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has become one of the primary endpoints of many clinical trials. Comparing treatments
and therapies using time-to-event (or “survival”) data requires some care, since
survival differences may occur either early or late in the follow-up period, depending
on various factors such as the initial potency or the duration of efficacy of
the drugs. In this work, we investigate the effect of the CIMAvax?EGF
vaccine therapy on the survival of patients with non-small cell lung cancer, using
stratified and unstratified weighted log-rank tests. Weighted log-rank tests are
designed to identify early and late survival differences
between treatments. Using these tests, we conclude that the vaccine is more
efficient than the standard therapy among patients less than 60 years of age.
Impairment of vascular smooth muscle cells (VSMC) is recognized as a predisposition factor for atherosclerosis development. We hypothesize that the metabolic syndrome has a direct impact on VSMC migration and phenotypic switching, which may increase the incidence of atherosclerotic events. Aortic VSMC were extracted from 10 weeks old C57BL6 mice and incubated for 24 hr in adipocytes conditioned cell culture medium. Adipocytes were extracted from diabetic C57BL6 male mice fed with either a vegetal or an animal High-Fat-Diet (HFD) for 20 weeks. Migration of VSMC in response to conditioned media stimulations was significantly modulated compared to control. The most extended effects on VSMC were triggered by adipocytes from mice fed with animal HFD. These effects were concurrent with increased leptin concentrations and decreased adiponectin levels in conditioned media. A significant up-regulation of CD36 mRNA level was found in VSMC treated with adipocytes from HFD-fed mice. In conclusion, we have shown that the development of adipocyte-induced VSMC alterations is linked to diet fatty acid composition and the degree of metabolic alterations. The modulation of adipokine secretions in the adipose tissue that is linked to metabolic alterations may alter the physiology of VSMC and thus accelerate the development of metabolic-related vascular diseases.