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These toxic effects induced by OTA and CsA could be reversed by knockdown of TLR4 and autophagy inhibitor 3-methyladenine in vitro. Furthermore, the renal injury and autophagy induced by OTA and CsA could be attenuated in TLR4-/- mice. It suggested that a chronic nephropathy model had been successfully developed by administration of nontoxic concentration of OTA and low dosage of CsA via TLR4-mediated autophagy. The side effects of current model were significantly lesser than those of the previous model induced by onefold CsA. It provided a new tool for exploring the pathogenesis and treatment of chronic kidney disease.BACKGROUND This study aimed to use bioinformatics analysis to compare data from tissue microarrays from patients with lung adenocarcinoma (LUAD) and normal lung tissue, and human lung adenocarcinoma cells with normal lung epithelial cells in vitro to investigate the role of synaptotagmin 12 (SYT12) gene expression in LUAD. MATERIAL AND METHODS Human lung adenocarcinoma cell lines (A549, SPC-A-1, H1299, H1975, and PC9) and the normal HBE cell line were compared, and tumor xenografts were developed in mice. The Cancer Genome Atlas (TCGA) tissue microarray data were used to compare SYT12 expression and overall survival (OS). The in vivo and in vitro effects of down-regulation and upregulation of SYT12 were studied using short-interfering RNA (si-RNA) and overexpression plasmids, respectively. The Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) pathway analysis, quantitative reverse transcription-polymerase chain reaction (qRT-PCR), and Western blot investigated the molecular mechanisms of SYT12 expression in LUAD. RESULTS SYT12 expression was increased in tissues from patients with LUAD from TCGA and was associated with advanced tumor stage and reduced prognosis. Knockdown of SYT12 suppressed the proliferation and migration of LUAD cells, and upregulation of SYT12 increased the proliferation and migration of LUAD cells in vitro. Phosphorylation of PIK3R3 activated the PI3K/AKT/mTOR pathway. In the mouse xenograft model, expression of SYT12 increased the volume and weight of the xenograft tumors. CONCLUSIONS Bioinformatics analysis, human LUAD cells, and mouse xenograft studies showed that SYT12 acted as a possible oncogene by phosphorylation of PIK3R3 to activate the PI3K/AKT/mTOR signaling pathway.AIMS We performed a meta-analysis of currently available studies investigating the impact of postprocedural thrombocytopenia on mortality after transcatheter aortic valve implantation (TAVI). METHODS All studies researching the impact of postprocedural thrombocytopenia on mortality after TAVI were identified after searching PubMed and Web of Science through July 2019. The outcome of interest was early (in-hospital or 30-day) and overall (1- to 2-year) all-cause mortality after TAVI. From each study, the number of deaths in both patients with major (moderate/severe or higher postprocedural drop platelet counts defined in each study) and nonmajor (no/minor or lower drop platelet counts defined in each study) postprocedural thrombocytopenia was extracted. Then, odds ratios (ORs) of mortality for major vs. no/minor thrombocytopenia and their confidence intervals were generated. Alternatively, ORs and hazard ratios of mortality for major vs. no/minor thrombocytopenia (if available, adjusted) were directly extracted. Study-specific estimates were pooled in both the fixed-effect and random-effects models. RESULTS The principal pooled analysis demonstrated that postprocedural thrombocytopenia was associated with statistically significant increases in early (OR, 3.79; P for effect less then 0.00001; P for heterogeneity = 0.89) and overall mortality (OR/hazard ratio, 1.22; P for effect = 0.009; P for heterogeneity = 0.17) in the fixed-effect model. All sensitivity analyses did not substantively alter the results of the principal analysis. No funnel plot asymmetry of the principal analysis was detected (P for early mortality = 0.88; P for overall mortality = 0.14), which suggested probably no publication bias. CONCLUSION Postprocedural thrombocytopenia is associated with increased early and overall mortality after TAVI.BACKGROUND AND AIM Cardiac resynchronization therapy (CRT) reduces mortality and morbidity in chronic heart failure symptomatic patients with broad QRS who are already undergoing optimal medical treatment. However, approximately one-third of implanted patients do not show any benefit from this treatment. Right ventricle (RV) dysfunction leads to a worse outcome in patients with heart failure, but its role in predicting the response to CRT has shown conflicting results. The purpose of our study was to investigate how the RV function, assessed by cardiac magnetic resonance (CMR), could influence the outcome of heart failure patients treated with CRT. DL-Alanine METHODS AND RESULTS We retrospectively enrolled 72 heart failure patients, 38 affected by dilated cardiomyopathy (DCM) and 34 by ischemic dysfunction, with left bundle branch block, QRS greater than 120 ms and standard indications to CRT. We defined the response to CRT as an improvement of at least 10% of the left ventricular ejection fraction (LVEF) or at least onunction less likely benefited from CRT. RV assessment, studied with CMR, appears to be a good predictor of the response to biventricular stimulation. The European Society of Cardiology guidelines for myocardial revascularization state that de-escalation of P2Y12 inhibitor treatment guided by platelet function testing may be considered for acute coronary syndrome (ACS) patients deemed unsuitable for 12-month potent platelet inhibition. De-escalation strategy aim is to harmonize the time-dependency of thrombotic risk, which is high in the first month after ACS, then decreases exponentially, with bleeding risk, which tends to remain more stable after the procedure-related peak. Harmonizing time-dependency of clinical events may be particularly relevant in those at high risk, such as the elderly patients with ACS in whom an individualized antiplatelet therapy may be more appropriate than a 'one-size-fits all' approach. In this review, we outline the current medical evidence on the topic of dual antiplatelet therapy de-escalation. In addition, we include insights from the Elderly ACS 2 study and recently published post-hoc analyses conducted by the authors' consortium, which further expands current knowledge.