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Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 01/2008, Volume 118, Issue 1, pp. 239 - 247
Sepsis is characterized by a systemic response to severe infection. Although the inflammatory phase of sepsis helps eradicate the infection, it can have... 
MEDICINE, RESEARCH & EXPERIMENTAL | CELLS | SIGNALING PATHWAYS | OXIDATIVE STRESS | TOLL-LIKE RECEPTORS | SEPTIC SHOCK | ACUTE LUNG INJURY | ORGAN DYSFUNCTION | OXYGENASE | EXPRESSION | INNATE IMMUNITY | Enterococcus faecalis | Inflammation - pathology | Fibroblasts - enzymology | Antimetabolites - immunology | Escherichia coli | Escherichia coli Infections - enzymology | Humans | Immunity, Innate - genetics | Myocytes, Smooth Muscle - pathology | Phagocytosis - genetics | Carbon Monoxide - metabolism | Heme Oxygenase-1 - genetics | Sepsis - drug therapy | Escherichia coli Infections - genetics | Sepsis - pathology | Carbon Monoxide - pharmacology | Gram-Positive Bacterial Infections - enzymology | Inflammation - drug therapy | Inflammation Mediators - metabolism | Gram-Positive Bacterial Infections - genetics | Inflammation Mediators - antagonists & inhibitors | Antimetabolites - pharmacology | Escherichia coli Infections - drug therapy | Gene Targeting | Inflammation - microbiology | Phagocytosis - drug effects | Immunity, Innate - drug effects | Myocytes, Smooth Muscle - enzymology | Fibroblasts - pathology | Sepsis - genetics | Mice, Knockout | Animals | Escherichia coli Infections - pathology | Sepsis - enzymology | Heme Oxygenase-1 - immunology | Inflammation - genetics | Mice | Gram-Positive Bacterial Infections - drug therapy | Inflammation - enzymology | Sepsis - microbiology | Polymerase chain reaction | Care and treatment | Mediators | Sepsis | Inflammation | Research | Health aspects | Risk factors
Journal Article
Journal Article
Nature Medicine, ISSN 1078-8956, 11/2007, Volume 13, Issue 11, pp. 1349 - 1358
Data providing direct evidence for a causative link between endothelial dysfunction, microvascular disease and diabetic end-organ damage are scarce. Here we... 
MEDICINE, RESEARCH & EXPERIMENTAL | POLY(ADP-RIBOSE) POLYMERASE INHIBITORS | ANTICOAGULANT PATHWAY | BIOCHEMISTRY & MOLECULAR BIOLOGY | MOUSE | ALPHA | CELL BIOLOGY | THROMBOMODULIN | INFLAMMATION | DYSFUNCTION | CELL | RECEPTOR-1 | SEVERE SEPSIS | Kidney Glomerulus - blood supply | Diabetic Nephropathies - enzymology | Protein C - physiology | Diabetes Mellitus, Experimental - enzymology | Humans | Diabetes Mellitus, Experimental - genetics | Podocytes - enzymology | Apoptosis - genetics | Endothelium, Vascular - enzymology | Thrombomodulin - physiology | Diabetes Mellitus, Experimental - prevention & control | Mice, Mutant Strains | Diabetic Nephropathies - prevention & control | Kidney Glomerulus - enzymology | Diabetic Nephropathies - pathology | Mice, Inbred C57BL | Cells, Cultured | Diabetic Nephropathies - genetics | Mice, Transgenic | Signal Transduction - genetics | Kidney Glomerulus - pathology | Podocytes - pathology | Protein C - biosynthesis | Animals | Microcirculation - pathology | Microcirculation - enzymology | Diabetes Mellitus, Experimental - pathology | Amino Acid Substitution - genetics | Cytoprotection - genetics | Endothelium, Vascular - pathology | Mice | Enzyme Activation - genetics | Cell Line, Transformed | Protein C - genetics | Proteins | Diabetes | Kidney diseases | Cellular biology | Rodents | Apoptosis
Journal Article
Science, ISSN 0036-8075, 6/2010, Volume 328, Issue 5983, pp. 1290 - 1294
During sepsis, activation of phagocytes leads to the overproduction of proinflammatory cytokines, causing systemic inflammation. Despite substantial... 
Bacteriophages | Cytokines | Antibiotics | REPORTS | Neutrophils | Small interfering RNA | Sepsis | Septic shock | Inflammation | Macrophages | Vehicles | ACTIVATION | THERAPY | CECAL LIGATION | INFLAMMATORY RESPONSES | MULTIDISCIPLINARY SCIENCES | RECEPTOR | FC-GAMMA-RI | SPHINGOSINE KINASE | CA2+ SIGNALS | MODULATION | PUNCTURE | Up-Regulation | Humans | Middle Aged | Endotoxins | Male | NF-kappa B - metabolism | Shock, Septic - immunology | Lipopolysaccharides - immunology | Young Adult | Sepsis - drug therapy | RNA Interference | Aged, 80 and over | Adult | Female | Bacterial Proteins - immunology | Macrophages - immunology | Cytokines - blood | Sepsis - immunology | Cytokines - metabolism | Neutrophils - enzymology | Signal Transduction | Enzyme Inhibitors - pharmacology | Macrophages, Peritoneal - enzymology | Neutrophils - immunology | Macrophages, Peritoneal - immunology | Phosphotransferases (Alcohol Group Acceptor) - genetics | Peritonitis - immunology | Enzyme Inhibitors - therapeutic use | Macrophages - enzymology | Phosphotransferases (Alcohol Group Acceptor) - metabolism | Protein Kinase C-delta - metabolism | Phosphotransferases (Alcohol Group Acceptor) - antagonists & inhibitors | Peritonitis - enzymology | Animals | Sepsis - enzymology | Adolescent | Aged | Mice | Shock, Septic - enzymology | Enzyme Activation | Lipoproteins - immunology | Phagocytes | Physiological aspects | Diagnosis | Research | Risk factors | Enzymes | Molecular biology | Immune system
Journal Article
American Journal of Physiology - Cell Physiology, ISSN 0363-6143, 04/2018, Volume 314, Issue 4, pp. C449 - C455
MicroRNA-199a (miR-199a) is a novel gene regulator with an important role in inflammation and lung injury. However, its role in the pathogenesis of... 
Sepsis | SIRT1 | MicroRNA-199a | ARDS | Macrophage | APOPTOSIS | PHYSIOLOGY | microRNA-199a | macrophage | FAILURE | RESPIRATORY-DISTRESS-SYNDROME | CELL-DEATH | PROTECTS | CELL BIOLOGY | MULTIPLE ORGAN DYSFUNCTION | PATHWAY | SEPTIC SHOCK | MICE | INFECTION | sepsis | Sirtuin 1 - metabolism | Lung - microbiology | Apoptosis - drug effects | Acute Lung Injury - genetics | Male | MicroRNAs - metabolism | Sirtuin 1 - genetics | Acute Lung Injury - enzymology | Lung - enzymology | Sepsis - drug therapy | Respiratory Distress Syndrome, Adult - genetics | Pseudomonas aeruginosa - pathogenicity | Respiratory Distress Syndrome, Adult - microbiology | Acute Lung Injury - prevention & control | Inflammation Mediators - metabolism | 3' Untranslated Regions | Binding Sites | Disease Models, Animal | Lung - pathology | Macrophages, Alveolar - microbiology | Cytokines - metabolism | Respiratory Distress Syndrome, Adult - prevention & control | Down-Regulation | Mice, Inbred C57BL | Burns - microbiology | Pseudomonas Infections - microbiology | Sirtuin 1 - antagonists & inhibitors | Sepsis - genetics | Macrophages, Alveolar - enzymology | Pseudomonas Infections - genetics | Gene Expression Regulation, Enzymologic | Acute Lung Injury - microbiology | Animals | Signal Transduction - drug effects | Macrophages, Alveolar - drug effects | Sepsis - enzymology | Lung - drug effects | Histone Deacetylase Inhibitors - pharmacology | MicroRNAs - genetics | Antagomirs - metabolism | Carbazoles - pharmacology | Respiratory Distress Syndrome, Adult - enzymology | Antagomirs - genetics | Pseudomonas Infections - enzymology | Sepsis - microbiology | Acute respiratory distress syndrome | Prevention | RNA sequencing | MicroRNA | Genetic aspects | Health aspects | Methods
Journal Article
Thrombosis and Haemostasis, ISSN 0340-6245, 09/2007, Volume 98, Issue 3, pp. 512 - 520
The plasminogen activation system is part of the fibrinolysis which is tightly regulated and protected against dysfunction by various activators and... 
Theme Issue Article | Bacterial infection | Inflammation | Plasminogen | Plasminogen activator inhibitor | Urokinase/receptor | BORRELIA-BURGDORFERI | ALPHA-ENOLASE | OUTER SURFACE PROTEIN | BINDING-PROTEIN | bacterial infection | BLOOD MONONUCLEAR-CELLS | plasminogen | GROUP-A STREPTOCOCCI | inflammation | YERSINIA-PESTIS | urokinase/receptor | UROKINASE RECEPTOR | PERIPHERAL VASCULAR DISEASE | plasminogen activator inhibitor | HEMATOLOGY | HELICOBACTER-PYLORI | PESTIS PLASMINOGEN-ACTIVATOR | Borrelia Infections - blood | Bacterial Infections - enzymology | Tissue Plasminogen Activator - metabolism | Humans | Plasminogen Activators - metabolism | Metalloendopeptidases - metabolism | Plasminogen - metabolism | Meningitis, Bacterial - blood | Receptors, Urokinase Plasminogen Activator | Borrelia Infections - microbiology | Plasminogen Activator Inhibitor 1 - metabolism | Bacterial Infections - microbiology | Disease Models, Animal | Pneumonia, Bacterial - blood | Bacteria - metabolism | Meningitis, Bacterial - microbiology | Pneumonia, Bacterial - microbiology | Meningitis, Bacterial - enzymology | Signal Transduction | Pneumonia, Bacterial - enzymology | Receptors, Cell Surface - metabolism | Fibrinolysis | Animals | Carrier Proteins - metabolism | Helicobacter pylori - metabolism | Urokinase-Type Plasminogen Activator - metabolism | Sepsis - enzymology | Bacteria - enzymology | Bacterial Proteins - metabolism | Bacteria - pathogenicity | Mice | Sepsis - blood | Bacterial Infections - blood | Borrelia Infections - enzymology | Sepsis - microbiology | Streptokinase - metabolism
Journal Article
Journal of Cellular Physiology, ISSN 0021-9541, 06/2018, Volume 233, Issue 6, pp. 4783 - 4790
Mammalian target of rapamycin (mTOR) signaling pathway controls cell energy metabolism. There is an interplay between mTOR and proinflammatory signaling... 
inflamatory diseases | pharmacological inhibitors | mammalian target of rapamycin | inflammation | MAMMALIAN TARGET | RHEUMATOID-ARTHRITIS | PHYSIOLOGY | DENDRITIC CELLS | HUMAN MACROPHAGES | TRANSLATION INITIATION | KAPPA-B | CELL BIOLOGY | SKELETAL-MUSCLE | MUSCLE PROTEIN-SYNTHESIS | INFLAMMATORY RESPONSE | INNATE IMMUNITY | TOR Serine-Threonine Kinases - metabolism | Humans | Molecular Targeted Therapy | Neurodegenerative Diseases - drug therapy | Neurodegenerative Diseases - immunology | TOR Serine-Threonine Kinases - antagonists & inhibitors | Sepsis - drug therapy | Atherosclerosis - enzymology | Arthritis, Rheumatoid - drug therapy | Inflammation - drug therapy | Inflammation Mediators - metabolism | Anti-Inflammatory Agents - therapeutic use | Inflammation Mediators - antagonists & inhibitors | Inflammation Mediators - immunology | Sepsis - immunology | Atherosclerosis - drug therapy | Atherosclerosis - immunology | Neoplasms - enzymology | Arthritis, Rheumatoid - enzymology | Inflammation - immunology | Neoplasms - drug therapy | TOR Serine-Threonine Kinases - immunology | Animals | Signal Transduction - drug effects | Neoplasms - immunology | Protein Kinase Inhibitors - therapeutic use | Sepsis - enzymology | Arthritis, Rheumatoid - immunology | Inflammation - enzymology | Neurodegenerative Diseases - enzymology | Rheumatoid factor | Care and treatment | Nervous system diseases | Health aspects | Atherosclerosis | TOR protein | Energy metabolism | Inhibitor drugs | Neurodegenerative diseases | Pathogenesis | Medical treatment | Pharmacology | Rapamycin | Arthritis | Metabolism | Inflammatory diseases | Diseases | Neurological diseases | Signal transduction | Signaling | Inhibitors | Rheumatoid arthritis | Arteriosclerosis | Sepsis | Cancer
Journal Article
Journal of Thrombosis and Haemostasis, ISSN 1538-7933, 06/2015, Volume 13, Issue 6, pp. 1090 - 1102
Summary Background and objectives Carboxypeptidase B2 (CPB2) is a basic carboxypeptidase with fibrin and complement C3a and C5a as physiological substrates. We... 
fibrinolysis | carboxypeptidase B2 | inflammation | anaphylatoxin | sepsis | Carboxypeptidase B2 | Sepsis | Inflammation | Anaphylatoxin | Fibrinolysis | ACTIVATABLE FIBRINOLYSIS INHIBITOR | MOUSE | INJURY | RECEPTOR | PROTECTS | TAFI | GENE-EXPRESSION | PERIPHERAL VASCULAR DISEASE | MICE | PROCARBOXYPEPTIDASE-B | HEMATOLOGY | Blood Coagulation Disorders - enzymology | Liver - microbiology | Complement C5a - metabolism | Male | Cecum - microbiology | Protective Factors | Blood Coagulation Disorders - genetics | Liver - immunology | Cecum - surgery | Time Factors | Peritonitis - genetics | Complement C3a - antagonists & inhibitors | Carboxypeptidase B2 - deficiency | Disease Models, Animal | Leukopenia - microbiology | Risk Factors | Macrophages, Peritoneal - enzymology | Macrophages, Peritoneal - immunology | Macrophage Activation | Mice, Knockout | Peritonitis - enzymology | Sepsis - enzymology | Complement C3a - immunology | Enzyme Activation | Fibrin - metabolism | Leukopenia - immunology | Liver - enzymology | Leukopenia - genetics | Peritonitis - microbiology | Thrombomodulin - metabolism | Ligation | Carboxypeptidase B2 - genetics | Complement C3a - metabolism | Sepsis - immunology | Mice, Inbred C57BL | Cells, Cultured | Inflammation Mediators - blood | Punctures | Blood Coagulation Disorders - microbiology | Peritonitis - immunology | Sepsis - genetics | Complement C5a - antagonists & inhibitors | Animals | Macrophages, Peritoneal - microbiology | Blood Coagulation Disorders - immunology | Antifibrinolytic Agents - pharmacology | Leukopenia - enzymology | Complement C5a - immunology | Thrombin - metabolism | Sepsis - microbiology | Fibrin | Thrombin | Analysis | Liver | Medical research | Rodents
Journal Article
Nature Medicine, ISSN 1078-8956, 08/2012, Volume 18, Issue 8, pp. 1217 - 1223
Sepsis, a systemic inflammatory response to infection, commonly progresses to acute lung injury (ALI), an inflammatory lung disease with high morbidity. We... 
MEDICINE, RESEARCH & EXPERIMENTAL | ACTIVATION | PROTEIN-KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | ICAM-1 | MODEL | MOLECULES | CELL BIOLOGY | LEUKOCYTES | IN-VIVO | HEPARAN-SULFATE | CELL | UNFRACTIONATED HEPARIN | Intestinal Perforation - complications | Humans | Heparitin Sulfate - antagonists & inhibitors | Male | Adoptive Transfer | Heparitin Sulfate - metabolism | Pulmonary Alveoli - enzymology | Glucuronidase - deficiency | Glucuronidase - analysis | Receptors, Tumor Necrosis Factor, Type I - deficiency | Glucuronidase - physiology | Respiratory Insufficiency - enzymology | Ventilator-Induced Lung Injury - enzymology | Acute Lung Injury - prevention & control | Endotoxemia - physiopathology | Intercellular Adhesion Molecule-1 - biosynthesis | Endothelium - enzymology | Disease Models, Animal | Acute Lung Injury - physiopathology | Lipopolysaccharides - toxicity | Pulmonary Alveoli - pathology | Mice, Inbred C57BL | Neutrophils - physiology | Ventilator-Induced Lung Injury - pathology | Lung - physiopathology | Mice, Knockout | Gene Expression Regulation - drug effects | Respiratory Insufficiency - pathology | Glycocalyx - physiology | Animals | Cell Adhesion - physiology | Endotoxemia - complications | Receptors, Tumor Necrosis Factor, Type I - physiology | Intercellular Adhesion Molecule-1 - genetics | Tumor Necrosis Factor-alpha - physiology | Mice | Enzyme Activation | Acute Lung Injury - etiology | Intestinal Perforation - microbiology | Endothelium - physiology | Care and treatment | Glycocalyx | Cellular control mechanisms | Neutrophils | Cell adhesion | Physiological aspects | Sepsis | Development and progression | Research | Properties | Respiratory physiology | Endothelium | Leucocytes | Glycoproteins | Lung diseases | Cell adhesion & migration | Immune system
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 11/2017, Volume 127, Issue 11, pp. 4124 - 4135
Journal Article