Stress preconditioning attenuates oxidative injury to the alveolar epithelium of the lung following haemorrhage in rats - Wikidata - wikimedia - TriplyDB

Stress preconditioning attenuates oxidative injury to the alveolar epithelium of the lung following haemorrhage in rats

Stress preconditioning attenuates oxidative injury to the alveolar epithelium of the lung following haemorrhage in rats

http://www.wikidata.org/entity/Q28345091

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Inducible heat shock protein 70 kD and inducible nitric oxide synthase in hemorrhage/resuscitation-induced injury Hyperthermia promotes and prevents respiratory epithelial apoptosis through distinct mechanisms Activation of the heat shock response attenuates the interleukin 1β-mediated inhibition of the amiloride-sensitive alveolar epithelial ion transport Heat-shock response increases lung injury caused by Pseudomonas aeruginosa via an interleukin-10-dependent mechanism in mice.Organ preconditioning: the past, current status, and related lung studies Nadph oxidase regulates alveolar epithelial sodium channel activity and lung fluid balance in vivo via O⁻₂ signaling Combination therapy with HSP90 inhibitor 17-DMAG reconditions the tumor microenvironment to improve recruitment of therapeutic T cells.Extracellular heat shock protein 72 is a marker of the stress protein response in acute lung injury.The role of heat shock protein 90 in modulating ischemia-reperfusion injury in the kidney.Activation of the stress protein response inhibits the STAT1 signalling pathway and iNOS function in alveolar macrophages: role of Hsp90 and Hsp70.Heat shock protein 90-binding agents protect renal cells from oxidative stress and reduce kidney ischemia-reperfusion injury.Impact of haemorrhagic shock intensity on the dynamic of alarmins release in porcine poly-trauma animal model.17-DMAG diminishes hemorrhage-induced small intestine injury by elevating Bcl-2 protein and inhibiting iNOS pathway, TNF-α increase, and caspase-3 activation.Heat shock treatment protects against angiotensin II-induced hypertension and inflammation in aorta.Activation of heat shock response augments fibroblast growth factor-1 expression in wounded lung epithelium.Geldanamycin treatment inhibits hemorrhage-induced increases in KLF6 and iNOS expression in unresuscitated mouse organs: role of inducible HSP70.Geldanamycin prevents hemorrhage-induced ATP loss by overexpressing inducible HSP70 and activating pyruvate dehydrogenase.

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Stress preconditioning attenuates oxidative injury to the alveolar epithelium of the lung following haemorrhage in rats

http://www.wikidata.org/entity/Q28345091

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2002 nî lūn-bûn

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2002 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2002 թվականի հունվարին հրատարակված գիտական հոդված

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2002年の論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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name

Stress preconditioning attenua ...... following haemorrhage in rats

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Stress preconditioning attenua ...... following haemorrhage in rats

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Stress preconditioning attenua ...... following haemorrhage in rats

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Stress preconditioning attenua ...... following haemorrhage in rats

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Stress preconditioning attenua ...... following haemorrhage in rats

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Stress preconditioning attenua ...... following haemorrhage in rats

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Stress preconditioning attenua ...... following haemorrhage in rats

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Stress preconditioning attenua ...... following haemorrhage in rats

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Stress preconditioning attenua ...... following haemorrhage in rats

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JPHYSIOL.2001.013102

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The Journal of Physiology

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Stress preconditioning attenua ...... following haemorrhage in rats

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J F Pittet

http://www.w3.org/2001/XMLSchema#string

L N Lu

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M A Matthay

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T Geiser

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W J Welch

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P2860

Transcriptional repression of the prointerleukin 1beta gene by heat shock factor 1

Repression of heat shock transcription factor HSF1 activation by HSP90 (HSP90 complex) that forms a stress-sensitive complex with HSF1

Induction of the stress response in vivo decreases nuclear factor-kappa B activity in jejunal mucosa of endotoxemic mice.

Clinical implications of the stress response

Heat shock induces resistance in rat pancreatic islet cells against nitric oxide, oxygen radicals and streptozotocin toxicity in vitro.

Stimulation of lung epithelial liquid clearance by endogenous release of catecholamines in septic shock in anesthetized rats.

Essential role of induced nitric oxide in the initiation of the inflammatory response after hemorrhagic shock

Stress response decreases NF-kappaB nuclear translocation and increases I-kappaBalpha expression in A549 cells.

Hemorrhage activates NF-kappa B in murine lung mononuclear cells in vivo.

Heat shock activates the I-kappaBalpha promoter and increases I-kappaBalpha mRNA expression.

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583-597

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10.1113/JPHYSIOL.2001.013102

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Pt 2

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538

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11567452

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11790821

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internal bleeding

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2290060

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