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Cardiovascular phenotype

In the past, cardiovascular functions of ai AR have generated the greated interest and research effort. However, cardiovascular phenotypes which have been observed in gene-targeted mouse models deficient in ai AR are beyond the scope of this review and have been reviewed elsewhere (Chen and Minneman 2005 Koshimizu et al. 2006 Piascik and Perez 2001 Tanoue et al. 2003). [Pg.276]

Joseph J, Loscalzo J. Selenistasis epistatic effects of selenium on cardiovascular phenotype. Nutrients 2013 5(2) 340-58. [Pg.321]

B2 knockout embryos subjected to salt stress in utero show suppressed renin expression and an abnormal kidney phenotype and develop early postnatal hypertension. Consistently, although basal bradykinin formation is defective tissue kallikrein-null mice have normal blood pressure however suffer from cardiovascular abnormalities. However suggesting a function of kinin signaling during development. [Pg.675]

Systolic pressure, or maximum blood pressure, occurs during left ventricular systole. Diastolic pressure, or minimum blood pressure, occurs during ventricular diastole. The difference between systolic and diastolic pressure is the pulse pressure. While diastolic blood pressure has been historically been used as the most relevant clinical blood pressure phenotype, it has now been clearly established that systolic blood pressure is the more important clinical predictor for cardiovascular morbidity and mortality. More recently, additional attention is focussed on the importance of pulse pressure, i.e. the blood pressure amplitude, as a predictive factor for cardiovascular disease. [Pg.1175]

Siest, G., Marteau, J.B., Maumus, S., et al. (2005) Pharmacogenomics and cardiovascular drugs need for integrated biological system with phenotypes and proteomic markers. Eur. J. Pharmacol. 527, 1-22. [Pg.21]

Wilkenson, P., Leach, C., Ah-Sing, E.E., Hussain, N., Miller, G.J., Millward, D.J., and Griffin, B.A. 2005. Influence of a-linolenic acid and fish-oil on markers of cardiovascular risk in subjects with an atherogenic lipoprotein phenotype. Atheroslerosis 181, 115-124. [Pg.98]

Nosadini R, Manzato E, Solini A, et al. Peripheral, rather than hepatic, insulin resistance and atherogenic lipoprotein phenotype predict cardiovascular complications in NIDDM. Eur J Clin Invest 1994 24 258-266. [Pg.100]

There have been numerous attempts to discover diagnostic procedures that would accurately predict cardiovascular disease risks in the general population. "Phenotyping" (i.e., electrophoresis) of lipoproteins has been used, as have determinations of total cholesterol, HDL cholesterol, triglyceride, and LDL cholesterol. "Normal" although not optimal values for these parameters are 140-310, 30-70, 60-300, and 90-200 mg/dl, respectively. These values are both age and sex related. LDL cholesterol cannot be determined directly but can be calculated from Equation (19.3) ... [Pg.506]

Gerety, S. S. et al. (1999). Symmetrical mutant phenotypes of the receptor EphB4 and its specific transmembrane ligand ephrin-B2 in cardiovascular development. Mol. Cell 4, 403-414. [Pg.101]


See other pages where Cardiovascular phenotype is mentioned: [Pg.253]    [Pg.52]    [Pg.178]    [Pg.272]    [Pg.374]    [Pg.386]    [Pg.253]    [Pg.52]    [Pg.178]    [Pg.272]    [Pg.374]    [Pg.386]    [Pg.178]    [Pg.475]    [Pg.573]    [Pg.700]    [Pg.714]    [Pg.251]    [Pg.252]    [Pg.252]    [Pg.5]    [Pg.274]    [Pg.20]    [Pg.217]    [Pg.307]    [Pg.494]    [Pg.15]    [Pg.191]    [Pg.506]    [Pg.357]    [Pg.372]    [Pg.101]    [Pg.115]    [Pg.544]    [Pg.368]    [Pg.385]    [Pg.89]    [Pg.201]    [Pg.40]    [Pg.313]    [Pg.657]    [Pg.475]    [Pg.573]    [Pg.700]    [Pg.714]   
See also in sourсe #XX -- [ Pg.253 ]




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Phenotype

Phenotype/phenotyping

Phenotypic

Phenotyping

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