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Nature, ISSN 0028-0836, 03/2010, Volume 464, Issue 7285, pp. 104 - 107
Injury causes a systemic inflammatory response syndrome (SIRS) that is clinically much like sepsis. Microbial pathogen-associated molecular patterns (PAMPs)... 
SHOCK | SIRS | OPERATED CALCIUM INFLUX | HUMAN NEUTROPHILS | PEPTIDES | MODELS | MOBILIZATION | CHEMOTAXIS | MULTIDISCIPLINARY SCIENCES | RECEPTORS | TRAUMA | Liver - pathology | Phosphorylation | Humans | Male | Mitochondria - immunology | Liver - injuries | N-Formylmethionine Leucyl-Phenylalanine - metabolism | Liver - immunology | Systemic Inflammatory Response Syndrome - blood | Muscle, Skeletal - immunology | Sepsis - metabolism | Receptors, Formyl Peptide - metabolism | Systemic Inflammatory Response Syndrome - immunology | Neutrophils - metabolism | Calcium Signaling | Femur - injuries | Sepsis - immunology | CpG Islands - immunology | Neutrophils - enzymology | Wounds and Injuries - pathology | Fractures, Bone - immunology | Wounds and Injuries - blood | Cells, Cultured | Neutrophils - immunology | Wounds and Injuries - complications | Rats | Wounds and Injuries - immunology | Acute Lung Injury - pathology | DNA, Mitochondrial - blood | Rats, Sprague-Dawley | DNA, Mitochondrial - immunology | Immunity, Innate - immunology | Systemic Inflammatory Response Syndrome - pathology | Animals | Mitochondria - secretion | Acute Lung Injury - immunology | Fractures, Bone - pathology | Systemic Inflammatory Response Syndrome - complications | Muscle, Skeletal - pathology | Toll-Like Receptor 9 - metabolism | Sepsis - microbiology | Mitogen-Activated Protein Kinases - metabolism | N-Formylmethionine Leucyl-Phenylalanine - immunology | Infection | Peptides | Physiological aspects | Mitochondrial DNA | Inflammation | Research | Risk factors | Fractures | Bacterial proteins | Rheumatoid arthritis | Trauma | Deoxyribonucleic acid--DNA
Journal Article
Journal Article
Cell Death and Differentiation, ISSN 1350-9047, 09/2016, Volume 23, Issue 9, pp. 1565 - 1576
Necroptosis is a caspase-independent form of cell death that is triggered by activation of the receptor interacting serine/threonine kinase 3 (RIPK3) and... 
MYOCARDIAL-INFARCTION | RECEPTOR-INTERACTING PROTEIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | DOMAIN-LIKE PROTEIN | REPERFUSION INJURY | MIXED LINEAGE KINASE | PROGRAMMED NECROSIS | MEDIATES NECROPTOSIS | TNF-ALPHA | NECROPTOTIC CELL-DEATH | NF-KAPPA-B | CELL BIOLOGY | Protein Kinases - metabolism | Receptor-Interacting Protein Serine-Threonine Kinases - metabolism | Inflammation - pathology | Protein Kinases - genetics | Sepsis - etiology | Apoptosis - drug effects | Colitis - pathology | Male | Inflammation - metabolism | Sepsis - pathology | Sepsis - metabolism | Colitis - chemically induced | Female | Protein Kinases - deficiency | Reperfusion Injury - metabolism | Disease Models, Animal | Systemic Inflammatory Response Syndrome - metabolism | Lipopolysaccharides - toxicity | Reperfusion Injury - pathology | Mice, Inbred C57BL | Ceruletide - toxicity | Reperfusion Injury - mortality | Pancreatitis - chemically induced | Dextran Sulfate - toxicity | Mice, Knockout | Tumor Necrosis Factor alpha-Induced Protein 3 - genetics | Receptor-Interacting Protein Serine-Threonine Kinases - genetics | Systemic Inflammatory Response Syndrome - pathology | Animals | Colitis - metabolism | Pancreatitis - pathology | Systemic Inflammatory Response Syndrome - etiology | Mice | Receptor-Interacting Protein Serine-Threonine Kinases - deficiency | Pancreatitis - metabolism | Receptor-Interacting Protein Serine-Threonine Kinases - antagonists & inhibitors | Tumor Necrosis Factor alpha-Induced Protein 3 - deficiency | Original Paper
Journal Article
Clinical Infectious Diseases, ISSN 1058-4838, 8/2010, Volume 51, Issue 3, pp. 350 - 358
Journal Article
Journal Article
Journal Article