Ucf-101 protects against cerebral oxidative injury and cognitive impairment in septic rat.

[1]  J. Quevedo,et al.  Caspase-3 Mediates In Part Hippocampal Apoptosis in Sepsis , 2013, Molecular Neurobiology.

[2]  Ye Chen,et al.  Hydrogen-rich saline reverses oxidative stress, cognitive impairment, and mortality in rats submitted to sepsis by cecal ligation and puncture. , 2012, The Journal of surgical research.

[3]  M. Ziaja.  Sepsis and septic encephalopathy: characteristics and experimental models. , 2012, Folia neuropathologica.

[4]  G. B. Young,et al.  Sepsis-associated encephalopathy , 2012, Nature Reviews Neurology.

[5]  Russell R. Miller,et al.  The association between brain volumes, delirium duration, and cognitive outcomes in intensive care unit survivors: The VISIONS cohort magnetic resonance imaging study* , 2012, Critical care medicine.

[6]  J. Frontera.  Metabolic Encephalopathies in the Critical Care Unit , 2012, Continuum.

[7]  M. Bonten,et al.  Classification of sepsis, severe sepsis and septic shock: the impact of minor variations in data capture and definition of SIRS criteria , 2012, Intensive Care Medicine.

[8]  Q. Guo,et al.  Epidemiological features and risk factors of sepsis-associated encephalopathy in intensive care unit patients: 2008-2011. , 2012, Chinese medical journal.

[9]  Yunlan Ni,et al.  Ghrelin prevents neuronal apoptosis and cognitive impairments in sepsis-associated encephalopathy , 2011, Neuroreport.

[10]  Dong Sun Kim,et al.  Omi/HtrA2 protease is associated with tubular cell apoptosis and fibrosis induced by unilateral ureteral obstruction. , 2010, American journal of physiology. Renal physiology.

[11]  Y. Lou,et al.  The induction of reactive oxygen species and loss of mitochondrial Omi/HtrA2 is associated with S-nitrosoglutathione-induced apoptosis in human endothelial cells. , 2010, Toxicology and applied pharmacology.

[12]  E. Masliah,et al.  Molecular mechanisms of neurodegeneration in Alzheimer's disease. , 2010, Human molecular genetics.

[13]  J. Downward,et al.  Enhanced HtrA2/Omi expression in oxidative injury to retinal pigment epithelial cells and murine models of neurodegeneration. , 2009, Investigative ophthalmology & visual science.

[14]  Shanshan Yang,et al.  UCF‐101, A Novel Omi/HtrA2 Inhibitor, Protects Against Cerebral Ischemia/Reperfusion Injury in Rats , 2009, Anatomical record.

[15]  K. Fukunaga,et al.  Mitochondrial serine protease HtrA2/Omi as a potential therapeutic target. , 2009, Current drug targets.

[16]  H. Sebai,et al.  Protective effect of resveratrol against lipopolysaccharide-induced oxidative stress in rat brain , 2009, Brain injury.

[17]  J. Quevedo,et al.  Mitochondrial respiratory chain and creatine kinase activities in rat brain after sepsis induced by cecal ligation and perforation. , 2008, Mitochondrion.

[18]  J. Downward,et al.  The protease inhibitor Ucf-101 induces cellular responses independently of its known target, HtrA2/Omi , 2006, Cell Death and Differentiation.

[19]  C. Vorhees,et al.  Morris water maze: procedures for assessing spatial and related forms of learning and memory , 2006, Nature Protocols.

[20]  J. Quevedo,et al.  Oxidative variables in the rat brain after sepsis induced by cecal ligation and perforation , 2006, Critical care medicine.

[21]  D. Rigamonti,et al.  Prevention of cytosolic IAPs degradation: a potential pharmacological target in Huntington's Disease. , 2005, Pharmacological research.

[22]  T. Evans,et al.  Redox regulation of neutrophil apoptosis and the systemic inflammatory response syndrome. , 2005, Clinical science.

[23]  E. Alnemri,et al.  Omi/HtrA2 protease mediates cisplatin-induced cell death in renal cells. , 2005, American journal of physiology. Renal physiology.

[24]  E. Alnemri,et al.  Role of Omi/HtrA2 in Apoptotic Cell Death After Myocardial Ischemia and Reperfusion , 2005, Circulation.

[25]  M. Deckert,et al.  An Essential Role for Tumor Necrosis Factor in the Formation of Experimental Murine Staphylococcus aureus-Induced Brain Abscess and Clearance , 2005, Journal of neuropathology and experimental neurology.

[26]  J. Quevedo,et al.  Cognitive impairment in sepsis survivors from cecal ligation and perforation* , 2005, Critical care medicine.

[27]  S. Moochhala,et al.  Role of inflammatory mediators in the pathophysiology of acute respiratory distress syndrome , 2004, The Journal of pathology.

[28]  G. Wenk.  Assessment of Spatial Memory Using the Radial Arm Maze and Morris Water Maze , 2004, Current protocols in neuroscience.

[29]  S. Srinivasula,et al.  Characterization of a Novel and Specific Inhibitor for the Pro-apoptotic Protease Omi/HtrA2* , 2003, The Journal of Biological Chemistry.

[30]  S. Husain,et al.  Oxidants, antioxidants and carcinogenesis. , 2002, Indian journal of experimental biology.

[31]  L. Martins.  The serine protease Omi/HtrA2: a second mammalian protein with a Reaper-like function , 2002, Cell Death and Differentiation.

[32]  Arthur S Slutsky,et al.  Oxygen free radicals in ARDS, septic shock and organ dysfunction , 2000, Intensive Care Medicine.

[33]  J C Reed,et al.  IAP family proteins--suppressors of apoptosis. , 1999, Genes & development.

[34]  S. Strickland,et al.  Neuronal Death in the Hippocampus Is Promoted by Plasmin-Catalyzed Degradation of Laminin , 1997, Cell.

[35]  A. Yakovlev,et al.  Activation of CPP32-Like Caspases Contributes to Neuronal Apoptosis and Neurological Dysfunction after Traumatic Brain Injury , 1997, The Journal of Neuroscience.

[36]  S. Leib,et al.  Reactive oxygen intermediates contribute to necrotic and apoptotic neuronal injury in an infant rat model of bacterial meningitis due to group B streptococci. , 1996, The Journal of clinical investigation.

[37]  M. Uchiyama,et al.  Determination of malonaldehyde precursor in tissues by thiobarbituric acid test. , 1978, Analytical biochemistry.

[38]  H. Aebi,et al.  Catalase in vitro. , 1984, Methods in enzymology.

[39]  G. Paxinos,et al.  The Rat Brain in Stereotaxic Coordinates , 1983 .