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1. Full Text Vasculitis Associated With Tumor Necrosis Factor-α Inhibitors
by Sokumbi, Olayemi, MD and Wetter, David A., MD and Makol, Ashima, MBBS and Warrington, Kenneth J., MD
Mayo Clinic Proceedings, ISSN 0025-6196, 2012, Volume 87, Issue 8, pp. 739 - 745
Abstract Objective To describe the clinical characteristics, histopathologic features, and outcomes of patients in whom vasculitis developed in association... 
Internal Medicine | MEDICINE, GENERAL & INTERNAL | SYSTEMIC-LUPUS-ERYTHEMATOSUS | AGENTS | TNF-TARGETED THERAPIES | Azathioprine - therapeutic use | Glucocorticoids - therapeutic use | Humans | Middle Aged | Antibodies, Monoclonal - adverse effects | Male | Methotrexate - therapeutic use | Cyclophosphamide - therapeutic use | Young Adult | Anti-Inflammatory Agents - adverse effects | Etanercept | Infliximab | Arthritis, Rheumatoid - drug therapy | Adult | Female | Retrospective Studies | Colitis, Ulcerative - drug therapy | Vasculitis - chemically induced | Proteinuria - etiology | Antibodies, Monoclonal, Humanized - adverse effects | Rituximab | Immunoglobulin G - adverse effects | Mycophenolic Acid - analogs & derivatives | Mycophenolic Acid - therapeutic use | Polyneuropathies - etiology | Receptors, Tumor Necrosis Factor | Crohn Disease - drug therapy | Vasculitis - drug therapy | Aged | Adalimumab | Prednisone - therapeutic use | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Antibodies, Monoclonal, Murine-Derived - therapeutic use | Hematuria - etiology | Immunologic Factors - therapeutic use | IBD, inflammatory bowel disease | TNF-α, tumor necrosis factor-α | RA, rheumatoid arthritis | Original
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2. Full Text A Paracrine Loop Between Adipocytes and Macrophages Aggravates Inflammatory Changes: Role of Free Fatty Acids and Tumor Necrosis Factor α
by Suganami, Takayoshi and Nishida, Junko and Ogawa, Yoshihiro
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 10/2005, Volume 25, Issue 10, pp. 2062 - 2068
OBJECTIVE—Weight gain is associated with infiltration of fat by macrophages, suggesting that they are an important source of inflammation in obese adipose... 
Adipocyte | Obesity | TNF-α | Fatty acids | Macrophage | 3T3-L1 ADIPOCYTES | METABOLIC SYNDROME | fatty acids | TNF-alpha | MONOCYTE CHEMOATTRACTANT PROTEIN-1 | WEIGHT-LOSS | macrophage | KAPPA-B | INDUCED INSULIN-RESISTANCE | HUMAN ADIPOSE-TISSUE | adipocyte | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | EXPRESSION | obesity | Tumor Necrosis Factor-alpha - metabolism | Cell Communication - immunology | Inflammation - pathology | Obesity - immunology | Coculture Techniques | Tumor Necrosis Factor-alpha - genetics | Adipocytes - cytology | Metabolic Syndrome - metabolism | Adipose Tissue - immunology | Paracrine Communication - immunology | Adipose Tissue - metabolism | Fatty Acids, Nonesterified - metabolism | Inflammation - metabolism | Chemokine CCL2 - metabolism | Metabolic Syndrome - immunology | Adipocytes - immunology | Macrophages - immunology | Atherosclerosis - pathology | Atherosclerosis - immunology | Gene Expression Regulation - immunology | Adipose Tissue - pathology | Chemokine CCL2 - genetics | Inflammation - immunology | Macrophages - cytology | 3T3-L1 Cells | Atherosclerosis - metabolism | Obesity - metabolism | Obesity - pathology | Macrophages - metabolism | Animals | Adipocytes - metabolism | Mice | Metabolic Syndrome - pathology | Hypertrophy
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3. Full Text Tumor necrosis factor‐α antagonists and neuropathy
by Stübgen, Joerg‐Patrick
Muscle & Nerve, ISSN 0148-639X, 03/2008, Volume 37, Issue 3, pp. 281 - 292
Tumor necrosis factor (TNF)‐α plays an important role in many aspects of immune system development, immune‐response regulation, and T‐cell–mediated tissue... 
TNF‐α antagonists | TNF‐α | neuropathy | TNF-α | TNF-α antagonists | Neuropathy | IMMUNE-MEDIATED DEMYELINATION | RHEUMATOID-ARTHRITIS | TNF-alpha | PERIPHERAL NERVOUS-SYSTEM | GUILLAIN-BARRE-SYNDROME | CONDUCTION BLOCK | INFLAMMATORY DEMYELINATING POLYRADICULONEUROPATHY | EXPERIMENTAL AUTOIMMUNE NEURITIS | NEUROSCIENCES | CLINICAL NEUROLOGY | MULTIFOCAL MOTOR NEUROPATHY | MULTIPLE-SCLEROSIS | TNF-alpha antagonists | Tumor Necrosis Factor-alpha - metabolism | Anti-Infective Agents - therapeutic use | Polyneuropathies - drug therapy | Models, Biological | Humans | Tumor Necrosis Factor-alpha - antagonists & inhibitors
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4. Full Text Tumour necrosis factor-α as a tumour promoter
by Szlosarek, Peter and Charles, Kellie A and Balkwill, Frances R
European Journal of Cancer, ISSN 0959-8049, 2006, Volume 42, Issue 6, pp. 745 - 750
It is becoming more evident that many aspects of tumour promotion arise from persistent and unresolving inflammation. One of the key molecules mediating the... 
TNF-α | Cancer | NUDE-MICE | CELLS | INTERFERON-GAMMA | ONCOLOGY | TNF-alpha | IFN-GAMMA | DNA-DAMAGE | RECEPTOR EXPRESSION | cancer | OVARIAN-CANCER | GROWTH-FACTOR | NF-KAPPA-B | Inflammation - complications | Inflammation - pathology | Animals | Neoplasms - etiology | Humans | Tumor Necrosis Factor-alpha - physiology | Mice, Transgenic | Models, Animal | Mice | Neoplasms - pathology | Chronic Disease | Necrosis - pathology
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5. Full Text Tumor necrosis factor-α, kidney function, and hypertension
by Mehaffey, Eamonn and Majid, Dewan S. A
American Journal of Physiology - Renal Physiology, ISSN 0363-6127, 10/2017, Volume 313, Issue 4, pp. F1005 - F1008
Hypertension is considered to be a lowgrade inflammatory condition characterized by the presence of various proinflammatory cytokines. Tumor necrosis factor... 
Inflammatory cytokines | Natriuresis | TNF-α | Renin-angiotensin system | natriuresis | PHYSIOLOGY | TNF-alpha | NITRIC-OXIDE SYNTHASE | HEART-FAILURE | INVOLVEMENT | RATS | inflammatory cytokines | BLOOD-PRESSURE | RESPONSES | UROLOGY & NEPHROLOGY | MICE | DYSFUNCTION | CONTRIBUTES | renin-angiotensin system | Blood Pressure | Inflammation Mediators - immunology | Tumor Necrosis Factor-alpha - metabolism | Signal Transduction | Humans | Sodium Chloride, Dietary - adverse effects | Kidney - immunology | Hypertension - immunology | Inflammation - immunology | Receptors, Tumor Necrosis Factor, Type I - metabolism | Hypertension - physiopathology | Hypertension - metabolism | Inflammation - metabolism | Kidney - metabolism | Animals | Renin-Angiotensin System | Receptors, Tumor Necrosis Factor, Type II - metabolism | Inflammation Mediators - metabolism | Tumor Necrosis Factor-alpha - immunology | Kidney - physiopathology | Inflammation - physiopathology | Review
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6. Full Text Curcumin downregulates human tumor necrosis factor-α levels: A systematic review and meta-analysis ofrandomized controlled trials
by Sahebkar, Amirhossein and Cicero, Arrigo F.G and Simental-Mendía, Luis E and Aggarwal, Bharat B and Gupta, Subash C
Pharmacological Research, ISSN 1043-6618, 05/2016, Volume 107, pp. 234 - 242
Tumor necrosis factor-α (TNF-α) is a key inflammatory mediator and its reduction is a therapeutic target in several inflammatory diseases. Curcumin, a... 
Curcumin | Inflammation | TNF-α | Curcuma longa | Randomized controlled trial | Meta-analysis | PLACEBO | TNF-alpha | PIPERINE | FACTOR-KAPPA-B | SUPPLEMENTATION | IN-VITRO | THERAPY | DOUBLE-BLIND | PHARMACOLOGY & PHARMACY | SUPPRESSES | MODULATION | Animals | Down-Regulation | Humans | Tumor Necrosis Factor-alpha - blood | Curcumin - pharmacology | Randomized Controlled Trials as Topic
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7. Full Text Depressive-like behavior induced by tumor necrosis factor-α in mice
by Kaster, Manuella P and Gadotti, Vinícius M and Calixto, João B and Santos, Adair R.S and Rodrigues, Ana Lúcia S
Neuropharmacology, ISSN 0028-3908, 01/2012, Volume 62, Issue 1, pp. 419 - 426
Pro-inflammatory cytokines are implicated in the pathogenesis of depression. However, few animal models of cytokine-induced depression well characterized... 
Depression | Inflammation | TNF-α | Antidepressants | HIPPOCAMPAL LESION | EXPRESSING TNF-ALPHA | TNF-alpha | SICKNESS BEHAVIOR | MAJOR DEPRESSION | MILD STRESS | FORCED SWIMMING TEST | NEUROSCIENCES | INTERFERON-GAMMA | NITRIC-OXIDE | PHARMACOLOGY & PHARMACY | RAT-BRAIN | NEUROBEHAVIORAL ALTERATIONS | Lymphotoxin-alpha - toxicity | Antibodies - therapeutic use | Mice, Inbred C57BL | Injections, Intraperitoneal | Male | Depression - genetics | Hindlimb Suspension - methods | Lymphotoxin-alpha - immunology | Mice, Knockout | Antidepressive Agents - therapeutic use | Dose-Response Relationship, Drug | Depression - drug therapy | Hindlimb Suspension - psychology | Receptors, Tumor Necrosis Factor, Type I - deficiency | Animals | Analysis of Variance | Swimming - psychology | Depression - chemically induced | Exploratory Behavior - drug effects | Mice | Thalidomide - therapeutic use | Disease Models, Animal
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8. Full Text Tumor necrosis factor α suppresses the mesenchymal stem cell osteogenesis promoter miR‐21 in estrogen deficiency–induced osteoporosis
by Yang, Nan and Wang, Guang and Hu, Chenghu and Shi, Yuanyuan and Liao, Li and Shi, Songtao and Cai, Yan and Cheng, Shuli and Wang, Xi and Liu, Yali and Tang, Liang and Ding, Yin and Jin, Yan
Journal of Bone and Mineral Research, ISSN 0884-0431, 03/2013, Volume 28, Issue 3, pp. 559 - 573
Inflammatory cytokines, especially tumor necrosis factor α (TNF‐α), have been shown to inhibit osteogenic differentiation of mesenchymal stem cells (MSCs) and... 
OSTEOGENESIS | miR‐21 | TNF‐α | MESENCHYMAL STEM CELL | OSTEOPOROSIS | miR-21 | TNF-α | Enzyme-Linked Immunosorbent Assay | Ovariectomy | Down-Regulation | Humans | Mesenchymal Stromal Cells - metabolism | Mesenchymal Stromal Cells - cytology | Animals | MicroRNAs | Tumor Necrosis Factor-alpha - physiology | Female | Cell Differentiation | Mice | Osteoblasts - cytology | Osteoblasts - metabolism | Osteogenesis - genetics | Cytokines | Mesenchyme | Estrogens | Inflammation | Bone diseases | Inflammatory diseases | Promoters | Osteoporosis | Osteoblastogenesis | Stem cells | miRNA | Osteogenesis | Tumor necrosis factor- alpha
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9. Full Text Bidirectional Role of Tumor Necrosis Factor-α in Coronary Microembolization: Progressive Contractile Dysfunction Versus Delayed Protection Against Infarction
by Skyschally, Andreas and Gres, Petra and Hoffmann, Simone and Haude, Michael and Erbel, Raimund and Schulz, Rainer and Heusch, Gerd
Circulation Research, ISSN 0009-7330, 01/2007, Volume 100, Issue 1, pp. 140 - 146
In patients with unstable angina, plaque rupture and coronary microembolization (ME) can precede complete coronary artery occlusion and impending infarction.... 
Myocardial infarction | Inflammation | Microembolization | TNF-α | ISCHEMIA/REPERFUSION INJURY | CARDIAC & CARDIOVASCULAR SYSTEMS | TNF-alpha | myocardial infarction | HEART-FAILURE | MONOCLONAL-ANTIBODY | BLOOD-FLOW | microembolization | FREE-RADICALS | THERAPY | inflammation | ACUTE MYOCARDIAL-INFARCTION | PERIPHERAL VASCULAR DISEASE | UNSTABLE ANGINA | HEMATOLOGY | PLAQUE RUPTURE | Tumor Necrosis Factor-alpha - metabolism | Myocardial Reperfusion Injury - complications | Cardiotonic Agents - metabolism | Coronary Disease - physiopathology | Systole | Embolism - physiopathology | Microspheres | Coronary Disease - metabolism | Time Factors | Swine | Myocardial Infarction - pathology | Myocardium - metabolism | Swine, Miniature | Tumor Necrosis Factor-alpha - immunology | Embolism - etiology | Myocardial Infarction - etiology | Heart - physiopathology | Myocardial Contraction | Coronary Disease - etiology | Myocardium - pathology | Embolism - metabolism | Antibodies - pharmacology | Animals | Heart - drug effects | Myocardial Infarction - prevention & control
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10. Full Text Tumor necrosis factor‐α synthesis inhibitor, 3,6′‐dithiothalidomide, reverses behavioral impairments induced by minimal traumatic brain injury in mice
by Baratz, Renana and Tweedie, David and Rubovitch, Vardit and Luo, Weiming and Yoon, Jeong Seon and Hoffer, Barry J and Greig, Nigel H and Pick, Chaim G
Journal of Neurochemistry, ISSN 0022-3042, 09/2011, Volume 118, Issue 6, pp. 1032 - 1042
Mild traumatic brain injury (mTBI) patients do not show clear structural brain defects and, in general, do not require hospitalization, but frequently suffer... 
thiothalidomide | traumatic brain injury | thalidomide | neuroinflammation | TNF‐α | etanercept | TNF-α | CELL-DEATH MECHANISMS | TNF-alpha | BIOCHEMISTRY & MOLECULAR BIOLOGY | FACTOR RECEPTORS | NEUROSCIENCES | CLOSED-HEAD INJURY | MESSENGER-RNA | MEMORY | SEQUELAE | RAT-BRAIN | COGNITIVE DEFICITS | Brain Chemistry - drug effects | Inflammation - chemically induced | Cell Line | Inflammation - pathology | Lipopolysaccharides - toxicity | Brain Injuries - drug therapy | Behavior, Animal - physiology | Male | Lipopolysaccharides - antagonists & inhibitors | Mice, Inbred ICR | Thalidomide - analogs & derivatives | Animals | Maze Learning | Recognition (Psychology) - drug effects | Behavior, Animal - drug effects | Avoidance Learning - drug effects | Inflammation - prevention & control | Mice | Thalidomide - therapeutic use | Brain Injuries - psychology | Tumor Necrosis Factor-alpha - biosynthesis | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Memory - physiology | Drugs | Emotional behavior | Neuroprotection | Animal models | Head | Traumatic brain injury | Cytokines | Cognitive ability | Inflammation | Pattern recognition | Brain injury | Tumor necrosis factor- alpha | Mild traumatic brain injury | tumor necrosis factor-α | infliximab | head injury | interleukin-1β
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11. Full Text Liver Injury From Tumor Necrosis Factor-α Antagonists: Analysis of Thirty-four Cases
by Ghabril, Marwan and Bonkovsky, Herbert L and Kum, Clarissa and Davern, Tim and Hayashi, Paul H and Kleiner, David E and Serrano, Jose and Rochon, Jim and Fontana, Robert J and Bonacini, Maurizio and US Drug-Induced Liver Injury Netwo and US Drug-Induced Liver Injury Network
Clinical Gastroenterology and Hepatology, ISSN 1542-3565, 2013, Volume 11, Issue 5, pp. 558 - 564.e3
Background & Aims Tumor necrosis factor (TNF)-α antagonists have been associated with drug-induced liver injury (DILI). We reviewed cases of DILI in the United... 
Gastroenterology and Hepatology | Autoimmunity | Drug-Induced Liver Injury | TNF-α Antagonists | Tumor Necrosis Factor | Hepatotoxicity | INDUCED AUTOIMMUNE HEPATITIS | RHEUMATOID-ARTHRITIS | CROHNS-DISEASE | TNF-alpha Antagonists | ANKYLOSING-SPONDYLITIS | INFLIXIMAB-INDUCED HEPATITIS | PSORIATIC-ARTHRITIS | NO RELAPSE | ALCOHOLIC HEPATITIS | SUCCESSFUL SWITCH | ETANERCEPT | GASTROENTEROLOGY & HEPATOLOGY | Severity of Illness Index | Antibodies, Monoclonal, Humanized - adverse effects | Liver - pathology | United States | Humans | Antibodies, Monoclonal - adverse effects | Immunologic Factors - administration & dosage | Male | Receptors, Tumor Necrosis Factor - administration & dosage | Cholestasis - chemically induced | Immunoglobulin G - administration & dosage | Immunoglobulin G - adverse effects | Antibodies, Monoclonal, Humanized - administration & dosage | Etanercept | Infliximab | Antibodies, Monoclonal - administration & dosage | Adult | Female | Chemical and Drug Induced Liver Injury | Immunologic Factors - adverse effects | Adalimumab | Autoimmune Diseases - chemically induced | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Index Medicus
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12. Full Text Anti-tumor necrosis factor-α antibody therapy management before and after intestinal surgery for inflammatory bowel disease: A CCFA position paper
by Holubar, Stefan D and Holder-Murray, Jennifer and Flasar, Mark and Lazarev, Mark
Inflammatory Bowel Diseases, ISSN 1078-0998, 07/2015, Volume 21, Issue 11, pp. 2658 - 2672
Biologic therapy with anti-tumor necrosis factor (TNF)-α antibody medications has become part of the standard of care for medical therapy for patients with... 
biologic therapy | complications | infliximab | colectomy | anti-TNF-α antibody | Crohn's disease | ulcerative colitis | proctectomy | ileal pouch-anal anastomosis | inflammatory bowel disease | surgery | TNF-A AGENTS | CROHNS-DISEASE | EARLY POSTOPERATIVE COMPLICATIONS | SURGICAL SITE INFECTION | IMMUNOSUPPRESSIVE MEDICATION | ULCERATIVE-COLITIS | RESTORATIVE PROCTOCOLECTOMY | GASTROENTEROLOGY & HEPATOLOGY | PREOPERATIVE INFLIXIMAB THERAPY | ABDOMINAL-SURGERY | POUCH-ANAL ANASTOMOSIS | Infliximab - adverse effects | Perioperative Period | Digestive System Surgical Procedures | Humans | Inflammatory Bowel Diseases - surgery | Inflammatory Bowel Diseases - complications | Postoperative Complications | Inflammatory Bowel Diseases - therapy | Infliximab - administration & dosage | Tumor Necrosis Factor-alpha - antagonists & inhibitors | anti–TNF-α antibody | ileal pouch–anal anastomosis | CCFA Position Paper
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