeled as spherical joints with distributed mass and spring-dampers with coupled nonlinear spring and damping coefficients, which models compliant mechanisms spatially distributed in the structure while greatly reducing computation time compared to a finite element model. The constraints are established, followed by the formulation of a state model used in conjunction with a forward time integrator, an experiment to verify a rigid-link assumption and determine a flapping angle function, and finally several example runs. Modeling the CJs as coupled bi-linear springs shows the wing is able to flex more during upstroke than downstroke. Coupling the spring stiffnesses allows an angular deformation about one axis to induce an angular deformation about another axis, where the magnitude is proportional to the coupling term. Modeling both the leading edge and diagonal spars shows that the diagonal spar changes the kinematics of the leading edge spar verses only considering the leading edge spar, causing much larger axial rotations in the leading edge spar. The kinematics are very sensitive to CJ location, where moving the CJ toward the wing root causes a stronger response, and adding multiple CJs on the leading edge spar with a CJ on the diagonal spar allows the wing to deform with larger magnitude in all directions. This model lays a framework for a tool which can be used to understand flapping wing flight.
C1 [Calogero, J. P.; Frecker, M. I.] Penn State Univ, Dept Mech & Nucl Engn, University Pk, PA 16802 USA.
[Hasnain, Z.; Hubbard, J. E., Jr.] Univ Maryland, Dept Aerosp Engn, Hampton, VA USA.
[Hasnain, Z.; Hubbard, J. E., Jr.] NIA, Hampton, VA USA.
RP Calogero, JP (reprint author), Penn State Univ, Dept Mech & Nucl Engn, University Pk, PA 16802 USA.
EM jc7@psu.edu
FU Air Force Office of Scientific Research (AFOSR) [FA9550-13-0126]
FX The authors gratefully acknowledge the support of the Air Force Office
of Scientific Research (AFOSR), grant number FA9550-13-0126 under the
direction of Dr David Stargel. We would like to thank James Lankford and
Kaleb Bordner from the Alfred Gessow Rotorcraft Center at The University
of Maryland for allowing us to use their facility and aiding us in the
experiment. The resources of the NASA Langley Research Center, The
Pennsylvania State University, University of Maryland and Morpheus Lab
are also appreciated. The first author would like to acknowledge Dr H J
Sommer for helping to understand the forward dynamic constraint method.
NR 48
TC 0
Z9 0
U1 4
U2 4
PU IOP PUBLISHING LTD
PI BRISTOL
PA TEMPLE CIRCUS, TEMPLE WAY, BRISTOL BS1 6BE, ENGLAND
SN 0964-1726
EI 1361-665X
J9 SMART MATER STRUCT
JI Smart Mater. Struct.
PD OCT
PY 2016
VL 25
IS 10
AR 104006
DI 10.1088/0964-1726/25/10/104006
PG 16
WC Instruments & Instrumentation; Materials Science, Multidisciplinary
SC Instruments & Instrumentation; Materials Science
GA DX0XG
UT WOS:000384089200006
ER
PT J
AU Miller, S
Suppes, T
Mintz, J
Hellemann, G
Frye, MA
McElroy, SL
Nolen, WA
Kupka, R
Leverich, GS
Grunze, H
Altshuler, LL
Keck, PE
Post, RM
AF Miller, Shefali
Suppes, Trisha
Mintz, Jim
Hellemann, Gerhard
Frye, Mark A.
McElroy, Susan L.
Nolen, Willem A.
Kupka, Ralph
Leverich, Gabriele S.
Grunze, Heinz
Altshuler, Lori L.
Keck, Paul E., Jr.
Post, Robert M.
TI Mixed Depression in Bipolar Disorder: Prevalence Rate and Clinical
Correlates During Naturalistic Follow-Up in the Stanley Bipolar Network
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID MANIC SYMPTOMS; AGITATED DEPRESSION; STATE; EPISODES; SYMPTOMATOLOGY;
PHENOMENOLOGY; INVENTORY; DIAGNOSIS
AB Objective: DSM-5 introduced the "with mixed features" specifier for major depressive episodes. The authors assessed the prevalence and phenomenology of mixed depression among bipolar disorder patients and qualitatively compared a range of diagnostic thresholds for mixed depression.
Method: In a naturalistic study, 907 adult outpatients with bipolar disorder participating in the Stanley Foundation Bipolar Network were followed longitudinally across 14,310 visits from 1995 to 2002. The Inventory of Depressive Symptomatology-Clinician-Rated Version (IDS-C) and the Young Mania Rating Scale (YMRS) were administered at each visit.
Results: Mixed depression, defined as an IDS-C score >= 15 and a YMRS score >2 and <12 at the same visit, was observed in 2,139 visits (14.9% of total visits, and 43.5% of visits with depression) by 584 patients (64.4% of all patients). Women were significantly more Likely than men to experience subthreshold hypomania during visits with depression (40.7% compared with 34.4%). Patients with one or more mixed depression visits had more symptomatic visits and fewer euthymic visits compared with those with no mixed depression visits. DSM-5-based definitions of mixed depression (ranging from narrower definitions requiring >= 3 non overlapping YMRS items concurrent with an IDS-C score >= 15 to broader definitions requiring >= 2 nonoverlapping YMRS items) yielded lower mixed depression prevalence rates (6.3% and 10.8% of visits, respectively) but were found to have similar relationships to gender and longitudinal symptom severity.
Conclusions: Among outpatients with bipolar disorder, concurrent hypomanic symptoms observed during visits with depression were common, particularly in women. The DSM-5 diagnostic criteria for depression with mixed features may yield inadequate sensitivity to detect patients with mixed depression.
C1 [Miller, Shefali] VA Pato Alto Hlth Care Syst, Palo Alto, CA 94304 USA.
Stanford Univ, Med Ctr, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA.
Univ Texas Hlth Sci Ctr San Antonio, Dept Psychiat, San Antonio, TX 78229 USA.
Univ Calif Los Angeles, Dept Psychiat, Los Angeles, CA USA.
Mayo Clin, Dept Psychiat, Rochester, MN USA.
Univ Cincinnati, Lindner Ctr HOPE, Mason, OH USA.
Univ Groningen, Univ Med Ctr Groningen, NL-9700 AB Groningen, Netherlands.
Altrecht Inst Mental Hlth Care, Utrecht, Netherlands.
Vrije Univ Amsterdam, VU Univ Med Ctr Amsterdam, Amsterdam, Netherlands.
NIMH, Biol Psychiat Branch, Bethesda, MD 20892 USA.
Paracelsus Med Univ, Dept Psychiat & Psychotherapy, Salzburg, Austria.
Christian Doppler Klin, Salzburg, Austria.
George Washington Univ, Sch Med & Hlth Sci, Washington, DC 20052 USA.
RP Miller, S (reprint author), VA Pato Alto Hlth Care Syst, Palo Alto, CA 94304 USA.
EM shefalis@stanford.edu
OI Grunze, Heinz/0000-0003-4712-8979
FU Stanley Medical Research Institute; Merck; Sunovion; AztraZeneca; H
Lundbeck; Elan Pharma International; NIMH; VA Cooperative Studies
Program; AssureRx Health; Janssen; Mayo Foundation; Myriad; National
Institute on Alcohol Abuse and Alcoholism; Pfizer; Agency for Heatthcare
Research and Quality; Alkermes; AstraZeneca; Cephalon; Eli Lilly;
Forest; Marriott Foundation; Naurex; Orexigen; Shire; Takeda; Transcept;
Johnson Johnson; National Institute for Health Research; Medical
Research Council; Northumberland; Tyne; Wear National Health Service
Foundation Trust; Otsuka Pharmaceuticals; American College of
Psychiatrists; GlaxoSmithKline; Ferrer; Janssen-Cilag; Lundbeck; Otsuka;
Servier
FX Grant support was provided by the Stanley Medical Research Institute.;
Dr. Miller has received grant support from Merck and Sunovion. Dr.
Suppes has received consulting fees from AztraZeneca, H Lundbeck, Merck,
and Sunovion; she has received research funding from Elan Pharma
International, NIMH, Sunovion, and the VA Cooperative Studies Program;
and she has received royalties from Jones and Bartlett and UpToDate. Dr.
Frye has received grant support from AssureRx Health, Janssen, the Mayo
Foundation, Myriad, the National Institute on Alcohol Abuse and
Alcoholism, NIMH, and Pfizer; he has been a consultant to Janssen,
Mitsubishi Tanabe Pharma, Myriad Genetics, Sunovion, Supernus, and Teva;
and he has received CME and travel support from CME Outfitters and the
American Psychiatric Association. Dr. McElroy is a consultant to or
member of scientific advisory boards of Alkermes, Bracket, Corcept,
Hoffmann-La Roche, MedAvante, Naurex, Novo Nordisk, Shire, Sunovion, and
Teva; she is a principal or coinvestigator on studies sponsored by the
Agency for Heatthcare Research and Quality, Alkermes, AstraZeneca,
Cephalon, Eli Lilly, Forest, the Marriott Foundation, NIMH, Naurex,
Orexigen, Pfizer, Shire, Takeda, and Transcept; and she is named as an
inventor on U.S. Patent No. 6,323,236 B2 (Use of Sulfamate Derivatives
for Treating Impulse Control Disorders), and along with the patent's
assignee, the University of Cincinnati, she has received payments from
Johnson & Johnson, the exclusive rightsholder. Dr. Grunze has received
grants from the National Institute for Health Research, the Medical
Research Council, the Northumberland, Tyne, and Wear National Health
Service Foundation Trust, and Otsuka Pharmaceuticals; he has received
honoraria for speaker bureaus or advisory panels from Bristol-Myers
Squibb, Desitin, Gedeon-Richter, Hoffmann-LaRoche, and Lundbeck; and he
has received honoraria for presenting at sponsored CME activities from
Eli Lilly, Ferrer, Janssen-Cilag, Lundbeck, Otsuka, Pfizer, and Servier.
Dr. Altshuler was on an advisory board for Takeda and Lundbeck and
attended an editorial board meeting sponsored by Sunovion; she received
an honorarium as part of the 2014 Award for Research in Mood Disorders
given by the American College of Psychiatrists; she performed a medical
records review for the law offices of Hughes Socol Piers Resnick and
Dym; and she was principal investigator and coinvestigator on research
studies sponsored by NIMH. Dr. Keck is or has been a principal or
coinvestigator on research studies sponsored by Alkermes, AstraZeneca,
Cephalon, GlaxoSmithKline, Eli Lilly, the Marriott Foundation, NIMH,
Orexigen, Pfizer, and Shire; he has been reimbursed for consulting to
Alkermes, Bristol-Myers Squibb, Forest, Merck, Otsuka, ProPhase, Shire,
Sunovion, Supernus, and Teva; he is listed as a coinventor on U.S.
Patent No. 6,387,956 (Methods of Treating Obsessive-Compulsive Spectrum
Disorders), and he has received no financial gain from this patent. Dr.
Post has been a speaker for AstraZeneca, Sunovion, and Validus. Dr.
Mintz, Dr. Hellemann, Dr. Nolen, Dr. Kupka, and Ms. Leverich report no
financial relationships with commercial interests.
NR 30
TC 1
Z9 1
U1 6
U2 6
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0002-953X
EI 1535-7228
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD OCT
PY 2016
VL 173
IS 10
BP 1015
EP 1023
DI 10.1176/appi.ajp.2016.15091119
PG 9
WC Psychiatry
SC Psychiatry
GA DX1WT
UT WOS:000384158400013
PM 27079133
ER
PT J
AU Preston, KL
Jobes, ML
Phillips, KA
Epstein, DH
AF Preston, Kenzie L.
Jobes, Michelle L.
Phillips, Karran A.
Epstein, David H.
TI Real-time assessment of alcohol drinking and drug use in
opioid-dependent polydrug users
SO BEHAVIOURAL PHARMACOLOGY
LA English
DT Article
DE alcohol; cocaine; craving; drug use; ecological momentary assessment;
heroin; human
ID ECOLOGICAL MOMENTARY ASSESSMENT; SELF-REPORT; COCAINE; HEROIN;
INTERVENTION; CONSUMPTION; PREDICTORS; SYMPTOMS
AB We investigated relationships between drinking, other drug use, and drug craving, using ecological momentary assessment (EMA), in a sample of polydrug users who were not heavy drinkers. In a prospective longitudinal cohort study, 114 heroin and cocaine users on methadone-maintenance treatment carried handheld electronic diaries during waking hours and were screened for drug and alcohol use for up to 25 weeks. Individuals who fulfilled the Diagnostic and Statistical Manual of Mental Disorders criteria for alcohol abuse or dependence were excluded. Participants responded to 2-5 random prompts per day to report on their moods, cravings, and activities and initiated entries when they used or acutely craved heroin or cocaine. Drinking alcohol was assessed in both types of entries. Breath alcohol was measured three times weekly. Participants reported drinking alcohol in 1.6% of random-prompt entries, 3.7% of event-contingent entries when craving cocaine and/or heroin, and 11.6% of eventcontingent entries when using cocaine and/or heroin. Alcohol drinking was also associated with higher craving ratings and prestudy alcohol use. More drinking was detected by ambulatory self-report than by in-clinic breath testing. Even though we had screened out heavy drinkers from our sample of polydrug users, drinking was associated with heroin and cocaine craving and actual use. Copyright (C) 2016 Wolters Kluwer Health, Inc.
C1 [Preston, Kenzie L.; Jobes, Michelle L.; Phillips, Karran A.; Epstein, David H.] NIDA, Clin Pharmacol & Therapeut Res Branch, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Preston, KL (reprint author), NIDA, Intramural Res Program, 251 Bayview Blvd,Suite 200, Baltimore, MD 21224 USA.
EM kpreston@intra.nida.nih.gov
FU National Institute on Drug Abuse Intramural Research Program; Intramural
Research Program, National Institute on Drug Abuse, National Institutes
of Health
FX This work was supported by the National Institute on Drug Abuse
Intramural Research Program.; This study was funded by the Intramural
Research Program, National Institute on Drug Abuse, National Institutes
of Health.
NR 31
TC 0
Z9 0
U1 3
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0955-8810
EI 1473-5849
J9 BEHAV PHARMACOL
JI Behav. Pharmacol.
PD OCT
PY 2016
VL 27
IS 7
BP 579
EP 584
DI 10.1097/FBP.0000000000000250
PG 6
WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy
SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy
GA DW1IW
UT WOS:000383397700003
PM 27579810
ER
PT J
AU Madan, RA
Karzai, FH
Ning, YM
Adesunloye, BA
Huang, X
Harold, N
Couvillon, A
Chun, G
Cordes, L
Sissung, T
Beedie, SL
Dawson, NA
Theoret, MR
McLeod, DG
Rosner, I
Trepel, JB
Lee, MJ
Tomita, Y
Lee, S
Chen, C
Steinberg, SM
Arlen, PM
Gulley, JL
Figg, WD
Dahut, WL
AF Madan, Ravi A.
Karzai, Fatima H.
Ning, Yang-Min
Adesunloye, Bamidele A.
Huang, Xuan
Harold, Nancy
Couvillon, Anna
Chun, Guinevere
Cordes, Lisa
Sissung, Tristan
Beedie, Shaunna L.
Dawson, Nancy A.
Theoret, Marc R.
McLeod, David G.
Rosner, Inger
Trepel, Jane B.
Lee, Min-Jung
Tomita, Yusuke
Lee, Sunmin
Chen, Clara
Steinberg, Seth M.
Arlen, Philip M.
Gulley, James L.
Figg, William D.
Dahut, William L.
TI Phase II trial of docetaxel, bevacizumab, lenalidomide and prednisone in
patients with metastatic castration-resistant prostate cancer
SO BJU INTERNATIONAL
LA English
DT Article
DE prostate cancer; angiogenesis inhibition; combinationation therapy;
metastatic castration resistant prostate cancer; docetaxel coimbination
ID DOUBLE-BLIND; GENE POLYMORPHISMS; MULTIPLE-MYELOMA; TUMOR; CHEMOTHERAPY;
THALIDOMIDE; EFFICACY; PLACEBO; GROWTH; MEN
AB Objective
To determine the safety and clinical efficacy of two anti-angiogenic agents, bevacizumab and lenalidomide, with docetaxel and prednisone.
Patients and methods
Eligible patients with metastatic castration-resistant prostate cancer enrolled in this open-label, phase II study of lenalidomide with bevacizumab (15 mg/kg), docetaxel (75 mg/m(2)) and prednisone (10 mg daily). Docetaxel and bevacizumab were administered on day 1 of a 3-week treatment cycle. To establish safety, lenalidomide dosing in this combination was escalated in a conventional 3 + 3 design (15, 20 and 25 mg daily for 2 weeks followed by 1 week off). Patients received supportive measures including prophylactic pegfilgrastim and enoxaparin. The primary endpoints were safety and clinical efficacy.
Results
A total of 63 patients enrolled in this trial. Toxicities were manageable with most common adverse events (AEs) being haematological, and were ascertained by weekly blood counts. Twenty-nine patients (46%) had grade 4 neutropenia, 20 (32%) had grade 3 anaemia and seven (11%) had grade 3 thrombocytopenia. Despite frequent neutropenia, serious infections were rare. Other common non-haematological grade 3 AEs included fatigue (10%) and diarrhoea (10%). Grade 2 AEs in > 10% of patients included anorexia, weight loss, constipation, osteonecrosis of the jaw, rash and dyspnoea. Of 61 evaluable patients, 57 (93%), 55 (90%) and 33 (54%) had PSA declines of > 30, > 50 and > 90%, respectively. Of the 29 evaluable patients, 24 (86%) had a confirmed radiographic partial response. The median times to progression and overall survival were 18.2 and 24.6 months, respectively.
Conclusions
With appropriate supportive measures, combination angiogenesis inhibition can be safely administered and potentially provide clinical benefit. These hypothesis-generating data would require randomized trials to confirm the findings.
C1 [Madan, Ravi A.; Karzai, Fatima H.; Ning, Yang-Min; Adesunloye, Bamidele A.; Huang, Xuan; Harold, Nancy; Couvillon, Anna; Chun, Guinevere; Cordes, Lisa; Sissung, Tristan; Beedie, Shaunna L.; Theoret, Marc R.; Steinberg, Seth M.; Arlen, Philip M.; Gulley, James L.; Figg, William D.; Dahut, William L.] NCI, Genitourinary Malignancies Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Dawson, Nancy A.] Georgetown Univ, Lombardi Comprehens Canc Ctr, Washington, DC USA.
[McLeod, David G.; Rosner, Inger] Walter Reed Natl Mil Med Ctr, Ctr Prostate Dis Res, Bethesda, MD USA.
[Trepel, Jane B.; Lee, Min-Jung; Tomita, Yusuke; Lee, Sunmin] NCI, Dev Therapeut Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Chen, Clara] NCI, Radiol & Imaging Sci, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Figg, WD (reprint author), Bldg 10 Rm 5A01,10 Ctr Dr, Bethesda, MD 20892 USA.
EM wdfigg@helix.nih.gov
NR 30
TC 2
Z9 2
U1 5
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1464-4096
EI 1464-410X
J9 BJU INT
JI BJU Int.
PD OCT
PY 2016
VL 118
IS 4
BP 590
EP 597
DI 10.1111/bju.13412
PG 8
WC Urology & Nephrology
SC Urology & Nephrology
GA DW8HQ
UT WOS:000383896300020
PM 26780387
ER
PT J
AU Liu, L
Messer, K
Baron, JA
Lieberman, DA
Jacobs, ET
Cross, AJ
Murphy, G
Martinez, ME
Gupta, S
AF Liu, Lin
Messer, Karen
Baron, John A.
Lieberman, David A.
Jacobs, Elizabeth T.
Cross, Amanda J.
Murphy, Gwen
Martinez, Maria Elena
Gupta, Samir
TI A prognostic model for advanced colorectal neoplasia recurrence
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Polyp surveillance; Risk stratification; Epidemiology; Colorectal
cancer; Colorectal polyps
ID GENERALIZED LINEAR-MODELS; SURVEILLANCE COLONOSCOPY;
LOGISTIC-REGRESSION; RISK STRATIFICATION; ADENOMA RECURRENCE; COLON
ADENOMAS; CANCER; PREDICTORS; POLYPECTOMY; TRIAL
AB Following colonoscopic polypectomy, US Multisociety Task Force (USMSTF) guidelines stratify patients based on risk of subsequent advanced neoplasia (AN) using number, size, and histology of resected polyps, but have only moderate sensitivity and specificity. We hypothesized that a state-of-the-art statistical prediction model might improve identification of patients at high risk of future AN and address these challenges.
Data were pooled from seven prospective studies which had follow-up ascertainment of metachronous AN within 3-5 years of baseline polypectomy (combined n = 8,228). Pooled data were randomly split into training (n = 5,483) and validation (n = 2,745) sets. A prognostic model was developed using best practices. Two risk cut-points were identified in the training data which achieved a 10 percentage point improvement in sensitivity and specificity, respectively, over current USMSTF guidelines. Clinical benefit of USMSTF versus model-based risk stratification was then estimated using validation data.
The final model included polyp location, prior polyp history, patient age, and number, size and histology of resected polyps. The first risk cut-point improved sensitivity but with loss of specificity. The second risk cut-point improved specificity without loss of sensitivity (specificity 46.2 % model vs. 42.1 % guidelines, p < 0.001; sensitivity 75.8 % model vs. 74.0 % guidelines, p = 0.64). Estimated AUC was 65 % (95 % CI: 62-69 %).
This model-based approach allows flexibility in trading sensitivity and specificity, which can optimize colonoscopy over- versus underuse rates. Only modest improvements in prognostic power are possible using currently available clinical data. Research considering additional factors such as adenoma detection rate for risk prediction appears warranted.
C1 [Liu, Lin; Messer, Karen; Martinez, Maria Elena] Univ Calif San Diego, Dept Family Med & Publ Hlth, Div Biostat & Bioinformat, La Jolla, CA 92093 USA.
[Liu, Lin; Messer, Karen; Martinez, Maria Elena; Gupta, Samir] Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA 92093 USA.
[Baron, John A.] Univ N Carolina, Sch Med, Dept Med, Chapel Hill, NC USA.
[Lieberman, David A.] Vet Affairs Med Ctr, Div Gastroenterol & Hepatol, Portland, OR USA.
[Lieberman, David A.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Jacobs, Elizabeth T.] Univ Arizona, Ctr Canc, Arizona Coll Publ Hlth, Tucson, AZ USA.
[Cross, Amanda J.] Imperial Coll London, Sch Publ Hlth, Dept Epidemiol & Biostat, London, England.
[Cross, Amanda J.] Imperial Coll London, Dept Surg & Canc, Canc Screening & Prevent Res Grp, London, England.
[Murphy, Gwen] NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Rockville, MD USA.
[Gupta, Samir] Vet Affairs San Diego Healthcare Syst, 3350 La Jolla Village Dr,MC 111D, San Diego, CA 92161 USA.
[Gupta, Samir] Univ Calif San Diego, Dept Internal Med, Div Gastroenterol, La Jolla, CA 92093 USA.
RP Gupta, S (reprint author), Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA 92093 USA.; Gupta, S (reprint author), Vet Affairs San Diego Healthcare Syst, 3350 La Jolla Village Dr,MC 111D, San Diego, CA 92161 USA.; Gupta, S (reprint author), Univ Calif San Diego, Dept Internal Med, Div Gastroenterol, La Jolla, CA 92093 USA.
EM s1gupta@ucsd.edu
FU Public Health Service Grants from the National Cancer Institute
[CA-41108, CA-23074, CA95060, CA37287, CA104869, CA23108, CA59005,
CA26852, 5R01CA155293]; Cooperative Studies Program, Department of
Veterans Affairs; UCSD Department of Family Medicine and Public Health;
United States Department of Veterans Affairs Health Services Research
and Development Service of the VA Office of Research and Development [1
I01 HX001574-01A1]
FX This work was supported in part by Public Health Service Grants,
CA-41108, CA-23074, CA95060, CA37287, CA104869, CA23108, CA59005,
CA26852, and 5R01CA155293 from the National Cancer Institute. Funding
for the Veteran's Affairs Study was supported by the Cooperative Studies
Program, Department of Veterans Affairs. The project described was also
supported by a pilot grant from the UCSD Department of Family Medicine
and Public Health (Liu, PI), as well as in part by Merit Review Award
number 1 I01 HX001574-01A1 (Gupta, PI) from the United States Department
of Veterans Affairs Health Services Research and Development Service of
the VA Office of Research and Development. The views expressed in this
article are those of the author(s) and do not necessarily represent the
views of the Department of Veterans Affairs.
NR 49
TC 0
Z9 0
U1 4
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
EI 1573-7225
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD OCT
PY 2016
VL 27
IS 10
BP 1175
EP 1185
DI 10.1007/s10552-016-0795-5
PG 11
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA DW6MY
UT WOS:000383766500001
PM 27517467
ER
PT J
AU Mazul, AL
Siega-Riz, AM
Weinberg, CR
Engel, SM
Zou, F
Carrier, KS
Basta, PV
Vaksman, Z
Maris, JM
Diskin, SJ
Maxen, C
Naranjo, A
Olshan, AF
AF Mazul, Angela L.
Siega-Riz, Anna Maria
Weinberg, Clarice R.
Engel, Stephanie M.
Zou, Fei
Carrier, Kathryn S.
Basta, Patricia V.
Vaksman, Zalman
Maris, John M.
Diskin, Sharon J.
Maxen, Charlene
Naranjo, Arlene
Olshan, Andrew F.
TI A family-based study of gene variants and maternal folate and choline in
neuroblastoma: a report from the Children's Oncology Group
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Neuroblastoma; Genetics; Folate; Choline; Case-parent triad
ID NEURAL-TUBE DEFECTS; GENOME-WIDE ASSOCIATION; CASE-PARENT TRIADS; ACUTE
LYMPHOBLASTIC-LEUKEMIA; FOLIC-ACID; RISK; CANCER; POLYMORPHISMS;
METAANALYSIS; SUSCEPTIBILITY
AB Neuroblastoma is a childhood cancer of the sympathetic nervous system with embryonic origins. Previous epidemiologic studies suggest maternal vitamin supplementation during pregnancy reduces the risk of neuroblastoma. We hypothesized offspring and maternal genetic variants in folate-related and choline-related genes are associated with neuroblastoma and modify the effects of maternal intake of folate, choline, and folic acid.
The Neuroblastoma Epidemiology in North America (NENA) study recruited 563 affected children and their parents through the Children's Oncology Group's Childhood Cancer Research Network. We used questionnaires to ascertain pre-pregnancy supplementation and estimate usual maternal dietary intake of folate, choline, and folic acid. We genotyped 955 genetic variants related to folate or choline using DNA extracted from saliva samples and used a log-linear model to estimate both child and maternal risk ratios and stratum-specific risk ratios for gene-environment interactions.
Overall, no maternal or offspring genotypic results met criteria for a false discovery rate (FDR) Q-value < 0.2. Associations were also null for gene-environment interaction with pre-pregnancy vitamin supplementation, dietary folic acid, and folate. FDR-significant gene-choline interactions were found for offspring SNPs rs10489810 and rs9966612 located in MTHFD1L and TYMS, respectively, with maternal choline dietary intake dichotomized at the first quartile.
These results suggest that variants related to one-carbon metabolism are not strongly associated with neuroblastoma. Choline-related variants may play a role; however, the functional consequences of the interacting variants are unknown and require independent replication.
C1 [Mazul, Angela L.; Siega-Riz, Anna Maria; Engel, Stephanie M.; Carrier, Kathryn S.; Basta, Patricia V.; Olshan, Andrew F.] Univ N Carolina, Gillings Sch Global Publ Hlth, Dept Epidemiol, Campus Box 7435,2106 McGavran Greenberg Hall, Chapel Hill, NC 27599 USA.
[Siega-Riz, Anna Maria] Univ N Carolina, Gillings Sch Global Publ Hlth, Dept Nutr, Chapel Hill, NC USA.
[Weinberg, Clarice R.] NIEHS, Biostat & Computat Biol Branch, POB 12233, Res Triangle Pk, NC 27709 USA.
[Zou, Fei] Univ N Carolina, Gillings Sch Global Publ Hlth, Dept Biostat, Chapel Hill, NC USA.
[Basta, Patricia V.] Univ N Carolina, Biospecimen Proc Ctr, Chapel Hill, NC USA.
[Vaksman, Zalman; Maris, John M.; Diskin, Sharon J.] Childrens Hosp Philadelphia, Div Oncol, Philadelphia, PA 19104 USA.
[Vaksman, Zalman; Maris, John M.; Diskin, Sharon J.] Childrens Hosp Philadelphia, Ctr Childhood Canc Res, Philadelphia, PA 19104 USA.
[Vaksman, Zalman] Childrens Hosp Philadelphia, Dept Biomed & Hlth Informat, Philadelphia, PA 19104 USA.
[Maris, John M.; Diskin, Sharon J.] Univ Penn, Dept Pediat, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Maxen, Charlene] Akron Childrens Hosp, Showers Ctr Childhood Canc & Blood Disorder, Akron, OH USA.
[Naranjo, Arlene] Univ Florida, Coll Med, Dept Biostat, Gainesville, FL USA.
[Naranjo, Arlene] Univ Florida, Coll Publ Hlth & Hlth Profess, Dept Biostat, Gainesville, FL USA.
RP Mazul, AL (reprint author), Univ N Carolina, Gillings Sch Global Publ Hlth, Dept Epidemiol, Campus Box 7435,2106 McGavran Greenberg Hall, Chapel Hill, NC 27599 USA.
EM amazul@unc.edu
FU National Cancer Institute [R01 CA 132887, R01 CA124709]; Lineberger
Cancer Control Education Program [R25 CA57726]
FX This research was supported in part by two grants from the National
Cancer Institute (R01 CA 132887 and R01 CA124709) and the Lineberger
Cancer Control Education Program (R25 CA57726).
NR 47
TC 0
Z9 0
U1 6
U2 6
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
EI 1573-7225
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD OCT
PY 2016
VL 27
IS 10
BP 1209
EP 1218
DI 10.1007/s10552-016-0799-1
PG 10
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA DW6MY
UT WOS:000383766500004
PM 27541142
ER
PT J
AU Dayan, E
Thompson, RM
Buch, ER
Cohen, LG
AF Dayan, Eran
Thompson, Ryan M.
Buch, Ethan R.
Cohen, Leonardo G.
TI 3D-printed head models for navigated non-invasive brain stimulation
SO CLINICAL NEUROPHYSIOLOGY
LA English
DT Letter
C1 [Dayan, Eran; Thompson, Ryan M.; Buch, Ethan R.; Cohen, Leonardo G.] NINDS, Human Cort Physiol & Neurorehabil Sect, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
RP Dayan, E; Cohen, LG (reprint author), NINDS, Human Cort Physiol & Neurorehabil Sect, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
EM eran_dayan@med.unc.edu; cohenl@ninds.nih.gov
FU Intramural NIH HHS [Z99 NS999999]
NR 6
TC 0
Z9 0
U1 5
U2 5
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 1388-2457
EI 1872-8952
J9 CLIN NEUROPHYSIOL
JI Clin. Neurophysiol.
PD OCT
PY 2016
VL 127
IS 10
BP 3341
EP 3342
DI 10.1016/j.clinph.2016.08.011
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA DX0BU
UT WOS:000384027300020
PM 27614003
ER
PT J
AU Shope, JT
Zakrajsek, JS
Finch, S
Bingham, CR
O'Neil, J
Yano, S
Wasserman, R
Simons-Morton, B
AF Shope, Jean T.
Zakrajsek, Jennifer S.
Finch, Stacia
Bingham, C. Raymond
O'Neil, Joseph
Yano, Stephen
Wasserman, Richard
Simons-Morton, Bruce
TI Translation to Primary Care of an Effective Teen Safe Driving Program
for Parents
SO CLINICAL PEDIATRICS
LA English
DT Article
DE translation of evidence-based injury prevention; brief intervention
study; teen driving; traffic accidents; Checkpoints(TM) program;
adolescent risk taking; parents; primary care; Graduated Driver
Licensing
ID INJURY-PREVENTION; DRIVER EDUCATION; INTERVENTION; HEALTH; RISK;
PEDIATRICS; ISSUES; LIMITS; CHILD
AB Addressing teen driver crashes, this study adapted an effective Checkpoints(TM) program for parents of teen drivers for dissemination by primary care practitioners (PCPs) and the web; distributed the PCP/web program through pediatric practices; and examined dissemination to/implementation by parents. The website, youngDRIVERparenting.org, and brief intervention protocol were developed. PCPs delivered interventions and materials to parents, referred them to the website, and completed follow-up surveys. Google Analytics assessed parents' website use. Most PCPs reported delivering interventions with fidelity, and thought the program important and feasible. Brief interventions/website referrals, averaging 4.4 minutes, were delivered to 3465 (87%) of 3990 eligible parents by 133 PCPs over an 18-week average. Website visits (1453) were made by 42% of parents, who spent on average 3:53 minutes viewing 4.2 topics. This program costs little (its website, training and promotional materials are available) and could be one component of a comprehensive approach to reducing teen driver crashes.
C1 [Shope, Jean T.; Zakrajsek, Jennifer S.; Bingham, C. Raymond] Univ Michigan, Transportat Res Inst, 2901 Baxter Rd, Ann Arbor, MI 48109 USA.
[Finch, Stacia; Wasserman, Richard] Amer Acad Pediat, Elk Grove Village, IL USA.
[O'Neil, Joseph] Riley Hosp Children, Indianapolis, IN USA.
[Yano, Stephen] Childrens Med Associates Inc, Aiea, HI USA.
[Wasserman, Richard] Univ Vermont, Coll Med, Burlington, VT USA.
[Simons-Morton, Bruce] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
RP Shope, JT (reprint author), Univ Michigan, Transportat Res Inst, 2901 Baxter Rd, Ann Arbor, MI 48109 USA.
EM jshope@umich.edu
OI Simons-Morton, Bruce/0000-0003-1099-6617
FU Centers for Disease Control and Prevention's National Center for Injury
Prevention and Control [1R18CE001730]; HRSA MCHB [HRSA 5-UA6-10-001];
American Academy of Pediatrics (AAP); National Institutes of Health
[UL1TR000005]
FX The author(s) disclosed receipt of the following financial support for
the research, authorship, and/or publication of this article: The study
was funded by a grant (1R18CE001730) from the Centers for Disease
Control and Prevention's National Center for Injury Prevention and
Control. The Pediatric Research in Office Settings (PROS) Network
receives core funding from the HRSA MCHB (HRSA 5-UA6-10-001) and the
American Academy of Pediatrics (AAP). Pediatric PittNet is supported by
the National Institutes of Health grant number UL1TR000005.
NR 24
TC 0
Z9 0
U1 4
U2 4
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0009-9228
EI 1938-2707
J9 CLIN PEDIATR
JI Clin. Pediatr.
PD OCT
PY 2016
VL 55
IS 11
BP 1026
EP 1035
DI 10.1177/0009922816665086
PG 10
WC Pediatrics
SC Pediatrics
GA DW1EQ
UT WOS:000383386200005
PM 27630004
ER
PT J
AU Cook, AJ
Delong, E
Murray, DM
Vollmer, WM
Heagerty, PJ
AF Cook, Andrea J.
Delong, Elizabeth
Murray, David M.
Vollmer, William M.
Heagerty, Patrick J.
TI Statistical lessons learned for designing cluster randomized pragmatic
clinical trials from the NIH Health Care Systems Collaboratory
Biostatistics and Design Core
SO CLINICAL TRIALS
LA English
DT Article; Proceedings Paper
CT 8th Annual Symposium on Statistical Issues in Clinical Trials
CY APR, 2015
CL Univ Penn, Philadelphia, PA
HO Univ Penn
DE Pragmatic clinical trials; cluster-randomized; group randomized;
electronic health record; NIH Collaboratory
ID COVARIATE ADJUSTMENT; LONGITUDINAL DATA; BREAKING; OUTCOMES; MATCHES;
MODELS; SIZE
AB Background/aims: Pragmatic clinical trials embedded within health care systems provide an important opportunity to evaluate new interventions and treatments. Networks have recently been developed to support practical and efficient studies. Pragmatic trials will lead to improvements in how we deliver health care and promise to more rapidly translate research findings into practice.
Methods: The National Institutes of Health (NIH) Health Care Systems Collaboratory was formed to conduct pragmatic clinical trials and to cultivate collaboration across research areas and disciplines to develop best practices for future studies. Through a two-stage grant process including a pilot phase (UH2) and a main trial phase (UH3), investigators across the Collaboratory had the opportunity to work together to improve all aspects of these trials before they were launched and to address new issues that arose during implementation. Seven Cores were created to address the various considerations, including Electronic Health Records; Phenotypes, Data Standards, and Data Quality; Biostatistics and Design Core; Patient-Reported Outcomes; Health Care Systems Interactions; Regulatory/Ethics; and Stakeholder Engagement. The goal of this article is to summarize the Biostatistics and Design Core's lessons learned during the initial pilot phase with seven pragmatic clinical trials conducted between 2012 and 2014.
Results: Methodological issues arose from the five cluster-randomized trials, also called group-randomized trials, including consideration of crossover and stepped wedge designs. We outlined general themes and challenges and proposed solutions from the pilot phase including topics such as study design, unit of randomization, sample size, and statistical analysis. Our findings are applicable to other pragmatic clinical trials conducted within health care systems.
Conclusion: Pragmatic clinical trials using the UH2/UH3 funding mechanism provide an opportunity to ensure that all relevant design issues have been fully considered in order to reliably and efficiently evaluate new interventions and treatments. The integrity and generalizability of trial results can only be ensured if rigorous designs and appropriate analysis choices are an essential part of their research protocols.
C1 [Cook, Andrea J.] Grp Hlth Res Inst, Biostat Unit, 1730 Minor Ave Suite 1600, Seattle, WA 98101 USA.
[Cook, Andrea J.; Heagerty, Patrick J.] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Delong, Elizabeth] Duke Univ, Sch Med, Dept Biostat & Bioinformat, Durham, NC USA.
[Delong, Elizabeth] Duke Clin Res Inst, Durham, NC USA.
[Murray, David M.] NIH, Off Dis Prevent, Div Program Coordinat Planning & Strateg Initiat, Off Director, Bldg 10, Bethesda, MD 20892 USA.
[Vollmer, William M.] Kaiser Permanente Ctr Hlth Res, Portland, OR USA.
RP Cook, AJ (reprint author), Grp Hlth Res Inst, Biostat Unit, 1730 Minor Ave Suite 1600, Seattle, WA 98101 USA.
EM cook.aj@ghc.org
FU NCCIH NIH HHS [UH2 AT007782, U54 AT007748, UH2 AT007755, UH2 AT007766,
UH2 AT007769, UH2 AT007784, UH2 AT007788, UH2 AT007797]; NCI NIH HHS
[UH3 CA188640]
NR 38
TC 1
Z9 1
U1 8
U2 8
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1740-7745
EI 1740-7753
J9 CLIN TRIALS
JI Clin. Trials
PD OCT
PY 2016
VL 13
IS 5
BP 504
EP 512
DI 10.1177/1740774516646578
PG 9
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA DW1GZ
UT WOS:000383392600006
PM 27179253
ER
PT J
AU Brittain, EH
Proschan, MA
AF Brittain, Erica H.
Proschan, Michael A.
TI Comments on Berry et al.'s response-adaptive randomization platform
trial for Ebola
SO CLINICAL TRIALS
LA English
DT Letter
C1 [Brittain, Erica H.; Proschan, Michael A.] NIAID, Biostat Res Branch, 9000 Rockville Pike, Bethesda, MD 20892 USA.
RP Brittain, EH (reprint author), NIAID, Biostat Res Branch, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM ebrittain@niaid.nih.gov
NR 4
TC 0
Z9 0
U1 1
U2 1
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1740-7745
EI 1740-7753
J9 CLIN TRIALS
JI Clin. Trials
PD OCT
PY 2016
VL 13
IS 5
BP 566
EP 567
DI 10.1177/1740774516654440
PG 2
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA DW1GZ
UT WOS:000383392600013
PM 27365017
ER
PT J
AU Berg, HE
Ballard, ED
Luckenbaugh, DA
Nugent, AC
Ionescu, DF
Zarate, CA
AF Berg, Hannah E.
Ballard, Elizabeth D.
Luckenbaugh, David A.
Nugent, Allison C.
Ionescu, Dawn F.
Zarate, Carlos A., Jr.
TI Recognition of emotional facial expressions in anxious and nonanxious
depression
SO COMPREHENSIVE PSYCHIATRY
LA English
DT Article
ID STAR-ASTERISK-D; MAJOR DEPRESSION; TRAIT ANXIETY; DISORDER;
IDENTIFICATION; OUTPATIENTS; PERCEPTION; BIASES; MOOD
AB Background: Anxiety and depression have each been independently associated with impairments in emotional face recognition. However, little is known about the nature of these impairments when anxiety and depression co-occur.
Methods: This post-hoc analysis evaluated the relationship between anxiety status and performance on the Emotional Expression Multimorph Task within a clinical sample of individuals with major depressive disorder (MDD).
Results: Participants with anxious depression (n = 14) and nonanxious depression (n = 14) completed the Emotional Expression Multimorph Task. Those with anxious depression required greater intensity of emotion to identify both happy (p = .01) and sad (p = .04) facial expressions than those with nonanxious depression. Severity of anxiety also correlated with greater intensity of emotion required to detect sad faces. Contrary to prediction, hypervigilance to angry and fearful facial expressions was not observed in anxious depression.
Limitations: The present study did not include an anxiety-only group for comparison, and did not assess state anxiety at time of administration. In addition, the extent to which the experimental task correlates with social functioning is not fully understood.
Conclusions: These findings suggest a diminished sensitivity to happy and sad facial expressions specific to anxious depression, but not a hypervigilance toward threatening facial expressions. Further research on the nature of emotion recognition in anxiety and depression may inform improved clinical interventions. Published by Elsevier Inc.
C1 [Berg, Hannah E.; Ballard, Elizabeth D.; Luckenbaugh, David A.; Nugent, Allison C.; Zarate, Carlos A., Jr.] NIMH, Expt Therapeut & Pathophysiol Branch, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
[Ionescu, Dawn F.] Massachusetts Gen Hosp, Depress Clin & Res Program, Boston, MA 02114 USA.
[Ionescu, Dawn F.] Harvard Med Sch, Boston, MA USA.
RP Ballard, ED (reprint author), Bldg 10,CRC Room 7-3345,10 Ctr Dr,MSC 1282, Bethesda, MD 20892 USA.
EM Elizabeth.Ballard@nih.gov
RI Ionescu, Dawn/K-5675-2015;
OI Berg, Hannah/0000-0002-8283-0133
FU Intramural Research Program at the National Institute of Mental Health,
National Institutes of Health IRP-NIMH-NIH; NCT [00,088,699]; ZIA
[MH002927]; NARSAD; Brain and Behavior Mood Disorders Research Award
FX Funding for this work was supported in part by the Intramural Research
Program at the National Institute of Mental Health, National Institutes
of Health IRP-NIMH-NIH; NCT#00,088,699; ZIA MH002927), by a NARSAD
Independent Investigator to Dr. Zarate, and by a Brain and Behavior Mood
Disorders Research Award to Dr. Zarate. These funding sources had no
further role in study design; in the collection, analysis, or
interpretation of data; in the writing of the report; or in the decision
to submit the paper for publication.
NR 27
TC 0
Z9 0
U1 11
U2 11
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 2016
VL 70
BP 1
EP 8
DI 10.1016/j.comppsych.2016.06.007
PG 8
WC Psychiatry
SC Psychiatry
GA DW8SJ
UT WOS:000383925500001
PM 27624417
ER
PT J
AU Gmeiner, WH
Gearhart, PJ
Pommier, Y
Nakamura, J
AF Gmeiner, William H.
Gearhart, Patricia J.
Pommier, Yves
Nakamura, Jun
TI F10 cytotoxicity via topoisomerase I cleavage complex repair consistent
with a unique mechanism for thymineless death
SO FUTURE ONCOLOGY
LA English
DT Editorial Material
DE DNA repair; DNA topoisomerase I; F10; thymineless death
ID DNA-DAMAGE; CELL; INHIBITORS; SCREEN; RNA
C1 [Gmeiner, William H.] Wake Forest Sch Med, Dept Canc Biol, Winston Salem, NC 27157 USA.
[Gearhart, Patricia J.] NIA, Lab Mol Biol & Immunol, NIH, Baltimore, MD 21224 USA.
[Pommier, Yves] NCI, Dev Therapeut Branch, NIH, Bethesda, MD 20892 USA.
[Pommier, Yves] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Nakamura, Jun] Univ N Carolina, Chapel Hill, NC 27599 USA.
RP Gmeiner, WH (reprint author), Wake Forest Sch Med, Dept Canc Biol, Winston Salem, NC 27157 USA.
EM bgmeiner@wakehealth.edu
FU NIEHS NIH HHS [P30 ES010126, P42 ES005948]
NR 21
TC 1
Z9 1
U1 0
U2 0
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 2016
VL 12
IS 19
BP 2183
EP 2188
DI 10.2217/fon-2016-0127
PG 6
WC Oncology
SC Oncology
GA DW2XG
UT WOS:000383504900003
PM 27333295
ER
PT J
AU Zhang, LJ
Bell, BA
Li, Y
Zhang, XM
Fung, JJ
Caspi, RR
Lin, F
AF Zhang, Lingjun
Bell, Brent A.
Li, Yan
Zhang, Xiaomin
Fung, John J.
Caspi, Rachel R.
Lin, Feng
TI The lectin but not classical pathway of activation is important for
complement to regulate the development of experimental autoimmune
uveitis
SO IMMUNOBIOLOGY
LA English
DT Meeting Abstract
C1 [Zhang, Lingjun; Zhang, Xiaomin] Tianjin Med Univ, Inst Eye, Hosp Eye, Tianjin, Peoples R China.
[Bell, Brent A.] Cleveland Clin, Cole Eye Inst, Cleveland, OH 44106 USA.
[Li, Yan; Caspi, Rachel R.] NEI, Immunol Lab, NIH, Bldg 10, Bethesda, MD 20892 USA.
[Fung, John J.] Cleveland Clin, Inst Digest Dis, Cleveland, OH 44106 USA.
[Zhang, Lingjun; Lin, Feng] Cleveland Clin, Dept Immunol, Cleveland, OH 44106 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER GMBH, URBAN & FISCHER VERLAG
PI JENA
PA OFFICE JENA, P O BOX 100537, 07705 JENA, GERMANY
SN 0171-2985
J9 IMMUNOBIOLOGY
JI Immunobiology
PD OCT
PY 2016
VL 221
IS 10
SI SI
MA 6
BP 1133
EP 1133
DI 10.1016/j.imbio.2016.06.021
PG 1
WC Immunology
SC Immunology
GA DV3ER
UT WOS:000382804300018
ER
PT J
AU Rus, V
Nguyen, V
Tatomir, A
Boodhoo, D
Mekala, AP
Cudrici, C
Badea, TC
Rus, H
AF Rus, Violeta
Vinh Nguyen
Tatomir, Alexandru
Boodhoo, Dallas
Mekala, Armugam P.
Cudrici, Cornelia
Badea, Tudor C.
Rus, Horea
TI RGC-32 promotes Th17 cell differentiation and enhances experimental
autoimmune encephalomyelitis
SO IMMUNOBIOLOGY
LA English
DT Meeting Abstract
C1 [Rus, Violeta; Vinh Nguyen] Univ Maryland, Sch Med, Dept Med, Div Rheumatol & Clin Immunol, Baltimore, MD 21201 USA.
[Tatomir, Alexandru; Boodhoo, Dallas; Mekala, Armugam P.] Sch Med, Dept Neurol, Baltimore, MD USA.
[Cudrici, Cornelia; Badea, Tudor C.] NIH, Bethesda, MD 20892 USA.
[Rus, Horea] Vet Adm Maryland Hlth Care Syst, Res Serv, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER GMBH, URBAN & FISCHER VERLAG
PI JENA
PA OFFICE JENA, P O BOX 100537, 07705 JENA, GERMANY
SN 0171-2985
J9 IMMUNOBIOLOGY
JI Immunobiology
PD OCT
PY 2016
VL 221
IS 10
SI SI
MA 94
BP 1173
EP 1173
DI 10.1016/j.imbio.2016.06.109
PG 1
WC Immunology
SC Immunology
GA DV3ER
UT WOS:000382804300106
ER
PT J
AU Ueda, Y
Nishimura, J
Sugimori, C
Hosokawa, K
Yonemura, Y
Obara, N
Noji, H
Nakamura, Y
Shirasugi, Y
Ando, K
Shichishima, T
Ninomiya, H
Chiba, S
Kawaguchi, T
Kanakura, Y
Nakao, S
AF Ueda, Yasutaka
Nishimura, Jun-ichi
Sugimori, Chiharu
Hosokawa, Kohei
Yonemura, Yuji
Obara, Naoshi
Noji, Hideyoshi
Nakamura, Yoshihiko
Shirasugi, Yukari
Ando, Kiyoshi
Shichishima, Tsutomu
Ninomiya, Haruhiko
Chiba, Shigeru
Kawaguchi, Tatsuya
Kanakura, Yuzuru
Nakao, Shinji
TI High sensitivity flow cytometry to detect small population of PNH clone
in bone marrow failure syndrome in Japan
SO IMMUNOBIOLOGY
LA English
DT Meeting Abstract
C1 [Ueda, Yasutaka; Nishimura, Jun-ichi; Kanakura, Yuzuru] Osaka Univ, Grad Sch Med, Hematol & Oncol, Suita, Osaka, Japan.
[Ueda, Yasutaka; Nishimura, Jun-ichi; Sugimori, Chiharu; Hosokawa, Kohei; Yonemura, Yuji; Obara, Naoshi; Noji, Hideyoshi; Nakamura, Yoshihiko; Shirasugi, Yukari; Ando, Kiyoshi; Shichishima, Tsutomu; Ninomiya, Haruhiko; Chiba, Shigeru; Kawaguchi, Tatsuya; Kanakura, Yuzuru; Nakao, Shinji] Japan PNH Study Grp, Tokyo, Japan.
[Sugimori, Chiharu] Ishikawa Prefectural Cent Hosp, Hematol, Kanazawa, Ishikawa, Japan.
[Hosokawa, Kohei] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Yonemura, Yuji] Kumamoto Univ Hosp, Transfus Med & Cell Therapy, Kumamoto, Japan.
[Obara, Naoshi; Chiba, Shigeru] Univ Tsukuba, Hematol, Tsukuba, Ibaraki, Japan.
[Noji, Hideyoshi] Fukushima Res Inst Environm & Med, Fukushima, Japan.
[Nakamura, Yoshihiko; Shirasugi, Yukari; Ando, Kiyoshi] Tokai Univ, Sch Med, Hematol & Oncol, Isehara, Kanagawa, Japan.
[Shichishima, Tsutomu] Fukushima Med Univ, Cardiol & Hematol, Fukushima, Japan.
[Ninomiya, Haruhiko] Univ Tsukuba, Med Sci, Tsukuba, Ibaraki, Japan.
[Kawaguchi, Tatsuya] Kumamoto Univ, Grad Sch Med Sci, Kumamoto, Japan.
[Nakao, Shinji] Kanazawa Univ, Grad Sch Med Sci, Cellular Transplantat Biol, Kanazawa, Ishikawa, Japan.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER GMBH, URBAN & FISCHER VERLAG
PI JENA
PA OFFICE JENA, P O BOX 100537, 07705 JENA, GERMANY
SN 0171-2985
J9 IMMUNOBIOLOGY
JI Immunobiology
PD OCT
PY 2016
VL 221
IS 10
SI SI
MA 122
BP 1186
EP 1186
DI 10.1016/j.imbio.2016.06.137
PG 1
WC Immunology
SC Immunology
GA DV3ER
UT WOS:000382804300134
ER
PT J
AU Kolev, M
Nova-Lamperti, E
Freeley, S
Smolarek, D
Chakraborthy, S
Mii, S
Takahashi, M
Smith, RA
Afzali, B
Kemper, C
AF Kolev, Martin
Nova-Lamperti, Estefania
Freeley, Simon
Smolarek, Dorota
Chakraborthy, Shinjini
Mii, Shinji
Takahashi, Masahide
Smith, Richard A.
Afzali, Behdad
Kemper, Claudia
TI The C3-like molecule CD109 controls Th1 versus Th17 induction in CD4(+)
T cells
SO IMMUNOBIOLOGY
LA English
DT Meeting Abstract
C1 [Kolev, Martin; Nova-Lamperti, Estefania; Freeley, Simon; Smolarek, Dorota; Chakraborthy, Shinjini; Smith, Richard A.; Afzali, Behdad; Kemper, Claudia] Kings Coll London, Guys Hosp Great Maze Pond, MRC Ctr Transplantat, Div Transplant Immunol & Mucosal Biol, London SE1 9RT, England.
[Mii, Shinji; Takahashi, Masahide] Nagoya Univ, Grad Sch Med, Dept Pathol, Nagoya, Aichi, Japan.
[Afzali, Behdad] NIAMSD, Mol Immunol & Inflammat Branch, NIH, 10 Ctr Dr, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER GMBH, URBAN & FISCHER VERLAG
PI JENA
PA OFFICE JENA, P O BOX 100537, 07705 JENA, GERMANY
SN 0171-2985
J9 IMMUNOBIOLOGY
JI Immunobiology
PD OCT
PY 2016
VL 221
IS 10
SI SI
MA 142
BP 1195
EP 1196
DI 10.1016/j.imbio.2016.06.157
PG 2
WC Immunology
SC Immunology
GA DV3ER
UT WOS:000382804300154
ER
PT J
AU Semba, RD
Zhang, P
Zhu, M
Geng-Spyropoulos, M
Shardell, M
Gonzalez-Freire, M
Eiriksdottir, G
Gudnason, V
Van Eyk, JE
Ferrucci, L
AF Semba, Richard D.
Zhang, Pingbo
Zhu, Min
Geng-Spyropoulos, Minghui
Shardell, Michelle
Gonzalez-Freire, Marta
Eiriksdottir, Gudny
Gudnason, Vilmunder
Van Eyk, Jennifer E.
Ferrucci, Luigi
TI A novel, multiplexed targeted mass spectrometry assay for quantification
of complement factor H (CFH) variants and CFH-related proteins 1-5 in
human plasma
SO IMMUNOBIOLOGY
LA English
DT Meeting Abstract
C1 [Semba, Richard D.; Zhang, Pingbo; Geng-Spyropoulos, Minghui] Johns Hopkins Univ, Sch Med, Wilmer Eye Inst, Baltimore, MD 21205 USA.
[Zhu, Min; Shardell, Michelle; Gonzalez-Freire, Marta; Ferrucci, Luigi] NIA, NIH, Baltimore, MD 21224 USA.
[Eiriksdottir, Gudny; Gudnason, Vilmunder] Iceland Heart Assoc, Reykjavik, Iceland.
[Eiriksdottir, Gudny; Gudnason, Vilmunder] Univ Iceland, Dept Med, Reykjavik, Iceland.
[Van Eyk, Jennifer E.] Cedars Sinai Med Ctr, Adv Clin BioSyst Res Inst, Inst Heart, Los Angeles, CA 90048 USA.
[Van Eyk, Jennifer E.] Cedars Sinai Med Ctr, Dept Med, Los Angeles, CA 90048 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER GMBH, URBAN & FISCHER VERLAG
PI JENA
PA OFFICE JENA, P O BOX 100537, 07705 JENA, GERMANY
SN 0171-2985
J9 IMMUNOBIOLOGY
JI Immunobiology
PD OCT
PY 2016
VL 221
IS 10
SI SI
MA 155
BP 1201
EP 1201
DI 10.1016/j.imbio.2016.06.170
PG 1
WC Immunology
SC Immunology
GA DV3ER
UT WOS:000382804300167
ER
PT J
AU Bigelow, RT
Semenov, YR
Anson, E
du Lac, S
Ferrucci, L
Agrawal, Y
AF Bigelow, Robin T.
Semenov, Yevgeniy R.
Anson, Eric
du Lac, Sascha
Ferrucci, Luigi
Agrawal, Yuri
TI Impaired Vestibular Function and Low Bone Mineral Density: Data from the
Baltimore Longitudinal Study of Aging
SO JARO-JOURNAL OF THE ASSOCIATION FOR RESEARCH IN OTOLARYNGOLOGY
LA English
DT Article
DE vestibular; bone mineral density; aging; osteoporosis
ID POSTMENOPAUSAL WOMEN; OLDER INDIVIDUALS; HEARING-LOSS; AGE; OSTEOPONTIN;
BALANCE; LABYRINTHECTOMY
AB Animal studies have demonstrated that experimentally induced vestibular ablation leads to a decrease in bone mineral density, through mechanisms mediated by the sympathetic nervous system. Loss of bone mineral density is a common and potentially morbid condition that occurs with aging, and we sought to investigate whether vestibular loss is associated with low bone mineral density in older adults. We evaluated this question in a cross-sectional analysis of data from the Baltimore Longitudinal Study of Aging (BLSA), a large, prospective cohort study managed by the National Institute on Aging (N = 389). Vestibular function was assessed with cervical vestibular evoked myogenic potentials (cVEMPs), a measure of saccular function. Bone mineral density was assessed using dual-energy X-ray absorptiometry (DEXA). In two-way t test analysis, we observed that individuals with reduced vestibular physiologic function had significantly lower bone mineral density. In adjusted multivariate linear regression analyses, we observed that older individuals with reduced vestibular physiologic function had significantly lower bone mineral density, specifically in weight-bearing hip and lower extremity bones. These results suggest that the vestibular system may contribute to bone homeostasis in older adults, notably of the weight-bearing hip bones at greatest risk of osteoporotic fracture. Further longitudinal analysis of vestibular function and bone mineral density in humans is needed to characterize this relationship and investigate the potential confounding effect of physical activity.
C1 [Bigelow, Robin T.; Semenov, Yevgeniy R.; Anson, Eric; du Lac, Sascha; Agrawal, Yuri] Johns Hopkins Univ, Sch Med, Dept Otolaryngol Head & Neck Surg, 601 N Caroline St, Baltimore, MD 21287 USA.
[du Lac, Sascha] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA.
[Ferrucci, Luigi] NIA, Longitudinal Studies Sect, Clin Res Branch, Baltimore, MD 21224 USA.
RP Bigelow, RT (reprint author), Johns Hopkins Univ, Sch Med, Dept Otolaryngol Head & Neck Surg, 601 N Caroline St, Baltimore, MD 21287 USA.
EM rbigelow@jhmi.edu; ysemeno1@jhmi.edu; eanson1@jhmi.edu; sascha@jhmi.edu;
ferruccilu@grc.nia.nih.gov; yagrawa1@jhmi.edu
FU National Institutes of Health [NIH/NIDCD K23 DC013056, 5T32
DC000023-30]; National Institute on Aging
FX This work was supported by the National Institutes of Health grant
NIH/NIDCD K23 DC013056 and 5T32 DC000023-30. The Baltimore Longitudinal
Study of Aging is supported by the National Institute on Aging.
NR 38
TC 0
Z9 0
U1 6
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1525-3961
EI 1438-7573
J9 JARO-J ASSOC RES OTO
JI JARO
PD OCT
PY 2016
VL 17
IS 5
BP 433
EP 440
DI 10.1007/s10162-016-0577-5
PG 8
WC Neurosciences; Otorhinolaryngology
SC Neurosciences & Neurology; Otorhinolaryngology
GA DW3BX
UT WOS:000383518200004
PM 27447468
ER
PT J
AU Sigurdardottir, LG
Markt, SC
Sigurdsson, S
Aspelund, T
Fall, K
Schernhammer, E
Rider, JR
Launer, L
Harris, T
Stampfer, MJ
Gudnason, V
Czeisler, CA
Lockley, SW
Valdimarsdottir, UA
Mucci, LA
AF Sigurdardottir, Lara G.
Markt, Sarah C.
Sigurdsson, Sigurdur
Aspelund, Thor
Fall, Katja
Schernhammer, Eva
Rider, Jennifer R.
Launer, Lenore
Harris, Tamara
Stampfer, Meir J.
Gudnason, Vilmundur
Czeisler, Charles A.
Lockley, Steven W.
Valdimarsdottir, Unnur A.
Mucci, Lorelei A.
TI Pineal Gland Volume Assessed by MRI and Its Correlation with
6-Sulfatoxymelatonin Levels among Older Men
SO JOURNAL OF BIOLOGICAL RHYTHMS
LA English
DT Article
DE pineal; melatonin; sleep; circadian; MRI
ID PLASMA MELATONIN; SLEEP DISRUPTION; PRIMARY INSOMNIA; PROSTATE-CANCER;
HUMANS; SUPPRESSION; SECRETION; AGE; CALCIFICATION; EXCRETION
AB The pineal gland produces the hormone melatonin, and its volume may influence melatonin levels. We describe an innovative method for estimating pineal volume in humans and present the association of pineal parenchyma volume with levels of the primary melatonin metabolite, 6-sulfatoxymelatonin. We selected a random sample of 122 older Icelandic men nested within the AGES-Reykjavik cohort and measured their total pineal volume, their parenchyma volume, and the extent of calcification and cysts. For volume estimations we used manual segmentation of magnetic resonance images in the axial plane with simultaneous side-by-side view of the sagittal and coronal plane. We used multivariable adjusted linear regression models to estimate the association of pineal parenchyma volume and baseline characteristics, including 6-sulfatoxymelatonin levels. We used logistic regression to test for differences in first morning urinary 6-sulfatoxymelatonin levels among men with or without cystic or calcified glands. The pineal glands varied in volume, shape, and composition. Cysts were present in 59% of the glands and calcifications in 21%. The mean total pineal volume measured 207 mm(3) (range 65-536 mm(3)) and parenchyma volume 178 mm(3) (range 65-503 mm(3)). In multivariable-adjusted models, pineal parenchyma volume was positively correlated with 6-sulfatoxymelatonin levels ( = 0.52, p < 0.001). Levels of 6-sulfatoxymelatonin did not differ significantly by presence of cysts or calcification. By using an innovative method for pineal assessment, we found pineal parenchyma volume to be positively correlated with 6-sulfatoxymelatonin levels, in line with other recent studies.
C1 [Sigurdardottir, Lara G.] Iceland Canc Soc, IS-108 Reykjavik, Iceland.
[Sigurdardottir, Lara G.; Aspelund, Thor; Valdimarsdottir, Unnur A.; Mucci, Lorelei A.] Univ Iceland, Ctr Publ Hlth Sci, Reykjavik, Iceland.
[Sigurdardottir, Lara G.; Gudnason, Vilmundur; Valdimarsdottir, Unnur A.] Univ Iceland, Fac Med, Reykjavik, Iceland.
[Markt, Sarah C.; Schernhammer, Eva; Rider, Jennifer R.; Stampfer, Meir J.; Valdimarsdottir, Unnur A.; Mucci, Lorelei A.] Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
[Sigurdsson, Sigurdur; Aspelund, Thor; Gudnason, Vilmundur] Iceland Heart Assoc, Kopavogur, Iceland.
[Fall, Katja] Univ Orebro, Sch Med Sci, Clin Epidemiol & Biostat, Orebro, Sweden.
[Schernhammer, Eva; Stampfer, Meir J.; Mucci, Lorelei A.] Harvard Med Sch, Brigham & Womens Hosp, Channing Div Network Med, Boston, MA USA.
[Schernhammer, Eva] Med Univ Vienna, Dept Epidemiol, Vienna, Austria.
[Launer, Lenore; Harris, Tamara] NIA, Lab Epidemiol & Populat Sci, Intramural Res Program, Bethesda, MD 20892 USA.
[Czeisler, Charles A.; Lockley, Steven W.] Brigham & Womens Hosp, Dept Med, Div Sleep & Circadian Disorders, 75 Francis St, Boston, MA 02115 USA.
[Czeisler, Charles A.; Lockley, Steven W.] Harvard Med Sch, Div Sleep Med, Boston, MA USA.
RP Sigurdardottir, LG (reprint author), Iceland Canc Soc, IS-108 Reykjavik, Iceland.
EM lara@sessionimpossible.com
OI Fall, Katja/0000-0002-3649-2639
FU RANNIS (the Icelandic Research Fund); National Institutes on Aging
Intramural Research Program [N01-AG-12100]; Hjartavernd (the Icelandic
Heart Association); Althingi (the Icelandic Parliament); Harvard
Catalyst Award; National Cancer Institute at the National Institutes of
Health Training Grant [NIH T32 CA09001]; Prostate Cancer Foundation
FX This study was supported by RANNIS (the Icelandic Research Fund). The
AGES-Reykjavik is supported by Contract N01-AG-12100 from the National
Institutes on Aging Intramural Research Program; Hjartavernd (the
Icelandic Heart Association); the Althingi (the Icelandic Parliament);
and the Harvard Catalyst Award. This study is approved by the Icelandic
National Bioethics Committee, VSN: 00-063. S.C.M. is supported by the
National Cancer Institute at the National Institutes of Health Training
Grant NIH T32 CA09001. L.A.M. and J.R.R. are supported by the Prostate
Cancer Foundation. The funding agencies had no role in the design of the
study, the collection of the data, or the data analysis.
NR 40
TC 1
Z9 1
U1 4
U2 4
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0748-7304
EI 1552-4531
J9 J BIOL RHYTHM
JI J. Biol. Rhythms
PD OCT
PY 2016
VL 31
IS 5
BP 461
EP 469
DI 10.1177/0748730416656948
PG 9
WC Biology; Physiology
SC Life Sciences & Biomedicine - Other Topics; Physiology
GA DW1XK
UT WOS:000383436700004
PM 27449477
ER
PT J
AU Canepa, M
Bezante, G
Vianello, P
Ameri, P
Milaneschi, Y
Aste, M
Cavalla, F
Bauckneht, M
Marini, C
Balbi, M
Brunelli, C
Sambuceti, G
AF Canepa, Marco
Bezante, Gianpaolo
Vianello, Pierfilippo
Ameri, Pietro
Milaneschi, Yuri
Aste, Milena
Cavalla, Francesca
Bauckneht, Matteo
Marini, Cecilia
Balbi, Manrico
Brunelli, Claudio
Sambuceti, Gianmario
TI Diagnostic value of ischemia severity at myocardial perfusion imaging in
elderly persons with suspected coronary disease
SO JOURNAL OF CARDIOVASCULAR MEDICINE
LA English
DT Article
DE coronary artery disease; diagnostic accuracy; ischemia; myocardial
perfusion scintigraphy; summed score
ID EMISSION COMPUTED-TOMOGRAPHY; ARTERY-DISEASE; CARDIAC DEATH; RISK
STRATIFICATION; PROGNOSTIC VALUE; MEDICAL THERAPY; GUIDELINES;
PREDICTION; EXERCISE; IMPACT
AB AimsMyocardial perfusion and ischemia scores obtained from myocardial perfusion scintigraphy (MPS) have strong independent prognostic value in elderly individuals without known coronary artery disease (CAD). Herein we aimed to assess their independent diagnostic value and accuracy for CAD while considering different thresholds of myocardial ischemia.MethodsWe estimated the summed rest score (SRS), summed stress score (SSS) and summed difference score (SDS) in 322 elderly individuals (mean age 727 years, 68% men) who underwent coronary angiography following an MPS. Abnormal perfusion at stress was defined as an SSS greater than 3, and ischemia as an SDS of at least 2, and further categorized as mild (2-4), moderate (5-7) or severe (>7). Multivariate logistic regressions were used to establish the independent diagnostic value and accuracy of MPS parameters.ResultsCAD was diagnosed in 182 individuals (56%). In multivariate analysis accounting for clinical variables associated with CAD including the Framingham risk score, both SRS [odds ratio (OR) 1.09, 95% confidence interval (CI) 1.01-1.18, P=0.03] and SSS (OR 1.10, 95% CI 1.04-1.16, P=0.0006) and SDS (OR 1.12, 95% CI 1.04-1.21, P=0.003) were independently associated with CAD. An SSS greater than 3 was also independently associated with CAD (OR 2.51, 95% CI 1.43-4.39, P=0.0013), whereas an SDS of 2 or greater was not (OR 1.62, 95% CI 0.89-2.93, P=0.12), but only when at least 5 (OR 2.31, 95% CI 1.32-4.03, P=0.003). The probability of CAD was proportional to the amount of myocardial ischemia in those with an SSS greater than 3, and lower and comparable in those with an SSS of at least 3 or an SSS greater than 3 with SDS of 1 or less (P=0.19). Increasing the threshold of myocardial ischemia determined a decrease in sensitivity and increase in specificity of MPS for both diagnosis and severity of CAD.ConclusionWe established the diagnostic value and accuracy of continuous scores and thresholds of abnormal myocardial perfusion and ischemia previously validated in prognostic studies. Their more widespread use could potentially improve the diagnostic yield of coronary angiography in elderly individuals with suspected CAD.
C1 [Canepa, Marco; Bezante, Gianpaolo; Vianello, Pierfilippo; Ameri, Pietro; Aste, Milena; Cavalla, Francesca; Balbi, Manrico; Brunelli, Claudio] Univ Genoa, Dept Internal Med, Cardiovasc Unit, Genoa, Italy.
[Canepa, Marco] NIA, Longitudinal Studies Sect, Translat Gerontol Branch, NIH, Baltimore, MD 21224 USA.
[Milaneschi, Yuri] Vrije Univ Amsterdam, Med Ctr GGZ Geest, Dept Psychiat, Amsterdam, Netherlands.
[Bauckneht, Matteo; Marini, Cecilia; Sambuceti, Gianmario] Univ Genoa, Dept Hlth Sci, Nucl Med, Genoa, Italy.
RP Canepa, M (reprint author), Univ Genoa, Cardiovasc Unit, Dept Internal Med, IRCCS AOU San Martino IST, Viale Benedetto 15,6, I-16132 Genoa, Italy.
EM marco.canepa@unige.it
OI Bauckneht, Matteo/0000-0002-1937-9116
NR 28
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1558-2027
EI 1558-2035
J9 J CARDIOVASC MED
JI J. Cardiovasc. Med.
PD OCT
PY 2016
VL 17
IS 10
BP 719
EP 728
DI 10.2459/JCM.0000000000000339
PG 10
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA DW9DE
UT WOS:000383954800002
PM 26599683
ER
PT J
AU Rozins, C
Day, T
AF Rozins, Carly
Day, Troy
TI Disease eradication on large industrial farms
SO JOURNAL OF MATHEMATICAL BIOLOGY
LA English
DT Article
DE Impulsive differential equation; Poultry; SIR; Infectious disease;
Livestock production; All-in-all-out; Indirect transmission
ID MAREKS-DISEASE; UNITED-STATES; SEA LICE; TRANSMISSION; WELFARE; VIRUS
AB Many modern farms exhibit all-in-all-out dynamics in which entire cohorts of livestock are removed from a farm before a new cohort is introduced. This industrialization has enabled diseases to spread rapidly within farms. Here we look at one such example, Marek's disease. Marek's disease is an economically important disease of poultry. The disease is transmitted indirectly, enabling the spread of disease between cohorts of chickens who have never come into physical contact. We develop a model which allows us to track the transmission of disease within a barn and between subsequent cohorts of chickens occupying the barn. It is described by a system of impulsive differential equations. We determine the conditions that lead to disease eradication. For a given level of transmission we find that disease eradication is possible if the cohort length is short enough and/or the cohort size is small enough. Marek's disease can also be eradicated from a farm if the cleaning effort between cohorts is large enough. Importantly complete cleaning is not required for eradication and the threshold cleaning effort needed declines as both cohort duration and size decrease.
C1 [Rozins, Carly; Day, Troy] Queens Univ, Dept Math & Stat, Kingston, ON, Canada.
[Day, Troy] NIH, Fogarty Int Ctr, Bldg 10, Bethesda, MD 20892 USA.
RP Rozins, C (reprint author), Queens Univ, Dept Math & Stat, Kingston, ON, Canada.
EM crozins@mast.queensu.ca
NR 20
TC 1
Z9 1
U1 7
U2 7
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0303-6812
EI 1432-1416
J9 J MATH BIOL
JI J. Math. Biol.
PD OCT
PY 2016
VL 73
IS 4
BP 885
EP 902
DI 10.1007/s00285-016-0973-9
PG 18
WC Biology; Mathematical & Computational Biology
SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational
Biology
GA DV5AH
UT WOS:000382937000005
PM 26898368
ER
PT J
AU Kraemmer, J
Smith, K
Weintraub, D
Guillemot, V
Nalls, MA
Cormier-Dequaire, F
Moszer, I
Brice, A
Singleton, AB
Corvol, JC
AF Kraemmer, Julia
Smith, Kara
Weintraub, Daniel
Guillemot, Vincent
Nalls, Mike A.
Cormier-Dequaire, Florence
Moszer, Ivan
Brice, Alexis
Singleton, Andrew B.
Corvol, Jean-Christophe
TI Clinical-genetic model predicts incident impulse control disorders in
Parkinson's disease
SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY
LA English
DT Article
ID DNA-SEQUENCING DATA; ASSOCIATION; RECEPTOR; POLYMORPHISMS; BEHAVIORS;
SUSCEPTIBILITY; ADDICTIONS; FRAMEWORK; SYMPTOMS; GRIN2B
AB Objectives Impulse control disorders (ICD) are commonly associated with dopamine replacement therapy (DRT) in patients with Parkinson's disease (PD). Our aims were to estimate ICD heritability and to predict ICD by a candidate genetic multivariable panel in patients with PD.
Methods Data from de novo patients with PD, drug-naive and free of ICD behaviour at baseline, were obtained from the Parkinson's Progression Markers Initiative cohort. Incident ICD behaviour was defined as positive score on the Questionnaire for Impulsive-Compulsive Disorders in PD. ICD heritability was estimated by restricted maximum likelihood analysis on whole exome sequencing data. 13 candidate variants were selected from the DRD2, DRD3, DAT1, COMT, DDC, GRIN2B, ADRA2C, SERT, TPH2, HTR2A, OPRK1 and OPRM1 genes. ICD prediction was evaluated by the area under the curve (AUC) of receiver operating characteristic (ROC) curves.
Results Among 276 patients with PD included in the analysis, 86% started DRT, 40% were on dopamine agonists (DA), 19% reported incident ICD behaviour during follow-up. We found heritability of this symptom to be 57%. Adding genotypes from the 13 candidate variants significantly increased ICD predictability (AUC=76%, 95% CI (70% to 83%)) compared to prediction based on clinical variables only (AUC=65%, 95% CI (58% to 73%), p=0.002). The clinical-genetic prediction model reached highest accuracy in patients initiating DA therapy (AUC=87%, 95% CI (80% to 93%)). OPRK1, HTR2A and DDC genotypes were the strongest genetic predictive factors.
Conclusions Our results show that adding a candidate genetic panel increases ICD predictability, suggesting potential for developing clinical-genetic models to identify patients with PD at increased risk of ICD development and guide DRT management.
C1 [Kraemmer, Julia; Guillemot, Vincent; Cormier-Dequaire, Florence; Moszer, Ivan; Brice, Alexis; Corvol, Jean-Christophe] Univ Paris 06, Sorbonne Univ, Paris, France.
[Kraemmer, Julia; Guillemot, Vincent; Cormier-Dequaire, Florence; Moszer, Ivan; Brice, Alexis; Corvol, Jean-Christophe] INSERM, UMRS 1127, Paris, France.
[Kraemmer, Julia; Guillemot, Vincent; Cormier-Dequaire, Florence; Moszer, Ivan; Brice, Alexis; Corvol, Jean-Christophe] CIC 1422, Paris, France.
[Kraemmer, Julia; Guillemot, Vincent; Cormier-Dequaire, Florence; Moszer, Ivan; Brice, Alexis; Corvol, Jean-Christophe] CNRS, UMR 7225, Paris, France.
[Kraemmer, Julia; Guillemot, Vincent; Cormier-Dequaire, Florence; Moszer, Ivan; Brice, Alexis; Corvol, Jean-Christophe] AP HP, Paris, France.
[Kraemmer, Julia; Guillemot, Vincent; Cormier-Dequaire, Florence; Moszer, Ivan; Brice, Alexis; Corvol, Jean-Christophe] ICM, Dept Malad Syst Nerveux, Paris, France.
[Kraemmer, Julia; Guillemot, Vincent; Cormier-Dequaire, Florence; Moszer, Ivan; Brice, Alexis; Corvol, Jean-Christophe] Hop La Pitie Salpetriere, Dept Genet, Paris, France.
[Kraemmer, Julia] Med Univ Vienna, Vienna, Austria.
[Smith, Kara; Weintraub, Daniel] Univ Penn, Perelman Sch Med, Dept Neurol, Philadelphia, PA 19104 USA.
[Weintraub, Daniel] Univ Penn, Dept Psychiat, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Weintraub, Daniel] Corporal Michael J Crescenz Dept Vet Affairs Med, Philadelphia, PA USA.
[Nalls, Mike A.; Singleton, Andrew B.] NIH, Lab Neurogenet, Bldg 10, Bethesda, MD 20892 USA.
RP Corvol, JC (reprint author), Hop La Pitie Salpetriere, ICM, CIC Neurosci, 47-83 Bd Hop, F-75013 Paris, France.
EM jean-christophe.corvol@aphp.fr
RI corvol, jean-christophe/I-6387-2012
OI corvol, jean-christophe/0000-0001-7325-0199
FU Michael J Fox Foundation for Parkinson's Research; AbbVie; Avid
Radiopharmaceuticals; Biogen; Bristol-Myers Squibb; Covance; GE
Healthcare; Genentech; GlaxoSmithKline; Lilly; Lundbeck; Merck; Meso
Scale Discovery; Pfizer; Piramal; Roche; Servier; UCB; programme
'Investissements d'Avenir' [ANR-10-IAIHU-06]; Medtronic Inc.
FX PPMI-a public-private partnership-is funded by the Michael J Fox
Foundation for Parkinson's Research and funding partners, including
AbbVie, Avid Radiopharmaceuticals, Biogen, Bristol-Myers Squibb,
Covance, GE Healthcare, Genentech, GlaxoSmithKline, Lilly, Lundbeck,
Merck, Meso Scale Discovery, Pfizer, Piramal, Roche, Servier and UCB.
J-CC, IM and VG were supported by a funding from the programme
'Investissements d'Avenir' ANR-10-IAIHU-06; and KS by Medtronic Inc.
NR 41
TC 7
Z9 7
U1 11
U2 11
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0022-3050
EI 1468-330X
J9 J NEUROL NEUROSUR PS
JI J. Neurol. Neurosurg. Psychiatry
PD OCT
PY 2016
VL 87
IS 10
BP 1106
EP 1111
DI 10.1136/jnnp-2015-312848
PG 6
WC Clinical Neurology; Psychiatry; Surgery
SC Neurosciences & Neurology; Psychiatry; Surgery
GA DW9OU
UT WOS:000383991400011
PM 27076492
ER
PT J
AU Lopker, MJ
Del Prete, GQ
Estes, JD
Li, H
Reid, C
Newman, L
Lipkey, L
Camus, C
Easlick, JL
Wang, SY
Decker, JM
Bar, KJ
Learn, G
Pal, R
Weiss, DE
Hahn, BH
Lifson, JD
Shaw, GM
Keele, BF
AF Lopker, Michael J.
Del Prete, Gregory Q.
Estes, Jacob D.
Li, Hui
Reid, Carolyn
Newman, Laura
Lipkey, Leslie
Camus, Celine
Easlick, Juliet L.
Wang, Shuyi
Decker, Julie M.
Bar, Katharine J.
Learn, Gerald
Pal, Ranajit
Weiss, Deborah E.
Hahn, Beatrice H.
Lifson, Jeffrey D.
Shaw, George M.
Keele, Brandon F.
TI Derivation and Characterization of Pathogenic Transmitted/Founder
Molecular Clones from Simian Immunodeficiency Virus SIVsmE660 and
SIVmac251 following Mucosal Infection
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID RHESUS MACAQUES; ENVELOPE PROTEIN; SUBOPTIMAL NUCLEOTIDES; INTRARECTAL
CHALLENGE; MONOCLONAL-ANTIBODIES; BIOLOGICAL PHENOTYPE; REPLICATIVE
FITNESS; VACCINE CHALLENGE; GENETIC IDENTITY; NONHUMAN PRIMATE
AB Currently available simian immunodeficiency virus (SIV) infectious molecular clones (IMCs) and isolates used in nonhuman primate (NHP) models of AIDS were originally derived from infected macaques during chronic infection or end stage disease and may not authentically recapitulate features of transmitted/founder (T/F) genomes that are of particular interest in transmission, pathogenesis, prevention, and treatment studies. We therefore generated and characterized T/F IMCs from genetically and biologically heterogeneous challenge stocks of SIVmac251 and SIVsmE660. Single-genome amplification (SGA) was used to identify full-length T/F genomes present in plasma during acute infection resulting from atraumatic rectal inoculation of Indian rhesus macaques with low doses of SIVmac251 or SIVsmE660. All 8 T/F clones yielded viruses that were infectious and replication competent in vitro, with replication kinetics similar to those of the widely used chronic-infection-derived IMCs SIVmac239 and SIVsmE543. Phenotypically, the new T/F virus strains exhibited a range of neutralization sensitivity profiles. Four T/F virus strains were inoculated into rhesus macaques, and each exhibited typical SIV replication kinetics. The SIVsm T/F viruses were sensitive to TRIM5 alpha restriction. All T/F viruses were pathogenic in rhesus macaques, resulting in progressive CD4(+) T cell loss in gastrointestinal tissues, peripheral blood, and lymphatic tissues. The animals developed pathological immune activation; lymphoid tissue damage, including fibrosis; and clinically significant immunodeficiency leading to AIDS-defining clinical endpoints. These T/F clones represent a new molecular platform for the analysis of virus transmission and immunopathogenesis and for the generation of novel "bar-coded" challenge viruses and next-generation simian-human immunodeficiency viruses that may advance the HIV/AIDS vaccine agenda.
IMPORTANCE
Nonhuman primate research has relied on only a few infectious molecular clones for a myriad of diverse research projects, including pathogenesis, preclinical vaccine evaluations, transmission, and host-versus-pathogen interactions. With new data suggesting a selected phenotype of the virus that causes infection (i.e., the transmitted/founder virus), we sought to generate and characterize infectious molecular clones from two widely used simian immunodeficiency virus lineages (SIVmac251 and SIVsmE660). Although the exact requirements necessary to be a T/F virus are not yet fully understood, we generated cloned viruses with all the necessary characteristic of a successful T/F virus. The cloned viruses revealed typical acute and set point viral-load dynamics with pathological immune activation, lymphoid tissue damage progressing to significant immunodeficiency, and AIDS-defining clinical endpoints in some animals. These T/F clones represent a new molecular platform for studies requiring authentic T/F viruses.
C1 [Lopker, Michael J.; Easlick, Juliet L.; Decker, Julie M.] Univ Alabama Birmingham, Birmingham, AL USA.
[Del Prete, Gregory Q.; Estes, Jacob D.; Reid, Carolyn; Newman, Laura; Lipkey, Leslie; Camus, Celine; Lifson, Jeffrey D.; Keele, Brandon F.] Leidos Biomed Res Inc, AIDS & Canc Virus Program, Frederick Natl Lab Canc Res, Frederick, MD USA.
[Li, Hui; Wang, Shuyi; Bar, Katharine J.; Learn, Gerald; Hahn, Beatrice H.; Shaw, George M.] Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Pal, Ranajit] Adv BioSci Labs Inc, Rockville, MD USA.
[Weiss, Deborah E.] Bioqual, Rockville, MD USA.
RP Keele, BF (reprint author), Leidos Biomed Res Inc, AIDS & Canc Virus Program, Frederick Natl Lab Canc Res, Frederick, MD USA.
EM keelebf@mail.nih.gov
FU HHS | NIH | National Cancer Institute (NCI) [HHSN261200800001E]; HHS |
NIH | National Institute of Allergy and Infectious Diseases (NIAID)
[AI087383]; NIAID [AI087383]; National Cancer Institute; National
Institutes of Health [HHSN261200800001E]
FX This work, including the efforts of Gregory Q. Del Prete, Jacob D.
Estes, Carolyn Reid, Laura Newman, Leslie Lipkey, Celine Camus, Jeffrey
Lifson, and Brandon F. Keele, was funded by HHS | NIH | National Cancer
Institute (NCI) (HHSN261200800001E). This work, including the efforts of
Michael Lopker, Beatrice H. Hahn, and George M. Shaw, was funded by HHS|
NIH | National Institute of Allergy and Infectious Diseases (NIAID)
(AI087383).; This work was supported in part with federal funds from
NIAID grant AI087383 and the National Cancer Institute; National
Institutes of Health under contract 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 63
TC 2
Z9 2
U1 5
U2 5
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD OCT
PY 2016
VL 90
IS 19
BP 8435
EP 8453
DI 10.1128/JVI.00718-16
PG 19
WC Virology
SC Virology
GA DW6LH
UT WOS:000383761900006
PM 27412591
ER
PT J
AU Gach, JS
Venzon, D
Vaccari, M
Keele, BF
Franchini, G
Forthal, DN
AF Gach, Johannes S.
Venzon, David
Vaccari, Monica
Keele, Brandon F.
Franchini, Genoveffa
Forthal, Donald N.
TI Relationship between Vaccine-Induced Antibody Capture of Infectious
Virus and Infection Outcomes following Repeated Low-Dose Rectal
Challenges with Simian Immunodeficiency Virus SIVmac251
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HIV-1 INFECTION; DEPENDENT ENHANCEMENT; MEDIATED ENHANCEMENT; TYPE-1;
TRIAL; PROTECTION; GP120; CD4; FC; ACQUISITION
AB Antibodies are known to enhance in vitro infection by human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV). We measured the ability of antibodies induced by ALVAC-SIV/gp120 vaccination, given with alum or MF59 adjuvant, to capture infectious SIVmac251 and determined the association between capture and infection outcomes following low-dose, repeated rectal challenge of rhesus macaques. We found that capture correlated with the number of transmitted/founder (T/F) variants that established infection, such that animals whose plasma captured more virus were infected with a higher number of T/F strains. Capture also correlated with results of Env binding assays, indicating that greater immunogenicity resulted in greater capture. Although vaccination elicited negligible neutralizing activity against the challenge strain (50% inhibitory dilutions of >1/80 in all cases), animals with low capture and whose plasma, at a fixed dilution, inhibited a higher fraction of virus were infected at a lower rate than animals with high capture and low neutralization (P = 0.039); only animals with the low capture/high neutralization response profile were protected compared with unvaccinated control animals (P = 0.026). In a sieve analysis, high capture and low capture were distinguishable on the basis of polymorphisms in the V1 loop of Env at amino acids 144 and 145. Our results indicate that vaccine-induced antibody that binds to and captures infectious virus but does not inhibit its infectivity may enhance the likelihood of infection following rectal challenge with SIVmac251. Higher immunogenicity resulting in better antibody capture but similar anti-infectivity may not improve vaccine efficacy.
IMPORTANCE
Vaccines generally prevent viral infections by eliciting antibodies that inhibit virus infectivity. However, antibodies, including those induced by vaccination, have the potential to enhance, rather than prevent infection. We measured the ability of vaccine-induced antibodies to capture infectious simian immunodeficiency virus (SIV) and explored the relationship between virus capture and infection outcomes. We found that capture correlated with the number of SIV variants that established infection, such that animals whose plasma captured more virus were infected with a higher number of unique strains. In addition, animals whose sera had high capture but weak anti-infectivity activity were infected at a higher rate than were animals with low capture and stronger anti-infectivity activity. These results suggest that vaccines that induce antibodies that bind to and capture infectious virus but do not inhibit virus infectivity will not be effective in preventing infection.
C1 [Gach, Johannes S.; Forthal, Donald N.] Univ Calif Irvine, Dept Med, Div Infect Dis, Irvine, CA 92717 USA.
[Gach, Johannes S.; Forthal, Donald N.] Univ Calif Irvine, Dept Mol Biol & Biochem, Div Infect Dis, Irvine, CA 92717 USA.
[Venzon, David] NCI, Biostat & Data Management Sect, Bethesda, MD 20892 USA.
[Vaccari, Monica; Franchini, Genoveffa] NCI, Anim Models & Vaccine Sect, Bethesda, MD 20892 USA.
[Keele, Brandon F.] Leidos Biomed Res Inc, AIDS & Canc Virus Program, Frederick Natl Lab, Frederick, MD USA.
RP Forthal, DN (reprint author), Univ Calif Irvine, Dept Med, Div Infect Dis, Irvine, CA 92717 USA.; Forthal, DN (reprint author), Univ Calif Irvine, Dept Mol Biol & Biochem, Div Infect Dis, Irvine, CA 92717 USA.
EM dnfortha@uci.edu
OI Gach, Johannes/0000-0002-5043-5710
FU HHS | NIH | National Cancer Institute (NCI) [HHSN261200800001E]; HHS |
NIH | National Institute of Allergy and Infectious Diseases (NIAID)
[R01AI102715, R01AI118581]; National Institute of Allergy and Infectious
Diseases of the National Institutes of Health [R01AI102715,
R01AI118581]; National Cancer Institute [HHSN261200800001E]
FX This work, including the efforts of Brandon F. Keele, was funded by HHS
| NIH | National Cancer Institute (NCI) (HHSN261200800001E). This work,
including the efforts of Donald N. Forthal, was funded by HHS | NIH |
National Institute of Allergy and Infectious Diseases (NIAID)
(R01AI102715 and R01AI118581).; Research reported in this publication
was supported by the National Institute of Allergy and Infectious
Diseases of the National Institutes of Health under award numbers
R01AI102715 and R01AI118581 and in part by federal funds from the
National Cancer Institute under contract HHSN261200800001E. The content
is solely the responsibility of the authors and does not necessarily
represent the official views of the National Institutes of Health.
NR 22
TC 0
Z9 0
U1 2
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD OCT
PY 2016
VL 90
IS 19
BP 8487
EP 8495
DI 10.1128/JVI.00812-16
PG 9
WC Virology
SC Virology
GA DW6LH
UT WOS:000383761900010
PM 27440881
ER
PT J
AU Iyer, SS
Gangadhara, S
Victor, B
Shen, XY
Chen, XM
Nabi, R
Kasturi, SP
Sabula, MJ
Labranche, CC
Reddy, PBJ
Tomaras, GD
Montefiori, DC
Moss, B
Spearman, P
Pulendran, B
Kozlowski, PA
Amara, RR
AF Iyer, Smita S.
Gangadhara, Sailaja
Victor, Blandine
Shen, Xiaoying
Chen, Xuemin
Nabi, Rafiq
Kasturi, Sudhir P.
Sabula, Michael J.
Labranche, Celia C.
Reddy, Pradeep B. J.
Tomaras, Georgia D.
Montefiori, David C.
Moss, Bernard
Spearman, Paul
Pulendran, Bali
Kozlowski, Pamela A.
Amara, Rama Rao
TI Virus-Like Particles Displaying Trimeric Simian Immunodeficiency Virus
(SIV) Envelope gp160 Enhance the Breadth of DNA/Modified Vaccinia Virus
Ankara SIV Vaccine-Induced Antibody Responses in Rhesus Macaques
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID T-CELL RESPONSES; HIV VACCINE; MUCOSAL CHALLENGE; DENDRITIC CELLS;
DNA/MVA VACCINE; PROTECTION; IMMUNOGENICITY; SIVMAC251; EFFICACY;
IMMUNITY
AB The encouraging results of the RV144 vaccine trial have spurred interest in poxvirus prime-protein boost human immunodeficiency virus (HIV) vaccine modalities as a strategy to induce protective immunity. Because vaccine-induced protective immunity is critically determined by HIV envelope (Env) conformation, significant efforts are directed toward generating soluble trimeric Env immunogens that assume native structures. Using the simian immunodeficiency virus (SIV)-macaque model, we tested the immunogenicity and efficacy of sequential immunizations with DNA(D), modified vaccinia virus Ankara (MVA) (M), and protein immunogens, all expressing virus-like particles (VLPs) displaying membrane-anchored trimeric Env. A single VLP protein boost displaying trimeric gp160 adjuvanted with nanoparticle-encapsulated Toll-like receptor 4/7/8 (TLR4/7/8) agonists, administered 44 weeks after the second MVA immunization, induced up to a 3-fold increase in Env-specific IgG binding titers in serum and mucosa. Importantly, the VLP protein boost increased binding antibody against scaffolded V1V2, antibody-dependent phagocytic activity against VLP-coated beads, and antibody breadth and neutralizing antibody titers against homologous and heterologous tier 1 SIVs. Following 5 weekly intrarectal SIVmac251 challenges, two of sevenDNA/MVA and VLP (DM + VLP)-vaccinated animals were completely protected compared to productive infection in all seven DM-vaccinated animals. Vaccinated animals demonstrated stronger acute viral pulldown than controls, but a trend for higher acute viremia was observed in the DM + VLP group, likely due to a slower recall of Gag-specific CD8 T cells. Our findings support immunization with VLPs containing trimeric Env as a strategy to augment protective antibody but underscore the need for optimal engagement of CD8 T cells to achieve robust early viral control.
IMPORTANCE
The development of an effective HIV vaccine remains a global necessity for preventing HIV infection and reducing the burden of AIDS. While this goal represents a formidable challenge, the modest efficacy of the RV144 trial indicates that multicomponent vaccination regimens that elicit both cellular and humoral immune responses can prevent HIV infection in humans. However, whether protein immunizations synergize withDNAprime-viral vector boosts to enhance cellular and humoral immune responses remains poorly understood. We addressed this question in a nonhuman primate model, and our findings show benefit for sequential protein immunization combined with a potent adjuvant in boosting antibody titers induced by a preceding DNA/MVA immunization. This promising strategy can be further developed to enhance neutralizing antibody responses and boost CD8 T cells to provide robust protection and viral control.
C1 [Iyer, Smita S.; Gangadhara, Sailaja; Victor, Blandine; Sabula, Michael J.; Reddy, Pradeep B. J.; Amara, Rama Rao] Emory Univ, Yerkes Natl Primate Res Ctr, Emory Vaccine Ctr, Dept Microbiol & Immunol, Atlanta, GA 30322 USA.
[Shen, Xiaoying; Tomaras, Georgia D.] Duke Univ, Med Ctr, Duke Human Vaccine Inst, Durham, NC USA.
[Chen, Xuemin; Spearman, Paul] Emory Univ, Sch Med, Dept Pediat, Atlanta, GA USA.
[Nabi, Rafiq; Kozlowski, Pamela A.] Louisiana State Univ, Hlth Sci Ctr, Dept Microbiol Immunol & Parasitol, New Orleans, LA USA.
[Kasturi, Sudhir P.; Pulendran, Bali] Emory Univ, Sch Med, Dept Pathol & Lab Med, Atlanta, GA 30322 USA.
[Labranche, Celia C.; Montefiori, David C.] Duke Univ, Med Ctr, Dept Surg, Durham, NC 27710 USA.
[Moss, Bernard] NIAID, Viral Dis Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
RP Amara, RR (reprint author), Emory Univ, Yerkes Natl Primate Res Ctr, Emory Vaccine Ctr, Dept Microbiol & Immunol, Atlanta, GA 30322 USA.
EM ramara@emory.edu
FU National Institute of Allergy and Infectious Diseases (NIAID) [P01
AI088575]; NIH [PO1 AI088575, P51 OD011132, P30 AI50409,
HHSN27201100016C]; Division of Intramural Research, NIAID, NIH
FX This work, including the efforts of Rama Rao Amara, was funded by
National Institute of Allergy and Infectious Diseases (NIAID) (P01
AI088575).; This study was supported in part by NIH grants PO1 AI088575
to R.R.A., P51 OD011132 to the Yerkes National Primate Research Center,
P30 AI50409 to the Emory Center for AIDS Research, and HHSN27201100016C
to D.C.M. Partial support was also provided by the Division of
Intramural Research, NIAID, NIH.
NR 40
TC 1
Z9 1
U1 6
U2 6
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD OCT
PY 2016
VL 90
IS 19
BP 8842
EP 8854
DI 10.1128/JVI.01163-16
PG 13
WC Virology
SC Virology
GA DW6LH
UT WOS:000383761900038
PM 27466414
ER
PT J
AU Sivan, G
Weisberg, AS
Americo, JL
Moss, B
AF Sivan, Gilad
Weisberg, Andrea S.
Americo, Jeffrey L.
Moss, Bernard
TI Retrograde Transport from Early Endosomes to the trans-Golgi Network
Enables Membrane Wrapping and Egress of Vaccinia Virus Virions
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID INTRACELLULAR ENVELOPED VIRIONS; COG COMPLEX INTERACTS; ACTIN-BASED
MOTILITY; EXTRACELLULAR VIRUS; PHOSPHOLIPASE-D; F13L PROTEIN;
TRAFFICKING INHIBITOR; SIRNA SCREEN; CELLS; RELEASE
AB The anterograde pathway, from the endoplasmic reticulum through the trans-Golgi network to the cell surface, is utilized by trans-membrane and secretory proteins. The retrograde pathway, which directs traffic in the opposite direction, is used following endocytosis of exogenous molecules and recycling of membrane proteins. Microbes exploit both routes: viruses typically use the anterograde pathway for envelope formation prior to exiting the cell, whereas ricin and Shiga-like toxins and some nonenveloped viruses use the retrograde pathway for cell entry. Mining a human genome-wide RNA interference (RNAi) screen revealed a need for multiple retrograde pathway components for cell-to-cell spread of vaccinia virus. We confirmed and extended these results while discovering that retrograde trafficking was required for virus egress rather than entry. Retro-2, a specific retrograde trafficking inhibitor of protein toxins, potently prevented spread of vaccinia virus as well as monkeypox virus, a human pathogen. Electron and confocal microscopy studies revealed that Retro-2 prevented wrapping of virions with an additional double-membrane envelope that enables microtubular transport, exocytosis, and actin polymerization. The viral B5 and F13 protein components of this membrane, which are required for wrapping, normally colocalize in the trans-Golgi network. However, only B5 traffics through the secretory pathway, suggesting that F13 uses another route to the trans-Golgi network. The retrograde route was demonstrated by finding that F13 was largely confined to early endosomes and failed to colocalize with B5 in the presence of Retro-2. Thus, vaccinia virus makes novel use of the retrograde transport system for formation of the viral wrapping membrane.
IMPORTANCE
Efficient cell-to-cell spread of vaccinia virus and other orthopoxviruses depends on the wrapping of infectious particles with a double membrane that enables microtubular transport, exocytosis, and actin polymerization. Interference with wrapping or subsequent steps results in severe attenuation of the virus. Some previous studies had suggested that the wrapping membrane arises from the trans-Golgi network, whereas others suggested an origin from early endosomes. Some nonenveloped viruses use retrograde trafficking for entry into the cell. In contrast, we provided evidence that retrograde transport from early endosomes to the trans-Golgi network is required for the membrane-wrapping step in morphogenesis of vaccinia virus and egress from the cell. The potent in vitro inhibition of this step by the drug Retro-2 suggests that derivatives with enhanced pharmacological properties might serve as useful antipoxviral agents.
C1 [Sivan, Gilad; Weisberg, Andrea S.; Americo, Jeffrey L.; 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
OI Moss, Bernard/0000-0002-2154-8564
FU Division of Intramural Research, National Institute of Allergy and
Infectious Diseases (DIR, NIAID) [1 ZIA AI001074]
FX This work, including the efforts of Bernard Moss, was funded by Division
of Intramural Research, National Institute of Allergy and Infectious
Diseases (DIR, NIAID) (1 ZIA AI001074).
NR 80
TC 3
Z9 3
U1 8
U2 8
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD OCT
PY 2016
VL 90
IS 19
BP 8891
EP 8905
DI 10.1128/JVI.01114-16
PG 15
WC Virology
SC Virology
GA DW6LH
UT WOS:000383761900042
PM 27466413
ER
PT J
AU Chung, JY
Choi, J
Sears, JD
Ylaya, K
Perry, C
Choi, CH
Hong, SM
Chol, H
Brown, KM
Hewitt, SM
AF Chung, Joon-Yong
Choi, Jiyeon
Sears, John D.
Ylaya, Kris
Perry, Candice
Choi, Chel H.
Hong, Seung-Mo
Chol, Hanbyoul
Brown, Kevin M.
Hewitt, Stephen M.
TI A melanin-bleaching methodology for molecular and histopathological
analysis of formalin-fixed paraffin-embedded tissue
SO LABORATORY INVESTIGATION
LA English
DT Article
ID PHASE PROTEIN ARRAY; PIGMENTED MELANOCYTIC NEOPLASMS; DILUTE
HYDROGEN-PEROXIDE; GROWTH-FACTOR; RNA; REMOVAL; IMMUNOPEROXIDASE;
POLYMERASE; EXTRACTION; DIAGNOSIS
AB Removal of excessive melanin from heavily pigmented formalin-fixed paraffin-embedded (FFPE) melanoma tissues is essential for histomorphological and molecular diagnostic assessments. Although there have been efforts to address this issue, current methodologies remain complex and time-consuming, and are not suitable for multiple molecular applications. Herein, we have developed a robust and rapid melanin-bleaching methodology for FFPE tissue specimens. Our approach is based on quick bleaching (15 min) at high temperature (80 degrees C) with 0.5% diluted hydrogen peroxide (H2O2) in Tris-HCl, PBS, or Tris/Tricine/SDS buffer. Immunostaining for Ki-67 and HMB45 was enhanced by bleaching with 0.5% H2O2 in Tris/Tricine/SDS and Tris-HCl, respectively. In addition to histopathological applications, our approach also facilitates recovery of protein and nucleic acid from archival melanin-rich FFPE tissue sections. Protein extracted from bleached FFPE tissues was compatible with western blotting using anti-human GAPDH and AKT antibodies. Our bleaching condition significantly improved RNA quality compared with unbleached tissues without compromising the yield. Notably, the RNA/DNA obtained from bleached tissues was suitable for end point PCR and real-time quantitative RT-PCR. In conclusion, this improved melanin-bleaching method enhances and simplifies immunostaining procedures, and facilitates the use of melanin-rich FFPE tissues for histomorphological and PCR amplification-based molecular assays.
C1 [Chung, Joon-Yong; Sears, John D.; Ylaya, Kris; Perry, Candice; Choi, Chel H.; Chol, Hanbyoul; Hewitt, Stephen M.] NCI, Expt Pathol Lab, Pathol Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Choi, Jiyeon; Brown, Kevin M.] NCI, Lab Translat Genom, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Perry, Candice] Leidos Biomed Res Inc, Antibody Characterizat Lab, Adv Technol Program, Frederick, MD USA.
[Choi, Chel H.] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Obstet & Gynecol, Seoul, South Korea.
[Hong, Seung-Mo] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Pathol, Seoul, South Korea.
[Chol, Hanbyoul] Yonsei Univ, Coll Med, Gangnam Severance Hosp, Dept Obstet & Gynecol, Seoul, South Korea.
RP Hewitt, SM (reprint author), NCI, Expt Pathol Lab, Pathol Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.; Hewitt, SM (reprint author), NCI, Expt Pathol Lab, Pathol Lab, Ctr Canc Res,NIH, MSC1500, Bethesda, MD 20892 USA.
EM genejock@helix.nih.gov
OI Chung, Joon-Yong/0000-0001-5041-5982
FU Intramural Research Program of the National Institutes of Health,
National Cancer Institute, Center for Cancer Research, and Division of
Cancer Epidemiology and Genetics
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute, Center for
Cancer Research, and Division of Cancer Epidemiology and Genetics.
NR 30
TC 0
Z9 0
U1 1
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
EI 1530-0307
J9 LAB INVEST
JI Lab. Invest.
PD OCT
PY 2016
VL 96
IS 10
BP 1116
EP 1127
DI 10.1038/labinvest.2016.90
PG 12
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA DX0EV
UT WOS:000384035500007
PM 27548802
ER
PT J
AU Burbelo, PD
Iadarola, MJ
Alevizos, I
Sapio, MR
AF Burbelo, Peter D.
Iadarola, Michael J.
Alevizos, Ilias
Sapio, Matthew R.
TI Transcriptomic Segregation of Human Autoantigens Useful for the
Diagnosis of Autoimmune Diseases
SO MOLECULAR DIAGNOSIS & THERAPY
LA English
DT Review
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; PRIMARY BILIARY-CIRRHOSIS; STIFF-PERSON
SYNDROME; I INTERFERON PATHWAY; RHEUMATOID-ARTHRITIS;
DERMATITIS-HERPETIFORMIS; SJOGRENS-SYNDROME; MEMBRANOUS NEPHROPATHY;
MICROARRAY ANALYSIS; CELIAC-DISEASE
AB The measurement of autoantibodies in the clinical care of autoimmune patients allows for diagnosis, monitoring, and even disease prediction. Despite their clinical utility, the functional significance of autoantibody target proteins in many autoimmune diseases remains unclear. Here we present a comprehensive review of 52 autoantigens commonly employed for the serological diagnosis of 24 autoimmune diseases. We discuss their function, whether they have extracellular-exposed epitopes, and whether antibodies to these proteins are known to be pathogenic. Transcriptomics (RNA-Seq) datasets were mined to display messenger RNA (mRNA) expression of the autoantigens across 32 tissues and organs. This analysis revealed that autoantigens cluster into one of three groups: expression in the tissue most strongly affected in the disease (Group I), ubiquitous expression with enrichment in immune tissues (Group II), or expression in other tissues not typically associated with the clinical presentation (Group III). Clustering demonstrated that the autoantigens within Group I were often proteins containing extracellular epitopes, many of which are targets of pathogenic autoantibodies. Group II autoantigens were targets for several rheumatological diseases, including Sjogren syndrome, systemic lupus erythematosus, myositis, and systemic sclerosis, and were ubiquitously expressed with enrichment in immune-rich tissues. This raises the possibility that immune cells in Group II disorders may be the source of autoimmunization and/or targets of immune cell responses. Since tissues showing enriched autoantigen gene expression may contribute to the development of autoantibodies and subsequent autoimmunity, the emergent patterns arising from the autoantigen transcriptomic profiles may provide a new heuristic framework to deconvolute these complex disorders.
C1 [Burbelo, Peter D.] Natl Inst Dent & Craniofacial Res, Dent Clin Res Core, NIH, Bldg 10,Rm 5N102, Bethesda, MD 20892 USA.
[Iadarola, Michael J.; Sapio, Matthew R.] NIH, Dept Perioperat Med, Ctr Clin, Bldg 10, Bethesda, MD 20892 USA.
[Alevizos, Ilias] Natl Inst Dent & Craniofacial Res, Sjogrens Syndrome & Salivary Gland Dysfunct Unit, NIH, Bethesda, MD USA.
RP Burbelo, PD (reprint author), Natl Inst Dent & Craniofacial Res, Dent Clin Res Core, NIH, Bldg 10,Rm 5N102, Bethesda, MD 20892 USA.
EM burbelop@nidcr.nih.gov
FU intramural research programs of the National Institute of Dental and
Craniofacial Research; National Institutes of Health Clinical Center
FX This work was supported by the intramural research programs of the
National Institute of Dental and Craniofacial Research and the National
Institutes of Health Clinical Center.
NR 76
TC 0
Z9 0
U1 4
U2 4
PU ADIS INT LTD
PI NORTHCOTE
PA 5 THE WAREHOUSE WAY, NORTHCOTE 0627, AUCKLAND, NEW ZEALAND
SN 1177-1062
EI 1179-2000
J9 MOL DIAGN THER
JI Mol. Diagn. Ther.
PD OCT
PY 2016
VL 20
IS 5
BP 415
EP 427
DI 10.1007/s40291-016-0211-6
PG 13
WC Genetics & Heredity; Pharmacology & Pharmacy
SC Genetics & Heredity; Pharmacology & Pharmacy
GA DW3BE
UT WOS:000383516300002
PM 27259330
ER
PT J
AU Chen, W
Liu, P
Volkow, ND
Pan, Y
Du, C
AF Chen, W.
Liu, P.
Volkow, N. D.
Pan, Y.
Du, C.
TI Cocaine attenuates blood flow but not neuronal responses to stimulation
while preserving neurovascular coupling for resting brain activity
SO MOLECULAR PSYCHIATRY
LA English
DT Article
ID POSITRON EMISSION TOMOGRAPHY; RAT SOMATOSENSORY CORTEX; FUNCTIONAL MRI;
IN-VIVO; ALPHA-CHLORALOSE; DOPAMINE; ABUSERS; SIGNAL; ABNORMALITIES;
COMPLICATIONS
AB Cocaine affects neuronal activity and constricts cerebral blood vessels, making it difficult to determine whether cocaine-induced changes in cerebral blood flow (CBF) reflect neuronal activation or its vasoactive effects. Here we assessed the effects of acute cocaine on both resting-state and stimulation responses to investigate cocaine's effects on neurovascular coupling and to differentiate its effects on neuronal activity from its vasoactive actions. We concurrently measured cortical field potentials via thinned-skull electroencephalography recordings and CBF with laser Doppler flowmetry in the rat's somatosensory cortex for both resting state and forepaw stimulation before and following cocaine administration (1 mg kg(-1), intravenously). Results show both resting-state field potentials and CBF were depressed after cocaine administration (19.8 +/- 4.7% and 52.1 +/- 13.4%, respectively) and these changes were strongly correlated with each other (r = 0.81, P<0.001), indicating that cocaine did not affect neurovascular coupling at rest and that the reduction in resting CBF reflected reduction in synchronized spontaneous neuronal activity rather than vasoconstriction. In contrast, the forepaw stimulation-evoked neuronal activity was not changed by cocaine (P = 0.244), whereas the CBF to the stimulation was reduced 49.9 +/- 2.6% (P = 0.028) gradually recovering similar to 20 min after cocaine injection, indicating that neurovascular coupling during stimulation was temporarily disrupted by cocaine. Neurovascular uncoupling by cocaine during stimulation but not during rest indicates that distinct processes might underlie neurovascular regulation for both stimulation and spontaneous activity. The greater reductions by cocaine to the stimulation-induced CBF increases than to the background CBF should be considered when interpreting functional MRI studies comparing activation responses between controls and cocaine abusers. Neurovascular uncoupling could contribute to cocaine's neurotoxicity, particularly for stimulation conditions when CBF might be insufficient to cover for the energetic demands of neuronal tissue.
C1 [Chen, W.; Liu, P.; Pan, Y.; Du, C.] SUNY Stony Brook, Dept Biomed Engn, Stony Brook, NY 11794 USA.
[Volkow, N. D.] NIAAA, NIH, Bethesda, MD 20892 USA.
RP Pan, Y; Du, C (reprint author), SUNY Stony Brook, Dept Biomed Engn, Stony Brook, NY 11794 USA.; Volkow, ND (reprint author), NIAAA, NIH, Bethesda, MD 20892 USA.
EM nvolkow@nida.nih.gov; yingtian.pan@stonybrook.edu;
congwu.du@stonybrook.edu
FU National Institutes of Health (NIH) [R21DA032228, 1R01DA029718,
R01NS084817]; NIH's Intramural Program
FX This work was supported, in part, by National Institutes of Health (NIH)
Grants R21DA032228 (YP/CD), 1R01DA029718 (CD/YP), R01NS084817 (CD) and
NIH's Intramural Program (NDV).
NR 47
TC 2
Z9 2
U1 2
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1359-4184
EI 1476-5578
J9 MOL PSYCHIATR
JI Mol. Psychiatr.
PD OCT
PY 2016
VL 21
IS 10
BP 1408
EP 1416
DI 10.1038/mp.2015.185
PG 9
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA DX1KT
UT WOS:000384127000012
PM 26666202
ER
PT J
AU Belinson, H
Nakatani, J
Babineau, BA
Birnbaum, RY
Ellegood, J
Bershteyn, M
McEvilly, RJ
Long, JM
Willert, K
Klein, OD
Ahituv, N
Lerch, JP
Rosenfeld, MG
Wynshaw-Boris, A
AF Belinson, H.
Nakatani, J.
Babineau, B. A.
Birnbaum, R. Y.
Ellegood, J.
Bershteyn, M.
McEvilly, R. J.
Long, J. M.
Willert, K.
Klein, O. D.
Ahituv, N.
Lerch, J. P.
Rosenfeld, M. G.
Wynshaw-Boris, A.
TI Prenatal beta-catenin/Brn2/Tbr2 transcriptional cascade regulates adult
social and stereotypic behaviors
SO MOLECULAR PSYCHIATRY
LA English
DT Article
ID AUTISM SPECTRUM DISORDERS; NEURONAL DIFFERENTIATION; INTERMEDIATE
PROGENITORS; DEVELOPING NEOCORTEX; GENE-EXPRESSION; MOUSE MODELS;
BETA-CATENIN; PATHWAY; CELLS; BRAIN
AB Social interaction is a fundamental behavior in all animal species, but the developmental timing of the social neural circuit formation and the cellular and molecular mechanisms governing its formation are poorly understood. We generated a mouse model with mutations in two Disheveled genes, Dvl1 and Dvl3, that displays adult social and repetitive behavioral abnormalities associated with transient embryonic brain enlargement during deep layer cortical neuron formation. These phenotypes were mediated by the embryonic expansion of basal neural progenitor cells (NPCs) via deregulation of a a-catenin/Brn2/Tbr2 transcriptional cascade. Transient pharmacological activation of the canonical Wnt pathway during this period of early corticogenesis rescued the beta-catenin/Brn2/Tbr2 transcriptional cascade and the embryonic brain phenotypes. Remarkably, this embryonic treatment prevented adult behavioral deficits and partially rescued abnormal brain structure in Dvl mutant mice. Our findings define a mechanism that links fetal brain development and adult behavior, demonstrating a fetal origin for social and repetitive behavior deficits seen in disorders such as autism.
C1 [Belinson, H.; Nakatani, J.; Babineau, B. A.; Bershteyn, M.; Wynshaw-Boris, A.] Univ Calif San Francisco, Sch Med, Dept Pediat, Inst Human Genet,Edyth & Eli Broad Inst Regenerat, San Francisco, CA USA.
[Birnbaum, R. Y.] Ben Gurion Univ Negev, Dept Life Sci, Beer Sheva, Israel.
[Ellegood, J.; Lerch, J. P.] Hosp Sick Children, Mouse Imaging Ctr, Toronto, ON, Canada.
[McEvilly, R. J.; Rosenfeld, M. G.] Univ Calif San Diego, Sch Med, Howard Hughes Med Inst, Dept Med, La Jolla, CA 92093 USA.
[Long, J. M.] NIA, Lab Behav Neurosci, NIH, Baltimore, MD 21224 USA.
[Willert, K.] Univ Calif San Diego, Sch Med, Inst Regenerat Med, Dept Cell & Mol Biol, La Jolla, CA 92093 USA.
[Klein, O. D.] Univ Calif San Francisco, Dept Orofacial Sci, San Francisco, CA 94143 USA.
[Klein, O. D.] Univ Calif San Francisco, Program Craniofacial & Mesenchymal Biol, San Francisco, CA 94143 USA.
[Ahituv, N.] Univ Calif San Francisco, Inst Human Genet, Dept Bioengn & Therapeut Sci, San Francisco, CA 94143 USA.
[Lerch, J. P.] Univ Toronto, Dept Med Biophys, Toronto, ON, Canada.
[Wynshaw-Boris, A.] Case Western Reserve Univ, Sch Med, Dept Genet & Genome Sci, 10900 Euclid Ave,BRB731, Cleveland, OH 44106 USA.
RP Wynshaw-Boris, A (reprint author), Case Western Reserve Univ, Sch Med, Dept Genet & Genome Sci, 10900 Euclid Ave,BRB731, Cleveland, OH 44106 USA.
EM ajw168@case.edu
FU NINDS [R01 NS073159, R01NS079231]; Simons Foundation SFARI [256769];
Ontario Brain Institute; Autism Speaks Translational Postdoctoral
Fellowship [7587]; NIH [P30NS065780]; NIH, National Institute on Aging
FX This research was supported by NINDS grants R01 NS073159 (AWB) and
R01NS079231 (RYB & NA), the Simons Foundation SFARI #256769 (NA), the
Ontario Brain Institute (JPL), and a Autism Speaks Translational
Postdoctoral Fellowship #7587 (HB). Behavioral data were obtained with
the help of the Gladstone Institute Behavioral Core (supported by NIH
grant P30NS065780). This research was supported in part by the
Intramural Research Program of the NIH, National Institute on Aging. We
thank Peter Scacheri for his critical comments on the manuscript.
NR 71
TC 4
Z9 4
U1 10
U2 10
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1359-4184
EI 1476-5578
J9 MOL PSYCHIATR
JI Mol. Psychiatr.
PD OCT
PY 2016
VL 21
IS 10
BP 1417
EP 1433
DI 10.1038/mp.2015.207
PG 17
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA DX1KT
UT WOS:000384127000013
PM 26830142
ER
PT J
AU Mastronardi, CA
Pillai, E
Pineda, DA
Martinez, AF
Lopera, F
Velez, JI
Palacio, JD
Patel, H
Easteal, S
Acosta, MT
Castellanos, FX
Muenke, M
Arcos-Burgos, M
AF Mastronardi, C. A.
Pillai, E.
Pineda, D. A.
Martinez, A. F.
Lopera, F.
Velez, J. I.
Palacio, J. D.
Patel, H.
Easteal, S.
Acosta, M. T.
Castellanos, F. X.
Muenke, M.
Arcos-Burgos, M.
TI Linkage and association analysis of ADHD endophenotypes in extended and
multigenerational pedigrees from a genetic isolate
SO MOLECULAR PSYCHIATRY
LA English
DT Article
ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; FAMILY-BASED ASSOCIATION;
GENERAL-CLASS; SUSCEPTIBILITY; EPILEPSY; CHILDREN; TRAITS; TESTS; POWER;
LOCI
AB Attention-deficit/hyperactivity disorder (ADHD) is a heritable, chronic, neurodevelopmental disorder with serious long-term repercussions. Despite being one of the most common cognitive disorders, the clinical diagnosis of ADHD is based on subjective assessments of perceived behaviors. Endophenotypes (neurobiological markers that cosegregate and are associated with an illness) are thought to provide a more powerful and objective framework for revealing the underlying neurobiology than syndromic psychiatric classification. Here, we present the results of applying genetic linkage and association analyses to neuropsychological endophenotypes using microsatellite and single nucleotide polymorphisms. We found several new genetic regions linked and/or associated with these endophenotypes, and others previously associated to ADHD, for example, loci harbored in the LPHN3, FGF1, POLR2A, CHRNA4 and ANKFY1 genes. These findings, when compared with those linked and/or associated to ADHD, suggest that these endophenotypes lie on shared pathways. The genetic information provided by this study offers a novel and complementary method of assessing the genetic causes underpinning the susceptibility to behavioral conditions and may offer new insights on the neurobiology of the disorder.
C1 [Mastronardi, C. A.; Pillai, E.; Velez, J. I.; Patel, H.; Arcos-Burgos, M.] Australian Natl Univ, John Curtin Sch Med Res, Genome Biol Dept, ANU Coll Med Biol & Environm,Genom & Predict Med, Bldg 131 Garran Rd, Canberra, ACT 2600, Australia.
[Pineda, D. A.; Lopera, F.; Palacio, J. D.; Arcos-Burgos, M.] Univ Antioquia, Grp Neurosci, Medellin, Colombia.
[Martinez, A. F.; Acosta, M. T.; Muenke, M.; Arcos-Burgos, M.] NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
[Easteal, S.] Australian Natl Univ, John Curtin Sch Med Res, Genome Biol Dept,Genom, ANU Coll Med Biol & Environm,Natl Ctr Indigenous, Canberra, ACT, Australia.
[Castellanos, F. X.] NYU, Ctr Child Study, Langone Med Ctr, New York, NY USA.
[Castellanos, F. X.] Nathan S Kline Inst Psychiat Res, Orangeburg, NY USA.
RP Arcos-Burgos, M (reprint author), Australian Natl Univ, John Curtin Sch Med Res, Genome Biol Dept, ANU Coll Med Biol & Environm,Genom & Predict Med, Bldg 131 Garran Rd, Canberra, ACT 2600, Australia.; Muenke, M; Arcos-Burgos, M (reprint author), NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
EM mamuenke@mail.nih.gov; Mauricio.Arcos-Burgos@anu.edu.au
OI Castellanos, Francisco/0000-0001-9192-9437
FU John Curtin School of Medical Research, ANU College of Medicine, Biology
and Environment, The Australian National University, Canberra, ACT,
Australia [R42100-12]; Division of Intramural Research, National Human
Genome Research Institutes, National Institutes of Health, Bethesda, MD,
USA; NHGRI-NIH; COLCIENCIAS [1115-04-18083, 459-2005]; University of
Antioquia; University of San Buenaventura
FX Claudio Mastronardi, Eva Pillai and Mauricio Arcos-Burgos are supported
by John Curtin School of Medical Research, ANU College of Medicine,
Biology and Environment, The Australian National University, Canberra,
ACT, Australia, Project R42100-12. Maximilian Muenke, Ariel F Martinez,
Maria T Acosta and Mauricio Arcos-Burgos are supported by the Division
of Intramural Research, National Human Genome Research Institutes,
National Institutes of Health, Bethesda, MD, USA. Part of this research
was funded by the NHGRI-NIH and by COLCIENCIAS which funded the Project:
'Genetica del Trastorno de Atencion-Hiperactividad: los fenotipos
complejos, los endofenotipos y la asociacion con genes mayores y de
susceptibilidad' Code: 1115-04-18083, Contract: 459-2005, to David
Pineda, University of Antioquia and University of San Buenaventura.
NR 32
TC 2
Z9 2
U1 10
U2 10
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1359-4184
EI 1476-5578
J9 MOL PSYCHIATR
JI Mol. Psychiatr.
PD OCT
PY 2016
VL 21
IS 10
BP 1434
EP 1440
DI 10.1038/mp.2015.172
PG 7
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA DX1KT
UT WOS:000384127000014
PM 26598068
ER
PT J
AU Zimmet, P
Alberti, KG
Magliano, DJ
Bennett, PH
AF Zimmet, Paul
Alberti, K. George
Magliano, Dianna J.
Bennett, Peter H.
TI Diabetes mellitus statistics on prevalence and mortality: facts and
fallacies
SO NATURE REVIEWS ENDOCRINOLOGY
LA English
DT Article
ID IMPAIRED GLUCOSE-TOLERANCE; ALL-CAUSE MORTALITY; FASTING GLUCOSE;
DIAGNOSTIC-CRITERIA; EXCESS MORTALITY; POOLED ANALYSIS; GLOBAL BURDEN;
LIFE-STYLE; POPULATION; RISK
AB Diabetes mellitus is one of the most important public health challenges of the twenty-first century. Until the past decade, it has been seriously underrated as a global health threat. Major gaps exist in efforts to comprehend the burden nationally and globally, especially in developing nations, due to a lack of accurate data for monitoring and surveillance. Early attempts to obtain accurate data, discussed in this article, seem to have been cast aside so, at present, these needs remain unmet. Existing international efforts to assemble information fall far short of requirements. Current estimates are imprecise, only providing a rough picture, and probably underestimate the disease burden. The methodologies that are currently used, and that are discussed in this Perspectives article, are inadequate for providing a complete and accurate assessment of the prevalence of diabetes mellitus. International consensus on uniform standards and criteria for reporting national data on diabetes mellitus prevalence as well as for common complications of diabetes mellitus and mortality need to be developed.
C1 [Zimmet, Paul] Monash Univ, Fac Med Nursing & Hlth Sci, 99 Commercial Rd, Melbourne, Vic 3004, Australia.
[Alberti, K. George] Imperial Coll, Dept Endocrinol & Metab, St Marys Campus,Norfolk Pl, London W2 1PG, England.
[Magliano, Dianna J.] Baker IDI Heart & Diabet Inst, 99 Commercial Rd, Melbourne, Vic 3004, Australia.
[Bennett, Peter H.] NIH, 1550 East Indian Sch Rd, Phoenix, AZ 85014 USA.
RP Zimmet, P (reprint author), Monash Univ, Fac Med Nursing & Hlth Sci, 99 Commercial Rd, Melbourne, Vic 3004, Australia.
EM paul.zimmet@monash.edu
NR 59
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Z9 4
U1 18
U2 18
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-5029
EI 1759-5037
J9 NAT REV ENDOCRINOL
JI Nat. Rev. Endocrinol.
PD OCT
PY 2016
VL 12
IS 10
BP 616
EP 622
DI 10.1038/nrendo.2016.105
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA DW7AR
UT WOS:000383803900007
PM 27388988
ER
PT J
AU Usdin, TB
Dimitrov, EL
AF Usdin, Ted B.
Dimitrov, Eugene L.
TI The Effects of Extended Pain on Behavior: Recent Progress
SO NEUROSCIENTIST
LA English
DT Review
DE Pain-related behavior; neuropathic pain; inflammatory pain; chronic
pain; pain model; affective pain
ID PERIPHERAL-NERVE INJURY; ANTERIOR CINGULATE CORTEX; MEDIAL PREFRONTAL
CORTEX; CHRONIC NEUROPATHIC PAIN; ANXIETY-LIKE BEHAVIOR;
NUCLEUS-ACCUMBENS; PERSISTENT PAIN; CENTRAL AMYGDALA; WORKING-MEMORY;
UP-REGULATION
AB Chronic pain is frequently associated with anxiety, depression, and cognitive dysfunction. This review discusses recent work in rodents that contributes to the understanding of their neurobiological links. Brain regions that contain circuits that mediate persistent changes in behavior that are caused by nerve injury or joint inflammation include the rostral anterior cingulate and other parts of the medial prefrontal cortex, the basolateral and central nucleus of the amygdala, and the nucleus accumbens. Functional changes, including increases in the activity within specific neuronal pathways and in the levels of specific synaptic components, that are associated with the behavior changes, or are in some cases necessary for them, have recently been identified. Broadly projecting modulatory systems and widely expressed factors such as cytokines and growth factors also contribute to pain-associated behavior. Integrating these observations and determining their causal relationships is now critical for the identification of therapeutic targets and the design of appropriate interventions.
C1 [Usdin, Ted B.] NIMH, Sect Fundamental Neurosci, Intramural Res Program, Bethesda, MD 20892 USA.
[Dimitrov, Eugene L.] Rosalind Franklin Univ Med & Sci, Dept Physiol & Biophys, N Chicago, IL USA.
RP Usdin, TB (reprint author), NIMH, Sect Fundamental Neurosci, Intramural Res Program, Bethesda, MD 20892 USA.
EM usdint@mail.nih.gov
FU NIMH Intramural Program [ZIA-MH002685]
FX The author(s) disclosed receipt of the following financial support for
the research, authorship, and/or publication of this article: Support
was provided by the NIMH Intramural Program (ZIA-MH002685).
NR 66
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U1 8
U2 8
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1073-8584
EI 1089-4098
J9 NEUROSCIENTIST
JI Neuroscientist
PD OCT
PY 2016
VL 22
IS 5
BP 521
EP 533
DI 10.1177/1073858416633104
PG 13
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA DV6DC
UT WOS:000383020100012
PM 27621368
ER
PT J
AU Kahler, CW
Caswell, AJ
Laws, MB
Walthers, J
Magill, M
Mastroleo, NR
Howe, CJ
Souza, T
Wilson, I
Bryant, K
Monti, PM
AF Kahler, Christopher W.
Caswell, Amy J.
Laws, M. Barton
Walthers, Justin
Magill, Molly
Mastroleo, Nadine R.
Howe, Chanelle J.
Souza, Timothy
Wilson, Ira
Bryant, Kendall
Monti, Peter M.
TI Using topic coding to understand the nature of change language in a
motivational intervention to reduce alcohol and sex risk behaviors in
emergency department patients
SO PATIENT EDUCATION AND COUNSELING
LA English
DT Article
DE Alcohol; Sex risk; HIV; Motivational interviewing; Dialogue coding
ID USE DISORDERS; HIV CARE; COMMITMENT LANGUAGE; MIXED METHODS; USE
OUTCOMES; METAANALYSIS; AGREEMENT
AB Objective: To elucidate patient language that supports changing a health behavior (change talk) or sustaining the behavior (sustain talk).
Methods: We developed a novel coding system to characterize topics of patient speech in a motivational intervention targeting alcohol and HIV/sexual risk in 90 Emergency Department patients. We further coded patient language as change or sustain talk.
Results: For both alcohol and sex, discussions focusing on benefits of behavior change or change planning were most likely to involve change talk, and these topics comprised a large portion of all change talk. Greater discussion of barriers and facilitators of change also was associated with more change talk. For alcohol use, benefits of drinking behavior was the most common topic of sustain talk. For sex risk, benefits of sexual behavior were rarely discussed, and sustain talk centered more on patterns and contexts, negations of drawbacks, and drawbacks of sexual risk behavior change.
Conclusions: Topic coding provided unique insights into the content of patient change and sustain talk.
Practice implications: Patients are most likely to voice change talk when conversation focuses on behavior change rather than ongoing behavior. Interventions addressing multiple health behaviors should address the unique motivations for maintaining specific risky behaviors. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
C1 [Kahler, Christopher W.; Caswell, Amy J.; Walthers, Justin; Magill, Molly; Mastroleo, Nadine R.; Souza, Timothy; Monti, Peter M.] Brown Univ, Ctr Alcohol & Addict Studies, Sch Publ Hlth, Providence, RI 02912 USA.
[Laws, M. Barton; Wilson, Ira] Brown Univ, Sch Publ Hlth, Dept Hlth Serv Policy & Practice, Providence, RI 02912 USA.
[Howe, Chanelle J.] Brown Univ, Sch Publ Hlth, Dept Epidemiol, Ctr Populat Hlth & Clin Epidemiol, Providence, RI 02912 USA.
[Bryant, Kendall] Natl Inst Alcohol Abuse & Alcoholism, 5635 Fishers Lane, Bethesda, MD USA.
RP Kahler, CW (reprint author), Brown Univ, Sch Publ Hlth, Ctr Alcohol & Addict Studies, Dept Behav & Social Sci, Box G-S121-4, Providence, RI 02912 USA.
EM Christopher_Kahler@brown.edu
FU National Institute on Alcohol Abuse and Alcoholism (NIAAA) [U24AA022003,
5R01AA009892-20, P01AA019072, K23AA018126]
FX Support for this work was provided by the National Institute on Alcohol
Abuse and Alcoholism (NIAAA), grants U24AA022003, 5R01AA009892-20,
P01AA019072, and K23AA018126. Dr. Bryant from NIAAA was involved in
conceptualizing and writing this manuscript. NIAAA did not have any
other involvement in the project.
NR 30
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U1 6
U2 6
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 2016
VL 99
IS 10
BP 1595
EP 1602
DI 10.1016/j.pec.2016.05.003
PG 8
WC Public, Environmental & Occupational Health; Social Sciences,
Interdisciplinary
SC Public, Environmental & Occupational Health; Social Sciences - Other
Topics
GA DW0VQ
UT WOS:000383361500008
PM 27161165
ER
PT J
AU Zweidler-McKay, PA
Hogan, MJS
Jubran, R
Black, V
Casillas, J
Harper, J
Malempati, S
Margolin, J
Felgenhauer, J
Sakamoto, KM
Franklin, J
Shah, M
Seibel, N
Buchanan, G
Vaiselbuh, SR
Hastings, C
Hilden, J
Stork, LC
AF Zweidler-McKay, Patrick A.
Hogan, Mary-Jane Staba
Jubran, Rima
Black, Vandy
Casillas, Jacqueline
Harper, James
Malempati, Suman
Margolin, Judith
Felgenhauer, Judy
Sakamoto, Kathleen M.
Franklin, Janet
Shah, Mona
Seibel, Nita
Buchanan, George
Vaiselbuh, Sarah R.
Hastings, Caroline
Hilden, Joanne
Stork, Linda C.
TI Navigating your career path in pediatric hematology/oncology: On and off
the beaten track
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
C1 [Zweidler-McKay, Patrick A.] Univ Texas MD Anderson Canc Ctr, Childrens Canc Hosp, Div Pediat, Houston, TX 77030 USA.
[Hogan, Mary-Jane Staba] Yale Univ, Sch Med, Dept Pediat, New Haven, CT 06510 USA.
[Jubran, Rima] Childrens Hosp Los Angeles, Div Hematol Oncol, Los Angeles, CA 90027 USA.
[Black, Vandy] Univ Florida, Coll Med, Dept Pediat, Pediat, Gainesville, FL USA.
[Casillas, Jacqueline] Univ Calif Los Angeles, Los Angeles Mattel Childrens Hosp, Div Hematol Oncol, Los Angeles, CA USA.
[Harper, James] Univ Nebraska Med Ctr, Dept Pediat, Omaha, NE USA.
[Malempati, Suman; Stork, Linda C.] Oregon Hlth & Sci Univ, Doernbecher Childrens Hosp, Div Hematol Oncol, Portland, OR 97201 USA.
[Margolin, Judith; Shah, Mona] Texas Childrens Hosp, Baylor Coll Med, Div Hematol Oncol, Houston, TX 77030 USA.
[Felgenhauer, Judy] Providence Sacred Heart Med Ctr, Spokane, WA USA.
[Felgenhauer, Judy] Childrens Hosp, Pediat, Spokane, WA USA.
[Sakamoto, Kathleen M.] Stanford Univ, Dept Pediat, Sch Med, Stanford, CA 94305 USA.
[Franklin, Janet] Amgen Inc, Thousand Oaks, CA USA.
[Seibel, Nita] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Buchanan, George] Univ Texas Southwestern Med Ctr Dallas, Dept Pediat, Dallas, TX USA.
[Vaiselbuh, Sarah R.] Staten Isl Univ Ctr Northwell Hlth, Childrens Canc Ctr, Staten Isl, NY USA.
[Hastings, Caroline] Childrens Hosp & Res Ctr, Div Hematol Oncol, Oakland, CA USA.
[Hilden, Joanne] Univ Colorado, Sch Med, Dept Pediat, Aurora, CO USA.
RP Stork, LC (reprint author), OHSU, CDRCP, Dept Pediat, 3181 SW Sam Jackson Pk Rd, Portland, OR 97239 USA.
EM storkl@ohsu.edu
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 1545-5009
EI 1545-5017
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD OCT
PY 2016
VL 63
IS 10
BP 1723
EP 1730
DI 10.1002/pbc.26094
PG 8
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA DW0ZE
UT WOS:000383371500006
PM 27295503
ER
PT J
AU Kang, MH
Reynolds, CP
Kolb, EA
Gorlick, R
Carol, H
Lock, R
Keir, ST
Maris, JM
Wu, JR
Lyalin, D
Kurmasheva, RT
Houghton, PJ
Smith, MA
AF Kang, Min H.
Reynolds, C. Patrick
Kolb, E. Anders
Gorlick, Richard
Carol, Hernan
Lock, Richard
Keir, Stephen T.
Maris, John M.
Wu, Jianwrong
Lyalin, Dmitry
Kurmasheva, Raushan T.
Houghton, Peter J.
Smith, Malcolm A.
TI Initial Testing (Stage 1) of MK-8242A Novel MDM2 Inhibitorby the
Pediatric Preclinical Testing Program
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
DE developmental therapeutics; pi3k inhibitor; preclinical testing
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; PHASE-I TRIAL; SOLID TUMORS; P53 PATHWAY;
DEDIFFERENTIATED LIPOSARCOMA; ANTAGONIST RG7112; XENOGRAFT MODELS; TP53
MUTATIONS; CHILDHOOD; CANCER
AB BackgroundMK-8242 is an inhibitor of MDM2 that stabilizes the tumor suppressor TP53 and induces growth arrest or apoptosis downstream of TP53 induction.
ProceduresMK-8242 was tested against the Pediatric Preclinical Testing Program (PPTP) in vitro cell line panel at concentrations from 1.0 nM to 10.0 M and against the PPTP in vivo xenograft panels using oral gavage on Days 1-5 and Day 15-19 at a dose of 125 mg/kg (solid tumors) or 75 mg/kg (acute lymphoblastic leukemia [ALL] models).
ResultsThe median IC50 for MK-8242 was 0.07 M for TP53 wild-type cell lines versus >10 M for TP53 mutant cell lines. MK-8242 induced a twofold or greater delay in time to event in 10 of 17 (59%) of TP53 wild-type solid tumor xenografts, excluding osteosarcoma xenografts that have very low TP53 expression. Objective responses were observed in seven solid tumor xenografts representing multiple histotypes. For the systemic-disease ALL panel, among eight xenografts there were two complete responses (CRs) and six partial responses (PRs). Two additional MLL-rearranged xenografts (MV4;11 and RS4;11) grown subcutaneously showed maintained CR and PR, respectively. The expected pharmacodynamic responses to TP53 activation were observed in TP53 wild-type models treated with MK-8242. Pharmacokinetic analysis showed that MK-8242 drug exposure in SCID mice appears to exceed that was observed in adult phase 1 trials.
ConclusionsMK-8242-induced tumor regressions across multiple solid tumor histotypes and induced CRs or PRs for most ALL xenografts. This activity was observed at MK-8242 drug exposures that appear to exceed those observed in human phase 1 trials.
C1 [Kang, Min H.; Reynolds, C. Patrick] Texas Tech Univ, Hlth Sci Ctr, Ctr Canc, 3601 4th St STOP 9445, Lubbock, TX 79430 USA.
[Kolb, E. Anders] Alfred I DuPont Hosp Children, Wilmington, DE USA.
[Gorlick, Richard] Childrens Hosp Montefiore, Bronx, NY USA.
[Carol, Hernan; Lock, Richard] Childrens Canc Inst Australia Med Res, Randwick, NSW, Australia.
[Keir, Stephen T.] Duke Univ, Med Ctr, Durham, NC USA.
[Maris, John M.] Univ Penn, Childrens Hosp Philadelphia, Sch Med, Philadelphia, PA 19104 USA.
[Maris, John M.] Abramson Family Canc Res Inst, Philadelphia, PA USA.
[Wu, Jianwrong] St Jude Childrens Res Hosp, 332 N Lauderdale St, Memphis, TN 38105 USA.
[Lyalin, Dmitry; Kurmasheva, Raushan T.; Houghton, Peter J.] Nationwide Childrens Hosp, Columbus, OH USA.
[Smith, Malcolm A.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
RP Kang, MH (reprint author), Texas Tech Univ, Hlth Sci Ctr, Ctr Canc, 3601 4th St STOP 9445, Lubbock, TX 79430 USA.
EM min.kang@ttuhsc.edu
RI Lock, Richard/G-4253-2013;
OI Reynolds, C. Patrick/0000-0002-2827-8536
FU National Cancer Institute [NO1-CM-42216, CA21765, CA108786]
FX Grant sponsor: National Cancer Institute; Grant numbers: NO1-CM-42216,
CA21765, and CA108786.
NR 41
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U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1545-5009
EI 1545-5017
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD OCT
PY 2016
VL 63
IS 10
BP 1744
EP 1752
DI 10.1002/pbc.26064
PG 9
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA DW0ZE
UT WOS:000383371500009
PM 27238606
ER
PT J
AU Stewart, DR
Givens, SS
Harris, AK
Williams, GM
Messinger, YH
Schultz, KAP
Hill, DA
AF Stewart, Douglas R.
Givens, Shannon S.
Harris, Anne K.
Williams, Gretchen M.
Messinger, Yoav H.
Schultz, Kris Ann P.
Hill, D. Ashley
TI Comment on: DICER1-Negative Pleuropulmonary Blastoma in a Patient With
Selective IgA Deficiency
SO PEDIATRIC BLOOD & CANCER
LA English
DT Letter
ID PREVALENCE; MUTATIONS
C1 [Stewart, Douglas R.; Givens, Shannon S.] NCI, Div Canc Epidemiol & Genet, Clin Genet Branch, NIH, Rockville, MD USA.
[Harris, Anne K.; Williams, Gretchen M.; Messinger, Yoav H.; Schultz, Kris Ann P.] Childrens Hosp & Clin Minnesota, Dept Canc & Blood Disorders, Minneapolis, MN USA.
[Harris, Anne K.; Williams, Gretchen M.; Messinger, Yoav H.; Schultz, Kris Ann P.] Int Pleuropulm Blastoma Registry, Minneapolis, MN USA.
[Harris, Anne K.; Schultz, Kris Ann P.] Int Ovarian & Testicular Stromal Tumor Registry, Minneapolis, MN USA.
[Hill, D. Ashley] Childrens Natl Hlth Syst, Med Genet Res Ctr, Div Pathol, Washington, DC USA.
[Hill, D. Ashley] George Washington Univ, Sch Med & Hlth Sci, Dept Integrat Syst Biol, Washington, DC 20052 USA.
RP Stewart, DR (reprint author), NCI, Div Canc Epidemiol & Genet, Clin Genet Branch, NIH, 9609 Med Ctr Dr,Rm 6E450, Bethesda, MD 20892 USA.
EM drstewart@mail.nih.gov
FU NCI NIH HHS [R01 CA143167]
NR 9
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U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1545-5009
EI 1545-5017
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD OCT
PY 2016
VL 63
IS 10
BP 1869
EP 1870
DI 10.1002/pbc.26075
PG 2
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA DW0ZE
UT WOS:000383371500031
PM 27238822
ER
PT J
AU Csermely, P
Korcsmaros, T
Nussinov, R
AF Csermely, Peter
Korcsmaros, Tamas
Nussinov, Ruth
TI Intracellular and intercellular signaling networks in cancer initiation,
development and precision anti-cancer therapy RAS acts as contextual
signaling hub
SO SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE Cancer attractors; Cancer stem cells; Combination therapies; N=1 trials;
RAS; Signaling networks
ID TUMOR MICROENVIRONMENT; CELL; PATHWAY; METASTASIS; EFFECTOR; DYNAMICS;
MODELS; DIFFERENTIATION; HETEROGENEITY; PROLIFERATION
AB Cancer initiation and development are increasingly perceived as systems-level phenomena, where intraand inter-cellular signaling networks of the ecosystem of cancer and stromal cells offer efficient methodologies for outcome prediction and intervention design. Within this framework, RAS emerges as a 'contextual signaling hub', i.e. the final result of RAS activation or inhibition is determined by the signaling network context. Current therapies often 'train' cancer cells shifting them to a novel attractor, which has increased metastatic potential and drug resistance. The few therapy-surviving cancer cells are surrounded by massive cell death triggering a primordial adaptive and reparative general wound healing response. Overall, dynamic analysis of patient- and disease-stage specific intracellular and intercellular signaling networks may open new areas of anticancer therapy using multitarget drugs, drugs combinations, edgetic drugs, as well as help design 'gentler', differentiation and maintenance therapies. (C) 2016 Elsevier Ltd. All rights reserved.
C1 [Csermely, Peter] Semmelweis Univ, Dept Med Chem, POB 2, H-1428 Budapest, Hungary.
[Korcsmaros, Tamas] Inst Food Res, Gut Hlth & Food Safety Programme, Norwich Res Pk, Norwich NR4 7UA, Norfolk, England.
[Korcsmaros, Tamas] Genome Anal Ctr, Earlham Inst TGAC, Norwich Res Pk, Norwich NR4 7UH, Norfolk, England.
[Nussinov, Ruth] NCI, Canc & Inflammat Program, Leidos Biomed Res Inc, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
[Nussinov, Ruth] Tel Aviv Univ, Sackler Sch Med, Dept Human Mol Genet & Biochem, IL-69978 Tel Aviv, Israel.
RP Csermely, P (reprint author), Semmelweis Univ, Dept Med Chem, POB 2, H-1428 Budapest, Hungary.
EM Csermely.Peter@med.semmelweis-univ.hu
FU Frederick National Laboratory for Cancer Research, National Institutes
of Health [HHSN261200800001E]; Biotechnology and Biological Sciences
Research Council, UK; Hungarian National Research, Development and
Innovation Office [K115378]; Intramural Research Program of NIH,
Frederick National Lab, Center for Cancer Research
FX The authors thank the authors of this special issue for their excellent
and timely contributions. Work in the authors' laboratory was supported
in part with Federal funds from the Frederick National Laboratory for
Cancer Research, National Institutes of Health, under contract
HHSN261200800001E. TK is a Computational Biology Fellow at The Genome
Analysis Centre in partnership with the Institute of Food Research
(Norwich, UK), and strategically supported by Biotechnology and
Biological Sciences Research Council, UK. Research in the lab of PC was
supported by the Hungarian National Research, Development and Innovation
Office (K115378). This research was supported in part by the Intramural
Research Program of NIH, Frederick National Lab, Center for Cancer
Research. The content of this publication does not necessarily reflect
the views or policies of the Department of Health and Human Services,
nor does mention of trade names, commercial products ororganizations
imply endorsement by the US Government.
NR 69
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PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1084-9521
J9 SEMIN CELL DEV BIOL
JI Semin. Cell Dev. Biol.
PD OCT
PY 2016
VL 58
BP 55
EP 59
DI 10.1016/j.semcdb.2016.07.005
PG 5
WC Cell Biology; Developmental Biology
SC Cell Biology; Developmental Biology
GA DV9TD
UT WOS:000383284000007
PM 27395026
ER
PT J
AU Nussinov, R
Tsai, CJ
Jang, H
Korcsmaros, T
Csermely, P
AF Nussinov, Ruth
Tsai, Chung-Jung
Jang, Hyunbum
Korcsmaros, Tamas
Csermely, Peter
TI Oncogenic KRAS signaling and YAP1/beta-catenin: Similar cell cycle
control in tumor initiation
SO SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE K-Ras; Cancer; Hippo; Myc; WNT; Cellular pathways; Proliferation; Drug
resistance
ID BETA-CATENIN ACTIVATION; REGULATES C-MYC; RESTRICTION POINT;
CANCER-THERAPIES; TARGETING RAS; PROTEIN INTERACTIONS;
PANCREATIC-CANCER; K-RAS; PATHWAY; RESISTANCE
AB Why are YAP1 and c-Myc often overexpressed (or activated) in KRAS-driven cancers and drug resistance? Here, we propose that there are two independent pathways in tumor proliferation: one includes MAPK/ERK and PI3K/A kt/mTOR; and the other consists of pathways leading to the expression ( or activation) of YAP1 and c-Myc. KRAS contributes through the first. MYC is regulated by e.g. beta-catenin, Notch and Hedgehog. We propose that YAP1 and ERK accomplish similar roles in cell cycle control, as do beta-catenin and PI3K. This point is compelling, since the question of how YAP1 rescues K-Ras or B-Raf ablation has recently captured much attention, as well as the mechanism of resistance to PI3K inhibitors. The similarity in cell cycle actions of beta-catenin and PI3K can also clarify the increased aggressiveness of lung cancer when both K-Ras and beta-catenin operate. Thus, we propose that the two pathways can substitute one another -or together amplify each other - in promoting proliferation. This new understanding of the independence and correspondence of the two pathways in cancer - MAPK/ERK and PI3K/Akt/mTOR; and YAP1 and c-Myc - provide a coherent and significant picture of signaling-driven oncogenic proliferation and may help in judicious, pathway-based drug discovery. (C) 2016 Ruth Nussinov. Published by Elsevier Ltd. All rights reserved.
C1 [Nussinov, Ruth; Tsai, Chung-Jung; Jang, Hyunbum] NCI, Canc & Inflammat Program, Leidos Biomed Res Inc, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
[Nussinov, Ruth] Tel Aviv Univ, Sackler Sch Med, Dept Human Mol Genet & Biochem, IL-69978 Tel Aviv, Israel.
[Korcsmaros, Tamas] Inst Food Res, Gut Hlth & Food Safety Programme, Norwich Res Pk, Norwich NR4 7UA, Norfolk, England.
[Korcsmaros, Tamas] TGAC, Norwich Res Pk, Norwich NR4 7UA, Norfolk, England.
[Korcsmaros, Tamas] Genome Anal Ctr, TGAC, Norwich Res Pk, Norwich NR4 7UH, Norfolk, England.
[Csermely, Peter] Semmelweis Univ, Dept Med Chem, POB 2, H-1428 Budapest, Hungary.
RP Nussinov, R (reprint author), NCI, Canc & Inflammat Program, Leidos Biomed Res Inc, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
EM NussinoR@helix.nih.gov
FU Frederick National Laboratory for Cancer Research, National Institutes
of Health [HHSN261200800001E]; Biotechnological and Biosciences Research
Council, UK; Hungarian National Research, Development and Innovation
Office [K115378]; Intramural Research Program of NIH, Frederick National
Lab, Center for Cancer Research
FX This project has been funded in whole or in part with Federal funds from
the Frederick National Laboratory for Cancer Research, National
Institutes of Health, under contract HHSN261200800001E. TK is a
Computational Biology Fellow at The Genome Analysis Centre in
partnership with the Institute of Food Research (Norwich, UK), and
strategically supported by Biotechnological and Biosciences Research
Council, UK. Research in the lab of PC was supported by the Hungarian
National Research, Development and Innovation Office (K115378). This
research was supported [in part] by the Intramural Research Program of
NIH, Frederick National Lab, Center for Cancer Research. The content of
this publication does not necessarily reflect the views or policies of
the Department of Health and Human Services, nor does mention of trade
names, commercial products or organizations imply endorsement by the US
Government.
NR 74
TC 5
Z9 5
U1 12
U2 12
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1084-9521
J9 SEMIN CELL DEV BIOL
JI Semin. Cell Dev. Biol.
PD OCT
PY 2016
VL 58
BP 79
EP 85
DI 10.1016/j.semcdb.2016.04.001
PG 7
WC Cell Biology; Developmental Biology
SC Cell Biology; Developmental Biology
GA DV9TD
UT WOS:000383284000010
PM 27058752
ER
PT J
AU Guven-Maiorova, E
Tsai, CJ
Nussinov, R
AF Guven-Maiorova, Emine
Tsai, Chung-Jung
Nussinov, Ruth
TI Pathogen mimicry of host protein-protein interfaces modulates immunity
SO SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE Molecular mimicry; Interface mimicry; Structure; Host-pathogen
interactions; Protein-protein interactions; Multi-organism
ID EPSTEIN-BARR-VIRUS; CONSTITUTIVE ACTIVATION; CRYSTAL-STRUCTURE;
CONFORMATIONAL SELECTION; MOLECULAR MIMICRY; COUPLED-RECEPTOR; VIRAL
CHEMOKINE; INDUCED FIT; TIR-DOMAIN; BACTERIAL
AB Signaling pathways shape and transmit the cell's reaction to its changing environment; however, pathogens can circumvent this response by manipulating host signaling. To subvert host defense, they beat it at its own game: they hijack host pathways by mimicking the binding surfaces of host-encoded proteins. For this, it is not necessary to achieve global protein homology; imitating merely the interaction surface is sufficient. Different protein folds often interact via similar protein-protein interface architectures. This similarity in binding surfaces permits the pathogenic protein to compete with a host target protein. Thus, rather than binding a host-encoded partner, the host protein hub binds the pathogenic surrogate. The outcome can be dire: rewiring or repurposing the host pathways, shifting the cell signaling landscape and consequently the immune response. They can also cause persistent infections as well as cancer by modulating key signaling pathways, such as those involving Ras. Mapping the rewired host-pathogen 'superorganism' interaction network - along with its structural details - is critical for in-depth understanding of pathogenic mechanisms and developing efficient therapeutics. Here, we overview the role of molecular mimicry in pathogen host evasion as well as types of molecular mimicry mechanisms that emerged during evolution. (C) 2016 Elsevier Ltd. All rights reserved.
C1 [Guven-Maiorova, Emine; Tsai, Chung-Jung; Nussinov, Ruth] NCI, Canc & Inflammat Program, Leidos Biomed Res Inc, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
[Nussinov, Ruth] Tel Aviv Univ, Sackler Sch Med, Dept Human Genet & Mol Med, Sackler Inst Mol Med, IL-69978 Tel Aviv, Israel.
RP Nussinov, R (reprint author), NCI, Canc & Inflammat Program, Leidos Biomed Res Inc, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
EM emine.guven-maiorov@nih.gov; tsaic@mail.nih.gov; nussinor@helix.nih.gov
OI Guven Maiorov, Emine/0000-0002-7388-9811
FU Federal funds from the National Cancer Institute, National Institutes of
Health [HHSN261200800001E]; Intramural Research Program of the 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, under
contract number 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.
This research was supported (in part) by the Intramural Research Program
of the NIH, National Cancer Institute, Center for Cancer Research.
NR 84
TC 0
Z9 0
U1 13
U2 13
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1084-9521
J9 SEMIN CELL DEV BIOL
JI Semin. Cell Dev. Biol.
PD OCT
PY 2016
VL 58
BP 136
EP 145
DI 10.1016/j.semcdb.2016.06.004
PG 10
WC Cell Biology; Developmental Biology
SC Cell Biology; Developmental Biology
GA DV9TD
UT WOS:000383284000016
PM 27287306
ER
PT J
AU Ahmed, MM
Narendra, A
Prasanna, P
Coleman, CN
Krishnan, S
AF Ahmed, Mansoor M.
Narendra, Amogh
Prasanna, Pataje
Coleman, C. Norman
Krishnan, Sunil
TI Current Insights in Radiation Combination Therapies: Influence of Omics
and Novel Targeted Agents in Defining New Concepts in Radiation Biology
and Clinical Radiation Oncology
SO SEMINARS IN RADIATION ONCOLOGY
LA English
DT Editorial Material
ID RADIOTHERAPY; EFFICACY
C1 [Ahmed, Mansoor M.; Narendra, Amogh; Prasanna, Pataje; Coleman, C. Norman] NCI, Div Canc Treatment & Diag, Radiat Res Program, Bethesda, MA 20892 USA.
[Krishnan, Sunil] Univ Texas Houston, Dept Radiat Oncol, MD Anderson Canc Ctr, Houston, TX 77030 USA.
RP Krishnan, S (reprint author), Univ Texas Houston, Dept Radiat Oncol, MD Anderson Canc Ctr, Houston, TX 77030 USA.; Ahmed, MM (reprint author), NCI, Div Canc Treatment & Diag, Radiat Res Program, Rockville, MD 20850 USA.
EM ahmedmm@mail.nih.gov; SKrishnan@mdanderson.org
NR 21
TC 0
Z9 0
U1 2
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 1053-4296
EI 1532-9461
J9 SEMIN RADIAT ONCOL
JI Semin. Radiat. Oncol.
PD OCT
PY 2016
VL 26
IS 4
BP 251
EP 253
DI 10.1016/j.semradonc.2016.07.002
PG 3
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA DW4UY
UT WOS:000383639700001
PM 27619246
ER
PT J
AU Makinde, AY
Eke, I
Aryankalayil, MJ
Ahmed, MM
Coleman, CN
AF Makinde, Adeola Y.
Eke, Iris
Aryankalayil, Molykutty J.
Ahmed, Mansoor M.
Coleman, C. Norman
TI Exploiting Gene Expression Kinetics in Conventional Radiotherapy,
Hyperfractionation, and Hypofractionation for Targeted Therapy
SO SEMINARS IN RADIATION ONCOLOGY
LA English
DT Article
ID NF-KAPPA-B; CANCER STEM-CELLS; FRACTIONATED RADIATION-THERAPY;
EPITHELIAL-MESENCHYMAL TRANSITION; RANDOMIZED MULTICENTER TRIAL;
RESIDUAL PANCREATIC-CANCER; PROSTATE-CANCER; BREAST-CANCER; LUNG-CANCER;
ACCELERATED RADIOTHERAPY
AB The dramatic changes in the technological delivery of radiation therapy, the repertoire of molecular targets for which pathway inhibitors are available, and the cellular and immunologic responses that can alter long-term clinical outcome provide a potentially unique role for using the radiation-inducible changes as therapeutic targets. Various mathematical models of dose and fractionation are extraordinarily useful in guiding treatment regimens. However, although the model may fit the clinical outcome, a deeper understanding of the molecular and cellular effect of the individual dose size and the adaptation to repeated exposure, called multifraction (MF) adaptation, may provide new therapeutic targets for use in combined modality treatments using radiochemotherapy and radioimmunotherapy. We discuss the potential of using different radiation doses and MF adaptation for targeting transcription factors, immune and inflammatory response, and cell "sternness." Given the complex genetic composition of tumors before treatment and their adaptation to drug treatment, innovative combinations using both the pretreatment molecular data and also the MF-adaptive response to radiation may provide an important role for focused radiation therapy as an integral part of precision medicine and immunotherapy. Published by Elsevier Inc.
C1 [Makinde, Adeola Y.; Eke, Iris; Aryankalayil, Molykutty J.; Coleman, C. Norman] NCI, Radiat Oncol Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
[Ahmed, Mansoor M.; Coleman, C. Norman] NCI, Radiat Res Program, NIH, Bethesda, MD 20892 USA.
RP Makinde, AY (reprint author), NCI, Radiat Oncol Branch, Ctr Canc Res, NIH, 10 Ctr Dr,Bldg 10 Room B3B406, Bethesda, MD 20892 USA.
EM adeola.makinde@nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 63
TC 2
Z9 2
U1 6
U2 6
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1053-4296
EI 1532-9461
J9 SEMIN RADIAT ONCOL
JI Semin. Radiat. Oncol.
PD OCT
PY 2016
VL 26
IS 4
BP 254
EP 260
DI 10.1016/j.semradonc.2016.07.001
PG 7
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA DW4UY
UT WOS:000383639700002
PM 27619247
ER
PT J
AU Takebe, N
Ahmed, MM
Vikram, B
Bernhard, EJ
Zwiebel, J
Coleman, CN
Kunos, CA
AF Takebe, Naoko
Ahmed, Mansoor M.
Vikram, Bhadrasain
Bernhard, Eric J.
Zwiebel, James
Coleman, C. Norman
Kunos, Charles A.
TI Radiation-Therapeutic Agent Clinical Trials: Leveraging Advantages of a
National Cancer Institute Programmatic Collaboration
SO SEMINARS IN RADIATION ONCOLOGY
LA English
DT Article
ID RIBONUCLEOTIDE REDUCTASE INHIBITOR; 3-AMINOPYRIDINE-2-CARBOXALDEHYDE
THIOSEMICARBAZONE 3-AP; SQUAMOUS-CELL CARCINOMA; HUMAN CERVICAL CANCERS;
PHASE-I TRIAL; DNA-DAMAGE; POLY(ADP-RIBOSE) POLYMERASE; WEEKLY
CISPLATIN; ONCOLOGY-GROUP; SOLID TUMORS
AB A number of oncology phase II radiochemotherapy trials with promising results have been conducted late in the overall experimental therapeutic agent development process. Accelerated development and approval of experimental therapeutic agents have stimulated further interest in much earlier radiation-agent studies to increase the likelihood of success in phase III trials. To sustain this interest, more forward-thinking preclinical radiobiology experimental designs are needed to improve discovery of promising radiochemotherapy plus agent combinations for clinical trial testing. These experimental designs should better inform next step radiation-agent clinical trial dose, schedule, exposure, and therapeutic effect. Recognizing the need for a better strategy to develop preclinical data supporting radiation-agent phase I or II trials, the National Cancer Institute (NCI)-Cancer Therapy Evaluation Program (CTEP) and the NCI-Molecular Radiation Therapeutics Branch of the Radiation Research Program have partnered to promote earlier radiobiology studies of CTEP portfolio agents. In this Seminars in Radiation Oncology article, four key components of this effort are discussed. First, we outline steps for accessing CTEP agents for preclinical testing. Second, we propose radiobiology studies that facilitate transition from preclinical testing to early phase trial activation. Third, we navigate steps that walk through CTEP agent strategic development paths available for radiation-agent testing. Fourth, we highlight a new NCI-sponsored cooperative agreement grant supporting in vitro and in vivo radiation-CTEP agent testing that informs early phase trial designs. Throughout the article, we include contemporary examples of successful radiation agent development initiatives. Published by Elsevier Inc.
C1 [Takebe, Naoko; Zwiebel, James; Kunos, Charles A.] NCI, Canc Therapy Evaluat Program, NIH, Bethesda, MD 20892 USA.
[Ahmed, Mansoor M.; Vikram, Bhadrasain; Bernhard, Eric J.; Coleman, C. Norman] NCI, Radiat Res Program, Bethesda, MD 20892 USA.
RP Takebe, N (reprint author), NCI, Canc Therapy Evaluat Program, NIH, Bethesda, MD 20892 USA.
NR 60
TC 2
Z9 2
U1 5
U2 5
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1053-4296
EI 1532-9461
J9 SEMIN RADIAT ONCOL
JI Semin. Radiat. Oncol.
PD OCT
PY 2016
VL 26
IS 4
BP 271
EP 280
DI 10.1016/j.semradonc.2016.06.005
PG 10
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA DW4UY
UT WOS:000383639700004
PM 27619249
ER
PT J
AU Ford, E
Deye, J
AF Ford, Eric
Deye, Jim
TI Current Instrumentation and Technologies in Modern Radiobiology
Research-Opportunities and Challenges
SO SEMINARS IN RADIATION ONCOLOGY
LA English
DT Article
ID RADIATION RESEARCH PLATFORM; SMALL ANIMAL IRRADIATOR; STEREOTACTIC BODY
RADIOTHERAPY; INDUCED LUNG INJURY; X-RAY; GOLD NANOPARTICLES;
CANCER-RESEARCH; DOSIMETRY STANDARDIZATION; SYNCHROTRON MICROBEAM;
CONFORMAL IRRADIATOR
AB There is a growing awareness of the gaps in the technical methods employed in radiation biology experiments. These quality gaps can have a substantial effect on the reliability and reproducibility of results as outlined in several recent meta-studies. This is especially true in the context of the newer laboratory irradiation technologies. These technologies allow for delivery of highly localized dose distributions and increased spatial accuracy but also present increased challenges of their own. In this article, we highlight some of the features of the new technologies and the experiments they support; this includes image-guided localized radiation systems, microirradiator systems using carbon nanotubes and physical radiation modifiers like gold nanoparticles. We discuss the key technical issues related to the consistency and quality of modern radiation biology experiments including dosimetry protocols that are essential to all experiments, quality assurance approaches, methods to validate physical radiation targeting including immunohistochemical assays and other biovalidation apprpaches. We highlight the future needs in terms of education and training and the creation of tools for cross-institutional benchmarking quality in preclinical studies. The demands for increased experimental rigor are challenging but can be met with an awareness and a systematic approach which ensures quality. (C) 2016 Published by Elsevier Inc.
C1 [Ford, Eric] Univ Washington, Med Ctr, Dept Radiat Oncol, Seattle, WA 98195 USA.
[Deye, Jim] NCI, Radiat Res Program, Bethesda, MD 20892 USA.
RP Ford, E (reprint author), Dept Radiat Oncol, Gox 356043,1959 NE Pacific St, Seattle, WA 98195 USA.
EM eford@uw.edu
NR 83
TC 2
Z9 2
U1 10
U2 10
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1053-4296
EI 1532-9461
J9 SEMIN RADIAT ONCOL
JI Semin. Radiat. Oncol.
PD OCT
PY 2016
VL 26
IS 4
BP 349
EP 355
DI 10.1016/j.semradonc.2016.06.002
PG 7
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA DW4UY
UT WOS:000383639700011
PM 27619256
ER
PT J
AU Mukherjee, S
Sirohi, D
Dowd, KA
Chen, ZG
Diamond, MS
Kuhn, RJ
Pierson, TC
AF Mukherjee, Swati
Sirohi, Devika
Dowd, Kimberly A.
Chen, Zhenguo
Diamond, Michael S.
Kuhn, Richard J.
Pierson, Theodore C.
TI Enhancing dengue virus maturation using a stable furin over-expressing
cell line
SO VIROLOGY
LA English
DT Article
DE Flavivirus; Dengue virus; West Nile virus; Virion maturation; Antibody
neutralization; Furin
ID WEST-NILE-VIRUS; BORNE ENCEPHALITIS-VIRUS; ANTIBODY-MEDIATED
NEUTRALIZATION; ENDOPLASMIC-RETICULUM; MONOCLONAL-ANTIBODY; ENVELOPE
PROTEIN; STRUCTURAL BASIS; FLAVIVIRUSES; INFECTION; PRM
AB Flaviviruses are positive-stranded RNA viruses that incorporate envelope (E) and premembrane (prM) proteins into the virion. Furin-mediated cleavage of prM defines a required maturation step in the flavivirus lifecycle. Inefficient prM cleavage results in structurally heterogeneous virions with unique antigenic and functional characteristics. Recent studies with dengue virus suggest that viruses produced in tissue culture cells are less mature than those produced in primary cells. In this study, we describe a Vero cell line that ectopically expresses high levels of human furin (Vero-furin) for use in the production of more homogenous mature flavivirus populations. Laboratory-adapted and clinical dengue virus isolates grow efficiently in Vero-furin cells. Biochemical and structural techniques demonstrate efficient prM cleavage in Vero-furin derived virus preparations. These virions also were less sensitive to neutralization by antibodies that bind efficiently to immature virions. This furin-expressing cell line will be of considerable utility for flavivirus neutralization and structural studies. Published by Elsevier Inc.
C1 [Mukherjee, Swati; Dowd, Kimberly A.; Pierson, Theodore C.] NIAID, Viral Pathogenesis Sect, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Sirohi, Devika; Chen, Zhenguo; Kuhn, Richard J.] Purdue Univ, Dept Biol Sci, W Lafayette, IN 47907 USA.
[Sirohi, Devika; Chen, Zhenguo; Kuhn, Richard J.] Purdue Univ, Purdue Inst Inflammat Immunol & Infect Dis, W Lafayette, IN 47907 USA.
[Diamond, Michael S.] Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA.
[Diamond, Michael S.] Washington Univ, Sch Med, Dept Mol Microbiol, St Louis, MO 63110 USA.
[Diamond, Michael S.] Washington Univ, Sch Med, Dept Pathol, St Louis, MO 63110 USA.
[Diamond, Michael S.] Washington Univ, Sch Med, Dept Immunol, St Louis, MO 63110 USA.
[Diamond, Michael S.] Washington Univ, Sch Med, Ctr Human Immunol & Immunotherapy Programs, St Louis, MO 63110 USA.
RP Pierson, TC (reprint author), NIH, Viral Pathogenesis Sect, Viral Dis Lab, Bldg 33,Room 2E19A-2, Bethesda, MD 20892 USA.
EM piersontc@mail.nih.gov
FU intramural program of the National Institute of Allergy and Infectious
Diseases; National Institutes of Health [R01AI073755]
FX This work was supported in part by the intramural program of the
National Institute of Allergy and Infectious Diseases and National
Institutes of Health (TCP) an extramural grant under award numbers
R01AI073755 (MSD and RJK). We are grateful to Heather Hickman for her
constructive comments on the manuscript. Finally, the authors are
grateful to members of their laboratories for helpful discussions.
NR 50
TC 2
Z9 2
U1 7
U2 7
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 2016
VL 497
BP 33
EP 40
DI 10.1016/j.virol.2016.06.022
PG 8
WC Virology
SC Virology
GA DW8RC
UT WOS:000383922200004
PM 27420797
ER
PT J
AU Liu, QP
Yan, YH
Kozak, CA
AF Liu, Qingping
Yan, Yuhe
Kozak, Christine A.
TI Permissive XPR1 gammaretrovirus receptors in four mammalian species are
functionally distinct in interference tests
SO VIROLOGY
LA English
DT Article
DE Mouse gammaretroviruses; Mouse leukemia viruses; XPR1 retrovirus
receptor; Gammaretrovirus interference
ID MURINE LEUKEMIA VIRUSES; CELL-SURFACE RECEPTOR; MOUSE XENOTROPIC
GAMMARETROVIRUSES; WILD MICE; RETROVIRUS XMRV; HOST-RANGE; INFECTION;
DETERMINANTS; GLYCOPROTEIN; VARIANTS
AB Xenotropic/polytropic mouse leukemia viruses (X/P-MLVs) use the XPR1 gammaretrovirus receptor for entry. X/P-MLV host range is defined by usage of naturally occurring restrictive XPR1 receptors, and is governed by polymorphisms in the virus envelope glycoprotein and in XPR1. Here, we examined receptors of four mammalian species permissive to all X/P-MLVs (Mus dunni, human, rabbit, mink). Interference assays showed the four to be functionally distinct. Preinfection with X-MLVs consistently blocked all nine XPR1-dependent viruses, while preinfection with P-MLVs and wild mouse X/P-MLVs produced distinctive interference patterns in the four cells. These patterns indicate shared usage of independent, but not always fully functional, receptor sites. XPR1 sequence comparisons identified candidate sites in receptor-determining regions that correlate with some interference patterns. The evolutionary record suggests that the X/P-MLV tropism variants evolved to adapt to host receptor polymorphisms, to circumvent blocks by competing viruses or to avoid host-encoded envelope glycoproteins acquired for defense. Published by Elsevier Inc.
C1 [Liu, Qingping; Yan, Yuhe; Kozak, Christine A.] NIAID, Mol Microbiol Lab, 9000 Rockville Pike, Bethesda, MD 20892 USA.
[Yan, Yuhe] Yisheng US Biopharma Inc, Gaithersburg, MD USA.
RP Kozak, CA (reprint author), NIAID, Mol Microbiol Lab, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM ckozak@niaid.nih.gov
FU Intramural Research Program of the National Institute of Allergy and
Infectious Diseases, Bethesda, MD
FX This work was supported by the Intramural Research Program of the
National Institute of Allergy and Infectious Diseases, Bethesda, MD. We
thank Venkat Yedavalli for assistance with figure preparation.
NR 49
TC 0
Z9 0
U1 1
U2 1
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD OCT
PY 2016
VL 497
BP 53
EP 58
DI 10.1016/j.virol.2016.06.026
PG 6
WC Virology
SC Virology
GA DW8RC
UT WOS:000383922200006
PM 27423269
ER
PT J
AU Blumberg, SJ
Zablotsky, B
Avila, RM
Colpe, LJ
Pringle, BA
Kogan, MD
AF Blumberg, Stephen J.
Zablotsky, Benjamin
Avila, Rosa M.
Colpe, Lisa J.
Pringle, Beverly A.
Kogan, Michael D.
TI Diagnosis lost: Differences between children who had and who currently
have an autism spectrum disorder diagnosis
SO AUTISM
LA English
DT Article
DE autism spectrum disorder; diagnosis; epidemiology; national surveys
ID DOUBLY ROBUST ESTIMATION; CAUSAL INFERENCE; FOLLOW-UP; STABILITY;
HISTORY; IDENTIFICATION; INTERVENTION; ADOLESCENTS; PREVALENCE; SYMPTOMS
AB Autism spectrum disorder diagnoses sometimes change due to misdiagnosis, maturation, or treatment. This study uses a probability-based national surveythe Survey of Pathways to Diagnosis and Servicesto compare currently diagnosed (n=1420) and previously diagnosed (n=187) children aged 6-17years based on retrospective parental reports of early concerns about their children's development, responses to those concerns by doctors and other healthcare providers, the type of provider who made the first autism spectrum disorder diagnosis, and the autism spectrum disorder subtype diagnoses received (if any). Propensity score matching was used to control for differences between the groups on children's current level of functioning and other current characteristics that may have been related to diagnosis loss. Approximately 13% of the children ever diagnosed with autism spectrum disorder were estimated to have lost the diagnosis, and parents of 74% of them believed it was changed due to new information. Previously diagnosed children were less likely to have parents with early concerns about verbal skills, nonverbal communication, learning, and unusual gestures or movements. They were also less likely to have been referred to and diagnosed by a specialist. Previously diagnosed children were less likely to have ever received a diagnosis of Asperger's disorder or autistic disorder.
C1 [Blumberg, Stephen J.; Zablotsky, Benjamin] Ctr Dis Control & Prevent, Hyattsville, MD USA.
[Avila, Rosa M.] Univ Washington, Seattle, WA 98195 USA.
[Colpe, Lisa J.; Pringle, Beverly A.] NIH, Bldg 10, Bethesda, MD 20892 USA.
[Kogan, Michael D.] Hlth Resources & Serv Adm, Rockville, MD USA.
RP Blumberg, SJ (reprint author), Ctr Dis Control & Prevent, Natl Ctr Hlth Stat, 3311 Toledo Rd, Hyattsville, MD 20782 USA.
EM sblumberg@cdc.gov
FU Intramural CDC HHS [CC999999]
NR 49
TC 0
Z9 0
U1 18
U2 18
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
EI 1461-7005
J9 AUTISM
JI Autism
PD OCT
PY 2016
VL 20
IS 7
BP 783
EP 795
DI 10.1177/1362361315607724
PG 13
WC Psychology, Developmental
SC Psychology
GA DV5JQ
UT WOS:000382963700002
PM 26489772
ER
PT J
AU Watson, DC
Bayik, D
Srivatsan, A
Bergamaschi, C
Valentin, A
Niu, G
Bear, J
Monninger, M
Sun, M
Morales-Kastresana, A
Jones, JC
Felber, BK
Chen, XY
Gursel, I
Pavlakis, GN
AF Watson, Dionysios C.
Bayik, Defne
Srivatsan, Avinash
Bergamaschi, Cristina
Valentin, Antonio
Niu, Gang
Bear, Jenifer
Monninger, Mitchell
Sun, Mei
Morales-Kastresana, Aizea
Jones, Jennifer C.
Felber, Barbara K.
Chen, Xiaoyuan
Gursel, Ihsan
Pavlakis, George N.
TI Efficient production and enhanced tumor delivery of engineered
extracellular vesicles
SO BIOMATERIALS
LA English
DT Article
DE Exosomes; Drug delivery; Biodistribution; Scavenger receptor;
Reticuloendothelial system; Dextran sulfate
ID CELL-DERIVED EXOSOMES; SCAVENGER RECEPTOR; IN-VIVO; B16BL6-DERIVED
EXOSOMES; CLASS-A; IL-15; MICE; BIODISTRIBUTION; IL-15R-ALPHA; CANCER
AB Extracellular vesicles (EV), including exosomes and microvesicles, are nano-sized intercellular communication vehicles that participate in a multitude of physiological processes. Due to their biological properties, they are also promising candidates for the systemic delivery of therapeutic compounds, such as cytokines, chemotherapeutic drugs, siRNAs and viral vectors. However, low EV production yield and rapid clearance of administered EV by liver macrophages limit their potential use as therapeutic vehicles. We have used a hollow-fiber bioreactor for the efficient production of bioactive EV bearing the heterodimeric cytokine complex Interleukin-15:Interleukin-15 receptor alpha. Bioreactor culture yielded-40fold more EV per mL conditioned medium, as compared to conventional cell culture. Biophysical analysis and comparative proteomics suggested a more diverse population of EV in the bioreactor preparations, while serum protein contaminants were detectable only in conventional culture EV preparations. We also identified the Scavenger Receptor Class A family (SR-A) as a novel monocyte/macrophage uptake receptor for EV. In vivo blockade of SR-A with dextran sulfate dramatically decreased EV liver clearance in mice, while enhancing tumor accumulation. These findings facilitate development of EV therapeutic methods. Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
C1 [Watson, Dionysios C.; Valentin, Antonio; Pavlakis, George N.] Natl Canc Inst Frederick, Ctr Canc Res, Vaccine Branch, Human Retrovirus Sect, Frederick, MD 21702 USA.
[Bayik, Defne] Natl Canc Inst Frederick, Ctr Canc Res, Canc & Inflammat Program, Frederick, MD 21702 USA.
[Bayik, Defne; Gursel, Ihsan] Bilkent Univ, Dept Mol Biol & Genet, TR-06800 Ankara, Turkey.
[Srivatsan, Avinash; Niu, Gang; Chen, Xiaoyuan] Natl Inst Biomed Imaging & Bioengn, Lab Mol Imaging & Nanomed, NIH, Bethesda, MD 20892 USA.
[Bergamaschi, Cristina; Bear, Jenifer; Felber, Barbara K.] Natl Canc Inst Frederick, Ctr Canc Res, Vaccine Branch, Human Retrovirus Pathogenesis Sect, Frederick, MD 21702 USA.
[Monninger, Mitchell; Sun, Mei] United States Army, Div Pathol, Med Res Inst Infect Dis, Frederick, MD 21702 USA.
[Morales-Kastresana, Aizea; Jones, Jennifer C.] NCI, Vaccine Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Pavlakis, GN (reprint author), Natl Canc Inst Frederick, Ctr Canc Res, Vaccine Branch, Human Retrovirus Sect, Frederick, MD 21702 USA.
EM George.pavlakis@nih.gov
RI Jones, Jennifer/C-8691-2015;
OI Jones, Jennifer/0000-0002-9488-7719; Watson,
Dionysios/0000-0002-9146-5641
FU Intramural Research Program of the National Institutes of Health,
National Cancer Institute, Center for Cancer Research; Admune/Novartis;
National Cancer Institute/NIH, USA
FX We thank William C. Kopp and Yanyt Wang for the IL-15 bioactivity
testing; Ming Zhou for mass spectrometry; John Cad well for discussions
and for providing Fibercell hollow-fiber materials; Joseph Meyer for
artwork; and Terry Jones for administrative support. Research supported
by the Intramural Research Program of the National Institutes of Health,
National Cancer Institute, Center for Cancer Research. Research also
supported by Admune/Novartis through a collaborative agreement with the
National Cancer Institute/NIH, USA. Opinions, interpretations,
conclusions, and recommendations are those of the authors and are not
necessarily endorsed by the U.S. Army.
NR 40
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U1 46
U2 48
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0142-9612
EI 1878-5905
J9 BIOMATERIALS
JI Biomaterials
PD OCT
PY 2016
VL 105
BP 195
EP 205
DI 10.1016/j.biomaterials.2016.07.003
PG 11
WC Engineering, Biomedical; Materials Science, Biomaterials
SC Engineering; Materials Science
GA DV9ZD
UT WOS:000383299800018
PM 27522254
ER
PT J
AU Burgess, AP
Fouquet, NC
Seri, S
Hawken, MB
Heard, A
Neasham, D
Little, MP
Elliott, P
AF Burgess, Adrian P.
Fouquet, Nathalie C.
Seri, Stefano
Hawken, Malcolm B.
Heard, Andrew
Neasham, David
Little, Mark P.
Elliott, Paul
TI Acute Exposure to Terrestrial Trunked Radio (TETRA) has effects on the
electroencephalogram and electrocardiogram, consistent with vagal nerve
stimulation
SO ENVIRONMENTAL RESEARCH
LA English
DT Article
DE Electromagnetic fields; Exposure; Neurophysiological effects;
Occupational cohort; Radio frequency
ID HEART-RATE-VARIABILITY; ELF MAGNETIC-FIELD; VAGUS NERVE;
ELECTROMAGNETIC-FIELDS; RESTING EEG; SLEEP EEG; BLOOD-PRESSURE; MOBILE
PHONES; HUMANS; POTENTIALS
AB Background: Terrestrial Trunked Radio (TETRA) is a telecommunications system widely used by police and emergency services around the world. The Stewart Report on mobile telephony and health raised questions about possible health effects associated with TETRA signals. This study investigates possible effects of TETRA signals on the electroencephalogram and electrocardiogram in human volunteers.
Methods: Blinded randomized provocation study with a standardized TETRA signal or sham exposure. In the first of two experiments, police officers had a TETRA set placed first against the left temple and then the upper-left quadrant of the chest and the electroencephalogram was recorded during rest and active cognitive processing. In the second experiment, volunteers were subject to chest exposure of TETRA whilst their electroencephalogram and heart rate variability derived from the electrocardiogram were recorded.
Results: In the first experiment, we found that exposure to TETRA had consistent neurophysiological effects on the electroencephalogram, but only during chest exposure, in a pattern suggestive of vagal nerve stimulation. In the second experiment, we observed changes in heart rate variability during exposure to TETRA but the electroencephalogram effects were not replicated.
Conclusions: Observed effects of exposure to TETRA signals on the electroencephalogram (first experiment) and electrocardiogram are consistent with vagal nerve stimulation in the chest by TETRA. However given the small effect on heart rate variability and the lack of consistency on the electroencephalogram, it seems unlikely that this will have a significant impact on health. Long-term monitoring of the health of the police force in relation to TETRA use is on-going. (C) 2016 The Authors. Published by Elsevier Inc.
C1 [Burgess, Adrian P.; Fouquet, Nathalie C.; Seri, Stefano] Aston Univ, Sch Life & Hlth Sci, Aston Brain Ctr, Birmingham B4 7ET, W Midlands, England.
[Hawken, Malcolm B.] Liverpool John Moores Univ, Res Inst Sport & Exercise Sci, Reilly Bldg,Byrom St, Liverpool L3 3AF, Merseyside, England.
[Heard, Andrew; Elliott, Paul] Imperial Coll London, Sch Publ Hlth, MRC PHE Ctr Environm & Hlth, St Marys Campus, London W2 1PG, England.
[Neasham, David] Creativ Ceut Ltd, Bank Chambers,10 Borough High St, London SE1 9QQ, England.
[Little, Mark P.] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Burgess, AP (reprint author), Aston Univ, Sch Life & Hlth Sci, Aston Brain Ctr, Birmingham B4 7ET, W Midlands, England.; Elliott, P (reprint author), Imperial Coll London, Sch Publ Hlth, MRC PHE Ctr Environm & Hlth, St Marys Campus, London W2 1PG, England.
EM a.p.burgess@aston.ac.uk; p.elliott@imperial.ac.uk
OI Burgess, Adrian P/0000-0002-0977-8105
FU UK Home Office [780-TETRA]; UK Department of Health Policy Research
Programme [RDD/091/210]; National Institute for Health Research (NIHR)
Biomedical Research Centre at Imperial College Healthcare NHS Trust and
Imperial College London; Medical Research Council - Public Health
England (MRC-PHE) Centre for Environment and Health; NIHR Health
Protection Research Unit on Health Impact of Environmental Hazards
FX This work was supported by the UK Home Office [780-TETRA; Experiment 1]
and the UK Department of Health Policy Research Programme [RDD/091/210;
Experiment 2]. P.E. is an NIHR senior investigator and is supported by
the National Institute for Health Research (NIHR) Biomedical Research
Centre at Imperial College Healthcare NHS Trust and Imperial College
London, the Medical Research Council - Public Health England (MRC-PHE)
Centre for Environment and Health and the NIHR Health Protection
Research Unit on Health Impact of Environmental Hazards.. The views
expressed in this publication are those of the authors and not
necessarily those of the Home Office, the Department of Health or the
NIHR.
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U1 1
U2 1
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0013-9351
EI 1096-0953
J9 ENVIRON RES
JI Environ. Res.
PD OCT
PY 2016
VL 150
BP 461
EP 469
DI 10.1016/j.envres.2016.06.031
PG 9
WC Environmental Sciences; Public, Environmental & Occupational Health
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health
GA DV4NU
UT WOS:000382903100056
PM 27419367
ER
PT J
AU Persky, S
Ferrer, RA
Klein, WMP
AF Persky, Susan
Ferrer, Rebecca A.
Klein, William M. P.
TI Nonverbal and paraverbal behavior in (simulated) medical visits related
to genomics and weight: a role for emotion and race
SO JOURNAL OF BEHAVIORAL MEDICINE
LA English
DT Article
DE Nonverbal behavior; Paraverbal behavior; Physician-patient interaction;
Genomics; Emotion; Obesity; Race
ID IMMERSIVE VIRTUAL ENVIRONMENT; HEALTH-CARE; CANCER-RISK; FAT PEOPLE;
COMMUNICATION; PREJUDICE; OUTCOMES; METAANALYSIS; ASSOCIATION;
INFORMATION
AB It is crucial to examine patient reactions to genomics-informed approaches to weight management within a clinical context, and understand the influence of patient characteristics (here, emotion and race). Examining nonverbal reactions offers a window into patients' implicit cognitive, attitudinal and affective processes related to clinical encounters. We simulated a weight management clinical interaction with a virtual reality-based physician, and experimentally manipulated patient emotional state (anger/fear) and whether the physician made genomic or personal behavior attributions for weight. Participants were 190 overweight females who racially identified as either Black or White. Participants made less visual contact when receiving genomic information in the anger condition, and Black participants exhibited lowered voice pitch when receiving genomic information. Black participants also increased their interpersonal distance when receiving genomic information in the anger condition. By studying non-conscious nonverbal behavior, we can better understand the nuances of these interactions.
Trial registry clinicaltrials.gov NCT01888913.
C1 [Persky, Susan] NHGRI, Social & Behav Res Branch, Bldg 31,Rm B1B36,31 Ctr Dr,MSC 2073, Bethesda, MD 20892 USA.
[Ferrer, Rebecca A.] NCI, Basic Biobehav & Psychol Sci Branch, Behav Res Program, Bethesda, MD 20892 USA.
[Klein, William M. P.] NCI, Behav Res Program, Bethesda, MD 20892 USA.
RP Persky, S (reprint author), NHGRI, Social & Behav Res Branch, Bldg 31,Rm B1B36,31 Ctr Dr,MSC 2073, Bethesda, MD 20892 USA.
EM perskys@mail.nih.gov
FU Intramural Research Program of the National Human Genome Research
Institute
FX This study was funded by the Intramural Research Program of the National
Human Genome Research Institute.
NR 51
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Z9 0
U1 10
U2 10
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0160-7715
EI 1573-3521
J9 J BEHAV MED
JI J. Behav. Med.
PD OCT
PY 2016
VL 39
IS 5
BP 804
EP 814
DI 10.1007/s10865-016-9747-5
PG 11
WC Psychology, Clinical
SC Psychology
GA DV4HS
UT WOS:000382887100006
PM 27146511
ER
EF