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Introduction:The effect of comorbid cardiometabolic diseases (CMDs), including diabetes, heart diseases, and stroke, on dementia remains unclear. Methods:A cohort of 2648 dementia-free adults aged ≥60 years was followed up for 12 years. An active lifestyle was defined in accordance with the engagement in leisure activities and/or a social network. Cox models were used in data analysis. Results:The multiadjusted hazard ratio (HR, 95% confidence interval) of dementia was 1.41 (1.07-1.86) for one, 2.38 (1.58-3.59) for two, and 4.76 (2.04-11.13) for three CMDs. In joint exposure analysis, the HR of dementia was 3.36 (2.14-5.30) for participants with CMDs plus an inactive lifestyle and 1.32 (0.95-1.84) for those with CMDs plus an active lifestyle (reference: no CMDs plus active lifestyle). An active lifestyle delayed dementia onset by 3.50 years in people with CMDs.Discussion: CMDs, especially when comorbid, are associated with increased dementia risk; however, leisure activities and social integration mitigate this risk.

Statins may decrease chronic kidney diseases (CKDs) risk, but their underlying molecular mechanisms are not completely understood. Recent studies indicate Endothelial-to-mesenchymal transition (EndMT) plays an important role contributing to renal interstitial fibrosis. In the present study, we first investigated whether lovastatin could ameliorate renal fibrosis via suppression of EndMT and its possible mechanism. In vitro experiments, lovastatin significantly ameliorated microalbuminuria and pathologic changes in diabetic rats. Double labeling immunofluorescence showed lovastatin could inhibit EndMT in glomeruli. Furthermore, lovastatin could inhibit oxidative stress and down-regulate TGF-β1-Smad signaling. Consistent alterations were observed in vivo that lovastatin substantially suppressed EndMT and TGF-β1 signaling induced by high glucose in glomerular endothelial cells (GEnCs). These data indicated that lovastatin could ameliorate EndMT in glomeruli in diabetic nephropathy, the mechanism of which might be at least partly through suppression of oxidative stress and TGF-β1/Smad signaling pathway.

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Currently, cerebral infarction (CI) is the leading cause of disability and the second leading cause of mortality in China, seriously affecting patient quality of life. Ischemia (IS) is considered to be the early stage of CI. The present study aims to investigate the variation of intestinal microbial communities in patients with CI and IS using high throughput sequencing technology, and then analyze the results to identify a novel potential pathogenic mechanism of CI and IS. In total, 8 patients with CI, 2 patients with IS and 10 healthy volunteers as a control were selected. Throughput sequencing technology was used to analyze the character and microbial population of the gut. The abundance of Escherichia, Bacteroides, Megamonas, Parabacteroides, Akkermansia, Prevotella, Faecalibacterium, Dialister, Bifidobacterium and Ruminococcus was the significant difference in the intestinal microbial communities of the CI and IS patients compared with the healthy group. It was also observed that CI and IS were closely associated with internal glucose metabolism. The intestinal gut disturbance of CI patients may be one of the causes inducing CI by glucose metabolism and maybe considered as a potential method to predict the disease.

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