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Publication DateGastroenterology, ISSN 0016-5085, 2010, Volume 138, Issue 6, pp. 2101 - 2114.e5
The connection between inflammation and tumorigenesis is well-established and in the last decade has received a great deal of supporting evidence from genetic,...
Gastroenterology and Hepatology | Inflammation | Cytokines | Immunity | Colon Cancer | CHRONIC INTESTINAL INFLAMMATION | COLITIS-ASSOCIATED CANCER | SEVERE CROHNS-DISEASE | EPITHELIAL-MESENCHYMAL TRANSITION | TUMOR-NECROSIS-FACTOR | NONSTEROIDAL ANTIINFLAMMATORY DRUGS | KINASE-I-EPSILON | TOLL-LIKE RECEPTORS | GASTROENTEROLOGY & HEPATOLOGY | NF-KAPPA-B | GENOME-WIDE ASSOCIATION | Colonic Neoplasms - genetics | Colonic Neoplasms - prevention & control | Colonic Neoplasms - drug therapy | Colorectal Neoplasms - genetics | Humans | Inflammatory Bowel Diseases - immunology | Gene Expression Regulation, Neoplastic | Colon - immunology | Cell Transformation, Neoplastic - genetics | Colonic Neoplasms - immunology | Colorectal Neoplasms - drug therapy | Inflammation Mediators - metabolism | Inflammatory Bowel Diseases - genetics | Anti-Inflammatory Agents - therapeutic use | Inflammatory Bowel Diseases - complications | Anticarcinogenic Agents - therapeutic use | Inflammatory Bowel Diseases - drug therapy | Genetic Predisposition to Disease | Cytokines - metabolism | Risk Assessment | Signal Transduction | Neoplasm Invasiveness | Risk Factors | Colorectal Neoplasms - prevention & control | Colonic Neoplasms - secondary | Cell Transformation, Neoplastic - immunology | Animals | Colorectal Neoplasms - immunology | Colorectal Neoplasms - secondary | Colon - microbiology | Dendritic cells | Measles-mumps-rubella vaccine | Biological response modifiers | Sulfates | Risk factors | Dextran | Prostaglandins | Colon cancer | Gastrointestinal diseases | Vascular endothelial growth factor | Growth factors | Tumors
Gastroenterology and Hepatology | Inflammation | Cytokines | Immunity | Colon Cancer | CHRONIC INTESTINAL INFLAMMATION | COLITIS-ASSOCIATED CANCER | SEVERE CROHNS-DISEASE | EPITHELIAL-MESENCHYMAL TRANSITION | TUMOR-NECROSIS-FACTOR | NONSTEROIDAL ANTIINFLAMMATORY DRUGS | KINASE-I-EPSILON | TOLL-LIKE RECEPTORS | GASTROENTEROLOGY & HEPATOLOGY | NF-KAPPA-B | GENOME-WIDE ASSOCIATION | Colonic Neoplasms - genetics | Colonic Neoplasms - prevention & control | Colonic Neoplasms - drug therapy | Colorectal Neoplasms - genetics | Humans | Inflammatory Bowel Diseases - immunology | Gene Expression Regulation, Neoplastic | Colon - immunology | Cell Transformation, Neoplastic - genetics | Colonic Neoplasms - immunology | Colorectal Neoplasms - drug therapy | Inflammation Mediators - metabolism | Inflammatory Bowel Diseases - genetics | Anti-Inflammatory Agents - therapeutic use | Inflammatory Bowel Diseases - complications | Anticarcinogenic Agents - therapeutic use | Inflammatory Bowel Diseases - drug therapy | Genetic Predisposition to Disease | Cytokines - metabolism | Risk Assessment | Signal Transduction | Neoplasm Invasiveness | Risk Factors | Colorectal Neoplasms - prevention & control | Colonic Neoplasms - secondary | Cell Transformation, Neoplastic - immunology | Animals | Colorectal Neoplasms - immunology | Colorectal Neoplasms - secondary | Colon - microbiology | Dendritic cells | Measles-mumps-rubella vaccine | Biological response modifiers | Sulfates | Risk factors | Dextran | Prostaglandins | Colon cancer | Gastrointestinal diseases | Vascular endothelial growth factor | Growth factors | Tumors
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Loading Rights2011, Recent results in cancer research, ISBN 3642035027, Volume 185., ix, 199
Inflammation in gastrointestinal mucosa is the single most common pathway for GI cancer. This book examines the relation between inflammation and GI cancer,...
Gastrointestinal mucosa | Gastrointestinal system | Cancer | Clinical & internal medicine | Chronic diseases | Inflammation | Digestive organs
Gastrointestinal mucosa | Gastrointestinal system | Cancer | Clinical & internal medicine | Chronic diseases | Inflammation | Digestive organs
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Gastroenterology, ISSN 0016-5085, 2011, Volume 140, Issue 6, pp. 1807 - 1816.e1
Patients with ulcerative colitis and Crohn's disease are at increased risk for developing colorectal cancer (CRC). Chronic inflammation is believed to promote...
Gastroenterology and Hepatology | Adaptive Immunity | IBD | Animal Model | Neoplasia | Intestine | Innate Immunity | NITRIC-OXIDE SYNTHASE | MICROSATELLITE INSTABILITY | ULCERATIVE-COLITIS | COLITIS-ASSOCIATED CARCINOGENESIS | BOWEL-DISEASE | COLON-CANCER | K-RAS GENE | EPITHELIAL-CELLS | COLORECTAL-CANCER | MOUSE MODEL | GASTROENTEROLOGY & HEPATOLOGY | Colitis, Ulcerative - complications | Oxidative Stress | Colitis, Ulcerative - metabolism | Humans | Risk Factors | Crohn Disease - metabolism | Gastrointestinal Tract - microbiology | Immunity, Innate | Crohn Disease - complications | Colonic Neoplasms - physiopathology | Bacterial Infections - complications | Animals | Colonic Neoplasms - pathology | Crohn Disease - drug therapy | Anti-Inflammatory Agents - therapeutic use | Colitis, Ulcerative - drug therapy | Colonic Neoplasms - etiology | Development and progression | Ursodiol | Crohn's disease | Inflammation | DNA binding proteins | Sulfates | Dextran | Colon cancer | Analysis | Nitric oxide | DNA | Genetically modified organisms | Tumor proteins | Ulcerative colitis | Cancer
Gastroenterology and Hepatology | Adaptive Immunity | IBD | Animal Model | Neoplasia | Intestine | Innate Immunity | NITRIC-OXIDE SYNTHASE | MICROSATELLITE INSTABILITY | ULCERATIVE-COLITIS | COLITIS-ASSOCIATED CARCINOGENESIS | BOWEL-DISEASE | COLON-CANCER | K-RAS GENE | EPITHELIAL-CELLS | COLORECTAL-CANCER | MOUSE MODEL | GASTROENTEROLOGY & HEPATOLOGY | Colitis, Ulcerative - complications | Oxidative Stress | Colitis, Ulcerative - metabolism | Humans | Risk Factors | Crohn Disease - metabolism | Gastrointestinal Tract - microbiology | Immunity, Innate | Crohn Disease - complications | Colonic Neoplasms - physiopathology | Bacterial Infections - complications | Animals | Colonic Neoplasms - pathology | Crohn Disease - drug therapy | Anti-Inflammatory Agents - therapeutic use | Colitis, Ulcerative - drug therapy | Colonic Neoplasms - etiology | Development and progression | Ursodiol | Crohn's disease | Inflammation | DNA binding proteins | Sulfates | Dextran | Colon cancer | Analysis | Nitric oxide | DNA | Genetically modified organisms | Tumor proteins | Ulcerative colitis | Cancer
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Loading Rights2012, ISBN 9814343595, xv, 361
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Immunological Reviews, ISSN 0105-2896, 03/2013, Volume 252, Issue 1, pp. 164 - 182
Summary Intestinal CD4+ T cells are essential mediators of immune homeostasis and inflammation. Multiple subsets of CD4+ T cells have been described in the...
intestinal inflammation | Th1 | T‐cell differentiation | Th17 | Treg | Intestinal inflammation | T-cell differentiation | PATHOGENIC T(H)17 CELLS | IMMUNOLOGY | ACTIVE CROHNS-DISEASE | CHRONIC MUCOCUTANEOUS CANDIDIASIS | SEGMENTED FILAMENTOUS BACTERIA | BOWEL-DISEASE | HYPER-IGE SYNDROME | IN-VIVO | LAMINA PROPRIA LYMPHOCYTES | CYTOKINE GM-CSF | TH17 CELLS | T-Lymphocyte Subsets - immunology | Intestines - pathology | Humans | Inflammatory Bowel Diseases - immunology | Immunity, Mucosal | Homeostasis - immunology | CD4-Positive T-Lymphocytes - pathology | Intestines - immunology | CD4-Positive T-Lymphocytes - immunology | T-Lymphocyte Subsets - pathology | Intestinal Mucosa - immunology | Inflammatory Bowel Diseases - pathology | Metagenome - immunology | Cytokines - immunology | Intestinal Mucosa - pathology | T cells | Gastrointestinal system | Inflammation | Inflammatory bowel diseases | Translation | Intestine | Homeostasis | Gastrointestinal tract | Lymphocytes T | CD4 antigen | Invited Reviews
intestinal inflammation | Th1 | T‐cell differentiation | Th17 | Treg | Intestinal inflammation | T-cell differentiation | PATHOGENIC T(H)17 CELLS | IMMUNOLOGY | ACTIVE CROHNS-DISEASE | CHRONIC MUCOCUTANEOUS CANDIDIASIS | SEGMENTED FILAMENTOUS BACTERIA | BOWEL-DISEASE | HYPER-IGE SYNDROME | IN-VIVO | LAMINA PROPRIA LYMPHOCYTES | CYTOKINE GM-CSF | TH17 CELLS | T-Lymphocyte Subsets - immunology | Intestines - pathology | Humans | Inflammatory Bowel Diseases - immunology | Immunity, Mucosal | Homeostasis - immunology | CD4-Positive T-Lymphocytes - pathology | Intestines - immunology | CD4-Positive T-Lymphocytes - immunology | T-Lymphocyte Subsets - pathology | Intestinal Mucosa - immunology | Inflammatory Bowel Diseases - pathology | Metagenome - immunology | Cytokines - immunology | Intestinal Mucosa - pathology | T cells | Gastrointestinal system | Inflammation | Inflammatory bowel diseases | Translation | Intestine | Homeostasis | Gastrointestinal tract | Lymphocytes T | CD4 antigen | Invited Reviews
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Loading RightsGastroenterology, ISSN 0016-5085, 2012, Volume 143, Issue 5, pp. 1158 - 1172
Inflammation In the absence of pathogens occurs in all tissues in response to a wide range of stimuli that cause tissue stress and injury. Such sterile...
Gastroenterology and Hepatology | Inflammasome | TLR | DAMPs | ACETAMINOPHEN-INDUCED HEPATOTOXICITY | INTERCELLULAR-ADHESION MOLECULE-1 | NLRP3 INFLAMMASOME | HEPATIC ISCHEMIA/REPERFUSION INJURY | TOLL-LIKE-RECEPTOR | GROUP BOX-1 PROTEIN | CELL-DEATH | NALP3 INFLAMMASOME | ISCHEMIA-REPERFUSION INJURY | GASTROENTEROLOGY & HEPATOLOGY | NF-KAPPA-B | Acetaminophen - adverse effects | Chemotaxis, Leukocyte | Hepatitis - etiology | Fatty Liver - metabolism | Inflammasomes - metabolism | Uric Acid - metabolism | Cytokines - metabolism | Signal Transduction | Humans | Neutrophils | Caspase 1 - metabolism | Nucleic Acids - metabolism | Fatty Liver, Alcoholic - metabolism | Hepatitis - drug therapy | Receptors, Pattern Recognition - metabolism | Chemical and Drug Induced Liver Injury - metabolism | Interleukin-1beta - metabolism | Adenosine Triphosphate - metabolism | HMGB1 Protein - metabolism | Hepatitis - metabolism | Non-alcoholic Fatty Liver Disease | Reperfusion Injury - complications | Reperfusion Injury - metabolism | Chromosomal proteins | Liver diseases | Interleukins | Alcoholics | Thrombin | Inflammation | Hyaluronic acid | Mitogens | Proteases | Gastrointestinal diseases | Index Medicus | Abridged Index Medicus
Gastroenterology and Hepatology | Inflammasome | TLR | DAMPs | ACETAMINOPHEN-INDUCED HEPATOTOXICITY | INTERCELLULAR-ADHESION MOLECULE-1 | NLRP3 INFLAMMASOME | HEPATIC ISCHEMIA/REPERFUSION INJURY | TOLL-LIKE-RECEPTOR | GROUP BOX-1 PROTEIN | CELL-DEATH | NALP3 INFLAMMASOME | ISCHEMIA-REPERFUSION INJURY | GASTROENTEROLOGY & HEPATOLOGY | NF-KAPPA-B | Acetaminophen - adverse effects | Chemotaxis, Leukocyte | Hepatitis - etiology | Fatty Liver - metabolism | Inflammasomes - metabolism | Uric Acid - metabolism | Cytokines - metabolism | Signal Transduction | Humans | Neutrophils | Caspase 1 - metabolism | Nucleic Acids - metabolism | Fatty Liver, Alcoholic - metabolism | Hepatitis - drug therapy | Receptors, Pattern Recognition - metabolism | Chemical and Drug Induced Liver Injury - metabolism | Interleukin-1beta - metabolism | Adenosine Triphosphate - metabolism | HMGB1 Protein - metabolism | Hepatitis - metabolism | Non-alcoholic Fatty Liver Disease | Reperfusion Injury - complications | Reperfusion Injury - metabolism | Chromosomal proteins | Liver diseases | Interleukins | Alcoholics | Thrombin | Inflammation | Hyaluronic acid | Mitogens | Proteases | Gastrointestinal diseases | Index Medicus | Abridged Index Medicus
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Loading RightsJournal of Clinical Investigation, ISSN 0021-9738, 11/2011, Volume 121, Issue 11, pp. 4503 - 4515
Tregs not only keep immune responses to autoantigens in check, but also restrain those directed toward pathogens and the commensal microbiota. Control of...
MEDICINE, RESEARCH & EXPERIMENTAL | THYMOCYTE DEVELOPMENT | CYTOKINE PRODUCTION | TH2 CELLS | TGF-BETA | IN-VIVO | SUPPRESSIVE FUNCTION | RETINOIC-ACID | HELPER-CELLS | CONTROL INTESTINAL INFLAMMATION | TRANSCRIPTION FACTOR GATA-3 | Forkhead Transcription Factors - immunology | GATA3 Transcription Factor - genetics | Inflammation - pathology | T-Lymphocytes, Regulatory - metabolism | Up-Regulation | GATA3 Transcription Factor - immunology | Humans | Male | Gastrointestinal Tract - pathology | T-Lymphocytes, Regulatory - pathology | T-Lymphocytes, Regulatory - immunology | Gastrointestinal Tract - immunology | Inflammation - metabolism | Female | Cytokines - genetics | Skin - pathology | Cytokines - immunology | Skin - immunology | Receptors, Antigen, T-Cell - metabolism | Mice, Inbred C57BL | Mice, Transgenic | Inflammation - immunology | GATA3 Transcription Factor - deficiency | Mice, Knockout | Animals | Cytokines - deficiency | Mice | Cytokines | Genetic aspects | Research | T cells | Properties | Genetic regulation | Gene expression
MEDICINE, RESEARCH & EXPERIMENTAL | THYMOCYTE DEVELOPMENT | CYTOKINE PRODUCTION | TH2 CELLS | TGF-BETA | IN-VIVO | SUPPRESSIVE FUNCTION | RETINOIC-ACID | HELPER-CELLS | CONTROL INTESTINAL INFLAMMATION | TRANSCRIPTION FACTOR GATA-3 | Forkhead Transcription Factors - immunology | GATA3 Transcription Factor - genetics | Inflammation - pathology | T-Lymphocytes, Regulatory - metabolism | Up-Regulation | GATA3 Transcription Factor - immunology | Humans | Male | Gastrointestinal Tract - pathology | T-Lymphocytes, Regulatory - pathology | T-Lymphocytes, Regulatory - immunology | Gastrointestinal Tract - immunology | Inflammation - metabolism | Female | Cytokines - genetics | Skin - pathology | Cytokines - immunology | Skin - immunology | Receptors, Antigen, T-Cell - metabolism | Mice, Inbred C57BL | Mice, Transgenic | Inflammation - immunology | GATA3 Transcription Factor - deficiency | Mice, Knockout | Animals | Cytokines - deficiency | Mice | Cytokines | Genetic aspects | Research | T cells | Properties | Genetic regulation | Gene expression
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Loading Rights2004, Progress in inflammation research, ISBN 9783764369101, x, 144
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Neurobiology of Disease, ISSN 0969-9961, 2012, Volume 50, Issue 1, pp. 42 - 48
Abstract Lewy pathology affects the gastrointestinal tract in Parkinson's disease (PD) and data from recent genetic studies suggest a link between PD and gut...
Neurology | Enteric nervous system | Tumor necrosis factor alpha | Parkinson's disease | Sox-10 | Glial fibrillary acidic protein | Inflammation | Colon | Interleukin-1 beta | Interleukin-6 | Interferon gamma | Glial flbrillary acidic protein | ENTERIC NERVOUS-SYSTEM | ULCERATIVE-COLITIS | NECROSIS-FACTOR-ALPHA | TIME QUANTITATIVE PCR | GLIAL-CELLS | CEREBROSPINAL-FLUID | NEUROSCIENCES | DETECT LEWY PATHOLOGY | MESSENGER-RNA | GROWTH-FACTOR-ALPHA | PROTEIN EXPRESSION | Inflammation - pathology | Parkinson Disease - complications | Parkinson Disease - pathology | Parkinson Disease - immunology | Humans | Middle Aged | RNA, Messenger - analysis | Colitis - pathology | Male | Inflammation - immunology | Inflammation - etiology | Colitis - etiology | Adult | Female | Aged | Colitis - immunology | Lewy Bodies - pathology | Real-Time Polymerase Chain Reaction | Cytokines - biosynthesis | RNA | Interferon alpha | Development and progression | Disease susceptibility | Biological response modifiers | Interleukins | Analysis | Gastrointestinal system | Dopa | Intermediate filament proteins
Neurology | Enteric nervous system | Tumor necrosis factor alpha | Parkinson's disease | Sox-10 | Glial fibrillary acidic protein | Inflammation | Colon | Interleukin-1 beta | Interleukin-6 | Interferon gamma | Glial flbrillary acidic protein | ENTERIC NERVOUS-SYSTEM | ULCERATIVE-COLITIS | NECROSIS-FACTOR-ALPHA | TIME QUANTITATIVE PCR | GLIAL-CELLS | CEREBROSPINAL-FLUID | NEUROSCIENCES | DETECT LEWY PATHOLOGY | MESSENGER-RNA | GROWTH-FACTOR-ALPHA | PROTEIN EXPRESSION | Inflammation - pathology | Parkinson Disease - complications | Parkinson Disease - pathology | Parkinson Disease - immunology | Humans | Middle Aged | RNA, Messenger - analysis | Colitis - pathology | Male | Inflammation - immunology | Inflammation - etiology | Colitis - etiology | Adult | Female | Aged | Colitis - immunology | Lewy Bodies - pathology | Real-Time Polymerase Chain Reaction | Cytokines - biosynthesis | RNA | Interferon alpha | Development and progression | Disease susceptibility | Biological response modifiers | Interleukins | Analysis | Gastrointestinal system | Dopa | Intermediate filament proteins
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