8 research outputs found
Co-ingestion of leucine with protein does not further augment post-exercise muscle protein synthesis rates in elderly men
Get PDFMurine muscles deficient in creatine kinase tolerate repeated series of high-intensity contractions
No full textCombined ingestion of protein and free leucine with carbohydrate increases postexercise muscle protein synthesis in vivo in male subjects
No full textCo-ingestion of leucine with protein does not further augment post-exercise muscle protein synthesis rates in elderly men
No full textDeletion of the hypoxia-response element in the vascular endothelial growth factor promoter causes motor neuron degeneration
No full textHypoxia stimulates angiogenesis through the binding of hypoxia-inducible factors to the hypoxia-response element in the vascular endothelial growth factor (Vegf) promotor. Here, we report that deletion of the hypoxia-response element in the Vegf promotor reduced hypoxic Vegf expression in the spinal cord and caused adult-onset progressive motor neuron degeneration, reminiscent of amyotrophic lateral sclerosis, The neurodegeneration seemed to be due to reduced neural vascular perfusion. In addition. Vegf(165) promoted survival of motor neurons during hypoxia through binding to Vegf receptor 2 and neuropilin 1. Acute ischemia is known to cause nonselective neuronal death. Our results indicate that chronic vascular insufficiency and, possibly, insufficient Vegf-dependent neuroprotection lead to the select degeneration of motor neurons
Co-ingestion of protein and leucine stimulates muscle protein synthesis rates to the same extent in young and elderly lean men
No full textDeletion of the hypoxia-response element in the vascular endothelial growth factor promoter causes motor neuron degeneration
No full textHypoxia stimulates angiogenesis through the binding of hypoxia-inducible factors to the hypoxia-response element in the vascular endothelial growth factor (Vegf) promotor. Here, we report that deletion of the hypoxia-response element in the Vegf promotor reduced hypoxic Vegf expression in the spinal cord and caused adult-onset progressive motor neuron degeneration, reminiscent of amyotrophic lateral sclerosis, The neurodegeneration seemed to be due to reduced neural vascular perfusion. In addition. Vegf(165) promoted survival of motor neurons during hypoxia through binding to Vegf receptor 2 and neuropilin 1. Acute ischemia is known to cause nonselective neuronal death. Our results indicate that chronic vascular insufficiency and, possibly, insufficient Vegf-dependent neuroprotection lead to the select degeneration of motor neurons
