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The aim of this study is to determine if the offspring of mothers with obesity, present disorders in the expression of genes related to atrophy or protein synthesis in the muscle and if these disorders are modified with the (−)-epicatechin (Epi) treatment. Six male offspring per group were randomly assigned to the control groups [C and offspring of maternal obesity (MO)] or the Epi intervention groups, Epi treatment for 13 weeks (C + Epi long or MO + Epi long), or Epi administration for two weeks (C + Epi short or MO + Epi short). The effect of Epi in the gastrocnemius tissue was evaluated, analyzing mRNA and protein levels of Murf1, MAFbx, Foxo1, NFkB, and p70S6K-alpha. After the analysis by two-way ANOVA, we found an influence of the Epi long treatment over the model, by decreasing the Murf1 gene expression in both groups treated with the flavonoid (C + Epi long and MO + Epi long) (p = 0.036). Besides, Epi long treatment over the NFκB expression, by decreasing the fold increase in both groups treated with the flavonoid (C + Epi long and MO + Epi long) (p = 0.038). We not find any interaction between the variables or changes in the MAFbx, Foxo1 mRNA, neither in the phosphorylated/total protein ratio of NFκB, Foxo1, or p70S6K-alpha. In conclusions, treatment with a long protocol of Epi, reduces the mRNA of the muscle atrophy genes Murf 1 and NFkB , in the gastrocnemius muscle; however, these changes are not maintained at protein level. [ABSTRACT FROM AUTHOR]

Introduction: Sporadic Parkinson's disease (PD) is a neurodegenerative disorder of unknown etiology. In recent years, it has been established that a genetic component underlies different forms of the disease. For instance, mitochondrial genome variants have been implicated in the pathogenesis of the PD. Aim of the study: To determine the association of tRNA(Gln) 4336 and 8701A>G (ATP6: Thr59Ala) mitochondrial DNA polymorphisms with the presence of PD in Mexican mestizo patients. Material and methods: This was a cross-sectional study in which patients were recruited from four tertiary-care level hospitals in Mexico. Genotyping was performed using real-time PCR with TaqMan genotyping assays. Genotypes were confirmed by automated sequencing. Results: The 4336C allele of the tRNAGln gene was present at a low frequency, and the 8701G allele of the MT-ATP6 gene was not associated with PD. Conclusions: The 4336C variant of the tRNAGln gene was uncommon in the study population, and 8701A/G of MT-ATP6 was not associated with PD in Mexican Mestizos. [ABSTRACT FROM AUTHOR]

The article discusses a study which explores the link between methylenetetrahydrofolate reductase (MTHFR) functional polymorphism and hypertension among Mexican-Mextizo population. The study case-control study to determine the effects of polymorphisms to hypertension. The study reveals the role of allele A of rs13306560 polymorphism for regulation of MTHFR.

The aim of this study is to determine if the offspring of mothers with obesity, present disorders in the expression of genes related to atrophy or protein synthesis in the muscle and if these disorders are modified with the (-)-epicatechin (Epi) treatment. Six male offspring per group were randomly assigned to the control groups [C and offspring of maternal obesity (MO)] or the Epi intervention groups, Epi treatment for 13 weeks (C + Epi long or MO + Epi long), or Epi administration for two weeks (C + Epi short or MO + Epi short). The effect of Epi in the gastrocnemius tissue was evaluated, analyzing mRNA and protein levels of Murf1, MAFbx, Foxo1, NFkB, and p70S6K-alpha. After the analysis by two-way ANOVA, we found an influence of the Epi long treatment over the model, by decreasing the Murf1 gene expression in both groups treated with the flavonoid (C + Epi long and MO + Epi long) (p = 0.036). Besides, Epi long treatment over the NFκB expression, by decreasing the fold increase in both groups treated with the flavonoid (C + Epi long and MO + Epi long) ( p = 0.038). We not find any interaction between the variables or changes in the MAFbx, Foxo1 mRNA, neither in the phosphorylated/total protein ratio of NFκB, Foxo1, or p70S6K-alpha. In conclusions, treatment with a long protocol of Epi, reduces the mRNA of the muscle atrophy genes Murf 1 and NFkB , in the gastrocnemius muscle; however, these changes are not maintained at protein level.

Epithelial ovarian cancer is the fifth most frequent cause of cancer death in women. In spite of the advantages in early detection and treatment options, overall survival rates have improved only slightly in the last decades. Therefore, alternative therapeutic approaches need to overcome resistance and improve the patient survival and outcome. MicroRNAs are evolutionary conserved small non-coding RNAs that function as negative regulators of gene expression by inhibiting translation or inducing degradation of messenger RNAs. In cancer, microRNAs are aberrantly expressed thus representing potential prognostic biomarkers and novel therapeutic targets. The knowledge of novel and unexpected functions of microRNAs is rapidly evolving and the advance in the elucidation of potential clinical applications deserves attention. Recently, a specific set of microRNAs dubbed as metastamiRs have been shown to initiate invasion and metastasis in diverse types of cancer. We reviewed the current status of microRNAs in development and progression of ovarian cancer with a special emphasis on tumor cells invasion and metastasis. Also, we show an update of microRNA functions in oncogenic pathways and discuss the current scenario for potential applications in clinical and translational research in ovarian cancer.

Scope: The flavanol (-)-epicatechin (Epi) has cardioprotective effects and improves physical capacity in normal mice. In addition, Epi increases nitric oxide (NO) production by activation of both PI3K/Akt or Ca 2+ /CaMI/CaMKII (where Akt is protein kinase B; PI3K is phosphoinositide 3-kinase; CaMI is calmodulin; CaMKII is Ca 2+ /calmodulin-dependent protein kinase II) signaling pathways, which have been associated with physiological and pathological cardiac hypertrophy, respectively. Notwithstanding all this information, few studies have been carried out that aimed to determine the potential beneficial effects that Epi may have in normal heart., Methods and Results: Mice were treated by oral gavage with the flavanol Epi. The treatment induced a significant increase in heart weight, size of the free walls, and size of the cardiac fibers. Also, no evidence of cardiac fibrosis was revealed. Furthermore, the phosphorylation level of PI3K/Akt/mTOR/p70S6K (where mTOR is mammalian target of rapamycin; p70S6K is ribosomal protein S6 kinase beta-1) proteins was significantly higher in the heart of Epi-treated animals. In contrast, a significantly decreased level of pathological cardiac hypertrophy markers atrial natriuretic peptide and brain natriuretic peptide was observed along with no modification in the level of β myosin heavy chain beta, calmodulin, and Ca 2+ /calmodulin-dependent protein kinase II proteins. Hemodynamic parameters indicated an improvement in mechanical heart performance after Epi treatment. Interestingly, morphometric parameters were similar between treated and untreated mice after 4 wk without treatment., Conclusion: These findings indicate that Epi treatment induced physiological cardiac growth in healthy mice by activation of the PI3K/Akt pathway., (© 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)