Metallothionein suppresses Ang II-induced NOX-dependent nitrosative damage and cell death in both nondiabetic and diabetic hearts early in the time course of injury and prevents the late development of Ang II-induced cardiomyopathy.

No abstract

Results of numerous studies have demonstrated a positive relation between religiosity and marital well-being. In this study, the authors examined direct effects on marital satisfaction of religious homogamy, prayer for spousal well-being, and forgiveness. They also examined the degree to which religiosity buffered against risks to marital well-being. The results indicated significant positive linear relations between each indicator of religiosity and marital satisfaction. Furthermore, religiosity moderated, or buffered against, the negative effects of risk factors; specifically, religious homogamy buffered against previous divorce; prayer buffered against having a high-stress marriage; and spousal forgiveness buffered

Marital satisfaction, marital adjustment, and problem areas experienced during the early months of marriage were examined using a sample of 1,010 newlywed husbands and wives. Results revealed that between 8% and 14% percent of newlyweds already scored in the distressed range on measures of marital satisfaction and adjustment, respectively. For both husbands and wives, the most problematic areas in the early months of marriage were balancing employment and marriage and debt brought into marriage. However, protective factors in the marriage, including respect, appreciation, commitment, mutual affection, and trust, were the strongest predictors of marital satisfaction and adjustment. Implications for future research and family life education are proposed.

In patients with hemochromatosis, cardiac dysfunction may appear years after they have reached a state of iron overload. We hypothesized that cumulative iron-catalyzed oxidant damage to mitochondrial DNA (mtDNA) might explain the cardiomyopathy of chronic iron overload. Mice were given repetitive injections of iron dextran for a total of 4 weeks after which the iron loaded mice had elevated cardiac iron, modest cardiac hypertrophy and cardiac dysfunction. qPCR amplification of near-full-length (~16 kb) mtDNA revealed >50% loss of full length product, whereas amounts of a qPCR product of a nuclear gene (13 kb region of beta globin) were unaffected. Quantitative rtPCR analyses revealed 60-70% loss of mRNA for proteins encoded by mtDNA with no change in mRNA abundance for nuclear encoded respiratory subunits. These changes coincided with proportionate reductions in complex I and IV activities and decreased respiration of isolated cardiac mitochondria. We conclude that chronic iron overload leads to cumulative iron-mediated damage to mtDNA and impaired synthesis of mitochondrial respiratory chain subunits. The resulting respiratory dysfunction may explain the slow development of cardiomyopathy in chronic iron overload and similar accumulation of damage to mtDNA may also explain the mitochondrial dysfunction observed in slowly progressing diseases such as neurodegenerative disorders.