Serum from human burn victims impairs myogenesis and protein synthesis in primary myoblasts
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S. Windham | J. Cross | M. Bamman | Michael J Stec | E. Merritt | Michael J. Stec | Steven J. Thomas | Katie L. Corrick
[1] David J. Kosek,et al. Heightened muscle inflammation susceptibility may impair regenerative capacity in aging humans. , 2013, Journal of applied physiology.
[2] S. Windham,et al. Increased Expression of Atrogenes and TWEAK Family Members after Severe Burn Injury in Nonburned Human Skeletal Muscle , 2013, Journal of burn care & research : official publication of the American Burn Association.
[3] T. Walters,et al. Skeletal muscle satellite cell activation following cutaneous burn in rats. , 2013, Burns : journal of the International Society for Burn Injuries.
[4] D. Herndon,et al. Whole body and skeletal muscle protein turnover in recovery from burns. , 2013, International journal of burns and trauma.
[5] M. Bamman,et al. Characterization and regulation of mechanical loading-induced compensatory muscle hypertrophy. , 2012, Comprehensive Physiology.
[6] Chibeza C. Agley,et al. An Image Analysis Method for the Precise Selection and Quantitation of Fluorescently Labeled Cellular Constituents , 2012, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.
[7] D. Sabatini,et al. mTOR Signaling in Growth Control and Disease , 2012, Cell.
[8] J. Cross,et al. Inflammatory and Protein Metabolism Signaling Responses in Human Skeletal Muscle After Burn Injury , 2012, Journal of burn care & research : official publication of the American Burn Association.
[9] D. Herndon,et al. Long-Term Persistance of the Pathophysiologic Response to Severe Burn Injury , 2011, PloS one.
[10] C. Lang,et al. mTor signaling in skeletal muscle during sepsis and inflammation: where does it all go wrong? , 2011, Physiology.
[11] D. Hatef,et al. Pathophysiologic Response to Severe Burn Injury , 2009 .
[12] Philippe Pierre,et al. SUnSET, a nonradioactive method to monitor protein synthesis , 2009, Nature Methods.
[13] C. Finnerty,et al. Burn size determines the inflammatory and hypermetabolic response , 2006, Critical care.
[14] D. Herndon,et al. Post burn muscle wasting and the effects of treatments. , 2005, The international journal of biochemistry & cell biology.
[15] D. Cooper,et al. IL-6-induced skeletal muscle atrophy. , 2005, Journal of applied physiology.
[16] M. Molinaro,et al. Tumor necrosis factor-alpha gene transfer induces cachexia and inhibits muscle regeneration. , 2005, Genesis.
[17] R. Tompkins,et al. Support of the metabolic response to burn injury , 2004, The Lancet.
[18] Valerie Horsley,et al. Forming a Multinucleated Cell: Molecules That Regulate Myoblast Fusion , 2004, Cells Tissues Organs.
[19] W. Mitch,et al. Activation of caspase-3 is an initial step triggering accelerated muscle proteolysis in catabolic conditions. , 2004, The Journal of clinical investigation.
[20] G. Pavlath,et al. IL-4 Acts as a Myoblast Recruitment Factor during Mammalian Muscle Growth , 2003, Cell.
[21] R. Slack,et al. Caspase 3 activity is required for skeletal muscle differentiation , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[22] D. Chinkes,et al. Persistence of muscle catabolism after severe burn. , 2000, Surgery.
[23] E. Engvall,et al. Binding of ADAM12, a Marker of Skeletal Muscle Regeneration, to the Muscle-specific Actin-binding Protein, α-Actinin-2, Is Required for Myoblast Fusion* , 2000, The Journal of Biological Chemistry.
[24] D. Chinkes,et al. Muscle protein catabolism after severe burn: effects of IGF-1/IGFBP-3 treatment. , 1999, Annals of surgery.
[25] R. Demling,et al. ANTICATABOLIC AND ANABOLIC STRATEGIES IN CRITICAL ILLNESS: A REVIEW OF CURRENT TREATMENT MODALITIES , 1998, Shock.
[26] E. Duda,et al. TNF inhibits myogenesis and downregulates the expression of myogenic regulatory factors myoD and myogenin. , 1997, European journal of cell biology.
[27] J. Darnell,et al. Maximal activation of transcription by statl and stat3 requires both tyrosine and serine phosphorylation , 1995, Cell.
[28] D. Ownby. The Whole Body , 1995 .
[29] M. Vance,et al. Growth hormone and cortisol secretion in patients with burn injury. , 1992, The Journal of burn care & rehabilitation.
[30] N. Skakkebaek,et al. Insulin-like growth factor 1 (IGF-1) in burn patients. , 1991, Burns : journal of the International Society for Burn Injuries.
[31] G. Gundersen,et al. Generation of a stable, posttranslationally modified microtubule array is an early event in myogenic differentiation , 1989, The Journal of cell biology.
[32] S. Shackford,et al. Cardiovascular and neurohumoral responses following burn injury. , 1989, Archives of surgery.
[33] R. Wolfe. Review: acute versus chronic response to burn injury. , 1981, Circulatory shock.
[34] D. Wilmore,et al. Metabolic changes in burned patients. , 1978, The Surgical clinics of North America.