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Cancer Cell, ISSN 1535-6108, 09/2016, Volume 30, Issue 3, pp. 377 - 390
Journal Article
Circulation, ISSN 0009-7322, 03/2007, Volume 115, Issue 12, pp. 1599 - 1608
Background-Stroke is the second to third leading cause of death. Toll-like receptor 4 (TLR4) is a signaling receptor in innate immunity that is a specific... 
Infection | Cerebral ischemia | Stroke | Nitric oxide synthase | Inflammation | Metalloproteinases | Immune system | infection | CARDIAC & CARDIOVASCULAR SYSTEMS | LIPID-PEROXIDATION | FOCAL CEREBRAL-ISCHEMIA | metalloproteinases | stroke | NITRIC-OXIDE-SYNTHASE | MATRIX METALLOPROTEINASES | TUMOR-NECROSIS-FACTOR | TOLL-LIKE RECEPTOR-4 | MESSENGER-RNA | inflammation | cerebral ischemia | immune system | GENE-EXPRESSION | PERIPHERAL VASCULAR DISEASE | nitric oxide synthase | HEMATOLOGY | PATTERN-RECOGNITION RECEPTORS | INNATE IMMUNITY | Interferons - biosynthesis | Nitric Oxide Synthase Type II - biosynthesis | Oxidative Stress | Tumor Necrosis Factor-alpha - genetics | Nitrobenzenes - therapeutic use | Male | NF-kappa B - metabolism | Interleukin-1beta - genetics | Cyclooxygenase 2 - biosynthesis | Toll-Like Receptor 4 - deficiency | Cyclooxygenase 2 - genetics | Infarction, Middle Cerebral Artery - complications | Matrix Metalloproteinase 9 - genetics | Cyclooxygenase 2 Inhibitors - therapeutic use | Brain Damage, Chronic - metabolism | Interferons - genetics | Interferon Regulatory Factor-1 - biosynthesis | Encephalitis - pathology | Mice, Knockout | Toll-Like Receptor 4 - physiology | Brain Damage, Chronic - etiology | Cerebral Infarction - etiology | Brain Chemistry | Mice | Tumor Necrosis Factor-alpha - biosynthesis | Brain Damage, Chronic - prevention & control | Encephalitis - etiology | Dinoprostone - analysis | Infarction, Middle Cerebral Artery - metabolism | Cerebral Infarction - metabolism | Encephalitis - drug therapy | Nitric Oxide Synthase Type II - antagonists & inhibitors | Encephalitis - metabolism | Inflammation Mediators - metabolism | Nerve Tissue Proteins - biosynthesis | Interleukin-1beta - biosynthesis | Brain Damage, Chronic - pathology | Cerebral Infarction - pathology | Matrix Metalloproteinase 9 - biosynthesis | Mice, Inbred C57BL | Gene Expression Regulation | Infarction, Middle Cerebral Artery - pathology | Nerve Tissue Proteins - genetics | Mice, Inbred C3H | Interferon Regulatory Factor-1 - genetics | Animals | Nitric Oxide Synthase Type II - genetics | Sulfonamides - therapeutic use | Lipid Peroxidation | Nitric Oxide - metabolism | Stroke (Disease) | Complications and side effects | Patient outcomes | Physiological aspects | Development and progression | Research | Chemokines | Index Medicus | Abridged Index Medicus
Journal Article
Journal Article
European Journal of Pharmacology, ISSN 0014-2999, 01/2012, Volume 674, Issue 2-3, pp. 73 - 79
Journal Article
Journal Article
Circulation, ISSN 0009-7322, 04/2013, Volume 127, Issue 15, pp. 1609 - 1619
Background-Atherosclerosis is a chronic inflammatory vascular disease driven by the subendothelial accumulation of macrophages. The mechanism regulating the... 
Macrophages | MicroRNAs | Atherosclerosis | atherosclerosis | microRNAs | CARDIAC & CARDIOVASCULAR SYSTEMS | PEROXYNITRITE | NITRIC-OXIDE SYNTHASE | LOW-DENSITY-LIPOPROTEIN | RECEPTOR | macrophages | REVERSE CHOLESTEROL TRANSPORT | NEGATIVE REGULATION | IN-VIVO | PERIPHERAL VASCULAR DISEASE | EXPRESSION | PROMOTES | CORONARY-ARTERY-DISEASE | Up-Regulation | Nitric Oxide Synthase Type II - biosynthesis | Carotid Stenosis - prevention & control | MicroRNAs - antagonists & inhibitors | Apolipoproteins E - deficiency | Oligonucleotides - therapeutic use | Vasculitis - physiopathology | Atherosclerosis - genetics | Vasculitis - pathology | RNA, Antisense - pharmacology | Tyrosine - analogs & derivatives | Vasculitis - genetics | Oligonucleotides - pharmacology | Carotid Stenosis - genetics | DEAD-box RNA Helicases - deficiency | Aortic Diseases - pathology | Atherosclerosis - pathology | Ribonuclease III - genetics | Bone Morphogenetic Protein Receptors, Type II - genetics | Interleukin-6 - genetics | Atherosclerosis - physiopathology | Carotid Stenosis - physiopathology | Chemokine CCL2 - genetics | MicroRNAs - biosynthesis | Proto-Oncogene Proteins c-akt - physiology | RNA, Antisense - therapeutic use | Carotid Stenosis - pathology | Ribonuclease III - deficiency | Disease Progression | Macrophage Activation | Mice, Knockout | Gene Expression Regulation - drug effects | DEAD-box RNA Helicases - genetics | Aortic Diseases - genetics | Aortic Diseases - physiopathology | Macrophages - metabolism | Tyrosine - metabolism | Animals | Nitric Oxide Synthase Type II - genetics | Chemokine CCL2 - biosynthesis | Interleukin-6 - biosynthesis | Signal Transduction - physiology | Mice | MicroRNAs - genetics | MicroRNAs - physiology | Bone Morphogenetic Protein Receptors, Type II - biosynthesis | MicroRNA | Physiological aspects | Development and progression | Genetic aspects | Cellular signal transduction | Research | Index Medicus | Abridged Index Medicus
Journal Article
Circulation Research, ISSN 0009-7330, 09/2007, Volume 101, Issue 7, pp. 692 - 702
Journal Article
Journal of Leukocyte Biology, ISSN 0741-5400, 04/2015, Volume 97, Issue 4, pp. 711 - 721
Post‐radiotherapeutic tumor re‐growth may be caused by interaction of irradiated cancer cells with macrophages, which induce TLR1‐mediated iNOS expression and... 
postradiotherapeutic effect | TLR1 | radiotherapy | iNOS | Postradiotherapeutic effect | Radiotherapy | MIGRATION | RADIATION RESPONSE | CHROMOSOMAL LOCALIZATION | MECHANISM | IMMUNOLOGY | CELL BIOLOGY | RADIOSENSITIZATION | GENE | MICROENVIRONMENT | IN-VIVO | HEMATOLOGY | EXPRESSION | PROGRESSION | Colonic Neoplasms - radiotherapy | Gamma Rays | Recurrence | Nitric Oxide Synthase Type II - biosynthesis | Adenocarcinoma - pathology | Coculture Techniques | Melanoma, Experimental - radiotherapy | Neoplasm Proteins - physiology | Cercopithecus aethiops | omega-N-Methylarginine - pharmacology | Nitric Oxide Synthase Type II - physiology | Melanoma, Experimental - immunology | Colonic Neoplasms - immunology | Neoplasm Proteins - genetics | Toll-Like Receptor 1 - biosynthesis | Adenocarcinoma - radiotherapy | Nitric Oxide - biosynthesis | Macrophages - classification | Neoplasm Proteins - biosynthesis | Adenocarcinoma - immunology | Enzyme Induction | Melanoma, Experimental - pathology | Nitric Oxide - physiology | Toll-Like Receptor 1 - physiology | Disease Progression | Toll-Like Receptor 1 - genetics | Tumor Microenvironment - radiation effects | Macrophages - metabolism | Animals | Colonic Neoplasms - pathology | Cell Line, Tumor | Mice | Mice, Inbred BALB C | Macrophages, Peritoneal - metabolism | COS Cells | 3T3 Cells | Bone Marrow Cells - metabolism | Index Medicus
Journal Article
British Journal of Pharmacology, ISSN 0007-1188, 04/2017, Volume 174, Issue 8, pp. 718 - 733
BACKGROUND AND PURPOSE Raloxifene can induce both endothelium- dependent and - independent relaxation in different arteries. However, the underlying mechanisms... 
ARTERIES | PUBLICATION | CONCISE GUIDE | CARDIOVASCULAR EVENTS | PHARMACOLOGY | ESTROGEN | PHARMACOLOGY & PHARMACY | RELEASE | HORMONE REPLACEMENT THERAPY | CORONARY-HEART-DISEASE | POSTMENOPAUSAL WOMEN | Raloxifene Hydrochloride - pharmacology | Nitric Oxide Synthase Type II - biosynthesis | Calcium - metabolism | Aorta - drug effects | RNA, Messenger - genetics | Rats | Male | Structure-Activity Relationship | Aorta - metabolism | Muscle, Smooth - metabolism | RNA, Messenger - metabolism | Rats, Sprague-Dawley | Dose-Response Relationship, Drug | Endothelium - drug effects | Muscle, Smooth - drug effects | Animals | Endothelium - metabolism | Nitric Oxide Synthase Type II - genetics | Nitric Oxide Synthase Type II - metabolism | Hormones, Sex | Gene expression | Nitric oxide | Endothelium | Immunohistochemistry | Transcription | Calcium | Nitrites | Estrogen receptors | Smooth muscle | Stimulation | Estradiol | Contraction | Channels | Calcium influx | Arteries | Vasodilation | Proteins | Receptors | Rodents | Radioimmunoassay | Cyclic GMP | Aorta | Inhibition | Calcium channels | Muscles | Protein biosynthesis | Tamoxifen | Ribonucleic acid--RNA | Muscle contraction | Nitric-oxide synthase | Calcium chloride | Sex hormones | Protein synthesis | Coronary vessels | Raloxifene | Calcium ions | Index Medicus | Research Papers | Research Paper
Journal Article
Nature, ISSN 0028-0836, 01/2012, Volume 481, Issue 7380, pp. 199 - 205
Journal Article
Journal Article