Artificial neuronal network analysis in investigating the relationship between oxidative stress and endoplasmic reticulum stress to address blocked vessels in cardiovascular disease.

Background: Cardiovascular disease is the leading cause of death in the world and is associated with significant morbidity. Atherosclerosis is the main cause of cardiovascular disease (CVD), including myocardial infarction (MI), heart failure, and stroke. The mechanism of atherosclerosis has not been well investigated in different aspects, such as the relationship between oxidative stress and endothelial function.

Effects of vitamin E on nicotine-induced lipid peroxidation in rat granulosa cells: Folliculogenesis.

In this study, we investigated the mechanism of oxidative damage induced by nicotine and the efficacy of vitamin E, an integral component of cellular membranes, against the damage in follicular/granulosa cells of rat ovaries. The animals were randomly divided into 4 groups; control, nicotine, nicotine + vitaminE, vitamin E (n = 8, per each group). Nicotine and vitamin E were administrated intraperitoneally 1 mg/kg/day and 200 mg/kg/day, respectively, once daily for 2 weeks.

In glomerular cells of puromycin aminonucleoside nephrosis rats both phosphorylated and total STAT3 levels increased during proteinuria.

Recent studies showed that JAK/STAT pathway plays role in glomerular damages. The fact that STAT3 could be activated also by oxidative stress make Puromycin Aminonucleoside (PAN) Nephrosis model very appropriate for examination of STAT3 expression changes in glomerular pathology. Along with a control group, three PAN groups sacrificed on different days were formed by the i.