Background: Type 1 diabetes (T1D) is caused by cell-mediated autoimmune attack on pancreatic beta-cells. Previous studies highlight the role of microRNAs (miRNAs) in the pathogenesis of T1D. MiRNAs are small non-coding RNAs involved in the regulation of gene expression post-transcriptionally. In this work, miR-18b was chosen and the differential expression of it was measured between T1D patients and healthy controls from Isfahan population.

Materials and Methods: MiR-18b was selected using Bioinformatics studies by miRWalk software. 22 T1D patients and 18 healthy controls from Isfahan population were enrolled in this study. Total RNA of the peripheral blood mononuclear cells (PBMCs) samples were extracted. After cDNA synthesis, the expression profile of miR-18b quantified by means of qPCR method in patients and controls. Finally the results were statistically analyzed.

Results: In this study despite our hypothesis, the expression levels of miR-18b didn’t show any significant difference between T1D patients and healthy controls (p value: 0.145).

Conclusion: Due to the results of our experimental analysis, it seems that miR-18b doesn’t have any association with T1D disease in Isfahan population.

MicroRNAs (mirNAs) have garnered tremendous interest in cancer biology research in the recent decade. mirNAs are a group of short non-coding RNAs,20–24 nucleotides in length, thatare found in animals and plants.Theycan reduce the expression of genes involved in numerous vital cell processes. Recent evidences indicate a key role played by mirNAs in the initiation and development of human carcinogenesis. These function including: the regulation of oncogenes, tumor suppressor genes, and several tumor-associated genes to that of processes such as cell proliferation, apoptosis, and angiogenesis. Clinical trials aimed at improving mirNA profiling for clinical diagnosis and prognosis of different disorders are now underway. In this review, we have summarized the physiological role of mirNAs and theirdiagnostic and therapeutic
potential inclinical assessment.

Background: Toll-like receptors (TLRs) detect diverse pathogen-associated molecular patterns and play a critical role in the innate immune response. Hosts should activate TLR-signaling pathways to eliminate invading pathogens. However, excessive activation of these pathways may interrupt immune homeostasis, leading to several diseases. Therefore precise regulation of TLR-signaling pathways is essential. Meanwhile, miRNAs (microRNAs) act similar to a class of small noncoding RNAs with gene regulatory functions. The regulation of TLR expression by miRNAs may be one of the valid points for targeting TLRs.
Materials and methods: In this study, we predicted most of the microRNAs bind to the TLRs pathway in the chicken, based on the bioinformatic methods. All genes involved in the TLR signaling pathway in chicken species were extracted from the KEGG database (Entry: gga04620) and analyzed based on different applications.
Results: We predicted 19 miRNAs for the 18 target genes of the TLR pathway that may provide essential clues for identifying novel drug targets for inflammatory diseases.
Conclusion: Substantial miRNA was found as gene regulators. As newly identified regulators, the performance mechanism of miRNAs in combination with other regulatory mechanisms will control the outcome of immune responses and these issues should be investigated in future studies

Background: Type 2 Diabetes (T2D) in the elderly is an epidemic that significantly impacts global health. This experimental study aimed to compare the responses of microRNA-133a (miR-133a) in different tissues and of Runt-related transcription factor 2 (Runx2) in bone marrow tissue following resistance and endurance training in old rats with High-Fat Diet and Streptozotocin (HFD/STZ)- induced type 2 diabetes.

Materials and Methods: T2D was induced by HFD/low-dose STZ in 30 male Wistar rats (21-monthold, Mean±SD weight 418±43 g). The rats received HFD (55%, 31%, and 14% of energy from fat, carbohydrate, and protein, respectively; 5.2 kcal/g). The diets continued for eight weeks in both groups. Over week four, the rats in the group with HFD/STZ-induced T2D received treatment with low-dose STZ. After one week of familiarity with the laboratory environment, they were randomly divided into three groups: Diabetic Endurance Training (DET, n=10), Diabetic Resistance Training (DRT, n=10), and Diabetic Control (DC, n=10). The eight weeks of endurance training protocol comprised five sessions of moderate-intensity training (60%-75% velocity at maximal oxygen uptake (vVO2max) and low intensity (30%-30% vVO2max). In 60% Maximum Voluntary Carrying Capacity (MVCC), the resistance group climbed the ladder 14-20 times with 1-minute rest, five days a week.

Results: The results of the 1-way ANOVA test showed no significant change in serum miR-133 expression (P=0.411) and muscle tissue (P=0.077) following resistance and endurance training. However, significant differences were observed in bone marrow miR-133 expression (P=0.003) and Runx2 gene expression (P=0.002) between groups. Tukey’s post hoc tests showed that the bone marrow miR-133 expression had a significant increase following eight weeks of resistance training compared to the endurance training (P=0.006) and control (P=0.002) groups, and bone marrow Runx2 gene expression in rats exposed to resistance training compared to the endurance training (P=0.044) and the control (P=0.018) groups.

Conclusion: It seems that longer periods of exercise are required for cellular changes in the metabolism of these tissues after these exercise protocols. This topic should be studied in future research.