Increased developmental potential this website correlated with significantly lower p66Shc content, significantly higher levels of catalase and MnSOD, and significantly lower intracellular ROS levels (MitoSOX staining) and reduced DNA damage (?-H2A.X(phospho S139) immunostaining). p66Shc content was increased by either high (20%) O2 culture or H2O2 treatment, and significantly decreased by supplementing culture media with the antioxidant polyethylene
glycol-conjugated catalase. While the abundance of p66Shc varied according to pro/anti-oxidant culture conditions, antioxidant content varied only according to developmental potential. This discrepancy has important implications regarding ongoing efforts towards maximizing in vitro embryo production. Mol.
Reprod. Dev. 80: 2234, 2013. (c) 2012 Wiley Periodicals, Inc.”
“Mitochondrial myopathies cover a diverse group of disorders in which ragged red and COX-negative fibers are common findings on muscle morphology. In contrast, muscle degeneration and regeneration, typically buy BEZ235 found in muscular dystrophies, are not considered characteristic features of mitochondrial myopathies. We investigated regeneration in muscle biopsies from 61 genetically well-defined patients affected by mitochondrial myopathy. Our results show that the perturbed energy metabolism in mitochondrial myopathies causes ongoing muscle regeneration in a majority of patients, and some were even affected by a dystrophic morphology. The results add to the complexity of the pathogenesis underlying mitochondrial myopathies, and expand the knowledge about the impact of energy deficiency on another aspect of muscle structure and function. (C) 2013
Elsevier B.V. and Mitochondria Research Society. All rights reserved.”
“The Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is the CaMK isoform predominantly found in the heart. Cardiac myocytes signaling during excitation-contraction coupling (ECC) is described by the increase in intracellular Ca(2+) concentration. In consequence, CaMKII is activated thereby phosphorylating several important Ca(2+) handling proteins with multiple functional consequences for cardiac myocytes. Specific CaMKII overexpression CX-6258 supplier in the heart and in isolated myocytes of animals can exert distinct and novel effects on ECC. CaMKII activity and expression are reported to be increased in cardiac hypertrophy, in human heart failure, as well as in animal models thereby contributing to cardiac disease through a regulation process termed excitation-transcription coupling (ETC). In the present review important aspects of the role of CaMKII in ECC and ETC are summarized with an emphasis on recent novel findings.”
“To investigate whether embryo shape is a useful morphologic predictor of developmental competence in IVF cycles.