Background and Objective: In this study the effect of high intensity interval training on miR-29 expression that is expressed in the heart and in the regulation of physiological processes, including extracellular matrix and cardiac hypertrophy of healthy male rats were examined. Materials and Methods: 16 Wistar rats were divided into training (n=8) and control (n=8) groups. After one week of familiarization, the training protocol was performed for 8 weeks. The progressive training protocol included 6 min warm up (with 50 to 60% of VO2max), 7 frequency (4 min with 80 to 90% of VO2max and 3 min with 50 to 60% of VO2max) and 5 min cool down with 50 to 60% of VO2max.The animals were sacrificed 24 hours after the last session of training program and cardiac samples were kept at a temperature of - 80 ° C and the variable expression levels (miR-29a، miR-29b and miR-29c) were measured by RT-PCR method. Analysis of the results was performed by independent t-test. Results: Training led to a significant increase in miR-29a (3.5 fold), miR-29b (2.24 fold) and miR-29c (9.77 fold) gene expression in the training group compared with the control group (p<0.001). Also training brought about 22% increase in heart weight to body weight ratio (HW/BW) in the training group (p<0.001). Conclusion: These results point out that training increases miR-29 expression which is associated with physiological cardiac hypertrophy and improved heart performance. 1- Rohini A, Agrawal N, Koyani C, et al. Molecular targets and regulators of cardiac hypertrophy. Pharmacological Research. 2010 61: 269-80. 2- Braun LT. Physiologic versus pathologic hypertrophy: endurance exercise and chronic pressure overload. J Cardiovasc Nurs. 1994 8: 39-56. 3- Gaeini AA, Kazemi F, Mehdiabadi J, et al. The effect of 8-week aerobic interval training and a detraining period on left ventricular structure and function in non-athlete healthy men. 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Background and Objective: Tamoxifen is the most commonly used treatment for the patients with breast cancer called ER +, which prevents the expression of genes that are effective in the growth and proliferation of cancer cells by estrogen. Resistant to Tamoxifen is a major clinical problem in breast cancer treatment. In recent studies, the role of microRNAs in tamoxifen resistance has been raised through the influence of regulation of cell cycle control genes. Throughout this study, the interactions of microRNAs with genes involved in tamoxifen resistance were investigated.
Materials and Methods: By comparing the gene expression data in samples of patients sensitive and resistant to Tamoxifen from the GEO database and searching in the database of articles, genes and microRNAs with significant expression variations were determined. Then, by examining the correlation between the expression of genes and microRNAs and bioinformatics by mirwalk software, the interconnection network between the genes and microRNAs was drawn.
Results: The results showed that 21 genes and 62 microRNAs altered in Tamoxifen resistant specimens. With miR342-3P/5P targeting the HOXB13, PRM2, and KLK3 genes, and MiR-520h and miR-582-5p microRNAs, targeting 5 reduced expression genes, can lead to recurrence of breast cancer.
Conclusion: The regulatory network mapped out between a set of genes and microRNAs that are potentially involved in the recurrence of breast cancer treated with Tamoxifen could clarify the role of the microRNAs in the recurrence of breast cancer.

Background and Objective: Ulcerative colitis (UC) is an unknown recurrent intestinal disease and a common cause of gastrointestinal disorders, which may lead to colorectal cancer if not diagnosed and treated in a timely manner. The beneficial effects of several probiotics in diseases like inflammatory bowel disease (IBD) have been investigated, although their mechanisms have not been yet fully understood. In this study, we investigated the possible association between the changes in the levels of the expression of miRNAs and the anti-inflammatory activity of the L. acidophilus as a probiotic model in Wistar rats suffering the acid-induced UC.
Materials and Methods: Twenty rats were randomly divided into four groups. To induce colitis, the rats were briefly anesthetized, and 1 ml of acetic acid (4%) was injected into their rectum using a Foley catheter, as explained previously.  L. acidophilus was given orally (3×10⁸ CCU/ml) for 10 days. The rats were monitored daily for clinical signs for 10 days. Following euthanasia, the macroscopic and microscopic pathological lesions in the intestinal tissues were examined. Additionally, the total RNA from specimens were extracted, and the expression levels of mRNAs for cytokines, including TNFα, IL-1β, IL-6, IL-10, IFN-γ, and the expression levels of miR-1, miR-155, miR-let7d, and miR-99a were determined using the qPCR method.
Results: The clinical signs and pathological damages induced by acid were ameliorated in the rats receiving L. acidophilus compared with rats that did not receive it, as evidenced by improved clinical signs and results of immunohistochemistry and chemical assays. miRNAs, including miR-1, miR-99, miR-Let7d and miR-155 and changes in the expression of mRNAs, including TNFα, IL-1β, IL-6, IL-10 and IFN-γ were significant. Changes in the amount of myeloperoxidase, nitrite oxide, and malondialdehyde were also significant (P ≤ 0.05). In pathological examination, immune cell infiltration and COX2 were different in colitis and treatment groups.
Conclusion: Therapeutic use of probiotics ameliorated UC by significantly changing the levels of miR-1, miR-99, miR-Let7d and miR-155.