Interleukine-17 (IL-17), a crucial component of the body's immune response against pathogens, is also implicated in various inflammatory processes. Notably, the skin of rosacea patients exhibits chronic inflammation, and IL-17 is known to induce the production of additional pro-inflammatory chemokines and cytokines. This inflammatory cascade can contribute to the hallmark features of rosacea, including dilated blood vessels, immune cell infiltration, and the development of papules and pustules. The study aimed to examine whether a specific genetic variation in the IL-17A gene (-197 G>A; rs2275913) is associated with rosacea susceptibility. We compared the IL-17A variant and rosacea risk in 31 healthy individuals and 25 with rosacea. Genotyping of the IL-17A variant was performed using the PCR-RFLP method. Genotype and allele frequency distributions were compared across groups using the chi-square test (χ2). Additionally, gene ontology (GO) analysis of the IL-17A gene using web-based tools is also demonstrated. No significant association between the rs2275913 polymorphism and rosacea susceptibility was observed in this study (p=0.124) but in silico analysis suggested that the IL-17A gene interaction network might play a role in the disease. Given its critical function in regulating IL-17A and related genes, particularly in immune defense and inflammatory processes, further investigation into its potential influence on rosacea development is required.

This study aimed to evaluate the mRNA and protein levels of SMURF1 and SMURF2 in breast cancer and to elucidate their potential biological roles through in silico analyses. Tumor and adjacent normal tissue samples were collected from 30 newly diagnosed breast cancer patients who underwent mastectomy. The mRNA expression levels of SMURF1 and SMURF2 were analyzed by quantitative PCR (qPCR), and their protein expression patterns were evaluated using immunohistochemistry (IHC). In addition, protein–protein interaction (PPI) and functional enrichment analyses were performed via the STRING database to identify potential molecular interactions and biological pathways associated with these genes. The mRNA expression level of SMURF1 was significantly downregulated in tumor tissues compared to normal breast tissues (p = 0.002), whereas no significant difference was observed in SMURF2 mRNA expression (p = 0.981). IHC results revealed that SMURF1 and SMURF2 protein levels did not differ significantly between tumor and normal samples. The in silico analysis demonstrated that SMURF1 and SMURF2 interact with multiple proteins involved in key signaling pathways, particularly the TGF-β/BMP and Wnt/β-catenin pathways. The findings suggest that the downregulation of SMURF1 in breast cancer may contribute to tumor progression by enhancing Wnt/β-catenin signaling activity. The interactions of SMURF1 and SMURF2 with TGF-β/BMP pathway regulators indicate that these genes may play dual roles in both tumor-suppressive and oncogenic mechanisms, depending on the cellular context.

Aim: Dopaminergic neurons and dopamine transporters show variations in Attention Deficit Hyperactivity Disorder (ADHD). Furthermore, Ghrelin and leptin, hormones recognized for their neurotrophic effects, are significant in central nervous system regulation, influencing neuronal survival and development. Material and Methods: This study aimed to examine the potential relationship between Attention Deficit Hyperactivity Disorder (ADHD) and polymorphisms in the GHRL (rs34911341) and LEP (rs7799039) genes. The research sample consisted of 29 children diagnosed with ADHD and 24 age-matched healthy controls. Genotypic analysis was conducted using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Results: A significant difference in genotype distribution for the GHRL gene rs34911341 polymorphism was observed between the ADHD group and healthy controls (p = 0.036), whereas allele frequencies did not show a statistically significant difference (p = 0.207). In contrast, analysis of the LEP gene rs7799039 polymorphism revealed no significant differences in either genotype (p = 0.579) or allele frequencies (p = 0.558) between the two groups. Conclusion: These findings suggest a potential role for the GHRL rs34911341 polymorphism in the development or presentation of ADHD. Further research is required to elucidate the mechanisms underlying this association.