scholarly article | Q13442814 |
P50 | author | Ruud Veldhuizen | Q60730440 |
Michael B Fessler | Q63363549 | ||
P2093 | author name string | Sanjay Mehta | |
Lefeng Wang | |||
Valeria Puntorieri | |||
Lynda McCaig | |||
Lijuan Yao | |||
Jennifer Madenspacher | |||
Cory M Yamashita | |||
Jim F Lewis | |||
Lakshman Vasanthamohan | |||
Joanne Lac | |||
P2860 | cites work | Contribution of alveolar macrophages to the response of the TIMP-3 null lung during a septic insult | Q80515924 |
Emerging therapies for treatment of acute lung injury and acute respiratory distress syndrome | Q83573197 | ||
Bench-to-bedside review: the role of the alveolar epithelium in the resolution of pulmonary edema in acute lung injury | Q24800694 | ||
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 | Q27861021 | ||
The acute respiratory distress syndrome | Q29615140 | ||
Obesity and pulmonary complications in critically injured adults | Q30440047 | ||
Emphysema is associated with increased inflammation in lungs of atherosclerosis-prone mice by cigarette smoke: implications in comorbidities of COPD. | Q34053824 | ||
eNOS protects from atherosclerosis despite relevant superoxide production by the enzyme in apoE mice. | Q34145922 | ||
Apolipoprotein E negatively regulates house dust mite-induced asthma via a low-density lipoprotein receptor-mediated pathway | Q34402431 | ||
The role of exogenous surfactant in the treatment of acute lung injury | Q35041169 | ||
LOX-1 deletion improves neutrophil responses, enhances bacterial clearance, and reduces lung injury in a murine polymicrobial sepsis model | Q35328629 | ||
Modified low density lipoprotein and its constituents augment cytokine-activated vascular cell adhesion molecule-1 gene expression in human vascular endothelial cells | Q35553734 | ||
Acid aspiration-induced lung injury in rabbits is mediated by interleukin-8-dependent mechanisms | Q35750001 | ||
Activation of the TLR4 signaling pathway and abnormal cholesterol efflux lead to emphysema in ApoE-deficient mice. | Q36045565 | ||
Understanding hyperlipidemia and atherosclerosis: lessons from genetically modified apoe and ldlr mice | Q36130584 | ||
ApoE controls the interface linking lipids and inflammation in atherosclerosis | Q38732861 | ||
Lung-derived mediators induce cytokine production in downstream organs via an NF-κB-dependent mechanism. | Q39825686 | ||
Involvement of ICAM-1 in the progression of atherosclerosis in APOE-knockout mice | Q40659567 | ||
Effect of mechanical ventilation on inflammatory mediators in patients with acute respiratory distress syndrome: a randomized controlled trial | Q40805989 | ||
The role of neutrophils, oxidants, and proteases in the pathogenesis of acid pulmonary injury | Q41098454 | ||
The effect of tidal volume on systemic inflammation in Acid-induced lung injury | Q42751385 | ||
Elevated endogenous surfactant reduces inflammation in an acute lung injury model | Q43258290 | ||
Prediction of outcome in patients with acute respiratory distress syndrome by bronchoalveolar lavage inflammatory mediators | Q43694492 | ||
Pathophysiology of apolipoprotein E deficiency in mice: relevance to apo E-related disorders in humans | Q43811092 | ||
Mortality of patients with respiratory insufficiency and adult respiratory distress syndrome after surgery: the obesity paradox | Q44331444 | ||
Septic pulmonary microvascular endothelial cell injury: role of alveolar macrophage NADPH oxidase | Q45266381 | ||
Transient increase in plasma oxidized LDL during the progression of atherosclerosis in apolipoprotein E knockout mice | Q46260958 | ||
Circulating oxidized LDL: determinants and association with brachial flow-mediated dilation | Q46359070 | ||
The ALIEN study: incidence and outcome of acute respiratory distress syndrome in the era of lung protective ventilation | Q46440662 | ||
Apolipoprotein E suppresses the type I inflammatory response in vivo | Q46716863 | ||
Apoetm1Unc mice have impaired alveologenesis, low lung function, and rapid loss of lung function. | Q51961868 | ||
Hyperoxia activates NF-kappaB and increases TNF-alpha and IFN-gamma gene expression in mouse pulmonary lymphocytes | Q71727800 | ||
Hyperoxia amplifies TNF-alpha production in LPS-stimulated human alveolar macrophages | Q72584576 | ||
ICAM-1 deficiency reduces atherosclerotic lesions in double-knockout mice (ApoE(-/-)/ICAM-1(-/-)) fed a fat or a chow diet | Q73295363 | ||
Resveratrol attenuates oxLDL-stimulated NADPH oxidase activity and protects endothelial cells from oxidative functional damages | Q79460195 | ||
Pulmonary neutrophil infiltration in murine sepsis: role of inducible nitric oxide synthase | Q79859249 | ||
P433 | issue | 5 | |
P304 | page(s) | 416-427 | |
P577 | publication date | 2014-03-22 | |
P1433 | published in | Respiration | Q15753091 |
P1476 | title | Apolipoprotein E-deficient mice are susceptible to the development of acute lung injury | |
P478 | volume | 87 |
Q52775785 | A New Frontier in Immunometabolism. Cholesterol in Lung Health and Disease. |
Q47265721 | Antibody Responses to Citrullinated and Non-Citrullinated Antigens in the Sputum of Subjects with and At-Risk for Rheumatoid Arthritis. |
Q38807248 | Emerging Roles of Apolipoprotein E and Apolipoprotein A-I in the Pathogenesis and Treatment of Lung Disease |
Q58722221 | Plasma proteomics reveals gestational age-specific responses to mechanical ventilation and identifies the mechanistic pathways that initiate preterm lung injury |
Q40835741 | Roles of the Mevalonate Pathway and Cholesterol Trafficking in Pulmonary Host Defense. |
Q35618507 | Serum apolipoprotein A-I and large high-density lipoprotein particles are positively correlated with FEV1 in atopic asthma |
Q58570133 | The APOE ε4 allele is associated with a reduction in FEV1/FVC in women: A cross-sectional analysis of the Long Life Family Study |
Q33924226 | The effect of matrix metalloproteinase-3 deficiency on pulmonary surfactant in a mouse model of acute lung injury. |
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