The promoter methylations of the autoimmune regulator (AIRE) gene and matrix metalloproteinase-3 (MMP-3) gene may have a role in gestational diabetes mellitus.

OBJECTIVE: Gestational diabetes mellitus (GDM) is characterized by new-onset glucose intolerance and is most common in the second and third trimesters of pregnancy. Epigenetic modifications regulate glucose and its cellular interactions with metabolic pathways. Emerging evidence suggests that epigenetic changes contribute to the pathophysiology of GDM. Since these patients have high glucose levels, the metabolic profiles of the fetus and the mother can affect these epigenetic changes. Therefore, we aimed to examine the potential alterations in the methylation profiles of three gene promoters: the autoimmune regulator (AIRE) gene, matrix metalloproteinase-3 (MMP-3), and calcium voltage-gated channel subunit alpha1 G (CACNA1G). PATIENTS AND METHODS: A total of 44 patients diagnosed with GDM and 20 controls were involved in the study. DNA isolation and bisulfite modification were performed from peripheral blood samples of all patients. Then, the promoter methylation status of the AIRE, MMP-3, and CACNA1G genes was determined by methylation-specific polymerase chain reaction (PCR) methylation-specific (MSP). RESULTS: Our results demonstrated that the methylation status of AIRE and MMP-3 changed to unmethylated in the GDM patients compared to healthy pregnant women (p<0.001). However, CACNA1G promoter methylation status failed to show a significant change between experimental groups (p>0.05). CONCLUSIONS: Our results indicated that AIRE and MMP-3 are the genes affected by epigenetic modification, which could be one of the causes of the long-term metabolic effects in maternal and fetal health and can be a target for prevention, diagnosis, or treatment for GDM in future studies.

An investigation of the relationship between rheumatological diseases and soluble receptor for advanced glycation end products.

OBJECTIVE: Soluble receptor for advanced glycation end products (sRAGE) is one of the forms of RAGE. It is a trap receptor that has a role in inhibiting pro-inflammatory processes that will occur with the combination of RAGE and its ligands. Our study aims to examine the level of sRAGE in rheumatological inflammatory diseases and its relationship with these diseases. PATIENTS AND METHODS: A total of 60 patients with Behçet's disease (BD), rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and 22 healthy control individuals were included in the study. Comorbidity status, sRAGE levels, disease activity scores, demographic and laboratory data of the patients were recorded. Serum sRAGE levels in these diseases and healthy controls were determined by Enzyme-Linked Immunosorbent Assay (ELISA) kit spectrophotometrically. RESULTS: Serum sRAGE levels in the patient groups were significantly higher when compared to the healthy control group (p < 0.001 for all). On the other hand, when the patient groups were compared with each other in terms of sRAGE levels, there was no significant difference (p > 0.05 for all). The serum sRAGE levels were not correlated with C-reactive protein (CRP) levels, erythrocyte sedimentation rate (ESR), and disease activity scores (p > 0.05 for all). CONCLUSIONS: Serum sRAGE levels increased in BD and in other inflammatory rheumatological diseases. However, this increase does not directly correlate with inflammatory markers and disease activity scores. These results suggest that serum sRAGE level may not be used as a biomarker for disease activity in BD and in other rheumatological diseases.

Genetic polymorphisms affecting antioxidant enzymes are present in tympanosclerosis patients.

BACKGROUND: This study investigated genetic polymorphisms affecting the inducible nitric oxide synthase, superoxide dismutase and catalase enzymes in chronic otitis media patients with and without tympanosclerosis, and the role of genetic susceptibility in the disease aetiology. METHODS: A total of 162 patients who underwent surgery for chronic otitis media were divided into two study groups: a tympanosclerosis group and a chronic otitis media group. A third, the control, group comprised 188 healthy volunteers. Venous blood samples were evaluated using reverse transcriptase polymerase chain reaction. RESULTS: There was a significant difference in GG genotype distribution of the -277A>G polymorphism in the NOS2 gene between the tympanosclerosis and control groups (p T) polymorphism in the SOD2 gene (p > 0.05). There were significant differences in the TT genotype distribution of the -21A>T polymorphism in the CAT gene between the tympanosclerosis and control groups, and between the chronic otitis media and control groups (p < 0.05). CONCLUSION: These results suggest that genetic predisposition may play a role in the aetiopathogenesis of tympanosclerosis.