Induction of mitochondrial dysfunction in patients under cardiopulmonary by-pass: preliminary results.
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R. Trentadue | G. Dipalma | F. Inchingolo | L. Santacroce | A. Gnoni | A. Ballini | N. Brienza | S. Scacco | N. Sardaro | A. Massari | P. Ferrara | F. Taurino | F. Massaro
[1] V. Rybakov,et al. Systemic inflammatory response in cardiac surgery , 2021, Anesteziologiya i reanimatologiya.
[2] Y. Wen,et al. Regulation by Pink1 on the mitochondrial dysfunction in endothelial cells post the hypoxia mimetic agent CoCl2 treatment. , 2018, European review for medical and pharmacological sciences.
[3] Q. He,et al. Mitochondria-mediated disturbance of fatty acid metabolism in proximal tubule epithelial cells leads to renal interstitial fibrosis. , 2018, European review for medical and pharmacological sciences.
[4] A. Gnoni,et al. Systematic review of plasma-membrane ecto-ATP synthase: A new player in health and disease. , 2018, Experimental and molecular pathology.
[5] All trans retinoic acid depresses the content and activity of the mitochondrial ATP synthase in human keratinocytes. , 2017, Biochemical and biophysical research communications.
[6] F. Damiano,et al. Acute administration of 3,5-diiodo-L-thyronine to hypothyroid rats stimulates bioenergetic parameters in liver mitochondria , 2016, Journal of Bioenergetics and Biomembranes.
[7] S. Papa,et al. Function and expression study uncovered hepatocyte plasma membrane ecto-ATP synthase as a novel player in liver regeneration. , 2016, The Biochemical journal.
[8] A. De Grassi,et al. Prediction of high- and low-affinity quinol-analogue-binding sites in the aa3 and bo3 terminal oxidases from Bacillus subtilis and Escherichia coli1. , 2014, The Biochemical journal.
[9] A. Corcelli,et al. Relationship between cardiolipin metabolism and oxygen availability in Bacillus subtilis☆ , 2013, FEBS open bio.
[10] S. Papa,et al. 3,5-Diiodo-L-Thyronine Administration To Hypothyroid Rats Rapidly Enhances Fatty Acid Oxidation Rate and Bioenergetic Parameters in Liver Cells , 2013, PloS one.
[11] R. Trentadue,et al. Induction of mitochondrial dysfunction and oxidative stress in human fibroblast cultures exposed to serum from septic patients. , 2012, Life sciences.
[12] S. Papa,et al. Mitochondrial proteome analysis reveals depression of the Ndufs3 subunit and activity of complex I in diabetic rat brain. , 2012, Journal of proteomics.
[13] Antonio Gnoni,et al. Respiratory chain complex I, a main regulatory target of the cAMP/PKA pathway is defective in different human diseases , 2012, FEBS letters.
[14] H. Tomita,et al. Novel pro-atherogenic molecule coupling factor 6 is elevated in patients with stroke: A possible linkage to homocysteine , 2010, Annals of medicine.
[15] S. Carr,et al. A Mitochondrial Protein Compendium Elucidates Complex I Disease Biology , 2008, Cell.
[16] N. Mariappan,et al. TNF-alpha-induced mitochondrial oxidative stress and cardiac dysfunction: restoration by superoxide dismutase mimetic Tempol. , 2007, American journal of physiology. Heart and circulatory physiology.
[17] R. Levy. MITOCHONDRIAL DYSFUNCTION, BIOENERGETIC IMPAIRMENT, AND METABOLIC DOWN-REGULATION IN SEPSIS , 2007, Shock.
[18] Chao-shu Tang,et al. Plasma level of mitochondrial coupling factor 6 increases in patients with type 2 diabetes mellitus. , 2007, International journal of cardiology.
[19] Chao-shu Tang,et al. Plasma level of mitochondrial coupling factor 6 increases in patients with coronary heart disease. , 2007, Circulation journal : official journal of the Japanese Circulation Society.
[20] V. Petruzzella,et al. Dysfunctions of Cellular Oxidative Metabolism in Patients with Mutations in the NDUFS1 and NDUFS4 Genes of Complex I* , 2006, Journal of Biological Chemistry.
[21] E. Holler,et al. Endothelial apoptosis and circulating endothelial cells after bypass grafting with and without cardiopulmonary bypass. , 2006, European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery.
[22] J. Parrillo,et al. Human Serum from Patients with Septic Shock Activates Transcription Factors STAT1, IRF1, and NF-κB and Induces Apoptosis in Human Cardiac Myocytes* , 2005, Journal of Biological Chemistry.
[23] M. Ranucci,et al. Oxygen delivery during cardiopulmonary bypass and acute renal failure after coronary operations. , 2005, The Annals of thoracic surgery.
[24] J. Vincent,et al. The SOFA (Sepsis-related Organ Failure Assessment) score to describe organ dysfunction/failure , 1996, Intensive Care Medicine.
[25] I. Chaudry,et al. THE ROLE OF THE MITOCHONDRION IN TRAUMA AND SHOCK , 2004, Shock.
[26] Chao-shu Tang,et al. Plasma mitochondrial coupling factor 6 in patients with acute myocardial infarction. , 2004, Hypertension research : official journal of the Japanese Society of Hypertension.
[27] M. Fink. Bench-to-bedside review: Cytopathic hypoxia , 2002, Critical care.
[28] John Land,et al. Association between mitochondrial dysfunction and severity and outcome of septic shock , 2002, The Lancet.
[29] J. Gellerich,et al. Mitochondrial Dysfunction in Sepsis: Evidence from Bacteraemic Baboons and Endotoxaemic Rabbits , 2002, Bioscience reports.
[30] T. Yau,et al. Cardiopulmonary bypass induced inflammation: pathophysiology and treatment. An update. , 2002, European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery.
[31] S. Trumbeckaite,et al. Different sensitivity of rabbit heart and skeletal muscle to endotoxin-induced impairment of mitochondrial function. , 2001, European journal of biochemistry.
[32] M. Fink. Cytopathic hypoxia. Mitochondrial dysfunction as mechanism contributing to organ dysfunction in sepsis. , 2001, Critical care clinics.
[33] R. Martineau,et al. Outcome with high blood lactate levels during cardiopulmonary bypass in adult cardiac operation. , 2000, The Annals of thoracic surgery.
[34] S. Kirchner,et al. Endothelial apoptosis is induced by serum of patients after cardiopulmonary bypass. , 2000, European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery.
[35] F L Grover,et al. The Society of Thoracic Surgeons National Database: current status and future directions. , 1999, The Annals of thoracic surgery.
[36] K. Werdan,et al. Impaired energy metabolism in hearts of septic baboons: diminished activities of Complex I and Complex II of the mitochondrial respiratory chain. , 1999, Shock.
[37] G. Kroemer,et al. A revolution in apoptosis: from a nucleocentric to a mitochondriocentric perspective. , 1998, Experimental gerontology.
[38] G. Kroemer,et al. The mitochondrial death/life regulator in apoptosis and necrosis. , 1998, Annual review of physiology.
[39] G. Rocker,et al. The Systemic Inflammatory Response to Cardiopulmonary Bypass: Pathophysiological, Therapeutic, and Pharmacological Considerations , 1997, Anesthesia and analgesia.
[40] M. Fink. Cytopathic hypoxia in sepsis , 1997, Acta anaesthesiologica Scandinavica. Supplementum.
[41] G. Hill. The Inflammatory Response to Cardiopulmonary Bypass , 1996, International anesthesiology clinics.
[42] M. Kollef,et al. Determinants of mortality and multiorgan dysfunction in cardiac surgery patients requiring prolonged mechanical ventilation. , 1995, Chest.
[43] C. Piantadosi,et al. Altered mitochondrial redox responses in gram negative septic shock in primates. , 1994, Circulatory shock.
[44] I. L. Cohen. Guidelines for the use of innovative therapies in sepsis. , 1993, Critical care medicine.
[45] A. Boveris,et al. Time course and mechanism of oxidative stress and tissue damage in rat liver subjected to in vivo ischemia-reperfusion. , 1993, The Journal of clinical investigation.
[46] E. Draper,et al. APACHE II: A severity of disease classification system , 1985, Critical care medicine.