[Expression and Regulatory Mechanism of Autophagy-related Genes in Synovial Tissues of Patients with Rheumatoid Arthritis].

Objective To investigate the expression regulation of autophagy-related genes(ATG)and the mechanism of autophagy in rheumatoid arthritis(RA).Methods The differentially expressed genes(DEG)of RA were identified from GSE55235 and GSE55457,on the basis of which the differentially expressed autophagy-related genes(DE-ATG)were selected from the Human Autophagy Database.STRING 11.

Expression of mA Methylation Regulator in Osteoarthritis and Its Prognostic Markers.

Objective: Osteoarthritis (OA) is a multifactorial disorder, in which genetic factors are strongly associated with its development. However, the pathogenesis of OA is still unclear, and recently it has been observed that epigenetic modifications are also involved in the pathogenesis of OA. This study aims to study the potential role of mA-related genes in the occurrence and development of OA.

The Role of Selenium-Mediated Notch/Hes1 Signaling Pathway in Kashin-Beck Disease Patients and Cartilage Injury Models.

Kashin-Beck disease (KBD) is a nutrition-related osteoarthropathy, and selenium (Se) deficiency is an environmental risk factor for KBD. Notch/Hes1 signaling pathway plays a vital role in regulating cartilage, but its exact mechanisms in KBD remain unknown. The Se contents were determined using the hydride atomic fluorescence spectrometry assay technique, and the mRNA levels were detected via quantitative real-time PCR.

Crosstalk between CpG Methylation and Polymorphisms (CpG-SNPs) in the Promotor Region of in Kashin-Beck Disease.

Objective This study was designed to determine the methylation profile of four CpGs and the genotypes of two CpG-SNPs located in promoter region of in patients with Kashin-Beck disease (KBD). We also analyzed the interaction between the CpGs methylations and CpG-SNPs. Methods Whole blood specimens were collected from 16 KBD patients and 16 healthy subjects.

Gene and prognostic value of N6-methyladenosine (m6A) modification regulatory factors in lung adenocarcinoma.

Lung cancer is the leading cause of death worldwide, and its incidence continues to increase. The treatment of lung cancer is related to the subtypes and stages of cancer, but the therapeutic effect is still unsatisfactory. We found that 10 of the 13 genes were differentially expressed in lung cancer, YTHDF1, RBM15, HNRNPC, KIAA1429, METTL3 and YTHDF2 are high expression while METTL14, ZC3H13, FTO and WTAP are low expression.

Dysregulation of Transcription Profile of Selenoprotein in Patients with Kashin-Beck Disease and Its Effect on Se Deficiency-Induced Chondrocyte Apoptosis.

Kashin-Beck disease (KBD) is a chronic, degenerative osteoarthropathy related to selenium (Se) deficiency. Se participates in the synthesis of selenoprotein in the form of selenocysteine. In total, 25 selenoproteins, encoded by 25 genes, are currently found in humans; however, the effects of selenoprotein genes on chondrocyte apoptosis, particularly in apoptosis-related genes, remain poorly elucidated.

Identification of differentially expressed and methylated genes associated with rheumatoid arthritis based on network.

Rheumatoid arthritis (RA) is a multi-systemic inflammatory autoimmune disease involving peripheral joints, and the pathogenesis is not clear. Studies showed that DNA methylation and expression might also be involved in the pathogenesis of RA. This study integrated three expression profile datasets (GSE55235, GSE12021, and GSE55457) and one methylation profile dataset GSE111942 to elucidate the potential essential candidate genes and pathways in RA.

Epidemic pattern of hand-foot-and-mouth disease in Xi'an, China from 2008 through 2015.

Background: Hand, foot and mouth disease (HFMD) is an infectious disease caused by enteroviruses that has a severely impair for those high incidence countries such as China.The current study aimed to investigate the epidemic pattern of HFMD by time and region in Northwestern China.

Methods: All reported HFMD cases from 2008 to 2015 were collected from local Disease Control and Prevention.

Analysis of gene expression and methylation datasets identified ADAMTS9, FKBP5, and PFKBF3 as biomarkers for osteoarthritis.

Background: Osteoarthritis (OA) is a kind of chronic osteoarthropathy and degenerative joint disease. Epigenetic regulation in the gene expression dynamics has become increasingly important in OA. We performed a combined analysis of two types of microarray datasets (gene expression and DNA methylation) to identify methylation-based key biomarkers to provide a better understanding of molecular biological mechanisms of OA.

The study of GPX3 methylation in patients with Kashin-Beck Disease and its mechanism in chondrocyte apoptosis.

Objective: Selenium deficiency is a risk factor for Kashin-Beck Disease (KBD), an endemic osteoarthropathy. Although promoter hypermethylation of glutathione peroxidase 3 (GPX3) (a selenoprotein) has been identified in several cancers, little is known about promoter methylation and expression of GPX3 and their relation to selenium in KBD. The present study was thus conducted to investigate this research question.

The study on polymorphisms of Sep15 and TrxR2 and the expression of AP-1 signaling pathway in Kashin-Beck disease.

The aim of the study was to investigate the association between rs5859 in Sep15, rs1139793 in TrxR2 polymorphisms with the risks of KBD and to detect the expression of AP-1 pathway in KBD subjects and in vitro. 208 KBD and 206 control subjects were included. PCR-Restriction Fragment Length Polymorphism (RFLP), Amplification Refractory Mutation Specific-PCR (ARMS-PCR) and Western Blotting were conducted.

The expression of ERK and JNK in patients with an endemic osteochondropathy, Kashin-Beck disease.

Kashin-Beck disease (KBD) is a chronic, endemic osteochondropathy. Its etiopathogenesis is still obscure until now. Epidemiological observation has shown that low selenium play a crucial role in the pathogenesis of KBD.

Epidemiological characteristics of measles from 2000 to 2014: Results of a measles catch-up vaccination campaign in Xianyang, China.

This study was a cross-sectional case-control study aimed at (1) identifying risk factors contributing to the measles epidemic and (2) evaluating the impacts of measles-containing vaccines (MCVs), with the goal of providing evidence-based recommendations for measles elimination strategies in China. Data on measles cases from 2000 to 2014 were obtained from a passive surveillance system at the Center for Diseases Prevention and Control in Xianyang. The effectiveness of MCVs was evaluated in 357 patients with a vaccination history and 503 healthy randomly selected controls.

Effects of sodium selenite on c-Jun N-terminal kinase signalling pathway induced by oxidative stress in human chondrocytes and c-Jun N-terminal kinase expression in patients with Kashin-Beck disease, an endemic osteoarthritis.

The c-Jun N-terminal kinases (JNK) are members of the mitogen-activated protein kinase family and are activated by environmental stress. Se plays an important role in the biological pathways by forming selenoprotein. Selenoproteins have been shown to exhibit a variety of biological functions including antioxidant functions and maintaining cellular redox balance, and compromise of such important proteins would lead to oxidative stress and apoptosis.

No Superiority of High-Flexion vs Standard Total Knee Arthroplasty: An Update Meta-Analysis of Randomized Controlled Trials.

This meta-analysis was performed using a Cochrane systematic review approach to examine published data with an aim to clarify whether standard or high flexion prostheses increase the range of knee motion and clinical outcomes. 1778 patients from 17 randomized controlled trials were identified. No significant differences in the range of motion, weight-bearing flexion and hip functions scores were found between treatment groups.

SNP-induced apoptosis may be mediated with caspase inhibitor by JNK signaling pathways in rabbit articular chondrocytes.

NO plays an important role in cartilage destruction by inducing apoptosis of chondrocytes. Here we investigated the role of c-Jun N-terminal kinase (JNK) signal transduction pathways in the apoptosis induced by NO donor sodium nitroprusside (SNP) in rabbit articular chondrocytes. We used Annexin V-FITC/PI flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL) assay to detect apoptosis rate.

SNP and mRNA expression for glutathione peroxidase 4 in Kashin-Beck disease.

Kashin-Beck disease (KBD) is a chronic endemic osteoarthropathy, which mainly occurs in West and Northeast China. Epidemiological studies suggest that Se deficiency is an important environmental factor for the incidence of KBD. Glutathione peroxidase 4 (GPx4) belongs to the glutathione peroxidase family, which is crucial for optimal antioxidant defences.

[TrxR2 gene polymorphisms may not be associated with the susceptibility to Kashin-Beck disease].

Objective: To study the association between single nucleotide polymorphisms of thioredoxin reductase-2 (TrxR2) gene and the susceptibility to Kashin-Beck disease (KBD).

Methods: Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to analyze the genotype frequencies of rs5748469 in TrxR2 gene in 84 KBD patients and 109 healthy control subjects.

Results: The genotype frequencies of A/A, A/C, and C/C in the KBD patients were 83.

[Dynamic effects of gallium chloride on osteoporotic rat model induced by tretinoin].

Objective: To investigate the effect of gallium salts on bone metabolism in osteoporosis rats caused by tretinoin.

Methods: After duplicating osteoporotic model of rats by using tretinoin, we observed the metabolism of blood, urine and bone in vivo. The rats were divided into control group, osteoporosis group, estrogen treated and gallium chloride treated group.

[The effect of retinoic acid on induction of osteoporotic model rats and the possible mechanism].

Objective: To observe the effect of retinoic acid on induction of osteoporotic model in rats and analyze the mechanism therein involved.

Methods: SD rats were treated with retinoic acid 80 mg/(kg x d) by gastrogavage for 15 days to induce osteoporosis and were killed in batches at 0, 30 and 60 days after drug withdrawal. The levels of Ca, P, BGP, E2, IGF-1, AKP and TRAP in serum were assayed, the collagen and proteoglycan contents of bone and bone mineral density (BMD) were determined, and the morphological changes in cancellous and cortical bone and growth plate cartilage (GPC) of femurs from the experimental rats were observed.