3′,4′-Dihydroxyflavonol Antioxidant Attenuates Diastolic Dysfunction and Cardiac Remodeling in Streptozotocin-Induced Diabetic m(Ren2)27 Rats

Diabetic cardiomyopathy (DCM) is an increasingly recognized cause of chronic heart failure amongst diabetic patients. Both increased reactive oxygen species (ROS) generation and impaired ROS scavenging have been implicated in the pathogenesis of hyperglycemia-induced left ventricular dysfunction, cardiac fibrosis, apoptosis and hypertrophy. We hypothesized that 3',4'-dihydroxyflavonol (DiOHF), a small highly lipid soluble synthetic flavonol, may prevent DCM by scavenging ROS, thus preventing ROS-induced cardiac damage.Six week old homozygous Ren-2 rats were randomized to receive either streptozotocin or citrate buffer, then further randomized to receive either DiOHF (1 mg/kg/day) by oral gavage or vehicle for six weeks. Cardiac function was assessed via echocardiography and left ventricular cardiac catheterization before the animals were sacrificed and hearts removed for histological and molecular analyses. Diabetic Ren-2 rats showed evidence of diastolic dysfunction with prolonged deceleration time, reduced E/A ratio, and increased slope of end-diastolic pressure volume relationship (EDPVR) in association with marked interstitial fibrosis and oxidative stress (all P<0.05 vs control Ren-2). Treatment with DiOHF prevented the development of diastolic dysfunction and was associated with reduced oxidative stress and interstitial fibrosis (all P<0.05 vs untreated diabetic Ren-2 rats). In contrast, few changes were seen in non-diabetic treated animals compared to untreated counterparts.Inhibition of ROS production and action by DiOHF improved diastolic function and reduced myocyte hypertrophy as well as collagen deposition. These findings suggest the potential clinical utility of antioxidative compounds such as flavonols in the prevention of diabetes-associated cardiac dysfunction

Changes to dryland rainfall result in rapid moss mortality and altered soil fertility

Arid and semi-arid ecosystems cover ~40% of Earth’s terrestrial surface1, but we know little about how climate change will affect these widespread landscapes. Like many drylands, the Colorado Plateau in southwestern United States is predicted to experience elevated temperatures and alterations to the timing and amount of annual precipitation2, 3, 4. We used a factorial warming and supplemental rainfall experiment on the Colorado Plateau to show that altered precipitation resulted in pronounced mortality of the widespread moss Syntrichia caninervis. Increased frequency of 1.2 mm summer rainfall events reduced moss cover from ~25% of total surface cover to \u3c2% after only one growing season, whereas increased temperature had no effect. Laboratory measurements identified a physiological mechanism behind the mortality: small precipitation events caused a negative moss carbon balance, whereas larger events maintained net carbon uptake. Multiple metrics of nitrogen cycling were notably different with moss mortality and had significant implications for soil fertility. Mosses are important members in many dryland ecosystems and the community changes observed here reveal how subtle modifications to climate can affect ecosystem structure and function on unexpectedly short timescales. Moreover, mortality resulted from increased precipitation through smaller, more frequent events, underscoring the importance of precipitation event size and timing, and highlighting our inadequate understanding of relationships between climate and ecosystem function in drylands

Neural Adaptations to Strength Training

Scientific study of strength training has revealed numerous physiological mechanisms that contribute to: (1) acute fatigue from a single strength training session and (2) chronic adaptation to repetitive and systematic strength training. Therefore, the purpose of this chapter is initially to discuss potential neural mechanisms that influence force production from the perspective of a single repetition. Thereafter, the chapter will highlight scientific evidence for candidate neural mechanisms that acutely limit force production during a single strength training session and long-term adaptations caused by strength training. For some of these potential neural mechanisms, there is strong scientific evidence and for others evidence has emerged in recent years and requires further investigation.peerReviewe