Genetic deletion of apolipoprotein A-I increases airway hyperresponsiveness, inflammation, and collagen deposition in the lung. - Wikidata - awgldk - TriplyDB

Genetic deletion of apolipoprotein A-I increases airway hyperresponsiveness, inflammation, and collagen deposition in the lung.

Genetic deletion of apolipoprotein A-I increases airway hyperresponsiveness, inflammation, and collagen deposition in the lung.

http://www.wikidata.org/entity/Q34053084

about

Lysophosphatidic acid and apolipoprotein A1 predict increased risk of developing World Trade Center-lung injury: a nested case-control study High-density Lipoproteins and Apolipoprotein A-I: Potential New Players in the Prevention and Treatment of Lung Disease Role of oxidized lipids in pulmonary arterial hypertension Regulation of Adaptive Immunity in Health and Disease by Cholesterol Metabolism Proteomic identification of novel differentiation plasma protein markers in hypobaric hypoxia-induced rat model.Identification of haptoglobin and apolipoprotein A-I as biomarkers for high altitude pulmonary edema.Apolipoprotein A-I, A-II, and H mRNA and protein accumulation sites in the developing lung in late gestation Genetic interactions between chromosomes 11 and 18 contribute to airway hyperresponsiveness in mice D-4F, an apoA-1 mimetic, decreases airway hyperresponsiveness, inflammation, and oxidative stress in a murine model of asthma.Serum apolipoprotein A-I and large high-density lipoprotein particles are positively correlated with FEV1 in atopic asthma Next stop for HDL: the lung.Apolipoprotein mimetic peptides: a new approach for the treatment of asthma.Scavenger receptor class B, type I-mediated uptake of A1AT by pulmonary endothelial cells The Mechanism of Proinflammatory HDL Generation in Sickle Cell Disease Is Linked to Cell-Free Hemoglobin via Haptoglobin.Emerging roles for cholesterol and lipoproteins in lung disease.Apolipoproteins and apolipoprotein mimetic peptides modulate phagocyte trafficking through chemotactic activity Carboxyl-Terminal Cleavage of Apolipoprotein A-I by Human Mast Cell Chymase Impairs Its Anti-Inflammatory Properties.An insight into the changes in human plasma proteome on adaptation to hypobaric hypoxia Microdomains, Inflammation, and Atherosclerosis.Examining the role of ABC lipid transporters in pulmonary lipid homeostasis and inflammation.Differential plasma proteome analysis in patients with high-altitude pulmonary edema at the acute and recovery phases.Apolipoprotein A-I inhibits LPS-induced atherosclerosis in ApoE(-/-) mice possibly via activated STAT3-mediated upregulation of tristetraprolin.Lipid-lowering drug therapies and chronic obstructive pulmonary disease: lung failure or just heart failure?Effects of human umbilical cord blood mononuclear cells on respiratory system mechanics in a murine model of neonatal lung injury.Emerging Roles of Apolipoprotein E and Apolipoprotein A-I in the Pathogenesis and Treatment of Lung Disease.Attenuation of Cigarette Smoke-Induced Emphysema in Mice by Apolipoprotein A-1 Overexpression.The A's Have It: Developing Apolipoprotein A-I Mimetic Peptides Into a Novel Treatment for Asthma.Roles of the Mevalonate Pathway and Cholesterol Trafficking in Pulmonary Host Defense.Effects of experimental asthma on inflammation and lung mechanics in sickle cell mice.Revisiting "Good" and "Bad" Cholesterol. The Battle over Flow through Arteries Now Shifts to Flow through Airways.Association between Allergies and Hypercholesterolemia: A Systematic Review.High-density lipoproteins potentiate α1-antitrypsin therapy in elastase-induced pulmonary emphysema.Apolipoprotein A1 potentiates lipoxin A4 synthesis and recovery of allergen-induced disrupted tight junctions in the airway epithelium.Eosinophil activation and novel mediators in the aspirin-induced nasal response in AERD.A New Frontier in Immunometabolism. Cholesterol in Lung Health and Disease.

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P2860

Genetic deletion of apolipoprotein A-I increases airway hyperresponsiveness, inflammation, and collagen deposition in the lung.

http://www.wikidata.org/entity/Q34053084

description

2010 nî lūn-bûn

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2010 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2010 թվականի մայիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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name

Genetic deletion of apolipopro ...... llagen deposition in the lung.

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Genetic deletion of apolipopro ...... llagen deposition in the lung.

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Genetic deletion of apolipopro ...... llagen deposition in the lung.

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type

label

Genetic deletion of apolipopro ...... llagen deposition in the lung.

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Genetic deletion of apolipopro ...... llagen deposition in the lung.

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Genetic deletion of apolipopro ...... llagen deposition in the lung.

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prefLabel

Genetic deletion of apolipopro ...... llagen deposition in the lung.

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Genetic deletion of apolipopro ...... llagen deposition in the lung.

@en

Genetic deletion of apolipopro ...... llagen deposition in the lung.

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P2860

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Journal of Lipid Research

P1476

Genetic deletion of apolipopro ...... ollagen deposition in the lung

@en

P2093

Deron W Jones

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Dorothee Weihrauch

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Haiqing Gao

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Hao Xu

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Hao Zhang

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Kirkwood A Pritchard

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Marie L Schulte

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Sandhya Nandedkar

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Thom Feroah

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Weiling Wang

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P2860

Contribution of nitric oxide synthases 1, 2, and 3 to airway hyperresponsiveness and inflammation in a murine model of asthma

Measuring the lung function in the mouse: the challenge of size

ApoA-I knockout mice: characterization of HDL metabolism in homozygotes and identification of a post-RNA mechanism of apoA-I up-regulation in heterozygotes

Marked reduction of high density lipoprotein cholesterol in mice genetically modified to lack apolipoprotein A-I

Nitric oxide, superoxide, and peroxynitrite: the good, the bad, and ugly

Proteomic identification of altered apolipoprotein patterns in pulmonary hypertension and vasculopathy of sickle cell disease

Oxygen radical inhibition of nitric oxide-dependent vascular function in sickle cell disease.

Overexpression of endothelial nitric oxide synthase accelerates atherosclerotic lesion formation in apoE-deficient mice.

Oxidant-mediated impairment of nitric oxide signaling in sickle cell disease--mechanisms and consequences.

Anti-inflammatory HDL becomes pro-inflammatory during the acute phase response. Loss of protective effect of HDL against LDL oxidation in aortic wall cell cocultures

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2560-2570

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10.1194/JLR.M004549

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9

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51

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Jason Jarzembowski

Mary G Sorci-Thomas

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2010-05-24T00:00:00Z

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20498409

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