Call to action: Better care, better health, and greater value in college health.

It is time for action by leaders across higher education to strengthen quality improvement (QI) in college health, in pursuit of better care, better health, and increased value - goals closely linked to students' learning and success. The size and importance of the college student population; the connections between wellbeing, and therefore QI, and student success; the need for improved standards and greater accountability; and the positive contributions of QI to employee satisfaction and professionalism all warrant a widespread commitment to building greater capacity and capability for QI in college health. This report aims to inspire, motivate, and challenge college health professionals and their colleagues, campus leaders, and national entities to take both immediate and sustainable steps to bring QI to the forefront of college health practice - and, by doing so, to elevate care, health, and value of college health as a key pathway to advancing student success.

Sarcopenia, age, atrophy, and myopathy: Mitochondrial oxidative enzyme activities.

Introduction: We studied mitochondrial impairment as a factor in the pathologic equivalent of sarcopenia, muscle fiber atrophy associated with increased age.

Methods: Mitochondrial oxidative enzyme activities and coenzyme Q10 levels were measured in frozen human proximal limb muscles with combined age and atrophy, age alone, atrophy alone, denervation, immune myopathies, and mitochondrial disorders with ophthalmoplegia.

Results: Sarcopenia (age and atrophy) had reduced mean activities of mitochondrial Complexes I, II, and II+III, with severe reduction of Complex I activity in 54% of patients.

Myovascular innervation: axon loss in small-fiber neuropathies.

Introduction: Vascular denervation occurs in some neuropathies, but measurement of small perivascular axons has been difficult.

Methods: We evaluated 31 consecutive patients who had both muscle and skin biopsies. We quantitated myovascular innervation by staining unmyelinated axons with peripherin and non-myelinating Schwann cells with neural cell adhesion molecule and comparing their areas.

Rapamycin nanoparticles target defective autophagy in muscular dystrophy to enhance both strength and cardiac function.

Duchenne muscular dystrophy in boys progresses rapidly to severe impairment of muscle function and death in the second or third decade of life. Current supportive therapy with corticosteroids results in a modest increase in strength as a consequence of a general reduction in inflammation, albeit with potential untoward long-term side effects and ultimate failure of the agent to maintain strength. Here, we demonstrate that alternative approaches that rescue defective autophagy in mdx mice, a model of Duchenne muscular dystrophy, with the use of rapamycin-loaded nanoparticles induce a reproducible increase in both skeletal muscle strength and cardiac contractile performance that is not achievable with conventional oral rapamycin, even in pharmacological doses.

Sensitive ultrasonic delineation of steroid treatment in living dystrophic mice with energy-based and entropy-based radio frequency signal processing.

Duchenne muscular dystrophy is a severe wasting disease, involving replacement of necrotic muscle tissue by fibrous material and fatty infiltrates. One primary animal model of this human disease is the X chromosome-linked mdx strain of mice. The goals of the present work were to validate and quantify the capability of both energy and entropy metrics of radio-frequency ultrasonic backscatter to differentiate among normal, dystrophic, and steroid-treated skeletal muscle in the mdx model.

RAG2 gene knockout in mice causes fatigue.

The effect of a disrupted immune system on the neuromuscular system is poorly characterized. We compared the strength and fatigue of RAG2(-/-) mice, which lack T-cells and B-cells, with immune intact controls. RAG2(-/-) mice demonstrated fatigue with shorter inverted hang-times (HT) and voluntary wheel-running (VWR) distance and total run times; they increased body weight more slowly but had proportionally normal forelimb grip strength (FGS) and VWR speed.

Strength and corticosteroid responsiveness of mdx mice is unchanged by RAG2 gene knockout.

Corticosteroids improve muscle function in boys with Duchenne muscular dystrophy and mdx mice possibly via effects on T-cell and B-cells. We quantified T-cell/B-cell functional effects and refined prednisolone's therapeutic mechanism in mdx mice. RAG2(-/-) mice, which produce no T-cells or B-cells, were crossed with mdx mice, which lack dystrophin protein.

Weekly oral prednisolone improves survival and strength in male mdx mice.

Although corticosteroids alleviate weakness in mdx mice, no long-term treatment has determined whether this benefit is maintained. We studied mdx mice forelimb grip strength and fatigue from 3 through 84 weeks and followed survival through 104 weeks. The mdx mice were given twice weekly oral prednisolone (5 mg/kg) beginning at 3 or 4 weeks.

Brain-derived neurotrophic factor and autoantibodies to neural antigens in sera of children with autistic spectrum disorders, Landau-Kleffner syndrome, and epilepsy.

Background: Brain derived neurotrophic factor (BDNF) elevation in newborn sera predicts intellectual/social developmental abnormalities. Other autoantibodies (AAs) to endothelial cells (ECs) and myelin basic protein (MBP) are also elevated in some children. We tested relationships between BDNF, BDNF AAs, and other AAs in children with these disorders.

Perception and reality: a national evaluation of social norms marketing interventions to reduce college students' heavy alcohol use.

Objective: To evaluate a widely used intervention to reduce college student alcohol use, we studied student drinking patterns at colleges that employed social norms marketing programs and those that did not.

Method: We examined responses of students in the Harvard School of Public Health College Alcohol Study (CAS) 1997, 1999 and 2001 data sets at 37 colleges that employed social norms marketing programs and at 61 that did not. Information about the students' drinking behavior and their familiarity with social norms marketing messages at their schools was analyzed, as were college administrators' reports about the implementation of social norms marketing campaigns.

Complement 3 deficiency and oral prednisolone improve strength and prolong survival of laminin alpha2-deficient mice.

Complement deposition and macrophages are common in biopsies of children with muscular dystrophy. While the presumed roles of complement and macrophages have been those of scavenger to remove and clear necrotic fibers, there is some evidence that they play a primary role in the pathogenesis of these diseases. Here, we explore the role of complement in the pathogenesis of the most severe animal model of congenital dystrophy, the dy-/- mouse, which is laminin alpha2-deficient.