Zobrazeno 1 - 10
of 23
pro vyhledávání: '"Faina Schwartz"'
Autor:
Fengzhu Sun, Orian S. Shirihai, Ramachandran S. Vasan, Andrew D. Johnson, Faina Schwartz, Qiong Yang, Chunyu Liu, Shih-Jen Hwang, Daniel Levy
Publikováno v:
Hypertension. 60:949-956
Elevated blood pressure (BP) is a major risk factor for cardiovascular disease. Several studies have noted a consistent maternal effect on BP; consequently, mitochondrial DNA variation has become an additional target of investigation of the missing B
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 287:H1957-H1966
Although the central role of ANG II in cardiovascular homeostasis is well appreciated, the molecular circuitry of its many actions is not completely understood. With the use of serial analysis of gene expression to assess global transcriptional chang
Publikováno v:
American Journal of Hypertension. 17:629-635
Human essential hypertension (HTN), a polygenic, multifactorial, and highly heterogeneous disorder of unknown etiology, has been shown to have excess maternal transmission in several studies, suggesting a possible mitochondrial involvement. In an eff
Autor:
Faina Schwartz, Xiaoming Li, Min-Xin Guan, Nathan Fischel-Ghodsian, Qingfeng Yan, Rick A. Friedman
Publikováno v:
Nucleic Acids Research. 32:867-877
We report here the biochemical characterization of the deafness-associated mitochondrial tRNA(Ser(UCN)) T7511C mutation, in conjunction with homoplasmic ND1 T3308C and tRNA(Ala) T5655C mutations using cybrids constructed by transferring mitochondria
Autor:
Lindsay A. Farrer, Faina Schwartz, Anita L. DeStefano, A.J. Manolis, Irene Gavras, Clinton T. Baldwin, Michael Bursztyn, H Gavras, Nancy L. Heard-Costa
Publikováno v:
Clinical Genetics. 60:13-21
To assess maternal versus paternal contributions to the familial aggregation of hypertension, we examined family history data from 344 hypertensive probands (69 African American, 153 US Caucasian, 122 Greek Caucasian) ascertained without respect to p
Publikováno v:
American Journal of Medical Genetics. 86:145-150
We determined the entire sequence of the mitochondrial genome in affected individuals from three families with idiopathic orthostatic hypotension. The disorder in two of these families was recently linked to chromosome arm 18q, while the third family
Autor:
Michael Burzstyn, Diane E. Handy, Lindsay A. Farrer, Haralambos Gavras, Anita L. DeStefano, Oscar Joost, Timothy Martel, Athanasios J. Manolis, Margaret Bresnahan, Michael Nicolaou, Jader Baima, Clinton T. Baldwin, Faina Schwartz, Irene Gavras
Publikováno v:
American Journal of Hypertension. 12:853-857
Essential hypertension, a clinically significant elevation in blood pressure with no recognizable cause, is believed to be attributable to the collective effect of genetic predisposing factors in combination with specific environmental factors, such
Autor:
Cheryl L. Laffer, Jader Baima, Michael Nicolaou, Anita L. DeStefano, Athanasios J. Manolis, Haralambos Gavras, Faina Schwartz, Fernando Elijovich, Clinton T. Baldwin, Lindsay A. Farrer, Irene Gavras
Publikováno v:
Scopus-Elsevier
Abstract —Several clinical and animal studies indicate that essential hypertension is inherited as a multifactorial trait with a significant genetic and environmental component. In the stroke-prone spontaneously hypertensive rat model, investigator
Autor:
Daniel Levy, Faina Schwartz, Fengzhu Sun, Ramachandran S. Vasan, Qiong Yang, Sung K. Kim, Jing Cui, Martin G. Larson
Publikováno v:
Journal of hypertension. 25(10)
OBJECTIVE To investigate the contribution of the mitochondrial genome to hypertension and quantitative blood pressure (BP) phenotypes in the Framingham Heart Study cohort, a randomly ascertained, community-based sample. METHODS Longitudinal BP values
Autor:
Faina Schwartz, Haralambos Gavras, Efthymia Melista, Irene Gavras, Conrado Johns, Irena Duka, Arvi Duka
Publikováno v:
American journal of hypertension. 19(3)
Objective In previous studies using serial analysis of gene expression for elucidation of the molecular pathways of angiotensin II (Ang II)-induced hypertensive/ischemic cardiomyopathy in mice, we found that a hitherto unknown transcript, designated