Background/aims: Preeclampsia (PE) is a life-threatening complication of pregnancy that is associated with a high rate of maternal and perinatal morbidity and/or mortality worldwide. If untreated, it can progress to eclampsia, which can result in the death of the mother, the fetus or both. The etiology of PE is still uncertain; however, recently the role of the immune system has gained in importance.
View Article and Find Full Text PDFIntroduction: We aimed to replicate a recent study which showed higher genetic risk load at 15 loci in men than in women with systemic lupus erythematosus (SLE). This difference was very significant, and it was interpreted as indicating that men require more genetic susceptibility than women to develop SLE.
Methods: Nineteen SLE-associated loci (thirteen of which are shared with the previous study) were analyzed in 1,457 SLE patients and 1,728 healthy controls of European ancestry.
Objectives: The goal of this clinical trial was to determine the incidence of undesirable side effects, and to ascertain any occurrence of genetic polymorphisms.
Material And Methods: Clinically, we looked for manifestations of a benign myositis and of serious rhabdomyolysis. We observed a group 198 patients treated with statins, primarially fluvastatin and rosuvastatin.
Am J Physiol Renal Physiol
March 2014
The posttranscriptional regulation of gene expression occurs through cis RNA regulatory elements by the action of trans factors, which are represented by noncoding RNAs (especially microRNAs) and turnover- and translation-regulatory (TTR) RNA-binding proteins (RBPs). These multifactorial proteins are a group of heterogeneous RBPs primarily implicated in controlling the decay and translation rates of target mRNAs. TTR-RBPs usually shuttle between cellular compartments (the nucleus and cytoplasm) in response to various stimuli and undergo posttranslational modifications such as phosphorylation or methylation to ensure their proper subcellular localization and function.
View Article and Find Full Text PDFAtherosclerosis is being nowadays defined as chronic subclinical inflammatory disease. Recently published clinical and laboratory studies have shown that subclinical inflammation represents main role in initiation of creation, in progress and destabilization of atherosclerotic plaque. Screening including traditional cardiovascular risk factors fails in identification in more than 50% of individuals with later development of acute coronary syndrome.
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