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Circulation, ISSN 0009-7322, 03/2013, Volume 127, Issue 10, pp. 1128 - 1138
Journal Article
Circulation Research, ISSN 0009-7330, 05/2012, Volume 110, Issue 11, pp. 1484 - 1497
RATIONALE:Pulmonary arterial hypertension (PAH) is a lethal syndrome characterized by pulmonary vascular obstruction caused, in part, by pulmonary artery... 
mitotic checkpoint | cyclin B1/cyclin-dependent kinase 1 | mitochondrial fission | hypoxia-inducible factor-1 | mitochondrial division inhibitor-1 | CARDIAC & CARDIOVASCULAR SYSTEMS | ENTRY | INDUCIBLE FACTOR 1-ALPHA | HYPOXIA | DRP1 | PATHWAY | ARTERIAL-HYPERTENSION | ENDOTHELIAL-CELLS | GENE-EXPRESSION | GERMLINE MUTATIONS | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | K+ CHANNELS | Antihypertensive Agents - pharmacology | Humans | Monocrotaline | Male | Cyclin B1 - metabolism | Cobalt | Hypertension, Pulmonary - therapy | CDC2 Protein Kinase - metabolism | RNA Interference | Time Factors | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Mitochondrial Proteins - metabolism | Myocytes, Smooth Muscle - drug effects | Hypertension, Pulmonary - enzymology | Disease Models, Animal | Muscle, Smooth, Vascular - drug effects | Myocytes, Smooth Muscle - enzymology | Dynamins - genetics | Rats | Familial Primary Pulmonary Hypertension | Hypoxia - complications | Rats, Sprague-Dawley | Pulmonary Artery - enzymology | Cell Cycle Checkpoints | GTP Phosphohydrolases - metabolism | GTP Phosphohydrolases - genetics | Mitochondria, Muscle - drug effects | Enzyme Activation | Hypertension, Pulmonary - etiology | Muscle, Smooth, Vascular - enzymology | Dynamins - metabolism | Phosphorylation | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Serine | Myocytes, Smooth Muscle - pathology | Mitochondrial Proteins - genetics | Case-Control Studies | Transfection | Quinazolinones - pharmacology | Mitochondria, Muscle - enzymology | Mitochondria, Muscle - pathology | Cells, Cultured | Muscle, Smooth, Vascular - pathology | Animals | Mitosis - drug effects | Glycolysis | Cell Proliferation - drug effects | Hypertension, Pulmonary - pathology | Pulmonary Artery - pathology | Genetic Therapy - methods | Hypoxia-inducible factor 1 | CDK1-cyclin B1 | Mitochondrial division inhibitor-1 (Mdivi-1) | Mitochondrial fission | Mitotic check point
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 07/2014, Volume 34, Issue 7, pp. 1446 - 1458
OBJECTIVE—Pulmonary vascular remodeling, the pathological hallmark of pulmonary arterial hypertension, is attributed to proliferation, apoptosis resistance,... 
anoxia | muscle | pulmonary | protein-lysine 6-oxidase | hypertension | extracellular matrix | smooth | COLLAGEN | muscle, smooth | AORTIC-ANEURYSMS | RAT | BONE MORPHOGENETIC PROTEIN | hypertension, pulmonary | PROLIFERATION | HYPOXIA | CROSS-TALK | GROWTH-FACTORS | ELASTIN | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | HEMATOLOGY | Antihypertensive Agents - pharmacology | Fibroblasts - enzymology | Humans | Middle Aged | Monocrotaline | Myocytes, Smooth Muscle - pathology | Male | Hypertrophy, Right Ventricular - etiology | RNA, Messenger - metabolism | Ventricular Dysfunction, Right - enzymology | Case-Control Studies | Cell Hypoxia | Young Adult | Aged, 80 and over | Adult | Female | Ventricular Dysfunction, Right - physiopathology | Hypertension, Pulmonary - drug therapy | Hypertension, Pulmonary - enzymology | Disease Models, Animal | Elastin - metabolism | Isoenzymes | Myocytes, Smooth Muscle - enzymology | Cells, Cultured | Enzyme Inhibitors - pharmacology | Rats | Familial Primary Pulmonary Hypertension | Hypertension, Pulmonary - genetics | Hypoxia - complications | Pulmonary Artery - drug effects | Fibroblasts - pathology | Hypertrophy, Right Ventricular - enzymology | Pulmonary Artery - enzymology | Gene Expression Regulation, Enzymologic | Ventricular Dysfunction, Right - prevention & control | Collagen - metabolism | Protein-Lysine 6-Oxidase - antagonists & inhibitors | Muscle, Smooth, Vascular - pathology | Animals | Ventricular Dysfunction, Right - etiology | Protein-Lysine 6-Oxidase - metabolism | Hypertrophy, Right Ventricular - prevention & control | Mice | Protein-Lysine 6-Oxidase - genetics | Hypertension, Pulmonary - etiology | Hypertension, Pulmonary - pathology | Muscle, Smooth, Vascular - enzymology | Pulmonary Artery - pathology
Journal Article
Circulation Research, ISSN 0009-7330, 08/2007, Volume 101, Issue 3, pp. 258 - 267
Nonphagocytic NADPH oxidases have recently been suggested to play a major role in the regulation of physiological and pathophysiological processes, in... 
Vascular smooth muscle cell proliferation | Hypoxia | Hypoxic pulmonary vasoconstriction | NADPH oxidase | Pulmonary hypertension | hypoxia | CARDIAC & CARDIOVASCULAR SYSTEMS | TGF-BETA | hypoxic pulmonary vasoconstriction | SUPEROXIDE-PRODUCTION | pulmonary hypertension | PROLIFERATION | vascular smooth muscle cell proliferation | NAD(P)H OXIDASE | ENDOTHELIAL-CELLS | GENE-EXPRESSION | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | CARDIOVASCULAR-DISEASES | ARTERY | HEMATOLOGY | VASOCONSTRICTION | Membrane Glycoproteins - analysis | Oxygen - pharmacology | Protein Subunits | Tunica Media - pathology | Humans | Myocytes, Smooth Muscle - pathology | Hypertension, Pulmonary - physiopathology | Male | Oxygen - metabolism | RNA, Messenger - biosynthesis | RNA Interference | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Cell Division | Drug Design | Superoxides - metabolism | NADPH Oxidases - genetics | Female | Hypertension, Pulmonary - drug therapy | NADPH Oxidases - biosynthesis | Hypertension, Pulmonary - enzymology | Endoplasmic Reticulum - enzymology | Cells, Cultured - drug effects | Hypoxia - enzymology | Myocytes, Smooth Muscle - enzymology | NADPH Oxidases - analysis | RNA, Small Interfering - pharmacology | Enzyme Induction | Nitric Oxide - physiology | Hypoxia - complications | NADPH Oxidase 4 | Organ Specificity | NADPH Oxidase 2 | Transforming Growth Factor beta1 - physiology | Cells, Cultured - enzymology | Pulmonary Artery - enzymology | Pulmonary Artery - cytology | Animals | Hypoxia - physiopathology | Lung - blood supply | Chronic Disease | Hypertension, Pulmonary - etiology | NADPH Oxidases - physiology | Tunica Media - enzymology | Hypertrophy
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 08/2014, Volume 34, Issue 8, pp. 1704 - 1715
OBJECTIVE—Pulmonary hypertension (PH) is a progressive disease arising from remodeling and narrowing of pulmonary arteries (PAs) resulting in high pulmonary... 
Adventitia | Fibroblast | NADPH oxidase | Pulmonary artery | pulmonary artery | ACTIVATION | adventitia | PROLIFERATION | FIBROBLASTS | NAD(P)H OXIDASE | fibroblast | CHRONIC HYPOXIA | MODELS | INFLAMMATION | NOX4 | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | HEMATOLOGY | MOLECULAR-MECHANISMS | Up-Regulation | Antihypertensive Agents - pharmacology | Fibroblasts - enzymology | Cell Proliferation | Reactive Oxygen Species - metabolism | Humans | Monocrotaline | NADPH Oxidases - metabolism | Pyrroles | Extracellular Matrix - metabolism | Male | Dose-Response Relationship, Drug | Extracellular Matrix - genetics | Transfection | Time Factors | HEK293 Cells | Adventitia - enzymology | NADPH Oxidases - genetics | Hypertrophy, Right Ventricular - pathology | Hypertension, Pulmonary - drug therapy | Indoles | Hypertension, Pulmonary - enzymology | Disease Models, Animal | Signal Transduction | Mice, Inbred C57BL | NADPH Oxidases - antagonists & inhibitors | Enzyme Inhibitors - pharmacology | Rats | Familial Primary Pulmonary Hypertension | Hypertension, Pulmonary - genetics | Hypoxia - complications | Adventitia - drug effects | NADPH Oxidase 4 | Pulmonary Artery - drug effects | Fibroblasts - pathology | Hypertrophy, Right Ventricular - enzymology | Rats, Sprague-Dawley | Pulmonary Artery - enzymology | Animals | Hypertrophy, Right Ventricular - prevention & control | Adventitia - pathology | Mice | Hypertension, Pulmonary - etiology | Hypertension, Pulmonary - pathology | Pulmonary Artery - pathology | Cell Movement | Index Medicus
Journal Article
Journal Article
Circulation, ISSN 0009-7322, 08/2012, Volume 126, Issue 9, pp. 1087 - 1098
Background-Pulmonary arterial hypertension (PAH) is a hyperproliferative vascular disorder observed predominantly in women. Estrogen is a potent mitogen in... 
Hypertension | Animal | Estrogens | Models | Cardiovascular diseases | Metabolism | Pulmonary | models animal | SEROTONIN TRANSPORTER | CARDIAC & CARDIOVASCULAR SYSTEMS | hypertension pulmonary | P450CYP1B1 | estrogens | cardiovascular diseases | P4501B1 CYP1B1 | HYPOXIA | BREAST-CANCER | IN-VIVO | ESTRADIOL | GENE-EXPRESSION | PERIPHERAL VASCULAR DISEASE | metabolism | MICE | 2-METHOXYESTRADIOL | Up-Regulation | Aryl Hydrocarbon Hydroxylases - biosynthesis | Humans | Aryl Hydrocarbon Hydroxylases - genetics | Myocytes, Smooth Muscle - pathology | Male | Stilbenes - pharmacology | Hypertension, Pulmonary - chemically induced | Lung - enzymology | Cell Hypoxia | Hydroxyestrones - toxicity | Aryl Hydrocarbon Hydroxylases - physiology | Female | Estrogens - metabolism | Myocytes, Smooth Muscle - metabolism | Estradiol - pharmacology | Hypertension, Pulmonary - enzymology | Aryl Hydrocarbon Hydroxylases - antagonists & inhibitors | Cells, Cultured - drug effects | Lung - pathology | Hydroxyestrones - pharmacology | Enzyme Induction | Hypoxia - complications | Hypertrophy, Right Ventricular - enzymology | Reverse Transcriptase Polymerase Chain Reaction | Pulmonary Artery - enzymology | Mice, Knockout | Animals | Aryl Hydrocarbon Hydroxylases - deficiency | Hydroxyestrones - metabolism | Cytochrome P-450 CYP1B1 | Cells, Cultured - metabolism | Mice | Chronic Disease | Hypertension, Pulmonary - etiology | Hypertension, Pulmonary - pathology | Pulmonary Artery - pathology | Physiological aspects | Development and progression | Research | Pulmonary hypertension | Cytochrome P-450 | Estrogen
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 12/2013, Volume 33, Issue 12, pp. 2780 - 2791
OBJECTIVE—Rho/Rho-kinase (ROCK) pathway in vascular smooth muscle cells (VSMCs) plays an important role in the pathogenesis of cardiovascular diseases,... 
Muscle, smooth, vascular | Rho-associated kinase | Hypertension, pulmonary | MIGRATION | ACTIVATION | METASTASIS | INVOLVEMENT | RHO-KINASE INHIBITOR | pulmonary | PROLIFERATION | vascular | VENTRAL BODY-WALL | rho-associated kinase | muscle | ARTERIAL-HYPERTENSION | PERIPHERAL VASCULAR DISEASE | HEME OXYGENASE-1 | HEMATOLOGY | hypertension | EXPRESSION | smooth | Phosphorylation | Cell Proliferation | Oxidative Stress | Humans | Middle Aged | Myocytes, Smooth Muscle - pathology | Child, Preschool | Ki-67 Antigen - metabolism | Male | Extracellular Signal-Regulated MAP Kinases - metabolism | Hypertension, Pulmonary - prevention & control | Young Adult | Transfection | RNA Interference | Time Factors | rho-Associated Kinases - metabolism | Inflammation Mediators - metabolism | Adult | Female | Child | rho-Associated Kinases - deficiency | Hypertension, Pulmonary - enzymology | Disease Models, Animal | Myocytes, Smooth Muscle - enzymology | Mice, Inbred C57BL | Cells, Cultured | rho-Associated Kinases - genetics | Familial Primary Pulmonary Hypertension | Hypertension, Pulmonary - genetics | Mice, Transgenic | Hypoxia - complications | Cell Adhesion Molecules - metabolism | Pulmonary Artery - enzymology | Mice, Knockout | Gene Expression Regulation, Enzymologic | Muscle, Smooth, Vascular - pathology | Animals | Adolescent | Heterozygote | Mice | Hypertension, Pulmonary - etiology | Hypertension, Pulmonary - pathology | Muscle, Smooth, Vascular - enzymology | Cell Movement | Index Medicus
Journal Article
Pediatric Research, ISSN 0031-3998, 12/2015, Volume 78, Issue 6, pp. 634 - 640
BACKGROUND: Pulmonary hypertension (PH) worsens clinical outcomes in former preterm infants with bronchopulmonary dysplasia (BPD). Oxidant stress disrupts... 
OVEREXPRESSION | VEGF | INFANTS | NITRIC-OXIDE | PEDIATRICS | MICE | HYPEROXIA | EXTRACELLULAR-SUPEROXIDE DISMUTASE | RAT LUNG | ENDOTHELIAL GROWTH-FACTOR | LUNG STRUCTURE | Bronchopulmonary Dysplasia - enzymology | Phosphorylation | Superoxide Dismutase - genetics | Vascular Remodeling | Oxidative Stress | Ventricular Dysfunction, Right - genetics | Bronchopulmonary Dysplasia - pathology | Hypertension, Pulmonary - physiopathology | Bronchopulmonary Dysplasia - physiopathology | Vascular Endothelial Growth Factor A - metabolism | Ventricular Dysfunction, Right - enzymology | Hypertension, Pulmonary - chemically induced | Pulmonary Alveoli - enzymology | Bronchopulmonary Dysplasia - genetics | Hypertrophy, Right Ventricular - physiopathology | Bleomycin | Ventricular Dysfunction, Right - physiopathology | Nitric Oxide Synthase Type III - metabolism | Ventricular Dysfunction, Right - chemically induced | Hypertension, Pulmonary - enzymology | Hypertrophy, Right Ventricular - genetics | Pulmonary Alveoli - blood supply | Animals, Newborn | Genetic Predisposition to Disease | Pulmonary Alveoli - pathology | Signal Transduction | Mice, Inbred C57BL | Vascular Endothelial Growth Factor Receptor-2 - metabolism | Hypertension, Pulmonary - genetics | Superoxide Dismutase - deficiency | Pulmonary Artery - physiopathology | Hypertrophy, Right Ventricular - enzymology | Pulmonary Artery - enzymology | Mice, Knockout | Phenotype | Animals | Bronchopulmonary Dysplasia - chemically induced | Hypertrophy, Right Ventricular - chemically induced | Ventricular Pressure | Endothelial Cells - pathology | Nitric Oxide - metabolism | Endothelial Cells - enzymology | Hypertension, Pulmonary - pathology | Pulmonary Artery - pathology | Ventricular Function, Right
Journal Article
by Hadinnapola, Charaka and Hadinnapola, Charaka and Bleda, Marta and Bleda, Marta and Haimel, Matthias and Haimel, Matthias and Screaton, Nicholas and Screaton, Nicholas and Swift, Andrew and Swift, Andrew and Dorfmüller, Peter and Dorfmüller, Peter and Preston, Stephen D and Preston, Stephen D and Southwood, Mark and Southwood, Mark and Hernandez-Sanchez, Jules and Hernandez-Sanchez, Jules and Martin, Jennifer and Martin, Jennifer and Treacy, Carmen and Treacy, Carmen and Yates, Katherine and Yates, Katherine and Bogaard, Harm and Bogaard, Harm and Church, Colin and Church, Colin and Coghlan, Gerry and Coghlan, Gerry and Condliffe, Robin and Condliffe, Robin and Corris, Paul A and Corris, Paul A and Gibbs, Simon and Gibbs, Simon and Girerd, Barbara and Girerd, Barbara and Holden, Simon and Holden, Simon and Humbert, Marc and Humbert, Marc and Kiely, David G and Kiely, David G and Lawrie, Allan and Lawrie, Allan and Machado, Rajiv and Machado, Rajiv and MacKenzie Ross, Robert and Ross, Robert Mackenzie and Moledina, Shahin and Moledina, Shahin and Montani, David and Montani, David and Newnham, Michael and Newnham, Michael and Peacock, Andrew and Peacock, Andrew and Pepke-Zaba, Joanna and Pepke-Zaba, Joanna and Rayner-Matthews, Paula and Rayner-Matthews, Paula and Shamardina, Olga and Shamardina, Olga and Soubrier, Florent and Soubrier, Florent and Southgate, Laura and Southgate, Laura and Suntharalingam, Jay and Suntharalingam, Jay and Toshner, Mark and Toshner, Mark and Trembath, Richard and Trembath, Richard and Noordegraaf, Anton Vonk and Vonk Noordegraaf, Anton and Wilkins, Martin R and Wilkins, Martin R and Wort, Stephen J and Wort, Stephen J and Wharton, John and Wharton, John and Gräf, Stefan and Gräf, Stefan and Morrell, Nicholas W and Morrell, Nicholas W and UK Natl Cohort Study Idiopathic He and BioResource-Rare Dis Consortium and NIHR BioResource–Rare Diseases Consortium; UK National Cohort Study of Idiopathic and Heritable PAH
Circulation, ISSN 0009-7322, 11/2017, Volume 136, Issue 21, pp. 2022 - 2033
Journal Article
Journal Article