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In conclusion, the present research revealed for the first time that baicalin acted as a therapeutic drug in IBD by suppression of the PI3K/AKT signaling pathway.Disruption of cell metabolism is a hallmark of cancer cells. selleck products Accumulating evidence suggests that microRNAs (miRNAs/miRs) are involved in almost all physiological and pathological processes. The aberrant expression of miRNAs induces metabolic reprogramming in cancer cells and thus, promotes proliferation. In the current study, miR-513a-3p was identified as a significantly downregulated miRNA in colorectal cancer cells and tumors. Overexpression of miR-513a-3p in colorectal cancer cells inhibited proliferation and glycolysis. A well-documented metabolic regulator, hexokinase 2 (HK2), was predicted and validated HK2to be a target gene of miR-513a-3p in colorectal cancer cells. In addition, overexpression of HK2 reversed the miR-513a-3p mimic-induced inhibition of proliferation. The association between HK2 and miR-513a-3p was further observed in tumors collected from patients with colorectal cancer. The findings suggest that miR-513a-5p may inhibit glycolysis in colorectal cancer cells via repressing HK2 expression, indicating that miR-513a-5p may be a tumor suppressor in colorectal cancer.Pre-participation sports examination (PPE) is a frequent reason for consultation. However, the exact role of cardiovascular magnetic resonance (CMR) in PPE remains undefined. The additive value of CMR in adolescent athletes with ventricular rhythm disturbances (VRDs) was investigated. We prospectively recruited and evaluated with CMR 50 consecutive, asymptomatic young athletes referred to our tertiary center after identification of VRDs on electrocardiogram (ECG) with otherwise normal standard PPE and echocardiography, and 20 age- and sex-matched healthy volunteer athletes who underwent the same evaluations. The primary outcome was case-control status and the secondary outcome was the discrimination between athletes with VRDs with and without non-sustained ventricular tachycardia (VT). CMR identified arrhythmogenic substrates in all athletes with VRDs. The predominant condition was myocarditis and arrhythmogenic right ventricular cardiomyopathy in patients with and without VT, respectively. Based on penalized regression analysis, late gadolinium enhancement (LGE), early gadolinium enhancement (EGE), extracellular volume fraction (ECV), and T2-mapping, best distinguished between case-control status. The aforementioned indices predicted case-control status independent of age and sex EGE [Odds ratio (95% confidence interval) 6.89 (2.19-21.62) per 0.5-unit, P less then 0.001], LGE (perfect prediction), ECV [1.66 (1.25-2.22), P less then 0.001] and T2 mapping [1.40 (1.13-1.72), P=0.002], among other independent CMR-derived predictors. Only indexed ventricular volumes independently discriminated between VRD patients with and without VT. In this study, asymptomatic young athletes with VRDs and normal PPE/echocardiography were optimally discriminated from healthy control athletes by CMR-derived indices, and CMR allowed for the identification of arrhythmogenic substrates in all cases.The development of abnormal lipid-induced atherosclerosis is initiated with endothelial cell apoptosis. Vascular endothelial cells possess highly developed endoplasmic reticulum (ER), which is involved in lipid metabolism, indicating that ER stress may contribute chiefly to the induction of endothelial cell apoptosis. Based on its ability to reduce cholesterol levels, rosuvastatin may play an endothelial and vascular protective role by regulating ER stress. In the present study, the involvement of the inhibition of the ER stress-induced endothelial injury was investigated in combination with the lipid lowering effects of rosuvastatin. This compound can be used to inhibit cholesterol synthesis in atherosclerosis. Rosuvastatin decreased the apoptotic rates of human umbilical vascular endothelial cells (HUVECs) that had been stimulated with ox-low density lipoprotein (LDL) in vitro and repressed the mRNA levels of CHOP, sXBP1 and caspase-12, and decreased caspase-12 activity, as well as the content of glucose-reortic intima. The data indicated that rosuvastatin could protect HUVECs from ER stress-induced apoptosis triggered by oxidized LDL. It could also inhibit atherosclerosis formation in ApoE-/- mice aorta by regulating the PERK/eIF2α/C/EBPα-homologous protein and IRE1α/sXBP1 signaling pathways. Taken collectively, the present study demonstrated the preventive and therapeutic effects of rosuvastatin in protecting from the development of endothelial cell dysfunction diseases.The aim of the present study was to analyze the sequence of the VP1 gene in enterovirus 71 (EV71) isolates and to explore their genetic evolution, so as to provide a scientific basis for the clinical prevention and treatment of hand, foot and mouth disease. The fecal samples of 590 patients with suspected hand, foot and mouth disease treated at Yan'an Hospital (Kunming, China) between January 2015 and December 2016 were collected and EV71 nucleic acid was detected by fluorescence PCR. The viral RNA of EV71-positive samples was extracted, the VP1 gene was amplified by PCR and the products were sequenced. The VP1 gene sequence was analyzed using DNAMAN and MEGA (version 4.0) software and homologous modeling was performed using Pymol software. A total of 50 EV71-positive samples were identified and the detection rate was 8.47% (50/590 cases). All of the 50 EV71 strains were of the C4 subtype. The genetic distance between the strains detected in the present study and EV71 strains detected in Beijing, Anhui and Malaysia was 0.01-0.03, while that between the strains detected in the present study and Australian strains was 2.11. Homologous modeling indicated that the amino acid sequence of the VP1 gene of the detected strains had a H144Y mutation. There was no significant genetic variation in the EV71 strain within the 2-year period. In conclusion, the EV71 strains detected in the present study was similar to that detected in Beijing, Anhui and Malaysia but different to that from Australia. A point mutation was present in the amino acid sequence of the VP1 gene.
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