Progress in clinical neurosciences: sepsis-associated encephalopathy: evolving concepts.
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The Optimal Management of Acute Febrile Encephalopathy in the Aged Patient: A Systematic ReviewYear in review 2010: Critical Care--Neurocritical careNeurodegenerative evidence in mice brains with cecal ligation and puncture-induced sepsis: preventive effect of the free radical scavenger edaravoneTranscranial doppler assessment of cerebral perfusion in critically ill septic patients: a pilot study.Assessment of blood-brain barrier function and the neuroinflammatory response in the rat brain by using cerebral open flow microperfusion (cOFM)Human severe sepsis cytokine mixture increases β2-integrin-dependent polymorphonuclear leukocyte adhesion to cerebral microvascular endothelial cells in vitro.Early prediction and outcome of septic encephalopathy in acute stroke patients with nosocomial coma.Sepsis: multiple abnormalities, heterogeneous responses, and evolving understanding.Metabolic theory of septic shock.No Awakening in Supratentorial Intracerebral Hemorrhage Is Potentially Caused by Sepsis-Associated Encephalopathy.Risk factors for nosocomial nontraumatic coma: sepsis and respiratory failure.Transcranial Doppler to assess sepsis-associated encephalopathy in critically ill patients.Assessment of cerebral circulation in a porcine model of intravenously given E. coli induced fulminant sepsis.Impaired cerebrovascular reactivity in sepsis-associated encephalopathy studied by acetazolamide test.Role of endothelial nitric oxide synthase-derived nitric oxide in activation and dysfunction of cerebrovascular endothelial cells during early onsets of sepsis.Methods of monitoring shock.Sepsis-associated encephalopathySepsis causes neuroinflammation and concomitant decrease of cerebral metabolism.Sparing brain damage in severe sepsis: a beginning.Endotoxemia-induced inflammation and the effect on the human brain.Endotoxin-induced lung alveolar cell injury causes brain cell damage.Agomelatine Protection in an LPS-Induced Psychosis-Relevant Behavior Model.Acetazolamide-induced cerebrovascular reactivity is impaired in sepsis-associated encephalopathy.Receptor for advanced glycation end products mediates sepsis-triggered amyloid-β accumulation, Tau phosphorylation, and cognitive impairment.Sepsis Associated Encephalopathy.Inhibition of microRNA-155 modulates endotoxin tolerance by upregulating suppressor of cytokine signaling 1 in microglia.
P2860
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P2860
Progress in clinical neurosciences: sepsis-associated encephalopathy: evolving concepts.
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2003 nî lūn-bûn
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2003 թուականի Մայիսին հրատարակուած գիտական յօդուած
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2003 թվականի մայիսին հրատարակված գիտական հոդված
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2003年の論文
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Progress in clinical neurosciences: sepsis-associated encephalopathy: evolving concepts.
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Progress in clinical neurosciences: sepsis-associated encephalopathy: evolving concepts.
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Progress in clinical neurosciences: sepsis-associated encephalopathy: evolving concepts.
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Progress in clinical neurosciences: sepsis-associated encephalopathy: evolving concepts.
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Progress in clinical neurosciences: sepsis-associated encephalopathy: evolving concepts.
@ast
Progress in clinical neurosciences: sepsis-associated encephalopathy: evolving concepts.
@en
P1476
Progress in clinical neurosciences: sepsis-associated encephalopathy: evolving concepts.
@en
P2093
G Bryan Young
John X Wilson
P304
P577
2003-05-01T00:00:00Z