Zobrazeno 1 - 10
of 60
pro vyhledávání: '"Richard J. Levine"'
Autor:
S. Ananth Karumanchi, Alice Wang, Mourad Toporsian, Richard J. Levine, Kai F. Yu, Jun Zhang, Alexander M. Holston
Publikováno v:
The Journal of Maternal-Fetal & Neonatal Medicine
Objective: To test the hypothesis that high circulating concen-trations of maternal anti-angiogenic factors are associated with increased risk of respiratory distress syndrome (RDS). Study Design: This is a nested case-control study of nulliparous wo
Autor:
Brett C. Young, Kee-Hak Lim, Cong Qian, Sarosh Rana, Richard J. Levine, S. Ananth Karumanchi, Saira Salahuddin
Publikováno v:
The Journal of Maternal-Fetal & Neonatal Medicine. :1-6
Preeclampsia (PE) is diagnosed using clinical criteria and in atypical cases the diagnosis may be inaccurate as there are no specific tests to confirm or exclude PE. This study sought to evaluate the utility of angiogenic biomarkers, sFlt1, sEng and
Autor:
Jose Alejandro Rauh-Hain, Shivalingappa Venkatesha, S. Ananth Karumanchi, Hector Tamez, Sarosh Rana, Richard J. Levine, Ravi Thadhani
Publikováno v:
Hypertension. 50:137-142
Concentrations of soluble fms-like tyrosine kinase 1 (sFlt1) and soluble endoglin (sEng) increase in maternal blood with the approach of clinical preeclampsia. Although alterations in these circulating antiangiogenic factors herald the signs and symp
Autor:
Sharon Maynard, Roberto Romero, S. Ananth Karumanchi, Franklin H. Epstein, Kai F. Yu, Richard J. Levine, Chun Lam, Cong Qian, Baha M. Sibai, Ravi Thadhani, Benjamin P. Sachs
Publikováno v:
New England Journal of Medicine. 355:992-1005
Alterations in circulating soluble fms-like tyrosine kinase 1 (sFlt1), an antiangiogenic protein, and placental growth factor (PlGF), a proangiogenic protein, appear to be involved in the pathogenesis of preeclampsia. Since soluble endoglin, another
Autor:
Franklin H. Epstein, Chun Lam, Cong Qian, Kai Yu, James L. Mills, Richard J. Levine, S. Ananth Karumanchi, Caroline Signore
Publikováno v:
Obstetrics & Gynecology. 108:338-344
Abnormalities in circulating angiogenic factors have been reported in diseases of abnormal placentation, such as preeclampsia and intrauterine growth restriction. Our objective was to determine whether circulating angiogenic factors are altered in an
Autor:
Franklin H. Epstein, Cong Qian, Kai F. Yu, Richard J. Levine, S. Ananth Karumanchi, Sharon Maynard
Publikováno v:
American Journal of Obstetrics and Gynecology. 194:1034-1041
Objective The purpose of this study was to determine whether serum fms-like tyrosine kinase 1 (sFlt1) concentration during preeclampsia were associated with mid trimester blood pressure, other maternal characteristics, or pregnancy outcomes. Study de
Autor:
Richard J. Levine, James E. Haddow, Yuval Yaron, Benjamin P. Sachs, Marlene B. Goldman, S. Ananth Karumanchi, Yuval Bdolah, Glenn E. Palomaki, Tali Bdolah-Abram
Publikováno v:
American Journal of Obstetrics and Gynecology. 194:239-245
Objective Women who are carrying a trisomy 13 fetus are more prone to develop preeclampsia. Excess circulating soluble fms-like tyrosine kinase-1 has been implicated recently in the pathogenesis of preeclampsia. Since the fms-like tyrosine kinase-1/s
Autor:
Marian G. Ewell, Kai F. Yu, Patrick M. Catalano, Cong Qian, Richard J Levine, Stephen P. Emery, Lucinda J England
Publikováno v:
BJOG: An International Journal of Obstetrics and Gynaecology. 112:1479-1485
Objective To evaluate levels of 24-hour urine insulin excretion before the onset of pre-eclampsia and gestational hypertension. Design Nested case–control study within the Calcium for Preeclampsia Prevention (CPEP) study cohort. Setting Five univer
Publikováno v:
Clinical Obstetrics and Gynecology. 48:372-386
Autor:
Lucinda England, Sharon Maynard, Vikas P. Sukhatme, Ravi Thadhani, Kai F. Yu, Franklin H. Epstein, Enrique F. Schisterman, Benjamin P. Sachs, Cong Qian, S. Ananth Karumanchi, Richard J. Levine, Kee-Hak Lim, Bahaeddine M Sibai
Publikováno v:
New England Journal of Medicine. 350:672-683
The cause of preeclampsia remains unclear. Limited data suggest that excess circulating soluble fms-like tyrosine kinase 1 (sFlt-1), which binds placental growth factor (PlGF) and vascular endothelial growth factor (VEGF), may have a pathogenic role.