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Small (Weinheim an der Bergstrasse, Germany), ISSN 1613-6810, 2014, Volume 10, Issue 6, pp. 1171 - 1183
Journal Article
Journal of Endodontics, ISSN 0099-2399, 2012, Volume 38, Issue 4, pp. 486 - 489
Journal Article
Journal Article
Journal of Leukocyte Biology, ISSN 0741-5400, 12/2005, Volume 78, Issue 6, pp. 1273 - 1280
Journal Article
PloS one, ISSN 1932-6203, 2016, Volume 11, Issue 7, p. e0158674
Modeling clinically relevant tissue responses using cell models poses a significant challenge for drug development, in particular for drug induced liver injury... 
SYSTEM | HEPATOCYTES | IDIOSYNCRASY | HEPATIC STELLATE CELLS | MULTIDISCIPLINARY SCIENCES | INJURY | LIPOPOLYSACCHARIDE | TROVAFLOXACIN HEPATOTOXICITY | CULTURE | RELEVANT | Bioprinting | Cell Proliferation | Albumins - metabolism | Humans | Liver - metabolism | Cells, Cultured | Lipopolysaccharides - metabolism | Hepatocytes - metabolism | Chemical and Drug Induced Liver Injury - diagnosis | Hepatocytes - cytology | Image Processing, Computer-Assisted | Liver - drug effects | Cytochrome P-450 CYP3A - metabolism | Platelet Endothelial Cell Adhesion Molecule-1 - metabolism | Drug-Related Side Effects and Adverse Reactions | Cell Culture Techniques | Imaging, Three-Dimensional | Naphthyridines - administration & dosage | Hepatocytes - drug effects | Levofloxacin - administration & dosage | Fluoroquinolones - administration & dosage | Drugs | Usage | Liver | Models | Diagnosis | Health aspects | 3D printing | Cytochrome | Cell culture | Levofloxacin | Enzyme activity | Toxicity | Smooth muscle | Research | Drug development | Macrophages | Mimicry | Toxicology | Enzymatic activity | Metabolites | Actin | Rodents | Biocompatibility | Physiology | Drug therapy | Trovafloxacin | Architecture | Tissue engineering | Muscles | Antimicrobial agents | Metabolism | Gene expression | Desmin | Three dimensional printing | Inventors | Hepatocytes | Human behavior | Three dimensional models | Pharmaceuticals
Journal Article
Journal of neurochemistry, ISSN 0022-3042, 2011, Volume 116, Issue 1, pp. 53 - 66
...‐cell autonomous fashion through the induction of TNF in mixed glial cultures. Here, we report that activation of oligodendroglial, but not astroglial and microglial, TNFR1 is required for LPS toxicity, and that astrocytes promote TNF... 
periventricular leukomalacia | cell death | oligodendrocyte precursors | inflammation | microglia | white matter injury | INDUCED CELL-DEATH | BIOCHEMISTRY & MOLECULAR BIOLOGY | NEUROSCIENCES | WHITE-MATTER INJURY | FACTOR-ALPHA | TUMOR-NECROSIS-FACTOR | MULTIPLE-SCLEROSIS | MICROGLIAL TOXICITY | CENTRAL-NERVOUS-SYSTEM | OXIDATIVE INJURY | TRANSGENIC MICE | Mice, Inbred C57BL | Astrocytes - pathology | Cells, Cultured | Mice, Transgenic | Receptors, Tumor Necrosis Factor, Type I - genetics | Tumor Necrosis Factor-alpha - toxicity | Mice, Knockout | Oligodendroglia - pathology | Astrocytes - physiology | Animals | Oligodendroglia - physiology | Receptors, Tumor Necrosis Factor, Type I - biosynthesis | Receptors, Tumor Necrosis Factor - biosynthesis | Stem Cells - pathology | Stem Cells - physiology | Mice | Receptors, Tumor Necrosis Factor - genetics | Nervous system diseases | Multiple sclerosis | Cell death | Mitogens | Neurochemistry | Cell culture | Cellular biology | Toxicity | Inflammatory diseases | Index Medicus | Tumor necrosis factor receptors | Astrocytes | Central nervous system | Cytotoxicity | Inflammation | Substantia alba | Glial stem cells | Lipopolysaccharides | Microglia | Neurological diseases | Tumor necrosis factor | Oligodendrocytes | Injuries
Journal Article
Journal Article
PloS one, ISSN 1932-6203, 2018, Volume 13, Issue 8, pp. e0201022 - e0201022
Hyperbilirubinemia (jaundice) is caused by raised levels of unconjugated bilirubin in the blood. When severe, susceptible brain regions including the... 
AUDITORY BRAIN-STEM | HYPERBILIRUBINEMIA | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | IN-VIVO | JAUNDICED GUNN-RATS | PNEUMOCOCCAL MENINGITIS | ENDOPLASMIC-RETICULUM | NF-KAPPA-B | NEURODEGENERATIVE DISEASES | DAMAGE | Bilirubin - metabolism | Hearing Loss - etiology | Humans | Ataxia - etiology | Male | NF-kappa B - metabolism | Hyperbilirubinemia - metabolism | Kernicterus - etiology | Hearing Loss - metabolism | Inflammation - metabolism | Evoked Potentials, Auditory, Brain Stem - drug effects | Mice, Inbred CBA | Female | Lipocalin-2 - genetics | Ataxia - metabolism | Kernicterus - metabolism | Disease Models, Animal | Cell Line | Acute Disease | Lipopolysaccharides - toxicity | Endoplasmic Reticulum Stress - drug effects | Anti-Inflammatory Agents - pharmacology | Bilirubin - toxicity | Hyperbilirubinemia - complications | Inflammation - etiology | Mice, Knockout | Neurotoxicity Syndromes - etiology | Animals | Neurotoxicity Syndromes - metabolism | Mice | Lipocalin-2 - deficiency | Hearing Loss - prevention & control | Care and treatment | Hyperbilirubinemia | Rattus | Causes of | Rats | Inflammation | Models | Research | Gene expression | Health aspects | Endoplasmic reticulum | Hearing loss | Cerebellum | Drugs | Brain | Oxidative stress | Neurosciences | Toxicity | Brain stem | Impairment | Immunoblotting | Inflammatory response | Genomes | Activation | Bilirubin | Lipopolysaccharides | Proteins | Thapsigargin | Signal transduction | Neurotoxicity | Protein folding | Biocompatibility | Ataxia | Stresses | Jaundice | NF-κB protein | Human motion | Lipocalin | Pharmacology | Exposure | Tumor necrosis factor-α | Hearing impairment | Chemical compounds | Anti-inflammatory agents | Brain research | Neurological complications | Auditory system | Brain damage | Human behavior | Apoptosis | Index Medicus
Journal Article
Journal Article
by Fan and Zhang and Luo and Wang and Tang and Chen and Yu
Molecules (Basel, Switzerland), ISSN 1420-3049, 2019, Volume 24, Issue 20, p. 3679
Journal Article
PLoS ONE, ISSN 1932-6203, 07/2013, Volume 8, Issue 7, p. e69452
Background/Aims: Septic cardiomyopathy is a severe condition that remains a challenge for clinical management. This study investigated whether the natural... 
CARDIAC-SPECIFIC OVEREXPRESSION | SIGNALING PATHWAY | INDUCED APOPTOSIS | MULTIDISCIPLINARY SCIENCES | REPERFUSION INJURY | HEART-FAILURE | MICROVASCULAR ENDOTHELIAL-CELLS | NECROSIS-FACTOR-ALPHA | TNF-ALPHA | PROTECTS CARDIOMYOCYTES | NF-KAPPA-B | Reactive Oxygen Species - metabolism | Myocytes, Cardiac - cytology | Apoptosis - drug effects | Humans | Mice, Inbred C57BL | Male | Mitochondria - metabolism | Cardiotonic Agents - pharmacology | Mitochondria - drug effects | Stilbenes - pharmacology | NF-E2-Related Factor 2 - deficiency | Gene Knockdown Techniques | Animals | Myocytes, Cardiac - drug effects | NF-E2-Related Factor 2 - metabolism | Lipopolysaccharides - pharmacology | Heart - drug effects | Myocytes, Cardiac - metabolism | NF-E2-Related Factor 2 - genetics | Mice | Cytokines - biosynthesis | Endotoxins - toxicity | Infection | Antioxidants | Cell death | Analysis | Resveratrol | Medicine, Preventive | Preventive health services | Heart | Transcription factors | Toxicity | Cardiomyopathy | Smooth muscle | Activation | Kinases | Lipopolysaccharides | Rodents | Tumor necrosis factor-TNF | Biocompatibility | Pretreatment | Cardiology | Heart diseases | Injuries | Heart failure | Echocardiography | Cytokines | Mortality | Cardiomyocytes | Inflammation | siRNA | Gene expression | Studies | Molecular modelling | Sepsis | In vivo methods and tests | Diabetes | Chemokines | Apoptosis | Structure-function relationships
Journal Article