Notes

Cecal volvulus: An uncommon post-partum side-effect.
Long non-coding RNAs (lncRNAs) serve major roles in diabetic nephropathy (DN). The present study investigated the regulatory mechanism of lncRNA non-coding RNA activated by DNA damage (NORAD) on DN in vitro. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of lncRNA NORAD, microRNA-485 (miR-485) and nuclear respiratory factor 1 (NRF1) in the tissues of patients with DN and high-glucose (HG)-induced human mesangial cells (HMCs). The viability of HMCs was determined using an MTT assay. The levels of inflammatory [tumour necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6] and fibrotic [type IV collagen (Col. IV), fibronectin (FN) and plasminogen activator inhibitor 1 (PAI-1)] factors in HMCs were measured by ELISA. The interactions between miR-485 and NORAD/NRF1 were predicted using StarBase and miRDB softwares and confirmed by a dual-luciferase reporter assay. Western blot analysis was utilized to measure NRF1 protein levels. lncRNA NORAD was highly expressed in tissues and HG-induced HMCs. NORAD knockdown suppressed cell viability in HG-induced HMCs. The levels of the inflammatory and fibrotic factors in HG-induced HMCs were inhibited by NORAD knockdown. miR-485 was the direct target of NORAD. NORAD reversed the inhibitory effects of miR-485 on HG-induced HMCs. Furthermore, NRF1 was the target gene of miR-485. Downregulation of miR-485 and upregulation of NRF1 reversed the inhibitory effects of NORAD knockdown on HG-induced HMCs. NORAD knockdown inhibited HG-induced HMC proliferation, inflammation and fibrosis by regulating miR-485/NRF1, providing a possible therapeutic strategy for DN.MicroRNAs (miRNAs/miRs) serve an important role in the pathogenesis of chronic heart failure (CHF). A number of reports have illustrated the regulatory effect of serum exosomal miRNA on myocardial fibrosis. The present study aimed to investigate the expression of miR-320a in serum exosomes, as well as the effect of miR-320a on myocardial fibroblast proliferation. Serum exosome samples from 10 patients with CHF and 5 healthy volunteers were obtained and characterized. mRNA and protein expression levels were measured via reverse transcription-quantitative PCR and western blotting, respectively. The content of soluble growth stimulation expressed gene 2 (sST2) was determined via ELISA. HEH2 cell viability and apoptosis were detected by performing MTT assays and flow cytometry, respectively. The results demonstrated that serum miR-320a expression levels and sST2 content were significantly increased in patients with CHF compared with healthy controls, and the expression of serum miR-320a was significantly correlat-320a promoted myocardial fibroblast proliferation via regulating the PIK3CA/Akt/mTOR signaling pathway in HEH2 cells, suggesting that serum exosomal miR-320a may serve as a potential biomarker for the diagnosis of CHF.Chronic exposure to inorganic arsenic (iAs) through contaminated drinking water is an important health problem in certain countries. The use of phytochemicals such as curcumin has recently emerged as an alternative strategy for preventing cellular damage caused by iAs. The Epstein-Barr virus (EBV) affects ~90% of the population and experimental evidence suggested that curcumin mediates cytotoxicity against EBV-infected cells. Due to the potential for an interaction of these factors, the aim of the present study was to evaluate the effect of this phytochemical on iAs-related toxicity in EBV-infected cells. Two independent EBV-immortalized human lymphoblastoid cell lines (LCLs) were used as the model. The cell lines were first incubated with increasing concentrations of curcumin or iAs for 24 and 15 h, respectively, to determine the individual effects of each exposure on cell death. In the next experiment, cell cultures were pre-incubated with 5 µM curcumin for 9 h prior to treatment with 10 µM iAs for 15 h, followed by evaluation of cell death and the cell cycle profile via flow cytometry. The results indicated that individual treatment with either curcumin or iAs induced cell death in a concentration-dependent manner. Furthermore, curcumin pre-treatment enhanced iAs-induced cell death and promoted cell cycle arrest in G1 phase. Taken together, these results suggested that curcumin sensitizes EBV-positive LCLs to the cytotoxic effects of iAs.Atherosclerosis (AS) is a chronic pathophysiological process that causes high mortality and morbidity. It has previously been reported that homeobox A9 (HOXA9) may participate in regulation of the cardiovascular system and the pathology of AS by upregulating E-selectin and vascular cell adhesion molecule-1 (VCAM-1). Thus, inhibiting HOXA9 could promote microcirculation of coronary arteries and could act as a potential therapy for AS treatment. Sprague-Dawley rats were randomly divided into four groups, as follows i) AS; ii) AS + HOXA9 inhibitor; iii) AS + small interfering RNA-HOXA9 and iv) normal control. ELISA was used to measure the levels of TNF-α, IL-1β, IL-12, C-C motif chemokine ligand 25 (CCL25), low-density lipoprotein (LDL), high-density lipoprotein (HDL) and very-low-density lipoprotein (VLDL). Flow cytometry was employed to detect the content of M1 macrophages. Hematoxylin & eosin (H&E) staining was performed to observe the morphology of the coronary arteries. Oil red O staining was conducted for coronary arteries of AS rats. These findings indicated that HOXA9 inhibitors may have the potential to succeed in the treatment of AS.Myocardial hypertrophy is an independent risk factor of cardiovascular diseases and is closely associated with the incidence of heart failure. In the present study, we hypothesized that difluoromethylornithine (DFMO) could attenuate cardiac hypertrophy through mitochondria-associated membranes (MAM) and autophagy. Cardiac hypertrophy was induced in male rats by intravenous administration of isoproterenol (ISO; 5 mg/kg/day) for 1, 3,7 and 14 days. MLi-2 cost For DFMO treatment group, rats were given ISO (5 mg/kg/day) for 14 days and 2% DFMO in their water for 4 weeks. The expression of atrial natriuretic peptide (ANP) mRNA,heart parameters, apoptosis rate, fibrotic area and protein expressions of cleaved caspase3/9, GRP75, Mfn2, CypD and VDAC1 were measured to confirm the development of cardiac hypertrophy, apoptosis and autophagy induced by ISO. ANP mRNA and MAM protein expression levels were assessed by reverse transcription-quantitative PCR and western blotting to evaluate hypertrophy and the effects of DFMO oral administration. The results demonstrated that heart parameters, ANP mRNA levels, fibrotic area and apoptosis rate were significantly increased in the heart tissue for ISO 7 and 14 day groups compared with the control group. Furthermore, treatment with DFMO significantly inhibited these indicators, and DFMO downregulated the MAM signaling pathway and upregulated the autophagy pathway in heart tissue compared with the ISO 14 day group. Overall, all ISO-induced changes analyzed in the present study were attenuated following treatment with DFMO. The findings form this study suggested that DFMO treatment may be considered as a potential strategy for preventing ISO-induced cardiac hypertrophy.Previous studies have reported that excess activation of autophagy in cardiomyocytes is associated with an increase in myocardial oxygen-glucose deprivation/reperfusion (OGD/R) injury. Ozone therapy affords significant cardio-protection against myocardial OGD/R injury. The present study was designed to determine whether ozone-induced tolerance to myocardial OGD/R injury was mediated by inhibiting autophagy. Subsequently, the rat cardio myoblast H9C2 cell line was used in the present study. A model of H9C2 cells under OGD/R was established. The cells were incubated with different concentrations of ozone (10-60 µg/ml) during reperfusion. Furthermore, to investigate the role of autophagy in OGD/R-induced injury, the autophagy inducer and inhibitor were applied. Cell viability was detected by Cell Counting kit-8 assay. Cell apoptosis was evaluated by flow cytometry. Oxidative stress was examined by superoxide dismutase, lactate dehydrogenase and malondialdehyde levels. The expressions of apoptosis regulator B-cel low concentrations could protect the myocardium from OGD/R-induced injury by inhibiting autophagy.Epithelial-mesenchymal transition (EMT) of retinal pigment epithelial (RPE) cells is considered to be the main mechanism of proliferative vitreoretinopathy (PVR). Our previous study demonstrated that microRNA-29b (miR-29b) and its target protein kinase B (Akt2) played vital roles in this process. miR-29b, a mesenchymal marker α-smooth muscle actin (α-SMA) and the epithelial marker E-cadherin were assessed in epiretinal membranes of patients with PVR. The potential mechanism of miR-29b and EMT was also investigated. The expression levels of miR-29b, E-cadherin, and α-SMA in PVR epiretinal membranes were measured using quantitative PCR. The expression levels of Akt2, phosphorylated (p)-Akt2, p65, p-p65, and Snail in ARPE-19 cells were assessed using western blotting. The expression levels of miR-29b were positively correlated with E-cadherin mRNA expression, while an inverse correlation was observed between miR-29b and α-SMA mRNA expression in epiretinal membranes of patients with PVR. When miR-29b was transfected into ARPE-19 cells, the expression levels of Akt2, p-Akt2, p-p65 and Snail were downregulated. shRNA-Akt2 inhibited p-p65 and Snail expression, while the NF-κB inhibitor BAY11-7082 reduced Snail expression. The Akt2/p-p65/Snail pathway may be the underlying mechanism of miR-29b in EMT of RPE cells. The results of the present study may provide a new strategy for prevention and therapy of PVR.Donor-specific human leukocyte antigen (HLA) antibodies (DSAs) have a significant role in graft survival after pediatric liver transplantation. To understand the significance of DSAs, a retrospective cohort study of 48 pediatric liver transplant recipients with posttransplant serum samples that were analyzed for DSAs was performed. According to their test results, the recipients were divided into a DSA-positive group and a DSA-negative group. Postoperative liver transplantation biopsies were performed in patients with abnormal liver function. The liver condition and prognosis of the recipients were recorded, and their association was analyzed. A total of 48 recipients were followed up for 2.7±0.8 years. DSA positivity was detected in 10 cases (20.8%). One case was positive for HLA class I and HLA class II antibodies, whereas 9 cases were positive for HLA class II antibodies, and the gene loci were HLA-DR and/or DQ. Antibody-mediated rejection (AMR) occurred in four of 10 patients in the DSA-positive group. Liver function was abnormal in 3 of 38 cases in the DSA-negative group. Multivariate analysis revealed that DSA positivity was an independent risk factor for liver insufficiency and long-term survival of recipients. In addition, Kaplan-Meier survival analysis demonstrated that there were significant differences in the survival of graft recipients between the DSA-positive group and the DSA-negative group (P less then 0.05). The positivity of DSAs after pediatric liver transplantation was closely related to the occurrence of AMR. These results suggested that DSAs should be routinely monitored post-operatively, and that DSA-positive recipients should be screened as soon as possible and given appropriate treatment.
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