Early thinning experiments established by the Fort Valley Experimental Forest

Between 1925 and 1936, the Fort Valley Experimental Forest (FVEF) scientists initiated a study to examine a series of forest thinning experiments in second growth ponderosa pine stands in Arizona and New Mexico. These early thinning plots furnished much of the early background for the development of methods used in forest management in the Southwest. The plots ranged from 0.1 ac to 5 ac (0.04 ha to 2.02 ha) in size and many of the thinning plots and control plots were remeasured at 2 to 10-year intervals until the 1940s. The first thinning plots in the Southwest, called the White Spar plots, were established in 1925 on the Prescott National Forest. The residual trees on the thinned White Spar plots maintained higher growth rates than the control until the mid 1970s. The results from these early stand thinning experiments led G.A. Pearson, Director of FVEF, and others to largely abandon uniform thinning treatments and adopt the crop-tree thinning method as an improved method for thinning southwestern ponderosa pine stands

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Statin-associated skeletal muscle damage and its interactions with novel or accustomed exercise

Statin drugs are a very commonly prescribed medication, and their most common side effect is some degree of skeletal muscle myopathy. Unfortunately, this side effect is more likely/severe in statin users who are also exercisers. Purpose: To examine the previously unaddressed interactions of statin treatment with novel vs. accustomed exercise, as well as to examine cellular markers of the stress response???heat shock proteins (Hsps)???and apoptosis???activated caspases. Methods: C57 mice were treated with daily cerivastatin (1/mg/kg/day) or saline for two weeks, with/without concomitant wheel running (RW) (Novel & Sedentary groups). Additional groups also performed two weeks of RW activity prior to the initiation of statin treatment (Accustomed groups). RW activity was tracked daily, and hindlimb plantarflexor maximal force and fatigue was measured at the end of the intervention. Hsp25, ??B-Crystallin, Caspase-3, and Caspase-9 were measured by western blot, plasma creatine kinase (CK) was assessed by activity assay. Results: Statin treatment did not significantly impact RW activity, however both sedentary and novel-exercise groups showed decrements in muscle force and fatigability with statin treatment. The effect on maximal force was more severe in the novel-exercise group, while accustomed exercise mice were protected from this decrement. Plasma creatine kinase levels did not correlate with functional outcomes. No significant effect of statin treatment was found for hsp25 or ??B-Crystallin expression, though both proteins were increased by both the novel and accustomed exercise interventions. A significant injection by activity interaction was found for active caspase-9 expression, with statins increasing expression in the sedentary and novel groups, but decreasing expression in the accustomed groups. Active caspase-3 was not detectable in any group. Conclusions: These results indicate that exercise training prior to statin treatment can protect against myopathy, rather than exacerbate it, as seen with novel exercise. Additionally, accustomed exercise was able to reverse statin treatment???s activation of caspase-9, though the physiological significance of this is unclear, as the lack of caspase-3 expression indicates that apoptosis did not in fact occur. An upregulation in Hsp expression with exercise may have contributed to the preservation of muscle force and decreased caspase-9 expression in the accustomed groups

Role of catecholate siderophores in gram-negative bacterial colonization of the mouse gut

We investigated the importance of the production of catecholate siderophores, and the utilization of their iron (III) complexes, to colonization of the mouse intestinal tract by Escherichia coli. First, a ΔtonB strain was completely unable to colonize mice. Next, we compared wild type E. coli MG1655 to its derivatives carrying site-directed mutations of genes for enterobactin synthesis (ΔentA::Cm; strain CAT0), ferric catecholate transport (Δfiu, ΔfepA, Δcir, ΔfecA::Cm; CAT4), or both (Δfiu, ΔfepA, ΔfecA, Δcir, ΔentA::Cm; CAT40) during colonization of the mouse gut. Competitions between wild type and mutant strains over a 2-week period in vivo showed impairment of all the genetically engineered bacteria relative to MG1655. CAT0, CAT4 and CAT40 colonized mice 10[superscript 1]-, 10[superscript 5]-, and 10[superscript 2]-fold less efficiently, respectively, than MG1655. Unexpectedly, the additional inability of CAT40 to synthesize enterobactin resulted in a 1000-fold better colonization efficiency relative to CAT4. Analyses of gut mucus showed that CAT4 hyperexcreted enterobactin in vivo, effectively rendering the catecholate transport-deficient strain iron-starved. The results demonstrate that, contrary to prior reports, iron acquisition via catecholate siderophores plays a fundamental role in bacterial colonization of the murine intestinal tract

The Impact of Exercise on Statin-Associated Skeletal Muscle Myopathy.

HMG-CoA reductase inhibitors (statins) are the most effective pharmacological means of reducing cardiovascular disease risk. The most common side effect of statin use is skeletal muscle myopathy, which may be exacerbated by exercise. Hypercholesterolemia and training status are factors that are rarely considered in the progression of myopathy. The purpose of this study was to determine the extent to which acute and chronic exercise can influence statin-induced myopathy in hypercholesterolemic (ApoE-/-) mice. Mice either received daily injections of saline or simvastatin (20 mg/kg) while: 1) remaining sedentary (Sed), 2) engaging in daily exercise for two weeks (novel, Nov), or 3) engaging in daily exercise for two weeks after a brief period of training (accustomed, Acct) (2x3 design, n = 60). Cholesterol, activity, strength, and indices of myofiber damage and atrophy were assessed. Running wheel activity declined in both exercise groups receiving statins (statin x time interaction, p<0.05). Cholesterol, grip strength, and maximal isometric force were significantly lower in all groups following statin treatment (statin main effect, p<0.05). Mitochondrial content and myofiber size were increased and 4-HNE was decreased by exercise (statin x exercise interaction, p<0.05), and these beneficial effects were abrogated by statin treatment. Exercise (Acct and Nov) increased atrogin-1 mRNA in combination with statin treatment, yet enhanced fiber damage or atrophy was not observed. The results from this study suggest that exercise (Nov, Acct) does not exacerbate statin-induced myopathy in ApoE-/- mice, yet statin treatment reduces activity in a manner that prevents muscle from mounting a beneficial adaptive response to training