Value of high-sensitivity C-reactive protein assays in predicting atrial fibrillation recurrence: a systematic review and meta-analysis

Objectives: We performed a systematic review and meta-analysis of studies on high-sensitivity C-reactive protein (hs-CRP) assays to see whether these tests are predictive of atrial fibrillation (AF) recurrence after cardioversion. Design: Systematic review and meta-analysis. Data sources PubMed, EMBASE and Cochrane databases as well as a hand search of the reference lists in the retrieved articles from inception to December 2013. Study eligibility criteria This review selected observational studies in which the measurements of serum CRP were used to predict AF recurrence. An hs-CRP assay was defined as any CRP test capable of measuring serum CRP to below 0.6 mg/dL. Primary and secondary outcome measures We summarised test performance characteristics with the use of forest plots, hierarchical summary receiver operating characteristic curves and bivariate random effects models. Meta-regression analysis was performed to explore the source of heterogeneity. Results: We included nine qualifying studies comprising a total of 347 patients with AF recurrence and 335 controls. A CRP level higher than the optimal cut-off point was an independent predictor of AF recurrence after cardioversion (summary adjusted OR: 3.33; 95% CI 2.10 to 5.28). The estimated pooled sensitivity and specificity for hs-CRP was 71.0% (95% CI 63% to 78%) and 72.0% (61% to 81%), respectively. Most studies used a CRP cut-off point of 1.9 mg/L to predict long-term AF recurrence (77% sensitivity, 65% specificity), and 3 mg/L to predict short-term AF recurrence (73% sensitivity, 71% specificity). Conclusions: hs-CRP assays are moderately accurate in predicting AF recurrence after successful cardioversion

Fourth Generation Leptons and Muon g−2g-2

We consider the contributions to $g_\mu-2$ from fourth generation heavy neutral and charged leptons, $N$ and $E$, at the one-loop level. Diagrammatically, there are two types of contributions: boson-boson-$N$, and $E$-$E$-boson in the loop diagram. In general, the effect from $N$ is suppressed by off-diagonal lepton mixing matrix elements. For $E$, we consider flavor changing neutral couplings arising from various New Physics models, which are stringently constrained by $\mu\to e\gamma$. We assess how the existence of a fourth generation would affect these New Physics models.Comment: Minor changes, with references update

Epidermal growth factor receptor regulates β-catenin location, stability, and transcriptional activity in oral cancer

<p>Abstract</p> <p>Background</p> <p>Many cancerous cells accumulate β-catenin in the nucleus. We examined the role of epidermal growth factor receptor (EGFR) signaling in the accumulation of β-catenin in the nuclei of oral cancer cells.</p> <p>Results</p> <p>We used two strains of cultured oral cancer cells, one with reduced EGFR expression (OECM1 cells) and one with elevated EGFR expression (SAS cells), and measured downstream effects, such as phosphorylation of β-catenin and GSK-3β, association of β-catenin with E-cadherin, and target gene regulation. We also studied the expression of EGFR, β-catenin, and cyclin D1 in 112 samples of oral cancer by immunostaining. Activation of EGFR signaling increased the amount of β-catenin in the nucleus and decreased the amount in the membranes. EGF treatment increased phosphorylation of β-catenin (tyrosine) and GSK-3β(Ser-(9), resulting in a loss of β-catenin association with E-cadherin. TOP-FLASH and FOP-FLASH reporter assays demonstrated that the EGFR signal regulates β-catenin transcriptional activity and mediates cyclin D1 expression. Chromatin immunoprecipitation experiments indicated that the EGFR signal affects chromatin architecture at the regulatory element of cyclin D1, and that the CBP, HDAC1, and Suv39h1 histone/chromatin remodeling complex is involved in this process. Immunostaining showed a significant association between EGFR expression and aberrant accumulation of β-catenin in oral cancer.</p> <p>Conclusions</p> <p>EGFR signaling regulates β-catenin localization and stability, target gene expression, and tumor progression in oral cancer. Moreover, our data suggest that aberrant accumulation of β-catenin under EGFR activation is a malignancy marker of oral cancer.</p

THE ANALYSIS OF PULLING FORCE CURVES IN TUG-OF-WAR

The purpose of this study is to analyze the pulling force curves in DFB and AFB movements that produced by elite tug-of-war athletes. The subjects are 11 female high school athletes who have been trained more than two years for tug-of-war. Data is analyzed by paired-sample t-test. The results show that force-related parameters are all different significantly between two movements, and time-related parameters are not significant. The DFB movement has higher value in MaxF, AveF, FS and lower value in MinF. We suggest to avoid the decay of pulling force while adopting DFB movement, and increase MaxF, AveF, and FS while adopting AFB movement. Within the start of 2sec we suggest the team to take the DFB movements in order to produce powerful pulling force, then transform to the AFB movements to keep the team formation

Association of Alzhemier\u27s Disease With Hepatitis C Among Patients With Bipolar Disorder

Associations of hepatitis C virus infection with Alzheimer’s disease have not been studied among higher risk, bipolar disorder patients. This population-based case-control study investigated the risks of hepatitis C virus infection among Alzheimer’s disease patients with bipolar disorder in the years preceding their Alzheimer’s disease diagnosis. We used 2000–2013 data from the Longitudinal Health Insurance Database in Taiwan. Among patients with bipolar disorder, 73 were diagnosed with Alzheimer’s disease (cases), who were compared with 365 individuals with bipolar disorder but without Alzheimer’s disease (randomly selected controls matched on sex, age, and index year with cases). Prior claims (before the diagnosis year/index year for controls) were screened for a diagnosis of hepatitis C virus infection. Conditional logistic regression models were used for analysis. We found that 23 (31.51%) and 60 (16.44%) patients with bipolar disease were identified with a hepatitis C diagnosis among those with and without Alzheimer’s disease, respectively. Compared to controls, patients with Alzheimer’s disease showed 2.31-fold (95% confidence interval = 1.28–4.16) increased risk of hepatitis C infections adjusted for demographics and socio-economic status. Findings suggest an association of Alzheimer’s disease with a preceding diagnosis of hepatitis C infection among patients with bipolar disorder. Findings may suggest a need for increased awareness of and appropriate surveillance for Alzheimer’s disease in patients with bipolar disorder diagnosed with hepatitis C infection