Sanford Levine

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BACKGROUND The combination of complete diaphragm inactivity and mechanical ventilation (for more than 18 hours) elicits disuse atrophy of myofibers in animals. We hypothesized that the same may also occur in the human diaphragm. METHODS We obtained biopsy specimens from the costal diaphragms of 14 brain-dead organ donors before organ harvest (case(More)
Glycolysis is the initial step of glucose catabolism and is up-regulated in cancer cells (the Warburg Effect). Such shifts toward a glycolytic phenotype have not been explored widely in other biological systems, and the molecular mechanisms underlying the shifts remain unknown. With proteomics, we observed increased glycolysis in disused human diaphragm(More)
BACKGROUND Patients with heart failure (HF) frequently experience exertional dyspnea. Using near-infrared spectroscopy, we have previously demonstrated accessory respiratory muscle deoxygenation during exercise in these patients by monitoring changes in light absorption at 760-800 nm. METHODS AND RESULTS To investigate whether low-frequency respiratory(More)
BACKGROUND In patients with severe chronic obstructive pulmonary disease, the diaphragm undergoes physiologic adaptations characterized by an increase in energy expenditure and relative resistance to fatigue. We hypothesized that these physiologic characteristics would be associated with structural adaptations consisting of an increased proportion of(More)
RATIONALE Patients on mechanical ventilation who exhibit diaphragm inactivity for a prolonged time (case subjects) develop decreases in diaphragm force-generating capacity accompanied by diaphragm myofiber atrophy. OBJECTIVES Our objectives were to test the hypotheses that increased proteolysis by the ubiquitin-proteasome pathway, decreases in myosin(More)
OBJECTIVES We sought to investigate whether reduced respiratory muscle endurance contributes to increased dyspnea and decreased exercise capacity in patients with chronic heart failure. BACKGROUND In patients with heart failure, the sensation of dyspnea may be related to abnormalities of respiratory muscle function, such as diminished strength or(More)
BACKGROUND During rest and exercise, patients with heart failure hyperventilate; therefore, the diaphragm can be viewed as undergoing constant moderate-intensity exercise. Accordingly, we hypothesized that heart failure elicits adaptations in the diaphragm similar to those elicited by endurance exercise in the limb muscles of normal subjects. METHODS AND(More)
BACKGROUND Diminished respiratory muscle strength and endurance have been demonstrated in patients with heart failure. This may contribute to exertional dyspnea and reduced exercise capacity in these patients. The purpose of this study was to investigate whether selective respiratory muscle training could alleviate dyspnea and improve exercise performance(More)
OBJECTIVES Previous workers have demonstrated that controlled mechanical ventilation results in diaphragm inactivity and elicits a rapid development of diaphragm weakness as a result of both contractile dysfunction and fiber atrophy. Limited data exist regarding the impact of pressure support ventilation, a commonly used mode of mechanical ventilation-that(More)