Background: The effective maintenance of genome integrity and delity is vital for the normal function of our tissues and organs, and the prevention of diseases. DNA repair pathways maintain genome stability, and the adequacy of genes acting in these pathways is essential for disease suppression and direct treatment responses. Chronic kidney disease is characterized by high levels of genomic damage. In this study, we examined the expression levels of the XPDgene, which plays a role in the NER repair mechanism, and the expression levels of miR-145 and miR-770 genes, which play a role in the regulation of the expression of the XPD gene, in hemodialysis patients with (n=42) and without malignancy (n=9) in pre-and post-dialysis conditions. We also evaluated these values with the clinical ndings of the patients.Methods & Results: Gene expression analysis was performed by real-time polymerase chain reaction (qRT-PCR). Compared to the control group (2.06 ± 0.32), the XPD gene expression was lower in the pre-dialysis condition both in hemodialysis patients without cancer (1.24 ± 0.18; p=0.02) and in hemodialysis patients with cancer (0.82 ± 0.114; p=0.001). On the other hand, we found that miR-145and miR-770 expression levels were high in both groups. We also found that expression levels were affected by dialysis processes. A statistically signi cant positive correlation was found between miR-145 and mir770 expression levels in the pre-dialysis group of patients with (r=-0.988. p=0.0001) and without (r=-0.934. p=0.0001) malignancy.Conclusions: Studies on DNA damage repair in the kidney will help develop strategies to protect kidney function against kidney diseases.

Background: STEMI (ST-elevation myocardial infarction) is one of the most severe forms of coronary artery disease, known to significantly contribute to DNA damage. There are very few publications in this field in the literature. In our study, we examined the association between four polymorphisms in repair enzymes (LIG4 Thr9Ile, XRCC6 promoter C-57G, XPA -4A/G, OGG1 Ser326Cys) involved in three distinct DNA repair mechanisms (NHEJ (non-homologous end joining), NER (nucleotide excision repair), and BER (base excision repair), and their impact on the risk of STEMI. Methods & Results: This study involved 185 patients diagnosed with STEMI and included 100 healthy controls. The genotyping of SNPs was conducted through the PCR-RFLP (Polymerase chain reaction-restriction fragment length polymorphism) method for the following variants: XRCC6 (rs2267437), XPA (rs1800975), LIG4 ( rs1805388), and OGG1 (rs1052133). No significant differences were observed in the genotype distributions of the XRCC6 and OGG1 variations between the control and patient groups. On the other hand, our findings indicate that individuals carrying the mutant G allele for XPA polymorphism and the mutant Tallele for LIG4 polymorphism are susceptible to STEMI. Conclusions: Our findings demonstrate the significance of NHEJ and NER DNA repair processes in the pathogenesis of STEMI, as evidenced by the observed relationship between LIG4 and XPA polymorphisms.

Background: The effective maintenance of genome integrity and fidelity is vital for the normal function of our tissues and organs, and the prevention of diseases. DNA repair pathways maintain genome stability, and the adequacy of genes acting in these pathways is essential for disease suppression and direct treatment responses. Chronic kidney disease is characterized by high levels of genomic damage. In this study, we examined the expression levels of the XPDgene, which plays a role in the NER repair mechanism, and the expression levels of miR-145 and miR-770 genes, which play a role in the regulation of the expression of the XPD gene, in hemodialysis patients with (n=42) and without malignancy (n=9) in pre- and post-dialysis conditions. We also evaluated these values with the clinical findings of the patients. Methods & Results: Gene expression analysis was performed by real-time polymerase chain reaction (qRT-PCR). Compared to the control group (2.06 ± 0.32), the XPD gene expression was lower in the pre-dialysis condition both in hemodialysis patients without cancer (1.24 ± 0.18; p=0.02) and in hemodialysis patients with cancer (0.82 ± 0.114; p=0.001). On the other hand, we found that miR-145and miR-770 expression levels were high in both groups. We also found that expression levels were affected by dialysis processes. A statistically significant positive correlation was found between miR-145 and mir770 expression levels in the pre-dialysis group of patients with (r=-0.988. p=0.0001) and without (r=-0.934. p=0.0001) malignancy. Conclusions: Studies on DNA damage repair in the kidney will help develop strategies to protect kidney function against kidney diseases.