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index medicus (17) 17
pulmonary hypertension (16) 16
humans (11) 11
animals (10) 10
abridged index medicus (8) 8
cardiac & cardiovascular systems (8) 8
male (8) 8
rats (8) 8
respiratory system (8) 8
arterial-hypertension (7) 7
hypertension (7) 7
peripheral vascular disease (7) 7
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female (6) 6
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hypertension, pulmonary - chemically induced (5) 5
hypertension, pulmonary - pathology (5) 5
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research (5) 5
health aspects (4) 4
hypertension, pulmonary - genetics (4) 4
hypertension, pulmonary - physiopathology (4) 4
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rats, wistar (4) 4
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vascular remodeling (4) 4
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hypertension, pulmonary (3) 3
hypertension, pulmonary - metabolism (3) 3
monocrotaline (3) 3
monocrotaline - toxicity (3) 3
mutation (3) 3
pathology (3) 3
proliferation (3) 3
pulmonary veno-occlusive disease - chemically induced (3) 3
rats, sprague-dawley (3) 3
risk factors (3) 3
rodents (3) 3
activation (2) 2
analysis (2) 2
antibiotics, antineoplastic - adverse effects (2) 2
biochemistry & molecular biology (2) 2
bone morphogenetic protein receptors, type ii - genetics (2) 2
breast-cancer cells (2) 2
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circulation (2) 2
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endothelial cells - pathology (2) 2
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gene mutations (2) 2
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neoplasms. tumors. oncology. including cancer and carcinogens (2) 2
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toxicity (2) 2
veno-occlusive disease (2) 2
5-bromo-2'-deoxyuridine (1) 1
5-ethynyl-2'-deoxyuridine (1) 1
acetylcysteine - pharmacology (1) 1
acetylcysteine - therapeutic use (1) 1
actins - biosynthesis (1) 1
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JACC (Journal of the American College of Cardiology), ISSN 0735-1097, 2015, Volume 65, Issue 7, pp. 668 - 680
Abstract Background Endothelial cell (EC) dysfunction plays a central role in the pathogenesis of pulmonary arterial hypertension (PAH), promoting... 
Cardiovascular | Internal Medicine | β-blocker | nebivolol | inflammation | endothelial dysfunction | pulmonary hypertension | CELLS | CARDIAC & CARDIOVASCULAR SYSTEMS | beta-blocker | RATS | CROSS-TALK | THERAPY | SMOOTH-MUSCLE HYPERPLASIA | ARTERIAL-HYPERTENSION | ANIMAL-MODELS | BLOCKADE | PROGRESSION | Ethanolamines - pharmacology | Benzopyrans - therapeutic use | Cell Proliferation | Rats, Wistar | Metoprolol - pharmacology | Humans | Monocrotaline | Adrenergic beta-1 Receptor Antagonists - pharmacology | Hypertension, Pulmonary - physiopathology | Endothelium, Vascular - drug effects | Male | Adrenergic beta-1 Receptor Antagonists - therapeutic use | Hypertension, Pulmonary - drug therapy | Cell Culture Techniques | Vascular Remodeling - drug effects | Benzopyrans - pharmacology | Disease Models, Animal | Nebivolol | Endothelium, Vascular - physiopathology | Rats | Metoprolol - therapeutic use | Pulmonary Artery - physiopathology | Pulmonary Artery - drug effects | Animals | Myocytes, Smooth Muscle | Cell Communication - drug effects | Endothelium, Vascular - pathology | Ethanolamines - therapeutic use | Hypertension, Pulmonary - pathology | Pulmonary Artery - pathology | Endothelial Cells - drug effects | Heart | Sects | Pulmonary hypertension | Endothelium | Studies | Cell growth | Pulmonary arteries | Mortality | Smooth muscle | Veins & arteries | Index Medicus | Abridged Index Medicus | Life Sciences
Journal Article
Journal Article
American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, 03/2019, Volume 199, Issue 6, pp. 799 - 802
[...]mean PApwa was increased in all PAH subtypes, and this observation could not be explained by differences in hematologic parameters or aortic radiodensity... 
RESPIRATORY SYSTEM | CRITICAL CARE MEDICINE | Hypertension | Medical imaging | Transplants & implants | Pulmonary arteries | Mortality | Coronary vessels | Calcification | Scleroderma | Age
Journal Article
Circulation, ISSN 0009-7322, 03/2015, Volume 131, Issue 11, pp. 1006 - 1018
BACKGROUND—The vascular remodeling responsible for pulmonary arterial hypertension (PAH) involves predominantly the accumulation of α-smooth muscle... 
Human | Hypertension | Vimentin | Sirolimus | Twist1 protein | Vascular remodeling | Epithelial-mesenchymal transition | Neointima | Animal | Type ii | Models | Bone morphogenetic protein receptors | Cardiovascular diseases | Pulmonary | RAPAMYCIN | MIGRATION | FIBROSIS | models, animal | CARDIAC & CARDIOVASCULAR SYSTEMS | neointima | hypertension, pulmonary | vimentin | cardiovascular diseases | vascular remodeling | DISCOVERY | bone morphogenetic protein receptors, type II | IN-VITRO | sirolimus | TWIST1 protein, human | ARTERIAL-HYPERTENSION | PERIPHERAL VASCULAR DISEASE | epithelial-mesenchymal transition | SMOOTH-MUSCLE-CELLS | KNOCKOUT RATS | TRANSDIFFERENTIATION | Vascular Remodeling | Humans | Gene Expression Profiling | Hypertension, Pulmonary - chemically induced | Actins - genetics | RNA, Messenger - biosynthesis | Vimentin - genetics | Cell Transdifferentiation | Lung - metabolism | Disease Models, Animal | Lung - pathology | Actins - biosynthesis | Bone Morphogenetic Protein Receptors, Type II - genetics | Vimentin - biosynthesis | Cells, Cultured | Rats | Hypertension, Pulmonary - genetics | Hypoxia - complications | Monocrotaline - toxicity | Sirolimus - pharmacology | Animals | Biomarkers | Mutation | Endothelial Cells - pathology | Lung - blood supply | Hypertension, Pulmonary - pathology | Mesoderm - pathology | Bone Morphogenetic Protein Receptors, Type II - biosynthesis | Cell Movement | Index Medicus | Abridged Index Medicus | Life Sciences
Journal Article
American Journal of Respiratory Cell and Molecular Biology, ISSN 1044-1549, 03/2017, Volume 56, Issue 3, pp. 402 - 405
[...]we hypothesized that bacterial translocation from gut lumen to bloodstream occurs in human and experimental PH, and that LPS translocation activates TLR4... 
CHRONIC HEART-FAILURE | CYTOKINES | RESPIRATORY SYSTEM | BIOCHEMISTRY & MOLECULAR BIOLOGY | ENDOTOXIN | IMMUNE ACTIVATION | RECEPTOR | DEATH | MICE | DYSFUNCTION | CD14 | CELL BIOLOGY | Hypotheses | Lungs | Cytokines | Pulmonary arteries | Pathogenesis | Rodents | Mutation | Permeability | Small intestine | Pulmonary hypertension | Veins & arteries | Index Medicus
Journal Article
Circulation, ISSN 0009-7322, 04/2016, Volume 133, Issue 14, pp. 1371 - 1385
BACKGROUND—Mutations in the KCNK3 gene have been identified in some patients suffering from heritable pulmonary arterial hypertension (PAH). KCNK3 encodes an... 
hypertension, pulmonary | pulmonary artery | cell proliferation | electrophysiology | ion channels | SIGNALING PATHWAYS | CARDIAC & CARDIOVASCULAR SYSTEMS | TYROSINE KINASE | RATS | pulmonary | MONOCROTALINE | FUNCTIONAL-PROPERTIES | MATRIX METALLOPROTEINASES | TO-MESENCHYMAL TRANSITION | ENDOTHELIAL-CELLS | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | hypertension | EXPRESSION | ortho-Aminobenzoates - pharmacology | Rats, Wistar | Humans | Myocytes, Smooth Muscle - pathology | Hypertension, Pulmonary - physiopathology | Male | Hypertrophy, Right Ventricular - etiology | Hypertension, Pulmonary - chemically induced | Cell Division | Nerve Tissue Proteins - biosynthesis | Nerve Tissue Proteins - antagonists & inhibitors | Genetic Predisposition to Disease | Nerve Tissue Proteins - physiology | Vascular Resistance | Bone Morphogenetic Protein Receptors, Type II - genetics | Potassium Channels, Tandem Pore Domain - genetics | Rats | Hypertension, Pulmonary - genetics | Inflammation | Monocrotaline - toxicity | Fibroblasts - pathology | Sulfonamides - pharmacology | Nerve Tissue Proteins - genetics | Rats, Sprague-Dawley | Patch-Clamp Techniques | Animals | Membrane Potentials | Potassium Channels, Tandem Pore Domain - physiology | Potassium Channels, Tandem Pore Domain - antagonists & inhibitors | Endothelium, Vascular - pathology | Adventitia - pathology | Potassium Channels, Tandem Pore Domain - biosynthesis | Hemodynamics | Mutation | Hypertension, Pulmonary - complications | Research | Gene mutations | Patients | Health aspects | Pulmonary hypertension | Index Medicus | Abridged Index Medicus
Journal Article
American Journal of Pathology, The, ISSN 0002-9440, 2015, Volume 185, Issue 2, pp. 356 - 371
Pulmonary veno-occlusive disease (PVOD) is an uncommon form of pulmonary hypertension (PH) characterized by progressive obstruction of small pulmonary veins... 
Pathology
Journal Article
Analytical cellular pathology (Amsterdam), 01/2017, Volume 2017, pp. 4697379 - 4697379
[This corrects the article DOI: 10.1155/2015/326385.]. 
Journal Article