Inflammation-Induced Acute Phase Response in Skeletal Muscle and Critical Illness Myopathy
暂无分享,去创建一个
G. Dittmar | H. Schulz | N. Hubner | C. Spies | G. Butler-Browne | V. Mouly | T. Wollersheim | S. Weber-Carstens | M. Boschmann | K. Saar | J. Spranger | S. Labeit | J. Fielitz | S. Spuler | S. Koch | M. Krebs | Jida Hamati | D. Lodka | Claudia Langhans | Xiaoxi Zhu | Melanie Kny | F. Schmidt | Franziska Schmidt
[1] U. Machado,et al. Identification of nuclear factor-κB sites in the Slc2a4 gene promoter , 2013, Molecular and Cellular Endocrinology.
[2] Andreas Marg,et al. Critical illness myopathy and GLUT4: significance of insulin and muscle contraction. , 2013, American journal of respiratory and critical care medicine.
[3] C. Sprung,et al. Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock, 2012 , 2013, Intensive Care Medicine.
[4] J. Kress,et al. Medical and Economic Implications of Physical Disability of Survivorship , 2012, Seminars in Respiratory and Critical Care Medicine.
[5] C. Spies,et al. Early type II fiber atrophy in intensive care unit patients with nonexcitable muscle membrane , 2012, Critical care medicine.
[6] F. Filippin-Monteiro,et al. Serum amyloid A is a growth factor for 3T3-L1 adipocytes, inhibits differentiation and promotes insulin resistance , 2011, International Journal of Obesity.
[7] T. Zimmers,et al. STAT3 Activation in Skeletal Muscle Links Muscle Wasting and the Acute Phase Response in Cancer Cachexia , 2011, PloS one.
[8] J. Kirk-Bayley,et al. Functional Disability 5 Years after Acute Respiratory Distress Syndrome , 2011 .
[9] Alexander Doyle,et al. Toll‐like receptor 4 mediates lipopolysaccharide‐induced muscle catabolism via coordinate activation of ubiquitin‐proteasome and autophagy‐lysosome pathways , 2011, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[10] K. Wernecke,et al. Critical illness myopathy is frequent: accompanying neuropathy protracts ICU discharge , 2010, Journal of Neurology, Neurosurgery & Psychiatry.
[11] C. Winkelman. The role of inflammation in ICU-acquired weakness , 2010, Critical care.
[12] K. Wernecke,et al. Risk factors in critical illness myopathy during the early course of critical illness: a prospective observational study , 2010, Critical care.
[13] J. Kinsella,et al. Nonexcitable muscle membrane predicts intensive care unit-acquired paresis in mechanically ventilated, sedated patients. , 2010, Critical care medicine.
[14] G. Supinski,et al. Sepsis-induced myopathy. , 2009, Critical care medicine.
[15] W. Mitch,et al. IL-6 and serum amyloid A synergy mediates angiotensin II-induced muscle wasting. , 2009, Journal of the American Society of Nephrology : JASN.
[16] G. Schuler,et al. Induction of MuRF1 is essential for TNF-alpha-induced loss of muscle function in mice. , 2008, Journal of molecular biology.
[17] S. Lemeshow,et al. Acquired weakness, handgrip strength, and mortality in critically ill patients. , 2008, American journal of respiratory and critical care medicine.
[18] D. Rittirsch,et al. Immunodesign of experimental sepsis by cecal ligation and puncture , 2008, Nature Protocols.
[19] Mi-Sung Kim,et al. Myosin accumulation and striated muscle myopathy result from the loss of muscle RING finger 1 and 3. , 2007, The Journal of clinical investigation.
[20] O. Friedrich. Critical illness myopathy: what is happening? , 2006, Current opinion in clinical nutrition and metabolic care.
[21] J. Lefaucheur,et al. Origin of ICU acquired paresis determined by direct muscle stimulation , 2005, Journal of Neurology, Neurosurgery & Psychiatry.
[22] D. West,et al. Serum Amyloid A-Luciferase Transgenic Mice: Response to Sepsis, Acute Arthritis, and Contact Hypersensitivity and the Effects of Proteasome Inhibition , 2005, The Journal of Immunology.
[23] C. Leeuwenburgh,et al. Muscle fiber‐specific apoptosis and TNF‐α signaling in sarcopenia are attenuated by life‐long calorie restriction , 2005, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[24] T. Zimmers,et al. Massive liver growth in mice induced by systemic interleukin 6 administration , 2003, Hepatology.
[25] Isabelle Durand-Zaleski,et al. Paresis acquired in the intensive care unit: a prospective multicenter study. , 2002, JAMA.
[26] A. Whitehead,et al. Serum amyloid A, the major vertebrate acute-phase reactant. , 1999, European journal of biochemistry.
[27] Griffiths,et al. Muscle fibre atrophy in critically ill patients is associated with the loss of myosin filaments and the presence of lysosomal enzymes and ubiquitin , 1998, Neuropathology and applied neurobiology.
[28] K. Sletten,et al. Mouse serum amyloid A (SAA) proteins isolated by two‐dimensional electrophoresis: characterization of isotypes and the effect of separate and combined administrations of cytokines, dexamethasone and lipopolysaccharide (LPS) on serum levels and isotype distribution , 1998, Clinical and experimental immunology.
[29] S. Anker,et al. Tumor necrosis factor and steroid metabolism in chronic heart failure: possible relation to muscle wasting. , 1997, Journal of the American College of Cardiology.
[30] M. Kindy,et al. Structure of the mouse Saa4 gene and its linkage to the serum amyloid A gene family. , 1996, Genomics.
[31] M. Rich,et al. Muscle is electrically inexcitable in acute quadriplegic myopathy , 1996, Neurology.
[32] M. Yano,et al. Interleukin 6 receptor antibody inhibits muscle atrophy and modulates proteolytic systems in interleukin 6 transgenic mice. , 1996, The Journal of clinical investigation.
[33] A. Whitehead,et al. A constitutively expressed serum amyloid A protein gene (SAA4) is closely linked to, and shares structural similarities with, an acute-phase serum amyloid A protein gene (SAA2). , 1993, Genomics.
[34] C. Bolton,et al. The neurological complications of sepsis , 1993, Annals of neurology.
[35] P Franchimont,et al. Cytokine serum level during severe sepsis in human IL-6 as a marker of severity. , 1992, Annals of surgery.
[36] J. Fischer,et al. Evidence that tumor necrosis factor participates in the regulation of muscle proteolysis during sepsis. , 1992, Archives of surgery.
[37] M. Goodman. Tumor necrosis factor induces skeletal muscle protein breakdown in rats. , 1991, The American journal of physiology.
[38] A. Waage,et al. ASSOCIATION BETWEEN TUMOUR NECROSIS FACTOR IN SERUM AND FATAL OUTCOME IN PATIENTS WITH MENINGOCOCCAL DISEASE , 1987, The Lancet.
[39] D. Potter,et al. Structure of the murine serum amyloid A gene family. Gene conversion. , 1986, The Journal of biological chemistry.
[40] A. Forrest,et al. Letter: Procaine and malignant hyperthermia. , 1974, Lancet.