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Nature, ISSN 0028-0836, 04/2013, Volume 496, Issue 7444, pp. 238 - 242
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 2016, Volume 311, Issue 4, pp. H871 - H880
We previously reported that endoplasmic reticulum (ER) stress is induced in the subfornical organ (SFO) and the hypothalamic paraventricular nucleus (PVN) of... 
Heart failure | Brain | Sympathetic activity | Hypothalamic paraventricular nucleus | Mitogen-activated protein kinase | Subfornical organ | Endoplasmic reticulum stress | heart failure | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | INDUCED PHOSPHORYLATION | MYOCARDIAL-INFARCTION | ER STRESS | subfornical organ | KINASE | RATS | sympathetic activity | KAPPA-B | brain | endoplasmic reticulum stress | hypothalamic paraventricular nucleus | mitogen-activated protein kinase | UNFOLDED PROTEIN RESPONSE | PERIPHERAL VASCULAR DISEASE | UP-REGULATION | Cholagogues and Choleretics - pharmacology | Tumor Necrosis Factor-alpha - genetics | Heart Failure - physiopathology | Male | NF-KappaB Inhibitor alpha - genetics | Peptidyl-Dipeptidase A - drug effects | Interleukin-1beta - genetics | Sympathetic Nervous System - physiopathology | RNA, Messenger - metabolism | Activating Transcription Factor 6 - genetics | Subfornical Organ - drug effects | Brain - metabolism | Heat-Shock Proteins - genetics | Inflammation - metabolism | Receptor, Angiotensin, Type 1 - genetics | Cyclooxygenase 2 - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | Real-Time Polymerase Chain Reaction | Echocardiography | Signal Transduction | Rats | Cyclooxygenase 2 - drug effects | Heart Failure - metabolism | Rats, Sprague-Dawley | Blotting, Western | Brain - drug effects | Tumor Necrosis Factor-alpha - drug effects | Mitogen-Activated Protein Kinase 3 - metabolism | Endoplasmic Reticulum Stress | Paraventricular Hypothalamic Nucleus - metabolism | Infusions, Intraventricular | Mitogen-Activated Protein Kinases - drug effects | Mitogen-Activated Protein Kinase 1 - metabolism | Interleukin-1beta - drug effects | Sympathetic Nervous System - drug effects | Mitogen-Activated Protein Kinase 1 - drug effects | X-Box Binding Protein 1 - drug effects | Sympathetic Nervous System - metabolism | Transcription Factor RelA - genetics | Activating Transcription Factor 6 - drug effects | Mitogen-Activated Protein Kinase 3 - drug effects | Taurochenodeoxycholic Acid - pharmacology | Peptidyl-Dipeptidase A - genetics | Renin-Angiotensin System | Receptor, Angiotensin, Type 1 - drug effects | RNA, Messenger - drug effects | Subfornical Organ - metabolism | Heat-Shock Proteins - drug effects | Activating Transcription Factor 4 - genetics | Activating Transcription Factor 4 - drug effects | NF-KappaB Inhibitor alpha - drug effects | Paraventricular Hypothalamic Nucleus - drug effects | p38 Mitogen-Activated Protein Kinases - drug effects | Animals | Transcription Factor RelA - drug effects | X-Box Binding Protein 1 - genetics | Mitogen-Activated Protein Kinases - metabolism | Physiological aspects | Cellular signal transduction | Endoplasmic reticulum | Health aspects | Mitogen-activated protein kinases | Cardiovascular Neurohormonal Regulation
Journal Article
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
Diabetes, ISSN 0012-1797, 04/2017, Volume 66, Issue 4, pp. 908 - 919
Journal Article
Nature, ISSN 0028-0836, 2014, Volume 512, Issue 1, pp. 78 - 81
Myeloproliferative neoplasms (MPNs) are diseases caused by mutations in the haematopoietic stem cell (HSC) compartment. Most MPN patients have a common... 
TYROSINE KINASE JAK2 | JAK2-V617F | ACTIVATING MUTATION | POLYCYTHEMIA-VERA | BONE | MULTIDISCIPLINARY SCIENCES | Neuroprotective Agents - therapeutic use | Apoptosis - drug effects | Neoplastic Stem Cells - drug effects | Sympathetic Nervous System - drug effects | Humans | Hematopoietic Stem Cells - pathology | Myeloproliferative Disorders - pathology | Sympathetic Nervous System - physiopathology | Adrenergic beta-3 Receptor Agonists - pharmacology | Neuroprotective Agents - pharmacology | Interleukin-1beta - metabolism | Neoplastic Stem Cells - pathology | Female | Sympathetic Nervous System - pathology | Schwann Cells - drug effects | Hematopoietic Stem Cells - drug effects | Nerve Fibers - pathology | Mesenchymal Stromal Cells - drug effects | Stem Cell Niche | Janus Kinase 2 - genetics | Nerve Fibers - drug effects | Schwann Cells - pathology | Myeloproliferative Disorders - drug therapy | Receptors, Adrenergic, beta-3 - metabolism | Disease Progression | Neoplasms - drug therapy | Nestin - metabolism | Adrenergic beta-3 Receptor Agonists - therapeutic use | Animals | Mice | Mesenchymal Stromal Cells - pathology | Neoplasms - pathology | Complications and side effects | Development and progression | Health aspects | Peripheral nerve diseases | Hematopoietic stem cells | Myeloproliferative disorders | Tumors | Studies | Mutation | Kinases | Rodents | Stem cells | Apoptosis
Journal Article
Journal of Periodontology, ISSN 0022-3492, 08/2013, Volume 84, Issue 8, pp. 1145 - 1157
Background: Simvastatin is a cholesterol‐lowering drug whose pleiotropic effects may have a therapeutic impact on bone. This study evaluates the effect of... 
hydroxymethylglutaryl‐CoA reductase inhibitors | inflammation | Alveolar bone loss | periodontitis | Inflammation | Hydroxymethylglutaryl-CoA reductase inhibitors | Periodontitis | OVARIECTOMIZED RATS | STATINS | IN-VITRO | METABOLISM | DENTISTRY, ORAL SURGERY & MEDICINE | NITRIC-OXIDE | hydroxymethylglutaryl-CoA reductase inhibitors | MEVALONATE PATHWAY | KAPPA-B LIGAND | PROTEIN PRENYLATION | Interleukin-1beta - drug effects | Simvastatin - therapeutic use | Bone Morphogenetic Protein 2 - drug effects | Rats, Wistar | Matrix Metalloproteinase 8 - drug effects | Alveolar Bone Loss - prevention & control | Receptor Activator of Nuclear Factor-kappa B - drug effects | RANK Ligand - drug effects | Malondialdehyde - analysis | Alanine Transaminase - drug effects | Gingiva - drug effects | Glutathione - drug effects | Anti-Inflammatory Agents - therapeutic use | Female | Osteoprotegerin - drug effects | Interleukin-10 - analysis | Nitrates - analysis | Peroxidase - drug effects | Matrix Metalloproteinase 1 - drug effects | Nitric Oxide Synthase Type II - drug effects | Rats | Aspartate Aminotransferases - drug effects | Alkaline Phosphatase - drug effects | Periodontitis - prevention & control | Antioxidants - therapeutic use | Animals | Tumor Necrosis Factor-alpha - drug effects | Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use | Nitrites - analysis | Oxidative Stress - drug effects
Journal Article
by Meng, S and Zhang, L and Tang, Y and Tu, Q and Zheng, L and Yu, L and Murray, D and Cheng, J and Kim, S.H and Zhou, X and Chen, J
Journal of Dental Research, ISSN 0022-0345, 7/2014, Volume 93, Issue 7, pp. 657 - 662
Journal Article
Nature, ISSN 0028-0836, 2014, Volume 505, Issue 7484, pp. 509 - 514
The pathway causing CD4 T-cell death in HIV-infected hosts remains poorly understood although apoptosis has been proposed as a key mechanism. We now show that... 
APOPTOSIS | ACTIVATION | HUMAN LYMPHOID-TISSUE | DENDRITIC CELLS | MEMORY | REVERSE TRANSCRIPTION | MULTIDISCIPLINARY SCIENCES | IMMUNODEFICIENCY-VIRUS TYPE-1 | X4 HIV-1 | EX-VIVO | CXCR4-TROPIC HIV-1 | Anti-HIV Agents - pharmacology | Spleen - virology | Inflammation - pathology | Caspase Inhibitors - pharmacology | HIV-1 - pathogenicity | Palatine Tonsil - drug effects | Inflammasomes - metabolism | Humans | Caspase 3 - metabolism | Caspase 1 - metabolism | Male | HIV Infections - enzymology | Spleen - drug effects | CD4-Positive T-Lymphocytes - pathology | Lymph Nodes - enzymology | HIV Infections - immunology | Inflammation - complications | HIV-1 - growth & development | HIV Infections - pathology | Adult | Interleukin-1beta - biosynthesis | Cell Death - drug effects | Interleukin-1beta - secretion | Caspase Inhibitors - administration & dosage | Administration, Oral | HIV-1 - drug effects | CD4-Positive T-Lymphocytes - cytology | Inflammation - virology | Inflammation - immunology | CD4-Positive T-Lymphocytes - secretion | Virus Replication | Protein Precursors - biosynthesis | Inflammasomes - immunology | Palatine Tonsil - virology | HIV Infections - drug therapy | In Vitro Techniques | CD4-Positive T-Lymphocytes - drug effects | Medical research | Cell death | Physiological aspects | Host-parasite relationships | Medicine, Experimental | Research | T cells | Health aspects | HIV infection | Infections | Kinases | Human immunodeficiency virus--HIV | Apoptosis | Immune system
Journal Article
Nature, ISSN 0028-0836, 10/2015, Volume 526, Issue 7575, pp. 666 - 671
Journal Article
Journal of the American Heart Association, ISSN 2047-9980, 09/2016, Volume 5, Issue 9, p. n/a
Background Activated T cells and dendritic cells (DCs) are colocalized in atherosclerotic plaques in association with plaque rupture. Oxidized low‐density... 
atherosclerosis | dendritic cells | statin | immune system | microRNA | oxidized low‐density lipoprotein | T cells | MicroRNA | Dendritic cells | Oxidized low-density lipoprotein | Atherosclerosis | Statin | Immune system | CARDIAC & CARDIOVASCULAR SYSTEMS | METAANALYSIS | INDUCTION | CANCER | ARTERIOSCLEROSIS | HEAT-SHOCK-PROTEIN | THERAPY | INHIBITION | INFLAMMATION | oxidized low-density lipoprotein | ASSOCIATION | LYMPHOCYTES | Interleukin-1beta - drug effects | Extracellular Signal-Regulated MAP Kinases - drug effects | Atorvastatin Calcium - pharmacology | Dendritic Cells - immunology | Humans | Interferon-gamma - drug effects | Interleukin-17 - immunology | Chaperonin 60 - immunology | Extracellular Signal-Regulated MAP Kinases - metabolism | Simvastatin - pharmacology | Th1 Cells - immunology | Mitochondrial Proteins - drug effects | Endarterectomy, Carotid | Lymphocyte Activation - immunology | Th17 Cells - drug effects | HSP90 Heat-Shock Proteins - immunology | T-Lymphocytes - drug effects | Nuclear Receptor Subfamily 1, Group F, Member 3 - metabolism | Tumor Necrosis Factor-alpha - immunology | Dendritic Cells - drug effects | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Real-Time Polymerase Chain Reaction | T-Box Domain Proteins - drug effects | Th1 Cells - drug effects | HSP90 Heat-Shock Proteins - drug effects | Interleukin-1beta - immunology | Lipoproteins, LDL - pharmacology | HSP27 Heat-Shock Proteins - immunology | Plaque, Atherosclerotic - immunology | MicroRNAs - immunology | Reverse Transcriptase Polymerase Chain Reaction | HSP27 Heat-Shock Proteins - drug effects | T-Box Domain Proteins - metabolism | Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology | Tumor Necrosis Factor-alpha - drug effects | Cell Differentiation - drug effects | Lymphocyte Activation - drug effects | Interferon-gamma - immunology | Interleukin-6 - immunology | MicroRNAs - drug effects | Th17 Cells - immunology | T-Lymphocytes - immunology | Chaperonin 60 - drug effects | Mitochondrial Proteins - immunology | Nuclear Receptor Subfamily 1, Group F, Member 3 - drug effects | Proto-Oncogene Proteins c-akt - drug effects
Journal Article