Investigating the association between the tissue expression of miRNA‐101, JAK2/STAT3 with TNF‐α, IL‐6, IL‐1β, and IL‐10 cytokines in the ulcerative colitis patients

Abstract Background Ulcerative colitis (UC) is a chronic inflammatory bowel disease caused by numerous factors, such as immune system dysfunction and genetic factors. MicroRNAs (miRNAs) play a crucial role in UC pathogenesis, particularly via the JAK‐STAT pathway. Our aim was to investigate the association between miRNA‐101 and JAK2‐STAT3 signaling pathway with inflammatory cytokines in UC patients. Methods We enrolled 35 UC patients and 35 healthy individuals as the control group, referred to Shariati Hospital, Tehran, Iran. Patients were diagnosed based on clinical, laboratory, histological, and colonoscopy criteria. RNA and protein extracted from tissue samples. Real‐time PCR was used to assess the expression levels of miRNA‐101, interleukin (IL)‐1β, IL‐6, tumor necrosis factor (TNF)‐α, and IL‐10 genes, while western blot was employed to measure levels of P‐STAT3, total STAT3, and JAK2 proteins. Results Expression of pro‐inflammatory cytokines TNF‐α, IL‐1β, and IL‐6 significantly increased, while the expression of IL‐10 significantly decreased in the case group versus controls. Additionally, miRNA‐101 expression was significantly higher in UC patients. A significant correlation between miRNA‐101 and IL‐6 expression was observed, indicating their relationship and possible impact on cell signaling pathways, JAK2‐STAT3. No significant changes were observed in phosphorylated and total STAT3 and JAK2 protein expression. Conclusion This study provides evidence of increased miRNA‐101 expression in UC tissue, suggesting a potential correlation between miRNA‐101 and IL‐6 expression and their involvement in the JAK2‐STAT3 pathway. The study confirms alterations in UC patients' pro‐inflammatory cytokines and anti‐inflammatory IL‐10. However, further investigations are needed to understand the exact role of miRNA‐101 in UC pathogenesis fully

Comparative genomics of the sperm mitochondria-associated cysteine-rich protein gene

AbstractThe sperm mitochondrial cysteine-rich protein (SMCP) is a rapidly evolving cysteine- and proline-rich protein that is localized in the mitochondrial capsule and enhances sperm motility. The sequences of the SMCP protein, gene, and mRNA in a variety of mammals have been compared to understand their evolution and regulation. SMCP can now be reliably identified by its tripartite structure including a short amino-terminal segment; a central segment containing short tandem repeats rich in cysteine, proline, glutamine, and lysine; and a C-terminal segment containing no repeats, few cysteines, and a C-terminal lysine. The SMCP gene is located in the epidermal differentiation complex (EDC), a large gene cluster that functions in forming epithelial barriers. Similarities in chromosomal location, molecular function, intron–exon structure, and protein organization argue that SMCP originated from an EDC gene and acquired spermatogenic cell-specific transcriptional and translational regulation and a novel cellular function in sperm motility. The SMCP 5′ UTR and 3′ UTR contain conserved elements and uORFs that may function in cytoplasmic regulation of gene expression, and the levels of SMCP mRNA in human are much lower than in other mammals, a feature of male-biased expression. The evolution of SMCP has been accompanied by changes in the sequence, number, and length of repeat units, including three alleles in dogs. The major proteins associated with the mitochondrial capsule, SMCP and phospholipid hydroperoxide glutathione peroxidase, provide outstanding examples of changes in cellular function driven by selective pressures on sperm motility, an important determinant of male reproductive success

Bone mass and microarchitecture in T2DM patients and corticosteroids therapy: the Bushehr Elderly Health program

Purpose Our study examined whether T2DM and glucocorticoids treatment affect bone quality and quantity that are measured by Bone Mineral Density (BMD) and Trabecular Bone Score (TBS). Materials & methods Participants in this study were 2294 women and men aged over 60 years who participated in stage II of the Bushehr Elderly Health (BEH) program. Patients with T2DM and those who received glucocorticoids were included. BMD was detected using the DXA method and the TBS of L1-L4 was evaluated by TBS iNsight® software. To evaluate the correlation between TBS and BMD levels with diabetes and taking corticosteroids sex-specific multivariable linear regression models were appplied. Results TBS and BMD were not significantly different in those who had received glucocorticoids versus those who did not.T2DM revealed a significant association with both BMD and TBS in men (beta = 0.12, p < 0.001 and beta = 0.063, p = 0.03, respectively). BMD values were significantly higher in diabetic women (beta = 0.073, p < 0.01). BMI had a significant association with both TBS and BMD but in an opposite direction, in women and men (BMD: beta = -0.22, -0.24, and regarding TBS: beta = 0.37, 0.25, all p-values < 0.001). Conclusion Our findings showed that T2DM had major effects on BMD in both men and women. However, T2DM only affects TBS in men. Furthermore, neither BMD nor TBS were affected by GC intake in men or women.Based on the variable importance of covariates, BMI was the most influential factor on both BMD and TBS, although in opposite directions, in both sexes

Systematic review of single and combined treatments for different types of striae : A comparison of striae treatments

Acknowledgements The authors would like to express their gratitude to the staff of Rasool Akram Medical Complex Clinical Research Development Center (RCRDC) for their technical and editorial assistance.Peer reviewedPostprin