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Gastroenterology, ISSN 0016-5085, 2014, Volume 146, Issue 7, pp. 1763 - 1774
Background & Aims The NACHT, LRR, and pyrin domain–containing protein 3 (NLRP3) inflammasome induces inflammation in response to organ injury, but little is... 
Gastroenterology and Hepatology | Innate Immune Response | Immune Regulation | Pancreas | Mouse Model | ACTIVATION | NLRP3 INFLAMMASOME | GPR81 | AGONISTS | GENE | TLR9 | MICE | HEPATOTOXICITY | GASTROENTEROLOGY & HEPATOLOGY | EXPRESSION | SEVERITY | Liver - pathology | Inflammasomes - metabolism | Receptors, G-Protein-Coupled - metabolism | NLR Family, Pyrin Domain-Containing 3 Protein | Humans | Male | NF-kappa B - metabolism | Monocytes - immunology | Lipopolysaccharides | Liver - immunology | Liver - drug effects | RNA Interference | Interleukin-1beta - metabolism | Toll-Like Receptors - drug effects | Anti-Inflammatory Agents - administration & dosage | Toll-Like Receptors - metabolism | Cytoprotection | Disease Models, Animal | Galactosamine | Chemical and Drug Induced Liver Injury - prevention & control | Anti-Inflammatory Agents - pharmacology | Down-Regulation | Liver - metabolism | Injections, Intraperitoneal | Pancreas - pathology | Pancreas - metabolism | Pancreas - immunology | Toll-Like Receptor 4 - metabolism | Chemical and Drug Induced Liver Injury - immunology | Monocytes - drug effects | Macrophages - metabolism | Signal Transduction - drug effects | Chemical and Drug Induced Liver Injury - metabolism | Sodium Lactate - pharmacology | beta-Arrestins | Mice | Receptors, G-Protein-Coupled - genetics | RNA, Small Interfering - metabolism | Monocytes - metabolism | Pancreatitis - prevention & control | Arrestins - metabolism | Dose-Response Relationship, Drug | Pancreatitis - genetics | Transfection | Inflammasomes - drug effects | Sodium Lactate - administration & dosage | Pancreatitis - immunology | Chemical and Drug Induced Liver Injury - pathology | Chemical and Drug Induced Liver Injury - etiology | Macrophages - immunology | Cell Line | Immunity, Innate - drug effects | Toll-Like Receptor 4 - drug effects | Mice, Inbred C57BL | Pancreas - drug effects | Chemical and Drug Induced Liver Injury - genetics | Pancreatitis - chemically induced | Animals | Carrier Proteins - metabolism | beta-Arrestin 2 | Inflammasomes - immunology | Macrophages - drug effects | Pancreatitis - pathology | Pancreatitis - metabolism | Ceruletide | Lactates | Gastrointestinal diseases | Inflammation
Journal Article
American Journal of Gastroenterology, ISSN 0002-9270, 02/2015, Volume 110, Issue 2, pp. 336 - 345
Journal Article
Molecular Biology of the Cell, ISSN 1059-1524, 12/2008, Volume 20, Issue 3, pp. 870 - 881
Journal Article
Gastroenterology, ISSN 0016-5085, 09/2016, Volume 151, Issue 3, pp. 526 - 539
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 03/2013, Volume 33, Issue 13, pp. 5603 - 5611
Visceral afferents expressing transient receptor potential (TRP) channels TRPV1 and TRPA1 are thought to be required for neurogenic inflammation and... 
ACTIVATION | SUBPOPULATIONS | PHOSPHORYLATION | SENSITIZATION | PROTEIN-KINASE | HYPERALGESIA | EXPRESSION | NEUROSCIENCES | SENSORY NEURONS | ERK | Calcium - metabolism | Male | Nodose Ganglion - metabolism | RNA, Messenger - metabolism | Amidines - metabolism | Time Factors | TRPV Cation Channels - antagonists & inhibitors | Pancreatitis, Chronic - drug therapy | Exploratory Behavior - drug effects | Monocytes - pathology | Pain - etiology | Sensory Receptor Cells - metabolism | Transient Receptor Potential Channels - metabolism | Calcitonin Gene-Related Peptide - metabolism | Neutrophil Infiltration - drug effects | Disease Models, Animal | Injections, Intraperitoneal | Pancreas - pathology | Analgesics, Opioid - therapeutic use | Pancreas - metabolism | Pain - pathology | Disease Progression | Pancreatitis, Chronic - pathology | Analysis of Variance | Transient Receptor Potential Channels - genetics | Ganglia, Spinal - pathology | Mice | Transient Receptor Potential Channels - antagonists & inhibitors | Oximes - therapeutic use | Pancreatitis, Chronic - chemically induced | Monocytes - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | TRPV Cation Channels - metabolism | Antigens, Differentiation - metabolism | Pyridines - therapeutic use | Sensory Receptor Cells - pathology | Pain - prevention & control | Mice, Inbred C57BL | Ceruletide - toxicity | Pancreas - drug effects | Pain Measurement - drug effects | TRPV Cation Channels - genetics | Gene Expression Regulation - drug effects | Nodose Ganglion - pathology | Animals | Sensory Receptor Cells - drug effects | Pancreatitis, Chronic - complications | TRPA1 Cation Channel | Morphine - therapeutic use | Ganglia, Spinal - metabolism | Peroxidase - metabolism
Journal Article
Journal Article
PLoS ONE, ISSN 1932-6203, 02/2016, Volume 11, Issue 2, p. e0148252
Fibroblast growth factor 21 (FGF21) is an important endocrine metabolic regulator expressed in multiple tissues including liver and adipose tissue. Although... 
PPAR-ALPHA | IMPROVES INSULIN SENSITIVITY | ACTIVATION | METABOLIC REGULATOR | FIBROBLAST-GROWTH-FACTOR-21 | MULTIDISCIPLINARY SCIENCES | LIVER | RECEPTOR | RESISTANT STATES | MICE | ADIPOSE-TISSUE | Tumor Necrosis Factor-alpha - metabolism | Pancreatitis - etiology | Tumor Necrosis Factor-alpha - genetics | Fibroblast Growth Factors - genetics | Male | Interferon-gamma - metabolism | Obesity - genetics | Fibroblast Growth Factors - metabolism | Pancreatitis - genetics | Hyperplasia - genetics | Forkhead Transcription Factors - metabolism | Islets of Langerhans - metabolism | Diet, High-Fat | Mitogen-Activated Protein Kinase 1 - genetics | Thy-1 Antigens - genetics | Obesity - etiology | Interferon-gamma - genetics | Hyperplasia - metabolism | Acinar Cells - metabolism | Dietary Fats - adverse effects | Fasting | Islets of Langerhans - pathology | Mitogen-Activated Protein Kinase 3 - genetics | Signal Transduction | Mice, Inbred C57BL | Gene Expression Regulation | Inflammation | Forkhead Transcription Factors - genetics | Organ Specificity | Receptors, Antigen, T-Cell, alpha-beta - genetics | Hyperplasia - etiology | Obesity - metabolism | Obesity - pathology | Hyperplasia - pathology | Thy-1 Antigens - metabolism | Acinar Cells - pathology | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Pancreatitis - pathology | Mice | Pancreatitis - metabolism | Receptors, Antigen, T-Cell, alpha-beta - metabolism | Mitogen-Activated Protein Kinase 1 - metabolism | Fibroblast growth factor | Phosphorylation | Adipose tissue | Laboratories | Liver | Hyperplasia | Lymphocytes T | Biology | Tissues | High fat diet | Infusion | Cell growth | Lymphocytes | Rodents | Interleukin 1 | Fibroblasts | Foxp3 protein | Physiology | Pancreas | Growth factors | Acinar cells | Cytokines | Immunoregulation | Extracellular signal-regulated kinase | Tumor necrosis factor-α | Metabolism | Fatty acids | Studies | Diet | γ-Interferon | Islet cells | Insulin resistance | Islets of Langerhans | Diabetes | Endocrinology
Journal Article
Gastroenterology, ISSN 0016-5085, 2009, Volume 137, Issue 1, pp. 350 - 360.e5
Background & Aims Acute pancreatitis constitutes a life-threatening condition in which pancreatic acinar cells undergo massive cell death. We investigated the... 
Gastroenterology and Hepatology | ACTIVATED PROTEIN-KINASE | INHIBITION | RAT PANCREAS | TRYPSINOGEN ACTIVATION | IN-VIVO | ENDOTOXIN | LIPOPOLYSACCHARIDE | CHRONIC ALCOHOL EXPOSURE | ACINAR-CELLS | GASTROENTEROLOGY & HEPATOLOGY | CELL-DEATH | Caspase 9 - metabolism | Pancreatitis - etiology | Humans | Caspase 3 - metabolism | Endotoxemia - chemically induced | Lysosomes - enzymology | Male | Endotoxemia - pathology | Autophagy | Lipopolysaccharides | Necrosis | Lysosomes - metabolism | Transfection | RNA Interference | Time Factors | Adenosine Triphosphate - metabolism | HMGB1 Protein - metabolism | Pancreatitis, Alcoholic - metabolism | Disease Models, Animal | Pancreas - enzymology | Pancreatitis, Alcoholic - etiology | Cell Line | Acute Disease | Lysosome-Associated Membrane Glycoproteins - metabolism | Ethanol | Down-Regulation | Lysosomal-Associated Membrane Protein 2 - genetics | Pancreas - pathology | Rats | Cathepsin B - metabolism | Pancreas - metabolism | Trypsin - metabolism | Rats, Sprague-Dawley | Animals | Endotoxemia - complications | Pancreatitis, Alcoholic - pathology | Pancreatitis - pathology | Pancreatitis - metabolism | Endotoxemia - metabolism | Lysosomal-Associated Membrane Protein 2 - metabolism | Apoptosis | Chromosomal proteins | Mitogens | Pancreatitis | Index Medicus | Abridged Index Medicus
Journal Article
SCIENCE, ISSN 0036-8075, 07/2017, Volume 357, Issue 6349
Kynurenine metabolites are generated by tryptophan catabolism and regulate biological processes that include host-microbiome signaling, immune cell response,... 
AMINO-ACID TRANSPORTER | QUINOLINIC ACID | DENDRITIC CELLS | ARYL-HYDROCARBON RECEPTOR | MULTIDISCIPLINARY SCIENCES | REGULATORY T-CELLS | ACUTE-PANCREATITIS | INDOLEAMINE 2,3-DIOXYGENASE ACTIVITY | TYPE-2 DIABETES-MELLITUS | BLOOD-BRAIN-BARRIER | IRRITABLE-BOWEL-SYNDROME | Neoplasms - metabolism | Signal Transduction | Humans | Liver - metabolism | Mental Disorders - metabolism | Gastrointestinal Microbiome | Muscle, Skeletal - metabolism | Mental Health | Tryptophan - metabolism | Gastrointestinal Tract - metabolism | Brain - metabolism | Depression - metabolism | Inflammation - metabolism | Exercise | Kynurenine - metabolism | Brain | Central nervous system | Disorders | Nervous system | Mental depression | Training | Physiology | Active control | Fitness training programs | Enzymes | Digestive system | Excitability | Bioavailability | Metabolism | Insulin | Substrates | Diseases | Probiotics | Physical fitness | Immunosuppression | Mood | Diet | Cell migration | Cell proliferation | Mental disorders | Mental health | Schizophrenia | Amino acids | Lymphocytes T | Tissues | Accumulation | Inflammatory diseases | Killer cells | Metabolites | Bioactive compounds | Intestine | Modulation | Bacteria | Nutrients | Digestive tract | Immune system | Biodegradation | Cues | Immune response | Dendritic cells | Secretion | Diabetes mellitus | Muscles | Inflammation | Pharmacology | Biological activity | Skeletal muscle | Musculoskeletal system | Monocytes | Acids | Catabolism | Diabetes | Tumors | Cancer
Journal Article
Journal Article
Endocrinology, ISSN 0013-7227, 11/2015, Volume 156, Issue 11, pp. 3937 - 3949
Journal Article
Molecular Biology of the Cell, ISSN 1059-1524, 01/2009, Volume 20, Issue 3, pp. 870 - 881
Using a bioinformatic approach, we identified a TP53INP1-related gene encoding a protein with 30% identity with tumor protein 53-induced nuclear protein 1... 
NERVOUS-SYSTEM | TUMOR-PROTEIN-53-INDUCED-NUCLEAR-PROTEIN-1 | MOLECULAR MACHINERY | GENE | MEMBRANE-TRANSPORT MODULATOR | PANCREATITIS | EXPRESSION | CANCER | LC3 | CONJUGATION SYSTEM | CELL BIOLOGY | Gene Silencing - drug effects | Microtubule-Associated Proteins - metabolism | Humans | Molecular Sequence Data | Protein Transport - drug effects | Luminescent Measurements | Phylogeny | Autophagy - drug effects | Protein Binding - drug effects | Cloning, Molecular | Conserved Sequence | Carrier Proteins - chemistry | Membrane Proteins - metabolism | Phagosomes - drug effects | Beclin-1 | Amino Acid Sequence | Cell Line | Heat-Shock Proteins - metabolism | Phagosomes - metabolism | Nuclear Proteins - metabolism | Nuclear Proteins - chemistry | Sirolimus - pharmacology | Apoptosis Regulatory Proteins - metabolism | Animals | Carrier Proteins - metabolism | Mice | Adaptor Proteins, Signal Transducing - metabolism | Heat-Shock Proteins - chemistry | Heat-Shock Proteins: chemistry,metabolism | Membrane Proteins: metabolism | Protein Binding: drug effects | Gene Silencing: drug effects | Adaptor Proteins, Signal Transducing: metabolism | Life Sciences | Phagosomes: drug effects,metabolism | Apoptosis Regulatory Proteins: metabolism | Nuclear Proteins: chemistry,metabolism | Autophagy: drug effects | Protein Transport: drug effects | Microtubule-Associated Proteins: metabolism | Sirolimus: pharmacology | Carrier Proteins: chemistry,metabolism | Other
Journal Article
Gut, ISSN 0017-5749, 06/2014, Volume 63, Issue 6, pp. 903 - 910
Objective Although polymorphisms of the NOD2 gene predispose to the development of ileal Crohn's disease, the precise mechanisms of this increased... 
INTESTINAL INFLAMMATION | HOMEOSTASIS | INFLAMMATORY-BOWEL-DISEASE | PEPTIDES | MICE | MICROBIOTA | DIVERSITY | GASTROENTEROLOGY & HEPATOLOGY | ILEAL CROHNS-DISEASE | ALPHA-DEFENSIN EXPRESSION | INNATE IMMUNITY | Defensins - metabolism | Defensins - genetics | Escherichia coli - drug effects | Peptides - genetics | Ileum - metabolism | Nod2 Signaling Adaptor Protein - genetics | RNA, Messenger - metabolism | alpha-Defensins - genetics | Microbial Sensitivity Tests | Salmonella enterica - drug effects | Feces - microbiology | Lectins, C-Type - metabolism | Peptides - metabolism | Antigens, Neoplasm - metabolism | Biomarkers, Tumor - metabolism | Transcription, Genetic | alpha-Defensins - metabolism | Ileum - cytology | Paneth Cells - metabolism | Protein Precursors - genetics | Mice, Inbred C57BL | Paneth Cells - cytology | Ribonuclease, Pancreatic - genetics | Muramidase - metabolism | Pancreatitis-Associated Proteins | Mice, Knockout | Protein Precursors - metabolism | alpha-Defensins - pharmacology | Animals | Nod2 Signaling Adaptor Protein - metabolism | Ribonuclease, Pancreatic - metabolism | Analysis | Antimicrobial peptides | Crohn's disease | Genetic aspects | Research | Gene expression | Risk factors | Genetic polymorphisms | Studies | Pathogenesis | Rodents | Antimicrobial agents | Inflammation | Clinical medicine | Laboratory animals | Crohns disease | IBD - GENETICS | INTESTINAL EPITHELIUM | BACTERIAL INTERACTIONS | CROHN'S DISEASE | Inflammatory Bowel Disease | 1506
Journal Article