Trimethylamine N-oxide serum levels have been associated with type 2 diabetes mellitus and its complications. The current study aimed to find out if plasma trimethylamine N-oxide level may be a novel marker in the diagnosis of diabetic retinopathy and if it can be used in the differential diagnosis of diabetic and nondiabetic retinopathy. The study included 30 patients with diabetic retinopathy, 30 patients with nondiabetic retinopathy, 30 patients with type 2 diabetes mellitus without retinopathy, and 30 healthy control participants. Biochemical parameters, serum IL-6, TNF-α, and trimethylamine N-oxide levels were measured in all participants. Trimethylamine N-oxide level was significantly higher in diabetic retinopathy than in the other groups (p<0.001). There was no significant difference in trimethylamine N-oxide levels between nondiabetic retinopathy and control or type 2 diabetes mellitus Groups. There was a significant positive correlation between trimethylamine N-oxide level and elevated FPG, BMI, HOMA-IR score, BUN, IL-6, and TNF-α levels. The current study showed that the trimethylamine N-oxide level is elevated in diabetic retinopathy. These findings suggest that serum trimethylamine N-oxide level might be a novel marker for diabetic retinopathy, and it might be used in the differential diagnosis of diabetic and nondiabetic retinopathy.

Background and Objectives: This study aimed to investigate the relationship between Maresin-1 (MaR1), Chitinase-3-like protein 1 (CHI3L1), and inflammatory as well as hematological markers in patients with type 2 diabetes mellitus (T2DM) and diabetic nephropathy (DN). Materials and Methods: This cross-sectional study included 90 participants divided into three groups: healthy controls (n = 30), patients with T2DM (n = 30), and patients with diabetic nephropathy (n = 30). The serum levels of MaR1 and CHI3L1 were measured using ELISA. Biochemical and hematological parameters were also assessed. Statistical comparisons were conducted using non-parametric tests, and correlations were analyzed via Spearman correlation. Results: Serum MaR1 levels were significantly higher in DN patients compared to both T2DM patients and controls (p < 0.01), while CHI3L1 levels were significantly lower in the DN group compared to controls (p = 0.007). MaR1 showed a positive correlation with CRP, BUN, and creatinine, and a negative correlation with GFR. CHI3L1 levels were positively correlated with GFR and negatively with BUN. Inflammatory markers such as CRP were elevated in the diabetic groups, while no significant differences were found in NLR values. Conclusions: Elevated MaR1 levels in DN patients and their correlation with renal dysfunction markers suggest that MaR1 may serve as a potential prognostic biomarker in diabetic nephropathy. The unexpected decrease in CHI3L1 levels in DN patients indicates the need for further research to clarify their role. These findings indicated that MaR1 and CHI3L1 should be further investigated in future studies as indicators for the early detection and monitoring of diabetic complications.

Purpose: In this study, we investigated the effect of ELF5 , KIF18A , NPTX1 and COL23A1 genes in residual processus vaginalis (PV) the main factor in the development of indirect inguinal hernia (IIH) in children. Methods: Cases operated for IIH in children aged 0–18 years between 2018 and 2021 constituted the study group, and cases with undescended testis without hernia the control group. Protein levels of KIF18A , which has the highest gene expression in tissue samples, were also analyzed by ELISA method. Polymorphisms of ELF5 , KIF18A and COL23A1 genes with the highest level of expression change in blood and tissue samples were analyzed by qRT-PCR. Statistical analysis was performed. Results: There were 186 patients in the study group and 26 patients in the control group. The results of ELF5 , KIF18A and COL23A1 genes were significantly higher in the study group than in the control group. There was a statistically significant positive correlation between GAPDH and ELF5 , KIF18A and NPTX1 in the study group. Also, a statistically significant positive correlation was found between KIF18A and ELF5 and between NPTX1 and ELF5 and COL23A1 . Conclusion: The present study may be the first study conducted in human tissue samples that we could access in the literature in terms of the genetic factors. It was predicted that ELF5 , KIF18A and COL23A1 genes may be counted among the effective factors in PV closure. This study may shed light on larger prospective genetic studies.

Objective: This study aims to evaluate the effects of the rs965623242 reference single nucleotide polymorphism (SNP) on the ZIC5 gene in patients with neural tube defect (NTD). Patients and Methods: One hundred sixty-eight controls and one hundred sixty-eight NTD patients were included in the study. Deoxyribonucleic acid (DNA) isolation from peripheral blood samples was carried out for all participants. rs965623242 polymorphic region was amplified by polymerase chain reaction (PCR) and then sequenced. Results: In the 5’ untranslated region (UTR) of the first exon, guanine (G) to adenine (A) base change was detected in the 38th base of NM_033132.5. G to A base change was determined as GG genotype in 117 (69.6%), AG genotype in 30 (17.86%), and AA genotype in 21 (12.5%) patients. In the control group, GG genotype in 107 (63.7%), AG genotype in 23 (13.7%) and AA genotype in 38 (22.7%) were observed. The statistically significant difference was observed between the NTD and the control groups in ZIC5 genotypes or allele frequencies [p=0.044, odds ratio (OR)=0.49 (0.27-0.88) and p=0.021, OR=0.65 (0.46-0.93), respectively]. Conclusion: ZIC5 rs965623242 polymorphism may have a protective role in the NTD development in the Eastern Anatolian population, in Turkey. Although, these findings demonstrate that the rs965623242 polymorphism is associated with NTD, we do not clarify how its expression is affected during the embryonic period and ongoing processes. We will need advanced ongoing genetic and clinical studies to obtain more detail.

Background/Objectives: This study aimed to evaluate serum fibroblast growth factor-23 (FGF-23) and α-Klotho levels in patients with prolactinoma and patients with non-tumoral hyperprolactinemia and to explore their discriminatory performance for prolactinoma. Methods: Seventy-three participants were included in this single-center, cross-sectional comparative study: non-tumoral hyperprolactinemia (n = 14), prolactinoma (n = 29), and healthy controls (n = 30). All patients with prolactinoma had received dopamine agonist therapy for at least six months. Serum FGF-23 and α-Klotho were measured by ELISA, and between-group comparisons, correlation analyses, linear regression analyses, and receiver operating characteristic (ROC) analyses were performed. Results: FGF-23 concentrations differed significantly among the groups (overall p < 0.001). Post hoc analysis showed that FGF-23 concentrations were significantly higher in the prolactinoma group [236.10 (107.70–667.90) pg/mL] than in healthy controls [138.75 (49.40–253.60) pg/mL] (adjusted p < 0.001), whereas the difference between the prolactinoma and non-tumoral hyperprolactinemia groups [166.20 (100.30–327.20) pg/mL] was not statistically significant (adjusted p = 0.075). α-Klotho concentrations were significantly higher in the prolactinoma group [2.908 (1.376–6.257) ng/mL] than in both the non-tumoral hyperprolactinemia group [2.244 (1.432–5.139) ng/mL] (adjusted p = 0.038) and healthy controls [2.204 (0.149–4.917) ng/mL] (adjusted p < 0.001). In pooled analyses, both biomarkers showed positive correlations with prolactin and weak negative correlations with hemoglobin. However, prolactin and hemoglobin were not independently associated with either biomarker after multivariable adjustment. The non-tumoral hyperprolactinemia group did not differ significantly from healthy controls for either biomarker. For distinguishing prolactinoma from non-tumoral hyperprolactinemia, the AUCs were 0.741 for FGF-23, 0.732 for α-Klotho, and 0.862 for the exploratory combined model. Conclusions : Dopamine agonist-treated prolactinoma was characterized by higher circulating FGF-23 concentrations than those in healthy controls and by higher α-Klotho concentrations than those in both healthy controls and patients with non-tumoral hyperprolactinemia. Exploratory ROC analyses suggested moderate discriminatory performance for the individual biomarkers and higher apparent performance for the combined model; however, these findings should be interpreted cautiously and require validation in larger, treatment-naïve cohorts.

MicroRNAs (miRNAs) are small, non-coding RNA molecules (~19–24 nucleotides) that post-transcriptionally regulate gene expression by inducing mRNA degradation or translational repression. Since the discovery of lin-4 in 1993, a milestone honored with the 2024 Nobel Prize, miRNAs have been estimated to regulate over 60% of human protein-coding genes. This review examines the canonical and non-canonical biogenesis pathways of miRNAs, emphasizing their role as homeostatic rheostats across major physiological systems, including embryogenesis, immunity, metabolism, neurobiology, and cardiovascular function. Dysregulation of these evolutionarily conserved regulatory networks contributes to the pathogenesis of human disorders, notably cancer, neurodegeneration, metabolic disorders, and autoimmune conditions. Given their stability in biofluids, circulating miRNAs have potential as diagnostic and prognostic biomarkers; however, most candidate signatures remain investigational and require prospective clinical validation. Therapeutic strategies based on miRNA mimics and inhibitors have reached preclinical and early-phase clinical testing, with outcomes ranging from completed proof-of-concept studies to terminated trials. Advances in nanotechnology, high-throughput sequencing, CRISPR-based tools, and precision medicine support the development of miRNA-based diagnostics and therapeutics, but routine clinical use still depends on standardized assays, reliable delivery, and evidence of safety and clinical benefit in the relevant biological context.