Sentence examples for development of cv from inspiring English sources

In support, previous studies identified inflammatory activity to be important for the development of CV disease in RA, even after adjustment for traditional CV risk factors [ 21- 24].

Although the increase in carotid IMT in this meta-analysis was much lower than expected in view of the almost doubled CV risk in RA patients [ 33], carotid IMT was proven to predict the development of CV events in RA patients [ 16].

Since CV disease is the most common cause of premature mortality in RA, an important step forward might be to identify high-CV risk RA patients who would benefit from active therapy to prevent the development of CV complications.

Angpt-2 levels have been found increased in recent onset RA patients with CV disease when compared with those without CV disease [ 97], which suggests that it could be a potential biomarker for the development of CV disease.

Widespread recognition of disease-specific risk profiles coupled with targeted therapeutic efforts among MAs may hold value for preventing the development of CV disease in this population.

Risk and preventative factors are considered to operate in a dynamic balance; dominance of thrombosis/vasoconstriction favors development of CV events, and dominance of anti-thrombosis/vasodilation favors prevention of CV events.

For this, the HUPO-PSI working groups defined some guidelines for the development of CVs (http://www.psidev.info/node/47).

There are three major categories involved in the development of CVs including gamete production, namely, gonadotropin releasing hormone (GnRH), follicle stimulating hormone (FSH), and luteinizing hormone (LH); gamete outcome, namely, human chorionic gonadotropin (hCG), or gamete function, namely, zona pellucida (ZP) and sperm antigens [ 7].

Risk factors in childhood create a life-long burden important in the development of cardiovascular (CV) disease in adulthood.

CRP may therefore facilitate the development of diverse CV diseases via its influence on the events mediated by NO, prostacyclin, and endothelin-1.

The progressive development of cardiovascular (CV) disease (CVD) resulting from pathophysiological changes mediated by angiotensin II in the presence of risk factors is well established [ 2] and local activation of RAS in the vascular walls is thought to contribute to atherosclerosis [ 5].