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Circulation Research, ISSN 0009-7330, 01/2009, Volume 104, Issue 1, pp. 15 - 18
Ischemic postconditioning (IPoC) reduces infarct size following ischemia/reperfusion. Whether or not phosphorylation of RISK (reperfusion injury salvage... 
PERMEABILITY TRANSITION PORE | CARDIAC & CARDIOVASCULAR SYSTEMS | PROTECTION | REPERFUSION | reperfusion injury | NECROSIS-FACTOR-ALPHA | ADENOSINE RECEPTORS | infarct size | INHIBITION | MYOCARDIAL INFARCT SIZE | cardioprotection | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | MOUSE HEARTS | SIGNAL TRANSDUCER | Glycogen Synthase Kinase 3 - physiology | MAP Kinase Kinase 2 - physiology | Nitriles - pharmacology | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Glycogen Synthase Kinase 3 beta | Ribosomal Protein S6 Kinases, 70-kDa - physiology | MAP Kinase Kinase 1 - physiology | Myocardial Reperfusion Injury - enzymology | Ribosomal Protein S6 Kinases, 70-kDa - biosynthesis | Protein Processing, Post-Translational - drug effects | Swine | Mitogen-Activated Protein Kinase 3 - biosynthesis | Myocardial Infarction - pathology | Swine, Miniature | Phosphorylation - drug effects | Myocardial Infarction - enzymology | MAP Kinase Kinase 1 - antagonists & inhibitors | Butadienes - pharmacology | Glycogen Synthase Kinase 3 - biosynthesis | Mitogen-Activated Protein Kinase 1 - physiology | Glycogen Synthase Kinase 3 - antagonists & inhibitors | Ribosomal Protein S6 Kinases, 70-kDa - antagonists & inhibitors | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Coronary Occlusion - enzymology | Enzyme Induction | Proto-Oncogene Proteins c-akt - physiology | Enzyme Activation - drug effects | Mitogen-Activated Protein Kinase 3 - physiology | Mitogen-Activated Protein Kinase 1 - biosynthesis | Proto-Oncogene Proteins c-akt - biosynthesis | Animals | Androstadienes - pharmacology | Myocardial Reperfusion | MAP Kinase Kinase 2 - antagonists & inhibitors | Coronary Occlusion - pathology | Phosphatidylinositol 3-Kinases - physiology | Protein Kinase Inhibitors - pharmacology | Myocardial Reperfusion Injury - prevention & control | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Index Medicus
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 11/2011, Volume 301, Issue 5, pp. 2130 - 2139
Cardioprotection by ischemic preconditioning (IPC) is impaired during hyperglycemia, but the mechanisms underlying this phenomenon are poorly understood. This... 
Endothelial nitric oxide synthase | Hyperglycemia | Tetrahydrobiopterin | Ischemia reperfusion | Nitric oxide | Heat shock protein | tetrahydrobiopterin | nitric oxide | A ADENOSINE RECEPTOR | ISCHEMIA/REPERFUSION INJURY | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | CARDIAC-SPECIFIC OVEREXPRESSION | NITRIC-OXIDE SYNTHASE | REPERFUSION INJURY | ischemia reperfusion | heat shock protein | HUMAN ENDOTHELIAL-CELLS | DIABETES-MELLITUS | hyperglycemia | SUPEROXIDE ANION | INFARCTION | IN-VIVO | endothelial nitric oxide synthase | PERIPHERAL VASCULAR DISEASE | Myocardial Reperfusion Injury - etiology | Phosphorylation | Immunoprecipitation | Protein Multimerization | Hyperglycemia - complications | Male | Biopterin - analogs & derivatives | Coronary Occlusion - complications | Myocardial Reperfusion Injury - enzymology | Biopterin - metabolism | Myocardial Reperfusion Injury - pathology | Time Factors | Myocardial Infarction - pathology | Nitric Oxide Synthase Type III - metabolism | Myocardial Infarction - etiology | Disease Models, Animal | Myocardial Infarction - enzymology | Rabbits | Endothelial Cells - metabolism | Mice, Inbred C57BL | Cells, Cultured | Coronary Occlusion - enzymology | Myocardium - pathology | Lactams, Macrocyclic - pharmacology | Blotting, Western | Benzoquinones - pharmacology | Myocardium - enzymology | Animals | Pterins - pharmacology | HSP90 Heat-Shock Proteins - antagonists & inhibitors | Ischemic Preconditioning, Myocardial | HSP90 Heat-Shock Proteins - metabolism | Hyperglycemia - enzymology | Mice | Myocardial Infarction - prevention & control | Blood Glucose - metabolism | Nitric Oxide - metabolism | Myocardial Reperfusion Injury - prevention & control | Physiological aspects | Heat shock proteins | Development and progression | Amino acids | Genetic aspects | Health aspects | Ischemia | Rodents | Cells | Index Medicus | Integrative Cardiovascular Physiology and Pathophysiology
Journal Article
Prostaglandins and Other Lipid Mediators, ISSN 1098-8823, 12/2012, Volume 99, Issue 3-4, pp. 68 - 78
► Global cerebral ischemia-reperfusion model was used to investigate the effect of CYP2J2. ► Transgenic mice with endothelial overexpression of CYP2J2 are more... 
Neuroprotection | Cytochrome P450 epoxygenase | Stroke | Arachidonic acid | Global cerebral ischemia | ISCHEMIA/REPERFUSION INJURY | SIGNALING PATHWAYS | ARTERY OCCLUSION | BIOCHEMISTRY & MOLECULAR BIOLOGY | COPPER/ZINC SUPEROXIDE-DISMUTASE | NEURONAL CELL-DEATH | BLOOD-FLOW | FOREBRAIN ISCHEMIA | CELL BIOLOGY | TEMPORAL PROFILE | FREE-RADICAL GENERATION | EPOXYEICOSATRIENOIC ACIDS | Gene Expression - drug effects | Apoptosis - drug effects | Coronary Occlusion - genetics | Brain Ischemia - genetics | Cytochrome P-450 Enzyme System - metabolism | Male | Phosphatidylinositol 3-Kinases - metabolism | 8,11,14-Eicosatrienoic Acid - metabolism | Cerebral Infarction - genetics | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - genetics | Cerebral Infarction - enzymology | Brain Ischemia - enzymology | Cell Hypoxia | 8,11,14-Eicosatrienoic Acid - analogs & derivatives | Cerebral Infarction - physiopathology | Apoptosis Regulatory Proteins - genetics | 8,11,14-Eicosatrienoic Acid - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | Astrocytes - cytology | Astrocytes - drug effects | Cells, Cultured | Coronary Occlusion - enzymology | Mice, Transgenic | Brain Ischemia - physiopathology | Cerebrovascular Circulation | Apoptosis Regulatory Proteins - metabolism | Phosphatidylinositol 3-Kinases - genetics | Glucose - deficiency | Animals | Signal Transduction - drug effects | Apoptosis Regulatory Proteins - antagonists & inhibitors | Cytochrome P-450 Enzyme System - genetics | Mice | Protein Kinase Inhibitors - pharmacology | Coronary Occlusion - physiopathology | Astrocytes - metabolism | Unsaturated fatty acids | Cerebral ischemia | Prostaglandins | Polyvinylidene fluoride | Analysis | Cytochrome P-450 | Dimethyl sulfoxide | DNA polymerases | Genetic engineering | Endothelium | Index Medicus | arachidonic acid | global cerebral ischemia | cytochrome P450 epoxygenase | stroke | neuroprotection
Journal Article
Journal Article
Journal of Vascular Surgery, ISSN 0741-5214, 2013, Volume 57, Issue 1, pp. 182 - 193.e10
Objective Intimal hyperplasia (IH) is the main cause of vein graft stenosis or failure after bypass surgery. Basic investigations are proceeding in an animal... 
Surgery | SURGERY | CONTROLLED-TRIAL | APOPTOSIS | CREB | PREVENTION | MUSCLE-CELL MIGRATION | PERIPHERAL VASCULAR DISEASE | GENE-THERAPY | BYPASS GRAFTS | EXPRESSION | E2F DECOY | INSITU | Genetic Therapy | Cell Proliferation | Oligonucleotide Array Sequence Analysis | Humans | Hyperplasia | Graft Occlusion, Vascular - prevention & control | Vascular Grafting - adverse effects | Vascular System Injuries - enzymology | Male | Intracellular Signaling Peptides and Proteins - metabolism | LIM Domain Proteins - metabolism | Vascular System Injuries - pathology | Neointima | Time Factors | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Disease Models, Animal | Myocytes, Smooth Muscle - enzymology | Graft Occlusion, Vascular - genetics | Cyclic AMP Response Element-Binding Protein - genetics | Mice | Mutation | Muscle, Smooth, Vascular - enzymology | Veins - pathology | Cell Movement | Phosphorylation | Constriction, Pathologic | Vascular System Injuries - genetics | Myocytes, Smooth Muscle - pathology | Veins - transplantation | Transfection | Veins - enzymology | Mice, Inbred C57BL | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Veins - injuries | Gene Expression Profiling - methods | Transcription Factors - genetics | Vascular System Injuries - prevention & control | Graft Occlusion, Vascular - enzymology | Transcription Factors - metabolism | Muscle, Smooth, Vascular - pathology | Animals | Graft Occlusion, Vascular - etiology | Graft Occlusion, Vascular - pathology | Cyclic AMP Response Element-Binding Protein - metabolism | Protein Binding | LIM Domain Proteins - genetics | Aged | Coronary artery bypass | Political corruption | Analysis | Chemical properties | Adenylic acid | Health aspects | Protein kinases | Protein binding | Index Medicus
Journal Article
Journal of Vascular Surgery, ISSN 0741-5214, 2009, Volume 49, Issue 3, pp. 750 - 758
Journal Article
Angiology, ISSN 0003-3197, 5/2013, Volume 64, Issue 4, pp. 293 - 299
Journal Article
Heart, Lung and Circulation, ISSN 1443-9506, 2013, Volume 22, Issue 9, pp. 751 - 758
Objective Following bypass surgery vein grafts undergo a remodelling process that can lead to restenosis and ultimately vein graft failure. Signalling through... 
Cardiovascular | Vein graft | p38 MAPK-inhibitor | Arterio-venous bypass | Medial hyperplasia | Intimal hypeplasia | Adventitia hyperplasia | P38 MAPK-inhibitor | ADVENTITIAL FIBROBLASTS | CARDIAC & CARDIOVASCULAR SYSTEMS | ATHEROSCLEROSIS | PORCINE CORONARY-ARTERIES | ARTERIOSCLEROSIS | BALLOON INJURY | DISEASE | RAT CAROTID ARTERIES | SAPHENOUS-VEIN | SMOOTH-MUSCLE-CELLS | ACTIVATED PROTEIN-KINASES | Graft Occlusion, Vascular - prevention & control | Tunica Intima - physiopathology | Rats | Male | Saphenous Vein - pathology | Tunica Intima - enzymology | Saphenous Vein - physiopathology | Graft Occlusion, Vascular - enzymology | Rats, Sprague-Dawley | Adventitia - physiopathology | Gene Expression Regulation - drug effects | Animals | Tunica Intima - pathology | Graft Occlusion, Vascular - pathology | Proliferating Cell Nuclear Antigen - biosynthesis | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Adventitia - enzymology | Coronary Artery Bypass | Adventitia - pathology | Protein Kinase Inhibitors - pharmacology | p38 Mitogen-Activated Protein Kinases - metabolism | Phosphorylation - drug effects | Saphenous Vein - enzymology | Graft Occlusion, Vascular - physiopathology | Platelet-derived growth factor | Coronary artery bypass | Mitogens | Coronary heart disease | Phosphotransferases | Index Medicus
Journal Article