Simvastatin provides long-term improvement of left ventricular function and prevents cardiac fibrosis in muscular dystrophy.

Duchenne muscular dystrophy (DMD), caused by absence of the protein dystrophin, is a common, degenerative muscle disease affecting 1:5000 males worldwide. With recent advances in respiratory care, cardiac dysfunction now accounts for 50% of mortality in DMD. Recently, we demonstrated that simvastatin substantially improved skeletal muscle health and function in mdx (DMD) mice.

Mice lacking α-, β1- and β2-syntrophins exhibit diminished function and reduced dystrophin expression in both cardiac and skeletal muscle.

Syntrophins are a family of modular adaptor proteins that are part of the dystrophin protein complex, where they recruit and anchor a variety of signaling proteins. Previously we generated mice lacking α- and/or β2-syntrophin but showed that in the absence of one isoform, other syntrophin isoforms can partially compensate. Therefore, in the current study, we generated mice that lacked α, β1 and β2-syntrophins [triple syntrophin knockout (tKO) mice] and assessed skeletal and cardiac muscle function.

Hydraulic redistribution affects modeled carbon cycling via soil microbial activity and suppressed fire.

Hydraulic redistribution (HR) of water from moist to drier soils, through plant roots, occurs world-wide in seasonally dry ecosystems. Although the influence of HR on landscape hydrology and plant water use has been amply demonstrated, HR's effects on microbe-controlled processes sensitive to soil moisture, including carbon and nutrient cycling at ecosystem scales, remain difficult to observe in the field and have not been integrated into a predictive framework. We incorporated a representation of HR into the Community Land Model (CLM4.

Validation of ultrasonography for non-invasive assessment of diaphragm function in muscular dystrophy.

Key Points: Duchenne muscular dystrophy (DMD) is a severe, degenerative muscle disease that is commonly studied using the mdx mouse. The mdx diaphragm muscle closely mimics the pathophysiological changes in DMD muscles. mdx diaphragm force is commonly assessed ex vivo, precluding time course studies.

Simvastatin offers new prospects for the treatment of Duchenne muscular dystrophy.

Duchenne muscular dystrophy (DMD) is the most common and severe inherited neuromuscular disorder. DMD is caused by mutations in the gene encoding the dystrophin protein in muscle fibers. Dystrophin was originally proposed to be a structural protein that protected the sarcolemma from stresses produced during contractions.

A new therapeutic effect of simvastatin revealed by functional improvement in muscular dystrophy.

Duchenne muscular dystrophy (DMD) is a lethal, degenerative muscle disease with no effective treatment. DMD muscle pathogenesis is characterized by chronic inflammation, oxidative stress, and fibrosis. Statins, cholesterol-lowering drugs, inhibit these deleterious processes in ischemic diseases affecting skeletal muscle, and therefore have potential to improve DMD.

Spatially nonrandom tree mortality and ingrowth maintain equilibrium pattern in an old-growth Pseudotsuga-Tsuga forest.

Mortality processes in old-growth forests are generally assumed to be driven by gap-scale disturbance, with only a limited role ascribed to density-dependent mortality, but these assumptions are rarely tested with data sets incorporating repeated measurements. Using a 12-ha spatially explicit plot censused 13 years apart in an approximately 500-year-old Pseudotsuga-Tsuga forest, we demonstrate significant density-dependent mortality and spatially aggregated tree recruitment. However, the combined effect of these strongly nonrandom demographic processes was to maintain tree patterns in a state of dynamic equilibrium.

The importance of large-diameter trees to forest structural heterogeneity.

Large-diameter trees dominate the structure, dynamics and function of many temperate and tropical forests. However, their attendant contributions to forest heterogeneity are rarely addressed. We established the Wind River Forest Dynamics Plot, a 25.

Mice lacking the Cβ subunit of PKA are resistant to angiotensin II-induced cardiac hypertrophy and dysfunction.

Background: PKA is a ubiquitous, multi-subunit cellular kinase that regulates a number of different physiological responses in response to cAMP, including metabolism, cell division, and cardiac function. Numerous studies have implicated altered PKA signaling in cardiac dysfunction. Recently, it has been shown that mice lacking the catalytic β subunit of PKA (PKA Cβ) are protected from age-related problems such as weight gain and enlarged livers, and we hypothesized that these mice might also be resistant to cardiomyopathy.