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Humans have generally evolved some adaptations to protect against UV and different levels of background ionizing radiation. Similarly, elephants and whales have evolved adaptations to protect against cancer, such as multiple copies of the tumor suppressor gene p53, due to their large size and long lifespan. The difference in cancer protection strategies between humans and elephants/whales depends on genetics, lifestyle, environmental exposures, and evolutionary pressures. In this paper, we discuss how the differences in evolutionary adaptations between humans and elephants could explain why elephants have evolved a protective mechanism against cancer, whereas humans have not. Humans living in regions with high levels of background radiation, e.g. in Ramsar, Iran where exposure rates exceed those on the surface of Mars, seem to have developed some kind of protection against the ionizing radiation. However, humans in general have not developed cancer-fighting adaptations, so they instead rely on medical technologies and interventions. The difference in cancer protection strategies between humans and elephants/whales depends on genetics, lifestyle, environmental exposures, and evolutionary pressures. In this paper, we discuss how the differences in evolutionary adaptations between humans and elephants could explain why elephants have evolved a protective mechanism against cancer, whereas humans have not. Studying elephant adaptations may provide insights into new cancer prevention and treatment strategies for humans, but further research is required to fully understand the evolutionary disparities. [ABSTRACT FROM AUTHOR]

Introduction: Cancer is considered one of the most significant causes of death worldwide. Probiotics are living microbes that play a significant role in protecting the host in various ways. The aim of this study was to investigate the cytotoxic effect of Bifidobacterium bifidum cell extract and supernatants as probiotic bacteria on the Adenocarcinoma gastric cancer cell line and analysis of Fas, P53, and Bcl2 gene expression. Materials & Methods: In this experimental study, the cell extract of heat-killed and supernatants Bifidobacterium bifidum was prepared. The cytotoxicity of cell extract and supernatants on AGS cell lines was evaluated in 24, 48, and 72 hours using a cytotoxicity assay. Moreover, the P53, Bcl2, and Fas apoptosis gene expression levels in the Adenocarcinoma gastric cancer cell line were analyzed using a molecular assay. The collected data were statistically analyzed using one-way ANOVA analysis with the Graph Pad Prism V.8 at the level of significance less than 0.05. Results: Supernatant (pH = 6), then supernatant (pH = 4), and then cell extracts of Bifidobacterium bifidum were able to reduce the survival rate of the AGS cell line in 48 and 72 hours. The results of gene expression by molecular method also showed an increase in Fas and P53 gene expression (p < 0.05) and a decrease in Bcl2 gene expression (p < 0.05) in the adenocarcinoma gastric cancer cell line compared to the reference GAPDH gene expression after 72 hours. Conclusion: Supernatant of Bifidobacterium bifidum with, respectively, pH = 6 and pH = 4, could induce apoptosis in the Adenocarcinoma gastric cancer cell line. So, it seems that Bifidobacterium bifidum has potential uses as a probiotic for pharmaceutical applications, including the prevention of gastric cancer. [ABSTRACT FROM AUTHOR]

Introduction: This study investigates the impact of two high-intensity interval training (HIIT) programs on PGC-1a, p53, and citrate synthase (CS) proteins within cardiomyocytes of male type 2 diabetic rats, aiming to discern potential molecular mechanisms influencing cardiac health. Material & Methods: Twenty-four male Wistar rats were randomly assigned to control (NC), diabetic control (DC), diabetic with type 1 HIIT (HIIT-1), and diabetic with type 2 HIIT (HIIT-2) groups. Streptozotocin (STZ) induced type 2 diabetes, excluding the NC group. A four-week HIIT intervention, six sessions per week, preceded the analysis of heart tissue for PGC-1a, p53, and CS protein levels. Statistical analysis employed GraphPad Prism software version 8 and one-way ANOVA (P < 0.05). Results: Both HIIT-1 (p=0.004) and HIIT-2 (p=0.007) groups exhibited significantly elevated cardiac PGC-1a levels compared to DC. CS levels increased notably in HIIT-1 (p=0.001) and HIIT-2 (p<0.001), with HIIT-2 surpassing HIIT-1 significantly (p=0.010). Concurrently, p53 levels significantly decreased in both HIIT-1 (p=0.005) and HIIT-2 (p=0.001) groups compared to DC. Conclusion: Exercise training (HIIT) positively influences cardiac metabolism, evident in PGC-1a and CS upregulation and p53 downregulation. While these findings provide valuable insights, further exploration is crucial for a comprehensive understanding of the underlying molecular mechanisms. This study advances our understanding of optimizing exercise interventions for improved cardiac health in type 2 diabetes. [ABSTRACT FROM AUTHOR]

Background: Chromodomain‐helicase 5 (CHD5) is a conventional tumor‐suppressing gene in many tumors. The CHD5 gene, as a key factor in the chromatin density process during sperm maturation, can affect the risk of infertility. This study aimed to determine whether CHD5 variants contribute to the risk of male infertility. Methods: Gene variants were identified using tetra primer‐ARMS‐PCR method on nonobstructive azoospermia and severe oligozoospermia in a case–control study. SPSS software 20 (SPSS Inc. Chicago, IL, USA) was used for data recording and statistical analysis. Results: In the codominant pattern, the rs12067480 TT variant versus CC significantly increased the risk of disease, and also, in the recessive pattern, TT variant versus CC + CT and T allele versus C. The rs2273032 variant was associated with the risk of infertility in codominant pattern AA versus GG and recessive pattern AA versus GG + GA and allele. We discovered that the rs12067480 T and rs2273032 A alleles increase the risk of male infertility. Also, the interaction of the CT/GA, CT/AA, TT/GA genotypes and rs12067480T/rs2273032A and rs12067480T/rs2273032G haplotypes significantly increased the risk of infertility. Conclusions: Our results suggest that the CHD5 gene polymorphisms contribute to the risk of male infertility. Our findings can be valuable in improving the diagnosis and treatment of infertility. [ABSTRACT FROM AUTHOR]

Background: Prostate cancer is an important disease whose many genetic aspects are still uncovered in spite of the wide spectrum of the studies previously performed on its genetic and environmental risk factors. According to the previous studies, KLF6, a suppressor gene dealing with prostate cancer, is exposed to genetic changes. Among all these changes, mutation of exon No. 2, which is in relation with disease prognosis, is common. The few studies conducted on the mutation of KLF6 gene have shown a relation between mutation and environmental factors as well as race and geographic conditions. The goal of this study was to investigate the mutation of exon No. 2 of KLF6 gene in people who suffer from prostate cancer in city of Isfahan, Iran. Methods: The study was carried out on microscopically and pathologically proved cases of prostate cancer in Isfahan, Iran, during 2009-2011. The samples were taken by prostatectomy or biopsy from 40 patients suffering the disease. A procedure including DNA extraction, determination of quality and quantity of DNA, PCR (using specific primers to replicate exon No. 2), polyacrylamide gel electrophoreses, and data analysis was performed on the samples to determine the mutation in exon No. 2 of KLF6 gene. Findings: Overall, 80% of the patients (32 people) were above 60 years of age. Only 17.5% of the patients (7 people) had mutation in exon No. 2 of KLF6 gene. There was no significant relation between the mutation of exon No. 2 of KLF6 gene and the age of the patients. A significant relation was found between the presence of mutation and tumor grading in the studied patients. Conclusion: The frequency of mutation in exon No. 2 of KLF6 gene was higher in cancer samples with higher grade. This finding can be a sign of weak prognosis in samples whose exon No. 2 of KLF6 gene has been mutated. [ABSTRACT FROM AUTHOR]