Myeloid disorders, especially myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML), cause significant mobility and high mortality worldwide. Despite numerous attempts, the common molecular events underlying the development of MDS and AML remain to be established. In the present study, 18 microarray datasets were selected, and a meta-analysis was conducted to identify shared gene signatures and biological processes between MDS and AML. Using NetworkAnalyst, 191 upregulated and 139 downregulated genes were identified in MDS and AML, among which, PTH2R, TEC, and GPX1 were the most upregulated genes, while MME, RAG1, and CD79B were mostly downregulated. Comprehensive functional enrichment analyses revealed oncogenic signaling related pathway, fibroblast growth factor receptor (FGFR) and immune response related events, ‘interleukine-6/interferon signaling pathway, and B cell receptor signaling pathway’, were the most upregulated and downregulated biological processes, respectively. Network based meta-analysis ascertained that HSP90AA1 and CUL1 were the most important hub genes. Interestingly, our study has largely clarified the link between MDS and AML in terms of potential pathways, and genetic markers, which shed light on the molecular mechanisms underlying the development and transition of MDS and AML, and facilitate the understanding of novel diagnostic, therapeutic and prognostic biomarkers.
A series of related electrophysiology phenomena can be caused by the occurrence of interpolated ventricular prematurecontraction. In our recent three-dimensional Lorenz R-R scatter plot research, we found that atrioventricular nodedouble path caused by interpolated ventricular premature contraction imprints a specific pattern on three-dimensionalLorenz plots generated from 24-hour Holter recordings. We found two independent subclusters separated from the interpolated premature beat precluster, the interpolated premature beat cluster, and the interpolated premature beat postcluster, respectively. Combined with use of the trajectory tracking function and the leap phenomenon, our results reveal the presence of the atrioventricular node double conduction path.
The occurrence of heart failure (HF) is closely correlated with the disturbance of mitochondrial energy metabolism, and trimetazidine (TMZ) has been regarded as an effective agent in treating HF. Intracellular potassium ion (K+) homeostasis, which is modulated by K+ channels and transporters, is crucial for maintaining normal myocardial function and can be disrupted by HF. This study is aimed at exploring the protective effect of TMZ on K+ homeostasis within myocardial tissue in mice with HF. We observed the pathological changes of myocardial tissue under microscopes and further measured the content of adenosine triphosphate (ATP), the activity of Na+-K+ ATPase, and the expression of ATP1α1 at the mRNA and protein levels. Moreover, we also analyzed the changes in K+ flux across the myocardial tissue in mice. As a result, we found that there was a large amount of myocardial fiber lysis and fracture in HF myocardial tissue. Meanwhile, the potassium flux of mice with HF was reduced, and the expression of ATP1α1, the activity of Na+-K+ ATPase, and the supply and delivery of ATP were also decreased. In contrast, TMZ can effectively treat HF by restoring K+ homeostasis in the local microenvironment of myocardial tissues.
Background: Mitral stenosis (MS) is related to prolonged inter- and intra-atrial electromechanical delays and increased P-wave dispersion. The objective of the current study was to investigate the correlation between the P-wave duration, P-wave dispersion (PWD), mitral stenosis (MS) and to explore the cut-off values for predicting the MS in the patients.Methods: We enrolled 62 patients with MS and sinus rhythm as test group, and 62 healthy subjects matched in age- and sex- were selected as control group. We conducted the 12-lead electrocardiogram and echocardiography for all the subjects. The maximum and the minimum P-wave duration and PWD were calculated. Univariate and multivariate logistic regression analyses were performed to demonstrate the correlation between P-wave duration and PWD and MS. The receiver operating characteristic (ROC) curve was drawn to detect the threshold of P-wave duration and PWD for predicting the MS.Results: There were significant differences in the left atrial diameter (45.00±5.78 vs. 32.31±4.24 cm2), pulmonary artery pressure (46.68±17.29 vs. 32.64±2.86 mm Hg), left ventricular end-diastolic diameter (47.57±4.80 vs. 45.58±5.04 cm), ejection fraction (63.10±3.05 vs. 65.13±2.56%), aortic root inside diameter (29.60±3.50 vs. 31.58±3.58) and pulmonary trunk (24.17±2.78 vs. 22.23±1.77) values between the test group and the control group. Besides, the test subjects had significantly longer maximum P-wave duration (123.42±12.33 vs. 108.18±9.07) and larger P-wave dispersion (47.24±13.61 vs. 28.94±9.19). In the multivariate analysis, maximum P-wave duration (OR:1.221, 95% CI:1.126-1.324) and P-wave dispersion (OR:1.164, 95% CI:1.094-1.238) were correlated with the occurrence of MS. The optimal threshold for the maximum P-wave duration and PWD were 119.50ms, and 42.50ms, respectively, and the areas under the curve were 0.859 and 0.865, respectively. Conclusions: A longer P-wave duration and a higher PWD are correlated with the increased risk of MS progression.
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