Rheumatoid arthritis (RA) is an autoimmune disease that involves T and B cells and their reciprocal immune interactions with proinflammatory cytokines. T cells, an essential part of the immune system, play an important role in RA. T helper 1 (Th1) cells induce interferon-γ (IFN-γ), tumour necrosis factor-α (TNF-α), and interleukin (IL)-2, which are proinflammatory cytokines, leading to cartilage destruction and bone erosion. Th2 cells primarily secrete IL-4, IL-5, and IL-13, which exert anti-inflammatory and anti-osteoclastogenic effects in inflammatory arthritis models. IL-22 secreted by Th17 cells promotes the proliferation of synovial fibroblasts through induction of the chemokine C-C chemokine ligand 2 (CCL2). T follicular helper (Tfh) cells produce IL-21, which is key for B cell stimulation by the C-X-C chemokine receptor 5 (CXCR5) and coexpression with programmed cell death-1 (PD-1) and/or inducible T cell costimulator (ICOS). PD-1 inhibits T cell proliferation and cytokine production. In addition, there are many immunomodulatory agents that promote or inhibit the immunomodulatory role of T helper cells in RA to alleviate disease progression. These findings help to elucidate the aetiology and treatment of RA and point us toward the next steps. Cite this article:
The aim of this study was to explore the genetic correlation and causal relationship between blood plasma proteins and rheumatoid arthritis (RA). Based on the genome-wide association studies (GWAS) summary statistics of RA from European descent and the GWAS summary datasets of 3,622 plasma proteins, we explored the relationship between RA and plasma proteins from three aspects. First, linkage disequilibrium score regression (LD score regression) was applied to detect the genetic correlation between RA and plasma proteins. Mendelian randomization (MR) analysis was then used to evaluate the causal association between RA and plasma proteins. Finally, GEO2R was used to screen the differentially expressed genes (DEGs) between patients with RA and healthy controls.Aims
Methods
Osteoarthritis (OA) is caused by complex interactions between genetic and environmental factors. Epigenetic mechanisms control the expression of genes and are likely to regulate the OA transcriptome. We performed integrative genomic analyses to define methylation-gene expression relationships in osteoarthritic cartilage. Genome-wide DNA methylation profiling of articular cartilage from five patients with OA of the knee and five healthy controls was conducted using the Illumina Infinium HumanMethylation450 BeadChip (Illumina, San Diego, California). Other independent genome-wide mRNA expression profiles of articular cartilage from three patients with OA and three healthy controls were obtained from the Gene Expression Omnibus (GEO) database. Integrative pathway enrichment analysis of DNA methylation and mRNA expression profiles was performed using integrated analysis of cross-platform microarray and pathway software. Gene ontology (GO) analysis was conducted using the Database for Annotation, Visualization and Integrated Discovery (DAVID).Aim
Patients and Methods
Total knee replacement has proven to be a very successful procedure. However, problems have been encountered in fitting standard femoral implants to distal femurs using various popular total knee replacement systems. Authors observed that difficulties matching femoral components with distal femurs most frequently occurred in female patients. In practice, as far as femoral sizing is concerned, women are just treated as small men. Despite an extensive English literature search, only a limited number of studies addressing the gender differences in distal femurs proportions were identified. In view of our experiences, we hypothesize that 1) Anterior-posterior (AP) dimensions do not increase in the same proportion to medial-lateral (ML) dimensions in men and women. 2) The AP/ML ratio is different in males and females. 3) Femoral implants AP/ ML ratios are more inline with men ratios then with women
Evaluation was focused on axial views of the distal femur. A cut with the maximum medial lateral dimensions of a studied femur was selected. The ML measurement was made along the epicondylar axis. The maximum AP dimension was obtained perpendicular to the epicondylar axis on the same cut. The ratios were then obtained. AP data for males and females was plotted against ML data. The data was found to approximate linear relation, permitting linear regression. Inside AP and ML dimensions of eight popular TKR systems produced by six manufactures were obtained. The AP vs. ML plots were made as well as ratios were calculated for each system. The implants data were compared with male and female data. A t-test was performed to demonstrate whether the AP/ML ratio was significantly different between males and females. In addition, ordinary least squares analyses were performed to establish whether the AP/ML ratios varied across different AP and ML sizes for both genders.
Dimensions propagation of femoral components for TKR fallowed significantly closer to males’ distal femur dimensions variation than to females’.
