Abstract

Pathogenic mechanisms for preeclampsia include end organ vasoconstriction , platelet aggregation, and reduced trophoblastic invasion of the uterine spinal arteries. This protocol aims to focus on activation of platelets in the pathogensis of preeclampsia by evaluating the levels of expression of P-selectin, CD 63, PAC platelet antigens and fibrinogen receptors in the whole blood of preeclamptic and control patients. Flow cytometry and monoclonal antibodies will be utilized. The etiology of platelet activation is most likely due to the placenta and will be evaluated by trophoblasts cultured under hypoxic conditions. Markers of platelet activation as above will be measured in trophoblastic cultured cells. Modulation of platelet activation as regulated by guanine nucleotide-binding proteins will be evaluated. The preeclamptic patients' blood will be obtained from blood that was banked in Protocol #733. The data base and statistical analysis provided by the GCRC will again be utilized. The core lab will be utilized for blood separation and laminar flow hoods.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
General Clinical Research Centers Program (M01)
Project #
5M01RR000096-39
Application #
6305939
Study Section
Project Start
1999-12-01
Project End
2000-11-30
Budget Start
1998-10-01
Budget End
1999-09-30
Support Year
39
Fiscal Year
2000
Total Cost
$21,006
Indirect Cost

  Institution

Name
New York University
Department
Type
DUNS #
City
New York
State
NY
Country
United States
Zip Code
10016

  Publications

Jun, Gyungah R; Chung, Jaeyoon; Mez, Jesse et al. (2017) Transethnic genome-wide scan identifies novel Alzheimer's disease loci. Alzheimers Dement 13:727-738
Homann, O R; Misura, K; Lamas, E et al. (2016) Whole-genome sequencing in multiplex families with psychoses reveals mutations in the SHANK2 and SMARCA1 genes segregating with illness. Mol Psychiatry 21:1690-1695
Ridge, Perry G; Hoyt, Kaitlyn B; Boehme, Kevin et al. (2016) Assessment of the genetic variance of late-onset Alzheimer's disease. Neurobiol Aging 41:200.e13-200.e20
Hohman, Timothy J; Bush, William S; Jiang, Lan et al. (2016) Discovery of gene-gene interactions across multiple independent data sets of late onset Alzheimer disease from the Alzheimer Disease Genetics Consortium. Neurobiol Aging 38:141-150
Jun, G; Ibrahim-Verbaas, C A; Vronskaya, M et al. (2016) A novel Alzheimer disease locus located near the gene encoding tau protein. Mol Psychiatry 21:108-17
Ebbert, Mark T W; Boehme, Kevin L; Wadsworth, Mark E et al. (2016) Interaction between variants in CLU and MS4A4E modulates Alzheimer's disease risk. Alzheimers Dement 12:121-129
Hohman, Timothy J; Cooke-Bailey, Jessica N; Reitz, Christiane et al. (2016) Global and local ancestry in African-Americans: Implications for Alzheimer's disease risk. Alzheimers Dement 12:233-43
Mukherjee, Shubhabrata; Walter, Stefan; Kauwe, John S K et al. (2015) Genetically predicted body mass index and Alzheimer's disease-related phenotypes in three large samples: Mendelian randomization analyses. Alzheimers Dement 11:1439-1451
Østergaard, Søren D; Mukherjee, Shubhabrata; Sharp, Stephen J et al. (2015) Associations between Potentially Modifiable Risk Factors and Alzheimer Disease: A Mendelian Randomization Study. PLoS Med 12:e1001841; discussion e1001841
Li, Yi; Tsui, Wai; Rusinek, Henry et al. (2015) Cortical laminar binding of PET amyloid and tau tracers in Alzheimer disease. J Nucl Med 56:270-3

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