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American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, 06/2012, Volume 185, Issue 11, pp. 1225 - 1234
Rationale: Despite advances in clinical management, there are currently no reliable diagnostic and therapeutic targets for acute respiratory distress syndrome... 
Acute respiratory distress syndrome | Inflammasome | Interleukin-18 | Mechanical ventilation | MORTALITY | ACTIVATION | IL-18 SECRETION | mechanical ventilation | CASPASE-1 | SEPSIS | RESPIRATORY-DISTRESS-SYNDROME | NALP3 INFLAMMASOME | interleukin-18 | INTENSIVE-CARE-UNIT | RESPIRATORY SYSTEM | inflammasome | IMMUNE-RESPONSES | acute respiratory distress syndrome | MICE | CRITICAL CARE MEDICINE | Critical Care - methods | Inflammasomes - metabolism | Respiration, Artificial - methods | Respiratory Distress Syndrome, Adult - physiopathology | Acute Lung Injury - therapy | Humans | Bronchoalveolar Lavage Fluid - immunology | Acute Lung Injury - genetics | Caspase 1 - metabolism | Male | Caspase 1 - immunology | Respiratory Distress Syndrome, Adult - genetics | Immunity, Innate - physiology | Microarray Analysis | Female | Acute Lung Injury - metabolism | Adaptive Immunity - immunology | Real-Time Polymerase Chain Reaction | Cytokines - immunology | Disease Models, Animal | Respiratory Distress Syndrome, Adult - therapy | Biomarkers - metabolism | Severity of Illness Index | Adaptive Immunity - physiology | Intensive Care Units | Cytokines - metabolism | Interleukin-18 - blood | Mice, Transgenic | Immunity, Innate - immunology | Animals | Inflammasomes - immunology | Mice | Cohort Studies | Index Medicus | Abridged Index Medicus
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 06/2012, Volume 122, Issue 6, pp. 1973 - 1990
EC activation and dysfunction have been linked to a variety of vascular inflammatory disease states. The function of microRNAs (miRNAs) in vascular EC... 
CELL-ADHESION MOLECULE-1 | TRANSCRIPTION FACTORS | MEDICINE, RESEARCH & EXPERIMENTAL | TUMOR-NECROSIS-FACTOR | DEPENDENT INDUCTION | LEUKOCYTE RECRUITMENT | HUMAN-ENDOTHELIAL-CELLS | ACUTE MYELOID-LEUKEMIA | PROGNOSTIC-SIGNIFICANCE | EXPRESSION PROFILES | SIGNAL-TRANSDUCTION PATHWAY | alpha Karyopherins - metabolism | Endotoxemia - therapy | Leukocytes - pathology | Vasculitis - metabolism | Acute Lung Injury - therapy | Endotoxemia - genetics | Humans | NF-kappa B - immunology | Critical Illness | Acute Lung Injury - genetics | MicroRNAs - metabolism | NF-kappa B - metabolism | Endotoxemia - pathology | Vasculitis - immunology | Leukocytes - immunology | Vasculitis - genetics | alpha Karyopherins - immunology | E-Selectin - genetics | Endotoxemia - immunology | Vascular Cell Adhesion Molecule-1 - genetics | Acute Lung Injury - metabolism | Vascular Cell Adhesion Molecule-1 - immunology | Vasculitis - therapy | Lipopolysaccharides - toxicity | Endothelial Cells - metabolism | E-Selectin - metabolism | E-Selectin - immunology | MicroRNAs - immunology | Acute Lung Injury - pathology | Endothelial Cells - immunology | Animals | NF-kappa B - genetics | alpha Karyopherins - genetics | Acute Lung Injury - immunology | Mice | MicroRNAs - genetics | Endothelial Cells - pathology | Endotoxemia - metabolism | Vascular Cell Adhesion Molecule-1 - metabolism | Leukocytes - metabolism | Index Medicus | Abridged Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 02/2013, Volume 8, Issue 2, pp. e56407 - e56407
Background: Nuclear factor-kappa B (NF-kappa B) is a central transcriptional factor and a pleiotropic regulator of many genes involved in acute lung injury.... 
INDUCED MITOGENIC FACTOR | IN-VITRO | ACTIVATION | INHIBITION | PI-3K/AKT-NF-KAPPA-B SIGNALING PATHWAY | MULTIDISCIPLINARY SCIENCES | ALVEOLAR FLUID CLEARANCE | EPITHELIAL SODIUM-CHANNEL | PANICULATA | EXPRESSION | RESPIRATORY-DISTRESS-SYNDROME | Bronchoalveolar Lavage Fluid | Protein Binding - genetics | Cell Count | Pneumonia - pathology | Cell Survival - genetics | Acute Lung Injury - genetics | Male | NF-kappa B - metabolism | Vascular Endothelial Growth Factor A - metabolism | Protective Agents - therapeutic use | Vascular Endothelial Growth Factor A - genetics | Lipopolysaccharides | Alveolar Epithelial Cells - pathology | Protective Agents - pharmacology | Protein Binding - drug effects | Pulmonary Edema - complications | Pulmonary Edema - pathology | Vascular Cell Adhesion Molecule-1 - genetics | Acute Lung Injury - drug therapy | Acute Lung Injury - metabolism | Alveolar Epithelial Cells - ultrastructure | Pneumonia - genetics | Diterpenes - pharmacology | Pulmonary Edema - genetics | Cell Survival - drug effects | Diterpenes - therapeutic use | Cytokines - metabolism | DNA - metabolism | Down-Regulation - drug effects | Acute Lung Injury - pathology | Pulmonary Edema - drug therapy | Gene Expression Regulation - drug effects | Animals | Pneumonia - drug therapy | Transcription Factor RelA - metabolism | Pneumonia - complications | Mice | Mice, Inbred BALB C | Vascular Cell Adhesion Molecule-1 - metabolism | Peroxidase - metabolism | Vascular cell adhesion molecule 1 | Phosphorylation | Epithelial cells | Lung | Kinases | Macrophages | Inactivation | Cell adhesion & migration | Interleukin 6 | Ultrastructure | Rodents | Inhibition | Alveoli | Vascular endothelial growth factor | Drug dosages | Deoxyribonucleic acid--DNA | Medicinal plants | Pathogens | Edema | NF-κB protein | Deactivation | Therapeutic applications | Traditional Chinese medicine | Leukocytes (neutrophilic) | Inflammation | Tumor necrosis factor-α | Gene expression | Medicine | Hospitals | Lungs | Respiratory distress syndrome | Rheumatoid arthritis | Hypoxia | In vivo methods and tests | Laboratory animals | In vitro methods and tests | Binding sites | Index Medicus | Deoxyribonucleic acid | DNA
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 03/2013, Volume 123, Issue 3, pp. 1019 - 1031
Acute lung injury (ALI) is an inflammatory disease with a high mortality rate. Although typically seen in individuals with sepsis, ALI is also a major... 
C-REACTIVE PROTEIN | INFLAMMATORY-RESPONSE | MEDICINE, RESEARCH & EXPERIMENTAL | APOPTOSIS | Acute lung injury (ALI) is an inflammatory disease with a high mortality rate. Although typically seen in individuals with sepsis | of STAT3 and production of the neutrophil attractant CXCL1 in pancreatic acinar cells. Examination of human samples revealed expression of IL-6 in combination with soluble IL-6 receptor was a reliable predictor of ALI in SAP. These results demonstrate that IL-6 trans-signaling is an essential mediator of ALI in SAP across | INTERLEUKIN-6 | RESPIRATORY-DISTRESS-SYNDROME | PREDICTION | species and suggest that therapeutic inhibition of IL-6 may prevent SAP-associated ALI | ACUTE-PHASE RESPONSE | ALI is also a major complication in severe acute pancreatitis (SAP). The pathophysiology of SAP-associated ALI is poorly understood, but elevated serum levels of IL-6 is a reliable marker for disease severity. Here, we used a mouse model of acute pancreatitis-associated (AP-associated) ALI to determine the role of IL-6 in ALI lethality. Il6-deficient mice had a lower death rate compared with wild-type mice with AP, while mice injected with IL-6 were more likely to develop lethal ALI. We found that inflammation-associated NF-kappa B induced myeloid cell secretion of IL-6, and the effects of secreted IL-6 were mediated by complexation with soluble IL-6 receptor, a process known as trans-signaling. IL-6 trans-signaling stimulated phosphorylation | BLOCKADE | INHIBITOR | SEVERITY | Phosphorylation | Humans | NF-kappa B - metabolism | Pancreatitis - complications | Receptors, Interleukin-8B - antagonists & inhibitors | Benzenesulfonates - pharmacology | Interleukin-6 - physiology | Pancreatitis - immunology | Acute Lung Injury - metabolism | Chemokine CXCL1 - metabolism | STAT3 Transcription Factor - metabolism | Acinar Cells - metabolism | Aminosalicylic Acids - pharmacology | Signal Transduction | Mice, Inbred C57BL | Pancreas - pathology | Mice, Transgenic | Acute Lung Injury - pathology | Interleukin-6 - secretion | Animals | Myeloid Cells - secretion | Receptors, Interleukin-8B - metabolism | Myeloid Cells - metabolism | Acute Lung Injury - immunology | Pancreatitis - pathology | Mice | Phenylurea Compounds - pharmacology | Protein Processing, Post-Translational | Pancreatitis - metabolism | STAT3 Transcription Factor - antagonists & inhibitors | Acute Lung Injury - etiology | Receptors, Interleukin-6 - metabolism | Lung diseases | Pancreatitis | Genetic aspects | Research | Health aspects | Risk factors | Interleukin-6 | Index Medicus | Abridged Index Medicus | Clinical Medicine | Medical and Health Sciences | Klinisk medicin | Medicin och hälsovetenskap | Surgery | Kirurgi
Journal Article
Journal Article
Proceedings of the National Academy of Sciences, ISSN 0027-8424, 01/2014, Volume 111, Issue 3, pp. E374 - E383
Journal Article
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 02/2015, Volume 125, Issue 2, pp. 652 - 664
Vascular endothelial barrier dysfunction underlies diseases such as acute respiratory distress syndrome (ARDS), characterized by edema and inflammatory cell... 
MEDICINE, RESEARCH & EXPERIMENTAL | HYPOXIA-INDUCIBLE FACTOR | ALVEOLAR HYPOXIA | FACTOR 1-ALPHA | ENDOTHELIAL-CELLS | IN-VIVO | LEUKOCYTE EXTRAVASATION | BARRIER FUNCTION | VE-CADHERIN | VASCULAR-PERMEABILITY | RESPIRATORY-DISTRESS-SYNDROME | Respiratory Distress Syndrome, Adult - pathology | Cadherins - metabolism | Humans | Hypoxia-Inducible Factor-Proline Dioxygenases - antagonists & inhibitors | Receptor-Like Protein Tyrosine Phosphatases, Class 3 - genetics | Respiratory Distress Syndrome, Adult - metabolism | Antigens, CD - genetics | Adherens Junctions - metabolism | Antigens, CD - metabolism | Phosphorylation - genetics | Respiratory Distress Syndrome, Adult - genetics | Basic Helix-Loop-Helix Transcription Factors - metabolism | Acute Lung Injury - metabolism | Cadherins - genetics | Adherens Junctions - genetics | Cell Line | Basic Helix-Loop-Helix Transcription Factors - genetics | Receptor-Like Protein Tyrosine Phosphatases, Class 3 - biosynthesis | Signal Transduction | Endothelial Cells - metabolism | Hypoxia-Inducible Factor-Proline Dioxygenases - genetics | Acute Lung Injury - pathology | Adherens Junctions - pathology | Mice, Knockout | Animals | Gene Expression Regulation, Enzymologic - genetics | Hypoxia-Inducible Factor-Proline Dioxygenases - metabolism | Mice | Endothelial Cells - pathology | Index Medicus | Abridged Index Medicus
Journal Article
Journal Article