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Journal Article
Circulation Research, ISSN 0009-7330, 02/2009, Volume 104, Issue 4, pp. 506 - 513
Cyclooxygenase (COX)-2 is among the endothelial genes upregulated by uniform laminar shear stress (LSS), characteristically associated with atherosclerotic... 
Shear stress | Cyclooxygenase | Prostaglandins | Tumor necrosis factor-α | Endothelial cells | Prostanoids | endothelial cells | CARDIAC & CARDIOVASCULAR SYSTEMS | HEALTHY-SUBJECTS | NITRIC-OXIDE SYNTHASE | cyclooxygenase | PROSTAGLANDIN ENDOPEROXIDE SYNTHASES | RECEPTOR | THROMBOXANE SYNTHASE | tumor necrosis factor-alpha | FLUID MECHANICAL STIMULI | shear stress | prostanoids | LOW-DOSE ASPIRIN | EPITHELIAL-CELLS | prostaglandins | CYCLOOXYGENASE-2 EXPRESSION | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | HEMATOLOGY | Inflammation - chemically induced | Nitrobenzenes - adverse effects | Propionates - pharmacology | Up-Regulation | Epoprostenol - metabolism | Heme Oxygenase-1 - metabolism | Receptors, Epoprostenol | Humans | Stress, Mechanical | Benzofurans - pharmacology | Dinoprost - metabolism | Nitrobenzenes - pharmacology | Receptors, Prostaglandin - metabolism | Atherosclerosis - enzymology | Aspirin - adverse effects | Prostaglandin D2 - metabolism | Epoprostenol - pharmacology | Aspirin - pharmacology | Receptors, Prostaglandin - drug effects | Atherosclerosis - chemically induced | Down-Regulation | Cells, Cultured | Sulfonamides - pharmacology | Cyclooxygenase Inhibitors - pharmacology | 6-Ketoprostaglandin F1 alpha | Dinoprostone - metabolism | Epoprostenol - analogs & derivatives | Perfusion | Cyclooxygenase 2 - metabolism | Sulfonamides - adverse effects | Cyclooxygenase 1 - metabolism | Cyclooxygenase Inhibitors - adverse effects | Endothelial Cells - enzymology | Inflammation - enzymology | Tumor Necrosis Factor-alpha - biosynthesis | Endothelial Cells - drug effects | Index Medicus
Journal Article
The Journal of Immunology, ISSN 0022-1767, 01/2004, Volume 172, Issue 1, pp. 567 - 576
The signaling mechanism by which the anti-inflammatory cytokine IL-10 mediates suppression of proinflammatory cytokine synthesis remains largely unknown.... 
RHEUMATOID-ARTHRITIS | TUMOR-NECROSIS-FACTOR | DNA-BINDING | HUMAN NEUTROPHILS | TYROSINE PHOSPHORYLATION | INTERLEUKIN-10 RECEPTOR | GENE-EXPRESSION | KAPPA-B-ALPHA | IMMUNOLOGY | HUMAN MONOCYTES | MONONUCLEAR PHAGOCYTES | Protein Binding - genetics | Protein Biosynthesis | Interleukin-6 - antagonists & inhibitors | Humans | Tumor Necrosis Factor-alpha - genetics | Immunoglobulins - genetics | Lipopolysaccharides - antagonists & inhibitors | RNA, Messenger - metabolism | Suppressor of Cytokine Signaling Proteins | Repressor Proteins - antagonists & inhibitors | Antigens, CD - metabolism | Trans-Activators - physiology | Protein Tyrosine Phosphatases - antagonists & inhibitors | RNA, Messenger - biosynthesis | Protein Tyrosine Phosphatases - genetics | Inflammation Mediators - physiology | Glycoproteins - genetics | DNA-Binding Proteins - physiology | Protein Tyrosine Phosphatases - biosynthesis | DNA-Binding Proteins - antagonists & inhibitors | Signal Transduction - genetics | DNA - metabolism | Down-Regulation - genetics | Macrophages - metabolism | Protein Tyrosine Phosphatase, Non-Receptor Type 2 | Repressor Proteins - biosynthesis | Up-Regulation - immunology | Interleukin-10 - antagonists & inhibitors | Lipopolysaccharides - pharmacology | Adenoviruses, Human - genetics | Interleukin-10 - immunology | Tumor Necrosis Factor-alpha - biosynthesis | Phosphorylation | Tissue Inhibitor of Metalloproteinase-1 - biosynthesis | Antigens, CD - biosynthesis | Receptors, Cell Surface | Receptors, IgG - biosynthesis | Receptors, IgG - antagonists & inhibitors | Interleukin-10 - physiology | Signal Transduction - immunology | Tissue Inhibitor of Metalloproteinase-1 - metabolism | Signaling Lymphocytic Activation Molecule Family Member 1 | Receptors, Tumor Necrosis Factor - antagonists & inhibitors | RNA, Messenger - antagonists & inhibitors | Receptors, Tumor Necrosis Factor, Type II | Trans-Activators - genetics | Inflammation Mediators - antagonists & inhibitors | Trans-Activators - biosynthesis | Immunoglobulins - biosynthesis | Macrophages - immunology | Inflammation Mediators - immunology | Receptors, Tumor Necrosis Factor - metabolism | Immune Sera - pharmacology | Proteins - physiology | Cells, Cultured | Glycoproteins - antagonists & inhibitors | Histocompatibility Antigens Class II - biosynthesis | Tissue Inhibitor of Metalloproteinase-1 - antagonists & inhibitors | Transcription Factors - antagonists & inhibitors | Transcription Factors - biosynthesis | Up-Regulation - genetics | DNA-Binding Proteins - genetics | DNA - antagonists & inhibitors | Glycoproteins - biosynthesis | Suppressor of Cytokine Signaling 3 Protein | Down-Regulation - immunology | Interleukin-6 - biosynthesis | Receptors, Tumor Necrosis Factor - biosynthesis | STAT3 Transcription Factor | Trans-Activators - antagonists & inhibitors | Genetic Vectors | DNA-Binding Proteins - biosynthesis | Tumor Necrosis Factor-alpha - antagonists & inhibitors | SOCS-3 protein | Index Medicus | Abridged Index Medicus
Journal Article
Journal of Clinical Immunology, ISSN 0271-9142, 6/2011, Volume 31, Issue 3, pp. 472 - 478
Leptin, one of the adipokines, functions as a hormone and a cytokine. In this investigation, we show for the first time that leptin, in a... 
Medical Microbiology | Biomedicine | Immunology | Internal Medicine | Infectious Diseases | activation markers | cytokines | B cells | PROTEIN-KINASE | TRANSDUCER | RECEPTOR | PROLIFERATION | IMMUNOLOGY | BLOOD MONONUCLEAR-CELLS | DEFICIENCY | PI3K/AKT | IMMUNE-RESPONSES | T-CELLS | Autoimmunity | Interleukin-6 - analysis | Janus Kinase 2 - biosynthesis | Mitogen-Activated Protein Kinase 3 - analysis | Humans | p38 Mitogen-Activated Protein Kinases - biosynthesis | p38 Mitogen-Activated Protein Kinases - analysis | Dose-Response Relationship, Drug | Signal Transduction - immunology | Inflammation - metabolism | Mitogen-Activated Protein Kinases - analysis | Mitogen-Activated Protein Kinase 3 - biosynthesis | Mitogen-Activated Protein Kinase 6 - analysis | Leptin - pharmacology | Phosphorylation - drug effects | Interleukin-10 - analysis | B-Lymphocytes - metabolism | Janus Kinase 2 - analysis | Enzyme-Linked Immunosorbent Assay | Lymphocyte Activation | Cells, Cultured | Mitogen-Activated Protein Kinases - biosynthesis | Receptors, Leptin - immunology | STAT3 Transcription Factor - analysis | Inflammation - immunology | Tumor Necrosis Factor-alpha - analysis | STAT3 Transcription Factor - biosynthesis | B-Lymphocytes - drug effects | B-Lymphocytes - immunology | Mitogen-Activated Protein Kinase 6 - biosynthesis | Interleukin-6 - biosynthesis | Interleukin-10 - biosynthesis | Receptors, Leptin - metabolism | Tumor Necrosis Factor-alpha - biosynthesis | Index Medicus
Journal Article
Journal Article
The Journal of Immunology, ISSN 0022-1767, 08/2005, Volume 175, Issue 4, pp. 2340 - 2348
ICOS is a new member of the CD28 family of costimulatory molecules that is expressed on activated T cells. Its ligand B7RP-1 is constitutively expressed on B... 
GERMINAL CENTER FORMATION | CXC CHEMOKINE RECEPTOR-5 | OX40 LIGAND | IMMUNE-RESPONSES | ACTIVATION MOLECULE | INDUCIBLE COSTIMULATOR | IMMUNOLOGY | LYMPHOID FOLLICLES | EXPRESSION | MICE LACKING | CUTTING EDGE | Spleen - immunology | Mice, Inbred A | Tumor Necrosis Factor-alpha - genetics | B-Lymphocyte Subsets - cytology | CD28 Antigens - genetics | Mice, Inbred CBA | CD40 Antigens - genetics | CD28 Antigens - physiology | CD40 Antigens - physiology | T-Lymphocytes, Helper-Inducer - metabolism | Membrane Proteins - genetics | Receptors, Cytokine - biosynthesis | Antibodies, Monoclonal - pharmacology | Antigens, Surface - biosynthesis | Spleen - cytology | Mice, Knockout | Cell Differentiation - immunology | Membrane Proteins - biosynthesis | Mice | Mice, Inbred BALB C | Antigens, Differentiation, T-Lymphocyte - biosynthesis | Tumor Necrosis Factor-alpha - biosynthesis | Receptors, CXCR5 | Inducible T-Cell Co-Stimulator Protein | Germinal Center - immunology | Tumor Necrosis Factors | Receptors, OX40 | Tumor Necrosis Factor-alpha - deficiency | Cell Differentiation - genetics | Membrane Proteins - deficiency | Immunization, Secondary | T-Lymphocytes, Helper-Inducer - immunology | Antigens, Differentiation, T-Lymphocyte - physiology | Receptors, Chemokine - biosynthesis | T-Lymphocytes, Helper-Inducer - cytology | B-Lymphocyte Subsets - immunology | Female | Mice, Inbred DBA | Receptors, Tumor Necrosis Factor - deficiency | Membrane Glycoproteins - immunology | Germinal Center - cytology | Receptors, Tumor Necrosis Factor - genetics | B7-1 Antigen - immunology | Mice, Inbred C57BL | Antigens, Surface - genetics | Mice, SCID | Mice, Inbred C3H | Animals | Inducible T-Cell Co-Stimulator Ligand | Spleen - metabolism | Antibodies, Monoclonal - administration & dosage | Antigens, Differentiation, T-Lymphocyte - genetics | Chemokines, CXC - metabolism | Receptors, Tumor Necrosis Factor - biosynthesis | Index Medicus | Abridged Index Medicus
Journal Article
The Journal of Immunology, ISSN 0022-1767, 08/2005, Volume 175, Issue 3, pp. 1665 - 1676
Independent studies have shown that CD27, 4-1BB, and OX40 can all promote survival of activated CD8+ T cells. We have therefore compared their impact on CD8+... 
B-CELLS | INFLUENZA-A | MURINE CD27 | CD8-T-CELL MEMORY | CLONAL EXPANSION | CD4-T-CELL HELP | IN-VIVO | CD27-CD70 INTERACTIONS | LIGAND | IMMUNOLOGY | MICE LACKING | CD8-Positive T-Lymphocytes - cytology | Genomic Imprinting | Cell Proliferation | Membrane Glycoproteins - biosynthesis | Antigens, CD - genetics | Receptors, Tumor Necrosis Factor - physiology | Orthomyxoviridae Infections - genetics | Lymphocyte Activation - genetics | Membrane Glycoproteins - physiology | CD8-Positive T-Lymphocytes - metabolism | Influenza A virus - immunology | Immunologic Memory - genetics | Antigen-Presenting Cells - metabolism | Receptors, Nerve Growth Factor - biosynthesis | T-Lymphocyte Subsets - transplantation | T-Lymphocyte Subsets - virology | Tumor Necrosis Factor Receptor Superfamily, Member 7 - physiology | Mice, Knockout | Antigens, CD - physiology | Ligands | Mice | CD8-Positive T-Lymphocytes - immunology | Receptors, Nerve Growth Factor - deficiency | Orthomyxoviridae Infections - virology | T-Lymphocyte Subsets - immunology | Antigens, CD - biosynthesis | Tumor Necrosis Factors | Receptors, Nerve Growth Factor - physiology | Adoptive Transfer | Receptors, OX40 | Tumor Necrosis Factor Receptor Superfamily, Member 9 | Immunization, Secondary | Receptors, Tumor Necrosis Factor - deficiency | Tumor Necrosis Factor Receptor Superfamily, Member 7 - biosynthesis | Receptors, Tumor Necrosis Factor - genetics | Antibodies, Viral - biosynthesis | Mice, Inbred C57BL | Tumor Necrosis Factor Receptor Superfamily, Member 7 - genetics | Administration, Intranasal | Antigen-Presenting Cells - immunology | Antigen-Presenting Cells - virology | Receptors, Nerve Growth Factor - genetics | Membrane Glycoproteins - genetics | Animals | CD8-Positive T-Lymphocytes - virology | T-Lymphocyte Subsets - metabolism | Receptors, Tumor Necrosis Factor - biosynthesis | Membrane Glycoproteins - deficiency | Orthomyxoviridae Infections - immunology | Index Medicus | Abridged Index Medicus
Journal Article
American Journal of Pathology, The, ISSN 0002-9440, 2013, Volume 182, Issue 6, pp. 2285 - 2297
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 11/2005, Volume 115, Issue 11, pp. 3083 - 3092
Journal Article
The New England Journal of Medicine, ISSN 0028-4793, 02/2006, Volume 354, Issue 7, pp. 697 - 708
Journal Article
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 | INFLAMMATORY DISEASES | BIOCHEMISTRY & MOLECULAR BIOLOGY | FACTOR RECEPTORS | NEUROSCIENCES | NEURODEGENERATIVE DISEASES | CLOSED-HEAD INJURY | MESSENGER-RNA | SPINAL-CORD-INJURY | 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 | Index Medicus | 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
Journal Article