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AD is a multigene disease, and thus there are many targets for regulation of expression of these genes which may contribute to the pathogenesis of AD. However, the epigenetic regulation of environmental factors in AD pathogenesis still needs to be further researched.Genomic predisposition fails to fully explain the onset of complex diseases, which is well illustrated by the largely incomplete concordance among monozygotic twins. Epigenetic mechanisms, including DNA methylation, chromatin remodeling, and non-coding RNA, are the link between environmental stimuli and disease onset on a permissive genetic background in autoimmune and chronic inflammatory diseases. Autoimmune diseases now include almost 100 conditions and are estimated to cumulatively affect up to 5% of the world population with a healthcare expenditure superior to cancer worldwide. Many advances in medicine have been made to treat these conditions but there are still gaps, and an innovative and efficient therapy is needed. Systemic autoimmune diseases include rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, Sjogren syndrome, polymyositis, and dermatomyositis. Monozygotic twins discordant for any disease offer an ideal study design as they are matched for many factors, including genetic variation and this is a real advantage for epigenetics study. We will herein discuss the available data in the epigenetic differences leading to disease discordance in MZ twins for systemic lupus erythematosus, rheumatoid arthritis, and systemic sclerosis.The study of epigenetics has its roots in the study of organism change over time and response to environmental change, although over the past several decades the definition has been formalized to include heritable alterations in gene expression that are not a result of alterations in underlying DNA sequence. In this chapter, we discuss first the history and milestones in the 100+ years of epigenetic study, including early discoveries of DNA methylation, histone posttranslational modification, and noncoding RNA. We then discuss how epigenetics has changed the way that we think of both health and disease, offering as examples studies examining the epigenetic contributions to aging, including the recent development of an epigenetic "clock", and explore how antiaging therapies may work through epigenetic modifications. We then discuss a nonpathogenic role for epigenetics in the clinic epigenetic biomarkers. We conclude by offering two examples of modern state-of-the-art integrated multi-omics studies of epigenetics in disease pathogenesis, one which sought to capture shared mechanisms among multiple diseases, and another which used epigenetic big data to better understand the pathogenesis of a single tissue from one disease.Epigenetic mechanisms, which include DNA methylation, histone modification, and microRNA (miRNA), can produce heritable phenotypic changes without a change in DNA sequence. Disruption of gene expression patterns which are governed by epigenetics can result in autoimmune diseases, cancers, and various other maladies. Mechanisms of epigenetics include DNA methylation (and demethylation), histone modifications, and non-coding RNAs such as microRNAs. Compared to numerous studies that have focused on the field of genetics, research on epigenetics is fairly recent. In contrast to genetic changes, which are difficult to reverse, epigenetic aberrations can be pharmaceutically reversible. The emerging tools of epigenetics can be used as preventive, diagnostic, and therapeutic markers. With the development of drugs that target the specific epigenetic mechanisms involved in the regulation of gene expression, development and utilization of epigenetic tools are an appropriate and effective approach that can be clinically applied to the treatment of various diseases.Vitamin D is involved in immune system modulation as well as in calcium and bone homeostasis, hence plays a role in rheumatoid arthritis (RA) etiopathogenesis. A bulk of studies in different populations have assessed the association between the vitamin D receptor (VDR) gene polymorphisms and the risk of RA, reporting conflicting results. Therefore, we designed a meta-analysis to comprehensively evaluate the association of VDR gene polymorphisms and RA risk. All potential studies reporting the association between VDR gene polymorphisms and susceptibility to RA published till February 2020 were retrieved through systematic search of database, including Scopus and MEDLINE. Strength of pooled association was determined through calculating the pooled odds ratios (ORs) and 95% confidence intervals (CIs). Subgroup analysis was performed by stratifying the studies by population type. This meta-analysis included 23 eligible studies (21 articles) overall. We noticed that FokI SNP had a significant protective association with susceptibility to RA in the overall analysis as well as in Europeans and Asians. TaqI SNP decreased the RA risk in Africans and Arabs, but not in the overall analysis. Likewise, BsmI SNP and RA risk in the overall population analysis was not significant. Interestingly, BsmI polymorphism increased RA risk in Africans. This meta-analysis offers a significant association between VDR gene polymorphism and susceptibility to RA in both overall and ethnic-specific analysis. However, different polymorphisms acted inversely in increasing or decreasing RA risk in different populations.Background Acute myocardial dysfunction is an uncommon but potentially fatal complication in systemic lupus erythematosus (SLE). We describe the outcome in a small series of Asian Indian patients and examine associated factors. Methods SLE patients who fulfilled the 2012 SLICC criteria and developed new-onset myocardial dysfunction were included in this retrospective case series. Acute myocardial dysfunction was defined as global hypokinesia and left ventricular ejection fraction (LVEF) less then 50% on echocardiography (with or without symptoms) in patients with SLE. Survival was assessed using Kaplan-Meier survival analysis and Cox regression. APX-115 mw Results This study included 37 patients with mean age 28.2 ± 11.2 years and median (range) LVEF of 35% (18-48%) at presentation. A majority had active disease, with SLEDAI-2k ≥ 5 in 26 (of 28). All patients received oral corticosteroids and a majority received additional immunosuppression, including pulse methylprednisolone in 28 and cyclophosphamide in 27. Nine patients died during hospitalisation (25%), a majority due to infections.