(1) Background: Obesity and mood disorders are considered as the most prevalent morbidities in many countries. We suppose that epigenetic mechanisms may induce higher rates of obesity in subjects who suffer from mood disorders. In this systematic review, we focused on the potential roles of DNA methylation on mood disorders and obesity development. (2) Methods: This systematic review was conducted in accordance with the PRISMA statement and registered in Prospero. A systematic search was conducted in MEDLINE, Scopus, Web of Science, Cochrane Central database, EMBASE, and CINHAL. We also conducted a Grey literature search, such as Google Scholar. (3) Results: After deduplication, we identified 198 potentially related citations. Finally, ten unique studies met our inclusion criteria. We have found three overlap genes that show significant DNA methylation changes, both in obesity and depression. Pathway analysis interaction for TAPBP, BDNF, and SORBS2 confirmed the relation of these genes in both obesity and mood disorders. (4) Conclusions: While mechanisms linking both obesity and mood disorders to epigenetic response are still unknown, we have already known chronic inflammation induces a novel epigenetic program. As the results of gene enrichment, pathways analysis showed that TAPBP, BDNF, and SORBS2 linked together by inflammatory pathways. Hypermethylation in these genes might play a crucial rule in the co-occurrence of obesity and mood disorders.

Thrombomodulin (THBD) gene plays an important role in activation and control of protein C. Regulation protein C levels as an important risk factor for cardiovascular disease. Mutations in this gene can affect Thrombomodulin levels. In this study, we aimed to investigate the role of single nucleotide polymorphism (SNP) in rs1042579 THBD gene in patients with cardiovascular disease. The samples of this case-control study consisted of 105 Iranian patients with cardiovascular disease and 95 healthy controls who enrolled from March 2017 to December 2018 in this study. Demographic data, medical history, and para-clinical were measured, and Sanger sequencing was used for allelic discrimination. Control samples were identified and then selected for genotyping of other ARMS-PCR technique. Data analysis revealed that the rs1042579 polymorphism of the THBD gene was associated with a risk of coronary heart disease. Sequencing results confirmed the existence of CC homozygous, heterozygous TC and TT homozygous genotypes. TT genotype is a risk factor in patients compared to healthy controls. The results of this study showed that the rs1042579 polymorphism was associated with an increased risk of cardiovascular disease.

Background and aims: Hearing loss (HL) is the most common sensorineural disorder affecting 1 in 1000 newborns. Autosomal recessive non-syndromic hearing loss (ARNSHL), which is the most common cause of severe HL, is caused by mutations in more than 80 loci. The OTOA gene located on DFNB22 is a rare cause of the disease and the gene studied less in Iranian ARNSHL families. Hence, limited information is available on the frequency and type of OTOA mutations in different populations. In this study, we investigated the role of DFNB22 locus in ARNSHL patients in Khuzestan province, Iran. Materials and Methods: In this descriptive-experimental study, 23 large families with pre-lingual ARNSHL from Khuzestan province were enrolled. Mutations in GJB2 were excluded by DNA sequencing followed by linkage analysis. Homozygosity mapping of DFNB22 was conducted using 6 short tandem repeat polymorphic markers via touch-down PCR and polyacrylamide gel electrophoresis. Homozygosityby-descent was identified by calculating two-point and multi-point LOD score and haplotype reconstruction. Results: Families were negative for GJB2 mutations. Genotyping the STRP markers, haplotype reconstruction, and two-point and multiplepoint LOD scores did not show homozygosity-by-descent in any of the pedigrees. Conclusion: Our findings suggest that OTOA mutations might not contribute significantly to the molecular pathophysiology of ARNSHL in Khuzestan province. However, extending the sample size can illuminate the role of this gene in Khuzestan province.

Background: Acute myocardial infarction refers to a reduction or amputation of coronary artery circulation leading to myocardial necrosis. BDNF is expressed in atherosclerotic arteries, vascular smooth muscle, and endothelial cells and is involved in angiogenesis, the inflammatory response, and apoptosis of myocardial regeneration after infarction. The aim of this study was to evaluate the effect of a cardiac rehabilitation period on changes in BDNF levels and functional capacity in patients with acute myocardial infarction. Methods: The present study was performed on 30 men with acute coronary syndrome with a pretest-posttest design and the samples were randomly divided into experimental and control groups. The experimental group performed a cardiac rehabilitation program for 6 weeks. The control group did not perform any training during this period. Before and after the rehabilitation program, BDNF levels were measured by the American Diaplus Kit in terms of picograms per milliliter and participants' functional capacity by a modified Bruce test. Analysis of covariance was used to compare BDNF levels and functional capacity of cardiac rehabilitation and control groups. Discussion & Conclusion: Data were analyzed by covariance and the results showed that cardiac rehabilitation training had a significant effect on increasing BDNF levels and functional capacity (P≤0.05). In general, it can be said that cardiac rehabilitation exercise program can play an important role in improving the physical and physiological condition of patients with acute myocardial infarction.