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Identification and Validation of Liver Transplantation-Induced Acute Lung Injury Biomarkers Using a Bioinformatics and Experimental Approach. [PDF]
Guiting Y +7 more
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Recruitment of CCR5<sup>+</sup> inflammatory monocytes in pulmonary tissue contributes to acute lung injury. [PDF]
Wei D +8 more
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The relationship between serum levels of miR-342 and miR-148a and acute lung injury in sepsis patients. [PDF]
Shen M, Cai T, Zhu J, Yin Z.
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The CXCL12/CXCR4 Axis in Sepsis-Induced Acute Lung Injury: Mechanisms and Therapeutic Potential. [PDF]
Luo R +5 more
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Mechanisms of Acute Lung Injury
Clinics in Laboratory Medicine, 1983The role of the complement system in generating an acute inflammatory response in the lung, manifested particularly by the presence of neutrophils, and the role of these neutrophils in altering lung microvascular permeability are examined. Although it is not possible at this time to reconcile all the experimental data so as to provide a unifying ...
G S, Worthen, P M, Henson
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Journal of Thoracic Imaging
Acute lung injury (ALI) is acute pulmonary inflammation with underlying pathology of disruption of the pulmonary vasculature endothelial and alveolar epithelial barriers. ALI is not an uncommon diagnosis and has a myriad of causes including pulmonary infection, (including sepsis), drugs, connective tissue disease, and polytrauma.
Nupur, Verma +4 more
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Acute lung injury (ALI) is acute pulmonary inflammation with underlying pathology of disruption of the pulmonary vasculature endothelial and alveolar epithelial barriers. ALI is not an uncommon diagnosis and has a myriad of causes including pulmonary infection, (including sepsis), drugs, connective tissue disease, and polytrauma.
Nupur, Verma +4 more
openaire +3 more sources
Microparticles and acute lung injury
American Journal of Physiology-Lung Cellular and Molecular Physiology, 2012The pathophysiology of acute lung injury (ALI) and its most severe form, acute respiratory distress syndrome (ARDS), is characterized by increased vascular and epithelial permeability, hypercoagulation and hypofibrinolysis, inflammation, and immune modulation.
Mark, McVey +2 more
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