Epithelial cell death is an important contributor to oxidant-mediated acute lung injury. - Wikidata - awgldk - TriplyDB

Epithelial cell death is an important contributor to oxidant-mediated acute lung injury.

Epithelial cell death is an important contributor to oxidant-mediated acute lung injury.

http://www.wikidata.org/entity/Q34914561

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Minimizing oxidation and stable nanoscale dispersion improves the biocompatibility of graphene in the lung Biphasic positive airway pressure minimizes biological impact on lung tissue in mild acute lung injury independent of etiology.Analysis of the transcriptome in hyperoxic lung injury and sex-specific alterations in gene expression.Taking a "good" look at free radicals in the aging process.Synchronizing allelic effects of opposing quantitative trait loci confirmed a major epistatic interaction affecting acute lung injury survival in mice.Mice deficient in the gene for cytochrome P450 (CYP)1A1 are more susceptible than wild-type to hyperoxic lung injury: evidence for protective role of CYP1A1 against oxidative stress.Sex-specific differences in hyperoxic lung injury in mice: implications for acute and chronic lung disease in humans.Developmental regulation of antioxidant enzymes and their impact on neonatal lung disease Nox2-dependent glutathionylation of endothelial NOS leads to uncoupled superoxide production and endothelial barrier dysfunction in acute lung injury.Protein expression profile of rat type two alveolar epithelial cells during hyperoxic stress and recovery.Flotillin-2 modulates fas signaling mediated apoptosis after hyperoxia in lung epithelial cells.Update in acute lung injury and critical care 2010.Augmented oxygen-mediated transcriptional activation of cytochrome P450 (CYP)1A expression and increased susceptibilities to hyperoxic lung injury in transgenic mice carrying the human CYP1A1 or mouse 1A2 promoter in vivo.Lung-specific loss of the laminin α3 subunit confers resistance to mechanical injury.Prenatal administration of the cytochrome P4501A inducer, Β-naphthoflavone (BNF), attenuates hyperoxic lung injury in newborn mice: implications for bronchopulmonary dysplasia (BPD) in premature infants.Disruption of cytochrome P4501A2 in mice leads to increased susceptibility to hyperoxic lung injury.Increased hyperoxia-induced lung injury in nitric oxide synthase 2 null mice is mediated via angiopoietin 2.Detoxification of Mitochondrial Oxidants and Apoptotic Signaling Are Facilitated by Thioredoxin-2 and Peroxiredoxin-3 during Hyperoxic Injury.Lung protection by inhalation of exogenous solubilized extracellular matrix.TLR signaling prevents hyperoxia-induced lung injury by protecting the alveolar epithelium from oxidant-mediated death Balancing the risks and benefits of oxygen therapy in critically III adults.TNF-induced death signaling triggers alveolar epithelial dysfunction in acute lung injury.Developmental differences in hyperoxia-induced oxidative stress and cellular responses in the murine lung.Inhibition of extracellular HMGB1 attenuates hyperoxia-induced inflammatory acute lung injury.IκBβ-mediated NF-κB activation confers protection against hyperoxic lung injury.Acute lung injury: how macrophages orchestrate resolution of inflammation and tissue repair NOX enzymes: potential target for the treatment of acute lung injury.Novel concepts of acute lung injury and alveolar-capillary barrier dysfunction.Potential contribution of type I alveolar epithelial cells to chronic neonatal lung disease.Leptin attenuates lipopolysaccharide or oleic acid-induced acute lung injury in mice.A novel fine tuning scheme of miR-200c in modulating lung cell redox homeostasis.miR-185 mediates lung epithelial cell death after oxidative stress Senegenin Ameliorate Acute Lung Injury Through Reduction of Oxidative Stress and Inhibition of Inflammation in Cecal Ligation and Puncture-Induced Sepsis Rats.Effective protection against acute respiratory distress syndrome/sepsis injury by combined adipose-derived mesenchymal stem cells and preactivated disaggregated platelets.Mitochondrial Dysfunction in Pulmonary Fibrosis.A role for heat shock factor 1 in hypercapnia-induced inhibition of inflammatory cytokine expression.Systemic combined melatonin-mitochondria treatment improves acute respiratory distress syndrome in the rat.Exogenous interleukin-10 attenuates hyperoxia-induced acute lung injury in mice.Effect of hyperoxia on the viability and proliferation of the primary type II alveolar epithelial cells.Efferocytosis of apoptotic alveolar epithelial cells is sufficient to initiate lung fibrosis

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Epithelial cell death is an important contributor to oxidant-mediated acute lung injury.

http://www.wikidata.org/entity/Q34914561

description

2010 nî lūn-bûn

@nan

2010 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի հոտեմբերին հրատարակված գիտական հոդված

@hy

2010年の論文

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2010年論文

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2010年論文

@zh-hant

2010年論文

@zh-hk

2010年論文

@zh-mo

2010年論文

@zh-tw

2010年论文

@wuu

name

Epithelial cell death is an important contributor to oxidant-mediated acute lung injury.

@ast

Epithelial cell death is an important contributor to oxidant-mediated acute lung injury.

@en

Epithelial cell death is an important contributor to oxidant-mediated acute lung injury.

@nl

type

label

Epithelial cell death is an important contributor to oxidant-mediated acute lung injury.

@ast

Epithelial cell death is an important contributor to oxidant-mediated acute lung injury.

@en

Epithelial cell death is an important contributor to oxidant-mediated acute lung injury.

@nl

prefLabel

Epithelial cell death is an important contributor to oxidant-mediated acute lung injury.

@ast

Epithelial cell death is an important contributor to oxidant-mediated acute lung injury.

@en

Epithelial cell death is an important contributor to oxidant-mediated acute lung injury.

@nl

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RCCM.201002-0181OC

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American Journal of Respiratory and Critical Care Medicine

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Epithelial cell death is an important contributor to oxidant-mediated acute lung injury

@en

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Daniela Urich

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G R Scott Budinger

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Gökhan M Mutlu

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Harris Perlman

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Hemant Agrawal

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James Eisenbart

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Kathryn A Radigan

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Keenan Hawkins

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Leonard J Buccellato

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Manu Jain

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P2860

Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function

Spatial and temporal association of Bax with mitochondrial fission sites, Drp1, and Mfn2 during apoptosis

Evolutionary conservation of the clk-1-dependent mechanism of longevity: loss of mclk1 increases cellular fitness and lifespan in mice

Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network

Proapoptotic Bcl-2 relative Bim required for certain apoptotic responses, leukocyte homeostasis, and to preclude autoimmunity

p53- and drug-induced apoptotic responses mediated by BH3-only proteins puma and noxa

Cell death: critical control points

Cyclophilin D-dependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell death

Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death

Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death

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1043-1054

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10.1164/RCCM.201002-0181OC

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8

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183

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Sergio E. Chiarella

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2010-10-19T00:00:00Z

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20959557

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3086743

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