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The analysis was adjusted for sociodemographic variables, health behaviors and health conditions. The seroprevalence of anti CMV and anti HSV-1 antibodies was 99.4% and 97.0%, respectively. Higher concentrations of CXCL8 and CCL5 chemokines were associated with lower antibody titers for CMV, and higher concentrations of CXCL9, IL-6 and CRP were associated with higher levels of antibodies to CMV. Moreover, intermediate levels of CXCL10 were also associated with higher levels of antibodies to CMV. In HSV-1 infection, intermediate levels of CXCL9, CCL5 and IL-6 were less likely to have higher antibody titers for this infection. On the other hand, higher levels of CXCL10 and CRP were positively associated with higher antibody titers for HSV-1. The results describe important immunological changes and reinforce the potential effect of CMV and HSV-1 on the immunosenescence process.Sphingosine-1-phosphate (S1P) is a bioactive lipid which regulates a series of physiological and pathological processes via binding to five S1P receptors (S1PR1-5). Although S1PR1-3 are widely expressed, the study of S1PRs, however, mainly addressed S1PR1 and S1PR2, and few studies focus on S1PR3-5. In recent years, a growing number of studies have shown that S1PR3 plays an important role in cell proliferation, differentiation, apoptosis, and migration, but its function is still controversial. This is the first comprehensive review paper about the role of S1PR3 signaling in cardiovascular function, tissue fibrosis, cancer, immune response, and neurological function. In addition, existing S1PR3 agonists and antagonists are listed at the end of the article, and we also put forward our opinion on the dispute of S1PR3 function.Polycystic ovary syndrome (PCOS), i.e., anovulation, hyperandrogenemia and polycystic ovary, is an endocrine-metabolic disease affecting reproductive aged women. Women with PCOS are likely to develop obesity, dyslipidemia, type 2 diabetes mellitus (T2DM) and cardiovascular diseases at a younger age. Despite high frequency and severe disease burden, the pathophysiological mechanisms of PCOS remain poorly defined and correspondingly have no therapeutic options. Emerging evidence has demonstrated that PCOS is accompanied with low-grade chronic inflammation and biomarkers thereof. Interestingly, serum amyloid A (SAA) has recently been identified as a potential marker of infection and inflammation and a number of studies have reported an association with PCOS. In this review, we explore the relationship between SAA and hyperandrogenemia, inflammation, obesity and insulin resistance, and provide convincing evidence for SAA as a potential inflammatory biomarker in PCOS.Exosomes, a subtype of extracellular vesicle secreted by cells, have been a subject of intense research interest. Unfortunately, a simple and reliable method to separate exosomes has yet to be developed. BI-3802 As can be expected, the lack of a standardized method for extraction and purification has contributed to suboptimal inter-laboratory correlation and difficulty in comparison studies. Traditional techniques such as centrifugation, immunoaffinity and size exclusion chromatography, suffer from low purity and tend to be labor intensive thus making their use limited. To mitigate these drawbacks, an integrated biosensor-based exosome separation and detection has recently been developed. In this review, we examine five biosensors that use a variety of detection technology (colorimetric, fluorescent, surface plasmon resonance, surface-enhanced Raman scattering and electrochemical) and propose thoughts on standardization of exosomal analysis.Intrinsic cardiac aging increases cardiovascular mortality and morbidity in the elderly. Estrogen helps reduce the risk of cardiovascular disease in women, with 17β-estradiol (17β-E2) activating the autophagy pathway and inhibiting vascular aging, mainly through estrogen receptor alpha (ER α) to prevent atherosclerosis. Abnormal methylation of autophagy-related genes can impact autophagic regulation. We hypothesized that 17β-E2, specifically 17β-E2 α, downregulates the methylation of autophagy factors and delays cardiac aging. Here, we used d-galactose, 17β-E2, and ER α receptor antagonist methyl-piperidino-pyrazole (MPP) to establish different aging models in mice divided into four groups, namely negative control, D.gal, D.gal + 17β-E2, and D.gal + 17β-E2 + MPP groups. Echocardiography showed that compared with the D.gal group group, the D.gal + 17β-E2 showed substantially increased cardiac function. The level of cardiac aging markers in mice in the D.gal + 17β-E2 group was lower than that in mice in the D.gal group. Beclin1, LC3, and Atg5 mRNA and protein expression levels in mice in the D.gal + 17β-E2 group were significantly increased compared with those in the D.gal group. Additionally, Beclin1, LC3, and Atg5 methylation levels were significantly decreased in the D.gal + 17β-E2 group. All the above values of the D.gal + 17β-E2 + MPP group were between those of the D.gal and D.gal + 17β-E2 groups. The expression of Dnmt1, Dnmt2, and Dnmt3A genes was the highest in the D.gal group. In summary, our results suggest that 17β-E2, specifically 17β-E2 α, promotes autophagy by downregulating the methylation of autophagy factors, thereby inhibiting galactose-induced cardiac aging in mice. 17β-E2 may be a potential therapeutic target to mitigate the effects of cardiac aging.The cellular chaperone machinery plays key role in the de novo formation and propagation of yeast prions (infectious protein). Though the role of Hsp70s in the prion maintenance is well studied, how Hsp90 chaperone machinery affects yeast prions remains unclear. In the current study, we examined the role of Hsp90 and its co-chaperones on yeast prions [PSI+] and [URE3]. We show that the overproduction of Hsp90 co-chaperone Tah1, cures [URE3] which is a prion form of native protein Ure2 in yeast. The Hsp90 co-chaperone Tah1 is involved in the assembly of small nucleolar ribonucleoproteins (snoRNP) and chromatin remodelling complexes. We found that Tah1 deletion improves the frequency of de novo appearance of [URE3]. The Tah1 was found to interact with Hsp70. The lack of Tah1 not only represses antagonizing effect of Ssa1 Hsp70 on [URE3] but also improves the prion strength suggesting role of Tah1 in both fibril growth and replication. We show that the N-terminal tetratricopeptide repeat domain of Tah1 is indispensable for [URE3] curing.