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ISSN 1932-6203, 08/2013
Angiogenesis is the result of the combined activity of the tumor microenvironment and signaling molecules. The angiogenic switch is represented as an imbalance... 
Endoteli | Sarcoma d'Ewing | Neovascularization | Angiogènesi | Ewing's sarcoma | Endothelium
Journal Article
ISSN 1932-6203, 05/2011
Understanding tumor induced angiogenesis is a challenging problem with important consequences for diagnosis and treatment of cancer. Recently, strong evidences... 
Models matemàtics | Cell proliferation | Proliferació cel·lular | Endoteli | Mathematical models | Neovascularization | Angiogènesi | Endothelium
Journal Article
Frontiers in Physiology, ISSN 1664-042X, 2012, Volume 3, p. 165
Aging is associated with structural and functional changes in the vasculature, including endothelial dysfunction, arterial stiffening and remodeling, impaired... 
Vascular protection | Estradiol | Menopause | Nitric oxide | Endothelium | endothelium | nitric oxide | PHYSIOLOGY | menopause | vascular protection | estradiol | Nitric Oxide
Journal Article
ISSN 1932-6203, 08/2012
Impaired hemostasis coexists with accelerated atherosclerosis in patients with chronic kidney disease (CKD). The elevated frequency of atherothrombotic events... 
Malalties del ronyó | Kidney diseases | Uremia | Urèmia | Endoteli | Endothelium
Journal Article
ISSN 1935-2735, 2011
Immunological pressure encountered by protozoan parasites drives the selection of strategies to modulate or avoid the immune responses of their hosts. Here we... 
Citoquines | Cytokines | Endoteli | Cytology | Citologia | Endothelium
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2012, Volume 7, Issue 4, p. e32785
Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. Most morbidity associated with the metabolic syndrome is... 
DIABETES-MELLITUS | METABOLIC SYNDROME | CCL4 CIRRHOTIC RATS | FATTY LIVER-DISEASE | INSULIN-RESISTANCE | IN-VIVO | BIOLOGY | NITRIC-OXIDE | NONALCOHOLIC STEATOHEPATITIS | STELLATE CELL ACTIVATION | PORTAL-HYPERTENSION | Metabolic Syndrome - etiology | Liver - pathology | Rats, Wistar | Diet - adverse effects | Fatty Liver - pathology | Fatty Liver - complications | Male | Liver - physiopathology | Inflammation - complications | Microcirculation | Metabolic Syndrome - physiopathology | Non-alcoholic Fatty Liver Disease | Obesity - etiology | Liver Cirrhosis - complications | Fatty Liver - physiopathology | Liver - metabolism | Rats | Obesity - physiopathology | Obesity - pathology | Liver - blood supply | Animals | Endothelium, Vascular - pathology | Splanchnic Circulation | Hemodynamics | Metabolic Syndrome - pathology | Fatty Liver - etiology | Obesity | Liver diseases | Dilatation | Fibrosis | Blood vessels | Insulin resistance | Models | Inflammation | Endothelium | Phosphorylation | Liver | Body weight | Clinical trials | AKT protein | Glucose | Metabolic syndrome | Vasodilation | Fatty liver | Rodents | Hepatology | Atherosclerosis | Hypertension | Complications | Metabolic diseases | Triglycerides | Insulin | Nitric-oxide synthase | Morbidity | Steatosis | Hospitals | Diet | Perfusion | Nitric oxide | Laboratory animals | Metabolic disorders | Fibrosi pulmonar | Malalties del fetge | Pulmonary fibrosis | Endoteli
Journal Article
Journal Article
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 05/2018, Volume 38, Issue 5, pp. 1216 - 1229
OBJECTIVE—ALK1 (activin-receptor like kinase 1) is an endothelial cell-restricted receptor with high affinity for BMP (bone morphogenetic protein) 9 TGF-β... 
endothelium | ARTERIOVENOUS-MALFORMATIONS | HEREDITARY HEMORRHAGIC TELANGIECTASIA | PROTEIN | telangiectasia | ANGIOGENESIS | ENDOTHELIAL-CELL MIGRATION | mice | hereditary hemorrhagic | rare diseases | RECEPTOR-LIKE KINASE-1 | GENE | retina | MOLECULAR REGULATION | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | humans | EXPRESSION | TYPE-2 | Growth Differentiation Factor 2 - pharmacology | Telangiectasia, Hereditary Hemorrhagic - pathology | Phosphatidylinositol 3-Kinase - antagonists & inhibitors | Humans | Hyperplasia | Neovascularization, Pathologic | Telangiectasia, Hereditary Hemorrhagic - genetics | Retinal Telangiectasis - genetics | Case-Control Studies | Gene Deletion | Phosphatidylinositol 3-Kinase - metabolism | Vascular Endothelial Growth Factor A - pharmacology | Genetic Predisposition to Disease | Signal Transduction | Mice, Inbred C57BL | Activin Receptors, Type I - deficiency | Cells, Cultured | Angiogenesis Inhibitors - pharmacology | Retinal Telangiectasis - enzymology | Telangiectasia, Hereditary Hemorrhagic - drug therapy | Telangiectasia, Hereditary Hemorrhagic - enzymology | Activin Receptors, Type I - genetics | Retinal Telangiectasis - drug therapy | Mice, Knockout | Phenotype | Animals | Human Umbilical Vein Endothelial Cells - enzymology | Activin Receptors, Type II - genetics | Retinal Telangiectasis - pathology | Human Umbilical Vein Endothelial Cells - pathology | Protein Kinase Inhibitors - pharmacology | Enzyme Activation | Mutation | Endothelial Cells - pathology | Endothelial Cells - enzymology | Endothelial Cells - drug effects | Proteïnes quinases | Rats as laboratory animals | Retina | Hemorrhage | Hemorràgia | Endothelium | Vascular endothelial growth factors | Vascular diseases | Factor de creixement de l'endoteli vascular | Malalties vasculars | Endoteli | Rates (Animals de laboratori) | Protein kinases
Journal Article
PLoS ONE, ISSN 1932-6203, 08/2013, Volume 8, Issue 8, p. e71449
Angiogenesis is the result of the combined activity of the tumor microenvironment and signaling molecules. The angiogenic switch is represented as an imbalance... 
TARGET | EPHA2 RECEPTOR | ACTIVATION | INVASION | TYROSINE KINASE | EWS/FLI-1 | MULTIDISCIPLINARY SCIENCES | EPHRINS | TUMOR | EXPRESSION | FAMILY | Humans | Receptor, EphA2 - metabolism | Sarcoma, Ewing - pathology | Bone Neoplasms - pathology | Cell Movement - genetics | Bone Neoplasms - metabolism | Heterografts | Female | Transcription, Genetic | Tumor Burden - genetics | Bone Neoplasms - genetics | Proto-Oncogene Proteins c-akt - metabolism | Disease Models, Animal | Sarcoma, Ewing - metabolism | Signal Transduction | Endothelial Cells - metabolism | Fibroblast Growth Factor 2 - biosynthesis | Gene Silencing | Caveolin 1 - genetics | Mice, Knockout | Protein Transport | Caveolin 1 - metabolism | Animals | Fibroblast Growth Factor 2 - genetics | Receptor, EphA2 - genetics | Cell Line, Tumor | Protein Binding | Neovascularization, Pathologic - genetics | Mice | Neovascularization, Pathologic - metabolism | Sarcoma, Ewing - genetics | Tyrosine | Development and progression | Fibroblast growth factors | Sarcoma | Phosphotransferases | Endothelium | Caveolin-1 | Laboratories | AKT protein | Biology | Metastasis | Kinases | Inactivation | Ewing's sarcoma | Cell adhesion & migration | Proteins | Angiogenesis | Signal transduction | Rodents | Fibroblasts | Protein-tyrosine kinase receptors | Nutrients | Children | Localization | Growth factors | Protein-tyrosine kinase | EphA2 protein | Fibroblast growth factor 2 | Ephrins | Young adults | Deactivation | Caveolin | Gene expression | Endothelial cells | Signaling | Neural networks | Ligands | Adults | Solid tumors | Prostate cancer | Cell migration | Tumors | Sarcoma d'Ewing | Neovascularization | Angiogènesi | Endoteli
Journal Article
Experimental Cell Research, ISSN 0014-4827, 2008, Volume 314, Issue 13, pp. 2448 - 2453
Journal Article