No abstract

The volume and complexity of their vascular systems make the dynamics of long-distance water transport in large trees difficult to study. We used heat and deuterated water (D 2 O) as tracers to characterize whole-tree water transport and storage properties in individual trees belonging to the coniferous species Pseudotsuga menziesii . Tracer residence time and half-life increased as tree diameter increased, independent of species. Species-independent scaling of tracer velocity with sapwood-specific conductivity was also observed. When data from this study were combined with similar data from an earlier study of four tropical angiosperm trees, species-independent scaling of tracer velocity and residence time with sapwood hydraulic capacitance was observed. Sapwood capacitance is an intrinsic tissue-level property that appears to govern whole-tree water transport in a similar manner among both tracheid-and vesselbearing species.

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. However, statins have not been considered for DMD, or other muscular dystrophies, principally because skeletal-muscle-related symptoms are rare, but widely publicized, side effects of these drugs. Here we show positive effects of statins in dystrophic skeletal muscle. Simvastatin dramatically reduced damage and enhanced muscle function in dystrophic (mdx) mice. Long-term simvastatin treatment vastly improved overall muscle health in mdx mice, reducing plasma creatine kinase activity, an established measure of muscle damage, to nearnormal levels. This reduction was accompanied by reduced inflammation, more oxidative muscle fibers, and improved strength of the weak diaphragm muscle. Shorter-term treatment protected against muscle fatigue and increased mdx hindlimb muscle force by 40%, a value comparable to current dystrophin gene-based therapies. Increased force correlated with reduced NADPH Oxidase 2 protein expression, the major source of oxidative stress in dystrophic muscle. Finally, in old mdx mice with severe muscle degeneration, simvastatin enhanced diaphragm force and halved fibrosis, a major cause of functional decline in DMD. These improvements were accompanied by autophagy activation, a recent therapeutic target for DMD, and less oxidative stress. Together, our findings highlight that simvastatin substantially improves the overall health and function of dystrophic skeletal muscles and may provide an unexpected, novel therapy for DMD and related neuromuscular diseases.statin | muscular dystrophy | fibrosis | inflammation | muscle force D uchenne muscular dystrophy (DMD) is a degenerative muscle disease caused by the absence of dystrophin, a large protein that links the cytoskeleton to the surface membrane in muscle cells. Loss of dystrophin causes widespread effects on muscle signaling and metabolic pathways, leading to cell death and progressive replacement of functional muscle fibers with fibrotic connective tissue. This process results in profound muscle weakness, usually leaving DMD boys wheelchair-bound by their early teenage years and leading to death from the consequences of respiratory and/or cardiac muscle failure by age 20-30. Current treatments, such as corticosteroids, slow disease progression only marginally (1), whereas gene-based approaches, such as exonskipping, although promising in preclinical studies, will need to overcome many technical and regulatory hurdles, as well becoming affordable, before they are a widely available therapy for DMD patients (2). Therefore, efficacious pharmaceutical agents that are cost-effective and already approved for human use are particularly attractive candidates for the current treatment of DM...

No abstract

Abstract. 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. Density-dependent mortality was most pronounced for the dominant latesuccessional species, Tsuga heterophylla. The long-lived, early-seral Pseudotsuga menziesii experienced an annual stem mortality rate of 0.84% and no new recruitment. Late-seral species Tsuga and Abies amabilis had nearly balanced demographic rates of ingrowth and mortality. The 2.34% mortality rate for Taxus brevifolia was higher than expected, notably less than ingrowth, and strongly affected by proximity to Tsuga. Large-diameter Tsuga structured both the regenerating conspecific and heterospecific cohorts with recruitment of Tsuga and Abies unlikely in neighborhoods crowded with large-diameter competitors (P , 0.001). Densitydependent competitive interactions strongly shape forest communities even five centuries after stand initiation, underscoring the dynamic nature of even equilibrial old-growth forests.