Previous observational studies have suggested a potential relationship between osteoarthritis (OA) and the risk of cardiovascular disease (CVD), with conflicting results. We aimed to provide a systematic and quantitative summary of the association between OA and the risk of CVD. We searched Medline and EMBASE to retrieve prospective and retrospective studies that reported risk estimates of the association between OA status and CVD risk. Pooled estimates were calculated by a random effects model. The search yielded 15 articles including a total of 358,944 participants, including 80,911 OA patients and 29,213 CVD patients. Overall, the risk of CVD was significantly increased by 24% (RR: 1.24, 95% CI: 1.12 to 1.37, P < 0.001) in patients with OA compared with the general population, with no significant publication bias. Furthermore, sensitivity analysis indicated that our results were robust and were not influenced by any one study. In conclusion, this meta-analysis provides strong evidence that OA is a significant risk factor for CVD.

Background: Several studies have suggested that cytomegalovirus infection is likely associated with an increased relative risk of cardiovascular disease ( CVD ); however, the results are inconsistent. We aimed to provide a systematic review and meta‐analysis of community‐based prospective studies assessing the association between cytomegalovirus infection and relative risk of CVD . Methods and Results: We searched Medline and EMBASE to retrieve prospective studies that reported risk estimates of the association between cytomegalovirus infection and relative risk of CVD . The search yielded 10 articles including a total of 34 564 participants and 4789 CVD patients. Overall, exposure to cytomegalovirus infection was associated with a 22% (relative risk: 1.22, 95% CI : 1.07–1.38, P =0.002) increased relative risk of future CVD . We estimated that 13.4% of CVD incidence could be attributable to cytomegalovirus infection. Conclusions: In conclusion, cytomegalovirus infection is associated with a significantly increased relative risk of CVD .

Background: Tumor necrosis factor-α (TNF-α) is one of the most typical pro-inflammatory cytokines with both beneficial and destructive properties for the central nervous system. Increasing evidences have demonstrated the important role of TNF-α in the development of ischemic stroke, but studies examining the possible association with stroke or direct functional effects of polymorphisms in TNF-α have been contradictory. Findings: In this study, a 2-kb length of the proximal promoter of the TNF-α was screened and four polymorphisms were investigated in the case–control study. Our data confirmed the association between -308G/A variant with stroke in 1,388 stroke patients and 1,027 controls and replicated in an independent population of 961 stroke patients and 821 controls (odds ratio (OR) = 1.34, 95% confidence interval (CI) =1.02 to 1.77 and OR = 1.56, 95% CI = 1.09 to 2.23, respectively). To reconcile the association between polymorphisms and stroke and to give a comprehensive picture of the genetic architecture of this important gene, we performed a meta-analysis of 15 published studies in an Asian population. Our results demonstrated an association between rs1800629 and ischemic stroke (OR = 1.43, 95% CI = 1.21 to 1.69). Another meta-analysis results of 14 studies demonstrated that ischemic stroke patients have higher serum TNF-α level than the control subjects (standardized mean difference (SMD) = 2.33, 95% CI = 1.85 to 2.81). In vitro evaluation of potential interaction between variants of the TNF-α gene (−308G/A, -857C/T, and -1031T/C) demonstrated that these three polymorphisms could interact together to determine the overall activity of the TNF-α gene. Conclusions: These findings strongly implicate the involvement of TNF-α in the pathogenesis of stroke.

Mesocorticolimbic dopaminergic (DA) neurons have been implicated in regulating nociception in chronic pain, yet the mechanisms are barely understood. Here, we found that chronic constructive injury (CCI) in mice increased the firing activity and decreased the KCNQ channel-mediated M-currents in ventral tegmental area (VTA) DA neurons projecting to the nucleus accumbens (NAc). Chemogenetic inhibition of the VTA-to-NAc DA neurons alleviated CCI-induced thermal nociception. Opposite changes in the firing activity and M-currents were recorded in VTA DA neurons projecting to the medial prefrontal cortex (mPFC) but did not affect nociception. In addition, intra-VTA injection of retigabine, a KCNQ opener, while reversing the changes of the VTA-to-NAc DA neurons, alleviated CCI-induced nociception, and this was abolished by injecting exogenous BDNF into the NAc. Taken together, these findings highlight a vital role of KCNQ channel-mediated modulation of mesolimbic DA activity in regulating thermal nociception in the chronic pain state.

Background:Several studies have suggested that snoring is associated with an increased risk of stroke; however, the results are inconsistent. We aim to conduct a systematic review and meta-analysis of observational studies assessing the association between snoring and the risk of stroke in adults.Methods:We searched PubMed for relevant studies. A random-effect model was adopted to summary relative risks (RRs), and forest plots from a cumulative meta-analysis method were used for a better presentation of how the pooled RRs changed as updated evidence accumulated.Results:The literature search yielded 16 articles that met our inclusion criteria, and a total of 3,598 stroke patients and 145,901 participants were finally included in our analysis. A consistent trend toward association was found after the initial discovery, and the summary analysis indicated that snoring is associated with a 46% (RR, 1.46; 95%CI, 1.29–1.63;p< 0.001) increased risk of stroke.Conclusions:Snoring is associated with a significantly increased risk for stroke, up to 46%. The importance of the current study lies in that we provide an imputes to take a more active approach against the increased risk of stroke in snorers.