Pathophysiological Response to Burn Injury in Adults
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[1] M. Jeschke,et al. Impaired Immune Response in Elderly Burn Patients: New Insights Into the Immune-senescence Phenotype , 2016, Annals of surgery.
[2] M. Jeschke,et al. Burned Adults Develop Profound Glucose Intolerance , 2016, Critical care medicine.
[3] M. Jeschke,et al. Burn Induces Browning of the Subcutaneous White Adipose Tissue in Mice and Humans , 2015, Cell reports.
[4] M. Jeschke,et al. Pathophysiologic Response to Burns in the Elderly , 2015, EBioMedicine.
[5] J. Lord,et al. The systemic immune response to trauma: an overview of pathophysiology and treatment , 2014, The Lancet.
[6] M. Jeschke,et al. Leukocyte Infiltration and Activation of the NLRP3 Inflammasome in White Adipose Tissue Following Thermal Injury* , 2014, Critical care medicine.
[7] D. Herndon,et al. Hypoglycemia Is Associated With Increased Postburn Morbidity and Mortality in Pediatric Patients* , 2014, Critical care medicine.
[8] L. Sidossis,et al. Browning of subcutaneous white adipose tissue in humans after severe adrenergic stress (1160.5) , 2014, Cell metabolism.
[9] D. Herndon,et al. Occurrence of Multiorgan Dysfunction in Pediatric Burn Patients: Incidence and Clinical Outcome , 2014, Annals of surgery.
[10] R. Gamelli,et al. Mild Obesity Is Protective After Severe Burn Injury , 2013, Annals of surgery.
[11] F. Sutterwala,et al. Mitochondrial cardiolipin is required for Nlrp3 inflammasome activation. , 2013, Immunity.
[12] Robert Kraft,et al. Burn size and survival probability in paediatric patients in modern burn care: a prospective observational cohort study , 2012, The Lancet.
[13] A. Tardivel,et al. ER stress activates the NLRP3 inflammasome via an UPR-independent pathway , 2012, Cell Death and Disease.
[14] J. Tschopp,et al. The inflammasome: an integrated view , 2011, Immunological reviews.
[15] D. Herndon,et al. Insulin increases resistance to burn wound infection-associated sepsis , 2010, Critical care medicine.
[16] D. Herndon,et al. THE ROLE OF HYPERGLYCEMIA IN BURNED PATIENTS: EVIDENCE-BASED STUDIES , 2010, Shock.
[17] D. Herndon,et al. The hypermetabolic response to burn injury and interventions to modify this response. , 2009, Clinics in plastic surgery.
[18] D. Hatef,et al. Pathophysiologic Response to Severe Burn Injury , 2009 .
[19] D. Herndon,et al. CHARACTERIZATION OF THE INFLAMMATORY RESPONSE DURING ACUTE AND POST-ACUTE PHASES AFTER SEVERE BURN , 2008, Shock.
[20] D. Herndon,et al. Insulin Resistance Postburn: Underlying Mechanisms and Current Therapeutic Strategies , 2008, Journal of burn care & research : official publication of the American Burn Association.
[21] D. Herndon,et al. Gender Differences in Pediatric Burn Patients: Does It Make a Difference? , 2008, Annals of surgery.
[22] D. Herndon,et al. Abnormal insulin sensitivity persists up to three years in pediatric patients post-burn. , 2009, The Journal of clinical endocrinology and metabolism.
[23] R. Gamelli,et al. American Burn Association Consensus Conference to Define Sepsis and Infection in Burns , 2007, Journal of burn care & research : official publication of the American Burn Association.
[24] R. Gamelli,et al. Inflammation and Sepsis: Past, Present, and the Future , 2007, Journal of burn care & research : official publication of the American Burn Association.
[25] D. Herndon,et al. Propranolol does not increase inflammation, sepsis, or infectious episodes in severely burned children. , 2007, The Journal of trauma.
[26] C. Finnerty,et al. Burn size determines the inflammatory and hypermetabolic response , 2006, Critical care.
[27] T. Evans,et al. Glucose control and mortality in critically ill patients. , 2004, JAMA.
[28] D. Herndon,et al. Fatty infiltration of the liver in severely burned pediatric patients: autopsy findings and clinical implications. , 2001, The Journal of trauma.
[29] P. Hasselgren. Glucocorticoids and muscle catabolism. , 1999, Current opinion in clinical nutrition and metabolic care.
[30] J. Wang,et al. DEXAMETHASONE STIMULATES PROTEASOME- AND CALCIUM‐DEPENDENT PROTEOLYSIS IN CULTURED L6 MYOTUBES , 1998, Shock.
[31] J. Wang,et al. Energy-ubiquitin-dependent muscle proteolysis during sepsis in rats is regulated by glucocorticoids. , 1996, The Journal of clinical investigation.
[32] P. Hasselgren. Muscle protein metabolism during sepsis. , 1995, Biochemical Society transactions.
[33] D. Wilmore,et al. Hormonal responses and their effect on metabolism. , 1976, The Surgical clinics of North America.
[34] A. Mason,et al. Catecholamines: Znediator of the Hypermetabolic Response to Thermal Injury , 1974, Annals of surgery.
[35] B. Haynes,et al. Urinary output of adrenaline and noradrenaline in severe thermal burns. , 1957, Annals of surgery.
[36] D. Herndon,et al. Association of postburn fatty acids and triglycerides with clinical outcome in severely burned children. , 2013, The Journal of clinical endocrinology and metabolism.
[37] M. Goodall. Sympathetic nerve and adrenal medullary response to thermal burn. Clinical analysis of adrenaline and noradrenaline depletion. , 1966, The American surgeon.