---

Background and Aim: Proliferate potential differentiate into different cell lineages and high self-renewal of Mesenchymal Stem Cells (MSCs); thus, they are ideal tools for regenerative medicine. However, a leading problem is an oxidative stress in the target tissue and the apoptosis of transplanted stem cells before tissue repair. The pretreatment of stem cells with antioxidants may make them resistant to oxidative stress. Ginger is the main medicinal plant with antioxidant properties. This study explored the antioxidant effects of ginger extract on bioavailability and oxidative stress-induced apoptosis in human adipose tissue-derived mesenchymal stem cells and rat bone marrow examined. 
Methods & Materials: In this study, human adipose tissue-derived mesenchymal stem cells and rat bone marrow were cultured in a DMEM medium with 20% FBS. The explored cells were incubated for 4 and 6 hours for pretreatment with different concentrations of ginger extract (50, 100, 200, & 400 mg/mL); then, they were treated with 200 μM H2O2 for 2 hours. Bioavailability was analyzed by ELISA reader using an MTS kit and apoptosis was analyzed by flow cytometry using an Annexin V-FITC/PI kit into the manufacturer’s protocol at both times. The obtained data were analyzed by Analysis of Variance (ANOVA) using SPSS. 
Ethical Considerations: This study was approved by the Ethics Research Committee of Shahrekord Branch, Islamic Azad University (Code: IR.IAU.SHK.REC.1397.028).
Results: The MTS results indicated a dose- and time-dependent manner increase in the bioavailability of human adipose tissue-derived mesenchymal treated stem cells. Ginger extract treatment also dose- and time-dependently decreased the rate of apoptosis in rat bone marrow mesenchymal stem cells. 
Conclusion: Ginger extract, by reducing the oxidative stress in mesenchymal stem cells, elevates their lifespan in the target tissue, and increases the efficiency of these cells in tissue regeneration.

---

Background and Aim: This study aimed to investigate the effect of exercise timing on elevated postprandial glucose and after brief interval exercises in women with obesity.
Methods & Materials: Ten women with obesity (Mean±SD age = 40.41±3.97 years; weight = 86.66±7.26 kg; and BMI = 33.22±2.20 kg/m2) participated in a crossover design exercise intervention: 1) postprandial aerobic exercise, 2) pre-prandial aerobic exercise, 3) brief periodic exercise, and 4) control. Pre- and postprandial exercise included 30 min of moderate-intensity walking on the treadmill before and after each main meal (1 minute of exercise -30 seconds rest). The brief periodic exercise had three one-minute reps of activity every 30 min for 20 times during the day. Twelve-hour continuous glucose monitoring and two-hour postprandial glucose levels were calculated to examine changes in blood glucose levels.
Ethical Considerations: This study was approved by the institutional review board of the University of Isfahan (Ethics Code: IR.UI.REC.1397.119) and conducted in agreement with the ethical principles for biomedical research involving human subjects outlined in the declaration of Helsinki.
Results: The findings of this study suggested that brief periodic exercise resulted in a significant decrease in continuous glucose monitoring levels and postprandial glucose compared to the control group as well as pre-prandial exercise (P˂0.05). However, pre- and postprandial exercise did not result in significant changes in continuous glucose monitoring (P˃0.05). In addition, postprandial exercise led to a significant decrease in postprandial glucose compared to the control group (P˂0.05).
Conclusion: It seems that brief periodic exercise can have more beneficial effects on postprandial glucose levels, probably due to improved glucose metabolism in skeletal muscle.

---

Introduction: Breast cancer is one of the most common cancers and the principal cause of death in women. One of the mechanisms of cancer cells for the lack of access to the immune system is the production of compounds suppressing immune responses, such as interleukin-10. On the other hand, vascular endothelial growth factor, by binding to its receptors on the surface of endothelial cells, plays a significant role in vascular permeability and tumor vascularity. In this study, the expression of interleukin-10 and vascular endothelial growth factor in breast tumor tissue was investigated in an experimental tumor model.
Methods: First, mammary tumors were experimentally induced in Balb/C mice, and RNA was extracted from the tumor tissue. cDNA was synthesized from the extracted RNAs, and the expression level of 10-IL and VEGF genes was evaluated by RT-PCR.
Results: The results of data analysis showed that the expression of IL-10 and VEGF genes in the tumor tissue was higher than in the cells of the control group, but this increase in expression was not statistically significant.
Conclusions: In general, the expression level of Interleukin-10 and VEGF genes was increased in the experimental tumor model, but broader research and the correlation with other involved factors seem necessary.