Barbourpehrson9439

Background Elderly patients, compared with the young, have a higher burden of surgical risk factors with reduced functional capacity and increased comorbidities conditions, and may have worse clinical outcomes. So far, few reports have focused on clinical outcomes of patients over 70 years of age with moderate chronic ischemic mitral regurgitation (IMR) undergoing mitral valve repair at the time of coronary artery bypass grafting (CABG). This single-center study of propensity-matched data attempts to answer a question compared with patients with age of 70 or less, whether patients over 70 years of age with moderate IMR undergoing CABG plus mitral valve repair receive poor outcomes. Methods All eligible patients were included in this study and were entered into either an elderly group (n=142) or a control group (n=182) according to patients' age. In-hospital outcomes (consisting of surgical mortality and major postoperative morbidity) and midterm clinical outcomes (including all-cause mortality and recurrent monic IMR undergoing combined CABG and mitral valve repair may receive favorable in-hospital and midterm clinical outcomes. 2019 Cardiovascular Diagnosis and Therapy. All rights reserved.Background Controlling blood lipid levels at the early stage of cardiovascular disease is a major focus of global disease prevention studies on atherosclerosis. The aim of our study was to investigate the effects of potassium selencyanoacetate on the blood lipid profiles and the formation of atherosclerotic plaques in mice fed with a high-fat diet. Methods Forty ApoE-/- male mice aged 8-10 weeks were randomly divided into the treatment group (n=20) and control group (n=20). The mice in the treatment group were given the high-fat diet supplemented with potassium selencyanoacetate (4.63 mg/kg/day) through a gavage, whereas the control group were fed with a same high-fat diet with 1.5 mL of normal saline only. After 16 weeks, the mice were euthanized using inhalation anesthetic methods. The aortas were isolated and stained with oil red O to observe the formation of plaques. Blood samples were collected from each animal to examine the levels of total cholesterol (TC), triacylglycerol (TG), HDL cholesterol (HDL-Ch), LDL cholesterol (LDL-Ch), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and plasma urea. Results The percentage of the atherosclerotic plaques area was significantly lower in the treatment group than the control group (P=0.017). The levels of TG, ALT, AST, and plasma urea were significantly lower in the treatment group than the control group (all P0.05). Conclusions Potassium selencyanoacetate could safely reduce the TG level and high-fat-diet induced atherosclerotic plaques in mice, which could be used as a potential drug to prevent cardiovascular atherosclerotic diseases. 2019 Cardiovascular Diagnosis and Therapy. All rights reserved.Background The molecular mechanism of quercetin in the prevention and treatment of AS has been widely reported. However, the microbial and metabolic characteristics of quercetin in AS treatment are still poorly understood. In this study, we aimed to explore the gut microbial and metabolic signatures of quercetin in AS treatment and conduct an integrative analysis on its biomechanism. Methods An atherosclerosis mouse model was induced by a high cholesterol diet (HCD). The duration of the quercetin treatment was 12 weeks. We measured TC, TG, HDL and LDL for plasma biochemical analysis and TNF-α and IL-6 for plasma inflammatory analysis. Haematoxylin-eosin (HE) staining was conducted to evaluate the aortic structure and atherosclerosis. Bacterial DNA, which was extracted from mouse faeces, was identified by the V3-V4 regions of the 16S rRNA for microbiological analysis. The HeatMap package of BTtools was applied to visualize the data of the microbial difference matrix according to the OTU results. Fecal metabolietabolic regulation. 2019 Cardiovascular Diagnosis and Therapy. All rights reserved.Background Heart failure (HF) is a progressive disease with relatively poor prognosis and lacks effective therapy, and the discovery of dysregulated microRNAs (miRNAs) and their role in cardiac fibroblasts have provided a new avenue for elucidating the mechanism involved in HF. Methods Two datasets of GSE53080 and GSE57338 were used to screen the miRNAs profiling and analysis the differentially expressed genes (DEGs) in HF. QRT-PCR was used to detect miR-216a between HF and healthy controls (HC). Cell counting kit-8 (CCK-8) assay and clonogenic assay were used to analyze the effect of proliferation and fibrogenesis. Then dual-luciferase activity assay and western blotting were used to confirm the key mechanism. Results In this study, the results showed that miR-216a was significantly up-regulated in HF and over-expression of miR-216a promoted proliferation and enhanced the fibrogenesis in the human cardiac fibroblasts (HCF) cells. Phosphatase and tensin homolog (PTEN) and mothers against decapentaplegic homolog 7 (SMAD7) were both validated as the direct target genes of miR-216a, which were confirmed by the dual-luciferase reporter assay. MiR-216a decreased the expression of PTEN and SMAD7 leading to the activation of Akt/mTOR and TGF-βRI/Smad2 in the HCF cells, which might act as a promoter of cardiac fibrosis. Conclusions Our study might provide a promising approach for the treatment of HF in the future. 2019 Cardiovascular Diagnosis and Therapy. All rights reserved.Detection of donor-specific antibodies (DSA) is an essential part of diagnosing antibody-mediated renal allograft rejection (ABMR). The role of solitary preformed, or post-transplant HLA-C antigens in solid organ transplantation is unclear, due to the less sensitive nature of the historical assays, lack of data, low expression level on the cell surface, and their co-existence with other anti-HLA DSA. PD-1/PD-L1 Inhibitor 3 supplier Herein, we present the case of a 39-year-old African American man, without prior history of pre-transplant sensitization that was diagnosed with biopsy-proven ABMR due to de novo donor-specific anti-HLA-C antibodies. This case report illustrates the role of HLA-C antibodies in causing ABMR if generated toward immunogenic-shared epitopes and demonstrates the need for their recognition in the pre- and post-transplant period. Another interesting aspect of this case is the incidental finding of Fabry-like zebra bodies, which we eventually determined to be of unclear etiology. © Dustri-Verlag Dr. K. Feistle.