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The Journal of biological chemistry, ISSN 1083-351X, 2015, Volume 290, Issue 22, pp. 13875 - 13887
Journal Article
Fluids and barriers of the CNS, ISSN 2045-8118, 2018, Volume 15, Issue 1, pp. 24 - 17
Breakdown of the blood-brain barrier (BBB) or inner blood-retinal barrier (BRB), induced by pathologically elevated levels of vascular endothelial growth... 
Plasmalemma vesicle-associated protein | Blood-brain barrier | Blood-retinal barrier | Cerebral edema | Diabetic macular edema | INDUCED RETINOPATHY | VASCULAR-PERMEABILITY | TRANSCELLULAR TRANSPORT | NEUROSCIENCES | DIFFERENTIATED MICRODOMAINS | MEDIATED TRANSCYTOSIS | FENESTRATED ENDOTHELIA | ANTIGEN PAL-E | LUMINAL SURFACE | CAPILLARY ENDOTHELIUM | ENDOTHELIAL GROWTH-FACTOR | Eye - metabolism | Brain Edema - metabolism | Capillary Permeability | Brain Edema - pathology | Diabetes Complications - metabolism | Humans | Macular Edema - pathology | Blood-Retinal Barrier - pathology | Macular Edema - metabolism | Blood-Brain Barrier - metabolism | Blood-Retinal Barrier - metabolism | Brain - metabolism | Blood-Brain Barrier - pathology | Animals | Carrier Proteins - metabolism | Macular Edema - complications | Membrane Proteins - metabolism | Diabetes Complications - pathology | Diabetic retinopathy | Brain | Nervous system diseases | Neurons | Mortality | Cell membranes | Permeability | Endothelium | Stroke (Disease) | Proteins | Health aspects | Vascular endothelial growth factor | Corticoids | Neuroprotection | Retinopathy | Brain cancer | Central nervous system | Retina | Angiogenesis | Ischemia | Protein transport | Edema | Stroke | Wound healing | Caveolae | Therapeutic applications | Diabetes mellitus | Morbidity | Endothelial cells | Plasma membranes | Diabetes | Cancer | Structure-function relationships | Blood–retinal barrier | Blood–brain barrier
Journal Article
JAMA ophthalmology, ISSN 2168-6165, 02/2013, Volume 131, Issue 2, pp. 160 - 165
Journal Article
PloS one, ISSN 1932-6203, 2016, Volume 11, Issue 1, p. e0146296
Naringenin (NGN) exhibits anti-inflammatory and antioxidant activities, but it remains undetermined its topical actions against ultraviolet B (UVB)-induced... 
ANTIOXIDANT ACTIVITY | HAIRLESS MICE | NADPH OXIDASE | IN-VITRO | LEUKOCYTE RECRUITMENT | INDUCED GENERATION | MULTIDISCIPLINARY SCIENCES | ANION-INDUCED PAIN | FACTOR-KAPPA-B | PIMENTA-PSEUDOCARYOPHYLLUS EXTRACT | HACAT HUMAN KERATINOCYTES | Tumor Necrosis Factor-alpha - metabolism | Heme Oxygenase-1 - metabolism | Gene Expression - drug effects | Edema - genetics | Glutathione - metabolism | Glutathione Reductase - metabolism | Skin - metabolism | Tumor Necrosis Factor-alpha - genetics | Administration, Cutaneous | Interleukin-1beta - genetics | Glutathione Reductase - genetics | Heme Oxygenase-1 - genetics | Interleukin-1beta - metabolism | Lipid Peroxidation - drug effects | Superoxides - metabolism | Interleukin-10 - metabolism | NF-E2-Related Factor 2 - genetics | Benzothiazoles - antagonists & inhibitors | Superoxides - antagonists & inhibitors | Hydroxyl Radical - antagonists & inhibitors | Benzothiazoles - metabolism | Interleukin-6 - metabolism | Skin - pathology | Edema - prevention & control | Glutathione Peroxidase - metabolism | Interleukin-6 - genetics | Catalase - genetics | Flavanones - pharmacology | Mice, Hairless | Hydroxyl Radical - metabolism | Inflammation | Antioxidants - pharmacology | Sulfonic Acids - metabolism | Glutathione Peroxidase - genetics | Sulfonic Acids - antagonists & inhibitors | Ultraviolet Rays - adverse effects | Catalase - metabolism | Edema - etiology | Animals | Skin - radiation effects | Interleukin-10 - genetics | NF-E2-Related Factor 2 - metabolism | Mice | Oxidative Stress - drug effects | Edema - pathology | Skin - drug effects | Antioxidants | Oxidative stress | Care and treatment | Ultraviolet radiation | Analysis | Lipid peroxidation | Dosage and administration | Skin | Research | Dermatitis | Risk factors | Naringenin | Life assessment | Iron | Interleukin 6 | Signal transduction | Mitochondria | Catalase | Glutathione reductase | Rodents | Heme | Hydroxyl radicals | Tumor necrosis factor-TNF | Peroxidase | Inhibition | Glutathione | Peroxidation | Citrus fruits | Formulations | Glutathione peroxidase | Edema | Cytokines | U.V. radiation | Heme oxygenase (decyclizing) | Superoxide | Stability analysis | Hairless | Gene expression | Sulfonic acid | Oxygenase | Flavonoids | Interleukin 10 | Irradiation | In vivo methods and tests | Topical application | Radiation damage | Reductase
Journal Article
American journal of physiology. Heart and circulatory physiology, ISSN 1522-1539, 2016, Volume 311, Issue 3, pp. H738 - H749
Journal Article
Arteriosclerosis, thrombosis, and vascular biology, ISSN 1524-4636, 2007, Volume 27, Issue 6, pp. 1312 - 1318
OBJECTIVES—S1P acts via the S1PR family of G protein–coupled receptors to regulate a variety of physiological responses. Whereas S1P1R activates Gi- and... 
PTEN | Rho | ROCK | Permeability | Sphingosine-1-phosphate | EDG-1 | MIGRATION | EXTRACELLULAR EXPORT | ANGIOGENESIS | PHOSPHORYLATION | permeability | MATURATION | SPHINGOSINE 1-PHOSPHATE RECEPTORS | PROTEIN-COUPLED RECEPTOR | ENDOTHELIAL-CELLS | PERIPHERAL VASCULAR DISEASE | sphingosine-1-phosphate | HEMATOLOGY | Lysophospholipids - metabolism | Phosphorylation | Receptors, Lysosphingolipid - antagonists & inhibitors | Cadherins - metabolism | Receptors, G-Protein-Coupled - metabolism | Humans | Hydrogen Peroxide | Capillary Permeability - drug effects | rac GTP-Binding Proteins - metabolism | Intracellular Signaling Peptides and Proteins - metabolism | Adherens Junctions - metabolism | Antigens, CD - metabolism | Pulmonary Edema - physiopathology | Transfection | Time Factors | rho-Associated Kinases | Receptors, Lysosphingolipid - genetics | Sphingosine - metabolism | Receptors, Lysosphingolipid - metabolism | Pulmonary Edema - metabolism | Protein-Serine-Threonine Kinases - metabolism | Disease Models, Animal | Pyrazoles - pharmacology | Endothelial Cells - metabolism | Cells, Cultured | PTEN Phosphohydrolase - metabolism | Rats | Pulmonary Edema - chemically induced | Sphingosine - analogs & derivatives | Stress Fibers - metabolism | Animals | Signal Transduction - drug effects | rho GTP-Binding Proteins - metabolism | Receptors, G-Protein-Coupled - antagonists & inhibitors | Pyridines - pharmacology | Receptors, G-Protein-Coupled - genetics | Endothelial Cells - drug effects
Journal Article
PloS one, ISSN 1932-6203, 2013, Volume 8, Issue 9, p. e74458
Status epilepticus (SE) induces vasogenic edema in the piriform cortex with disruptions of the blood-brain barrier (BBB). However, the mechanisms of vasogenic... 
NADPH-OXIDASE | PERMEABILITY | MULTIDISCIPLINARY SCIENCES | SEIZURE | RAT PIRIFORM CORTEX | NITRIC-OXIDE | RECEPTOR | KAINIC ACID | ENDOTHELIN | BLOOD-BRAIN-BARRIER | FACTOR-ALPHA | Tumor Necrosis Factor-alpha - metabolism | Neurons - pathology | Reactive Oxygen Species - metabolism | Tumor Necrosis Factor-alpha - genetics | Astrocytes - pathology | Cerebral Cortex - pathology | NADPH Oxidases - metabolism | Male | Status Epilepticus - genetics | Cerebral Cortex - metabolism | Brain Edema - genetics | NADPH Oxidases - genetics | Status Epilepticus - complications | Neurons - metabolism | Nitric Oxide Synthase Type III - metabolism | Disease Models, Animal | Brain Edema - metabolism | Brain Edema - etiology | Signal Transduction | Endothelial Cells - metabolism | Endothelin-1 - genetics | Endothelin-1 - metabolism | Brain Edema - pathology | Gene Expression Regulation | Status Epilepticus - pathology | Rats | Receptor, Endothelin A - genetics | Nitric Oxide Synthase Type III - genetics | Rats, Sprague-Dawley | Blood-Brain Barrier - metabolism | Stereotaxic Techniques | Blood-Brain Barrier - pathology | Animals | Microdialysis | Receptor, Endothelin A - metabolism | Endothelial Cells - pathology | Status Epilepticus - metabolism | Astrocytes - metabolism | Reactive oxygen species | Neurosciences | Phosphorylation | Laboratories | Epilepsy | Neurobiology | Oxidase | Membrane permeability | Activation | Cortex (piriform) | NAD(P)H oxidase | Blood-brain barrier | Rodents | Surgery | Tumor necrosis factor-TNF | Edema | Stroke | Astrocytes | Mortality | Endothelin 1 | Permeability | Tumor necrosis factor-α | Nitric-oxide synthase | Endothelial cells | Neurological diseases | Medicine | Brain research | Nitric oxide | TNF inhibitors | Receptor mechanisms
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2013, Volume 8, Issue 4, p. e61440
Human parvovirus B19 (B19V) is the causative agent of erythema infectiosum in humans. B19 infection also causes severe disease manifestations, such as chronic... 
APOPTOSIS | REPLICATION | MULTIDISCIPLINARY SCIENCES | ERYTHROID PROGENITOR CELLS | DISEASE | NONSTRUCTURAL PROTEIN | VP1 UNIQUE REGION | INFECTION | KAPPA-B | MINOR CAPSID PROTEIN | Consensus Sequence | Tumor Necrosis Factor-alpha - metabolism | Humans | Transcriptional Activation | NF-kappa B - metabolism | Female | Cell Membrane - metabolism | Phospholipases A2 - chemistry | Signal Transduction | Capsid Proteins - metabolism | Cells, Cultured | Models, Molecular | Phospholipases A2 - metabolism | Parvovirus B19, Human - genetics | Amino Acid Motifs | Protein Transport | Pregnancy | Erythema Infectiosum | Protein Conformation | Mutation | Enzyme Activation - genetics | Amino Acid Substitution | Capsid Proteins - genetics | Parvovirus B19, Human - enzymology | Phospholipases A2 - genetics | Proteins | Amino acids | Phospholipases | Anemia | Fatty acids | Bioengineering | VP1 protein | Transcription factors | Enzyme activity | Capsid protein | Transcription | Erythrocytes | Cytology | Chronic infection | Viruses | Genomes | Infections | Turnover rate | Cell morphology | Signal transduction | Red blood cells | E coli | Enzymatic activity | Cell cycle | Tumor necrosis factor-TNF | Life sciences | Localization | Edema | Enzymes | NF-κB protein | Phospholipase A2 | Blood & organ donations | Cytokines | Blood cells | Tumor necrosis factor-α | Patients | Virology | Mutants | Phospholipase | Hydrops fetalis | Determinants | Immunocompromised hosts | Erythema | Erythema infectiosum | Apoptosis | Capsid Proteins/metabolism | Parvovirus B19, Human/enzymology | Parvovirus B19, Human/genetics | Cellular Biology | Life Sciences | Phospholipases A2/genetics | Tumor Necrosis Factor-alpha/metabolism | Enzyme Activation/genetics | Microbiology and Parasitology | Cell Membrane/metabolism | Capsid Proteins/genetics | Phospholipases A2/metabolism | NF-kappa B/metabolism | Phospholipases A2/chemistry
Journal Article
PloS one, ISSN 1932-6203, 2017, Volume 12, Issue 11, p. e0187637
Background Hypoxia preconditioning has been proven to be an effective method to enhance the therapeutic action of mesenchymal stem cells (MSCs). However, the... 
ISCHEMIA-REPERFUSION INJURY | SURVIVAL | EMBOLISM | DEXAMETHASONE | THERAPY | INCREASE | MULTIDISCIPLINARY SCIENCES | MICE | MARROW STROMAL CELLS | DELIVERY | Bronchoalveolar Lavage Fluid | Protein Carbonylation | Lung Injury - pathology | Capillaries - pathology | Glutathione - metabolism | Antioxidants - metabolism | Caspase 3 - metabolism | Male | NF-kappa B - metabolism | Pulmonary Embolism - pathology | Cell Hypoxia | Proto-Oncogene Proteins c-bcl-2 - metabolism | Lung Injury - therapy | Mesenchymal Stromal Cells - cytology | Leukocyte Count | Reperfusion Injury - complications | Biomarkers - metabolism | Pulmonary Embolism - complications | Reperfusion Injury - therapy | Capillaries - physiopathology | Thrombosis - physiopathology | Reperfusion Injury - pathology | Signal Transduction | Cytochromes c - metabolism | Organ Size | Thiobarbituric Acid Reactive Substances - metabolism | Rats, Sprague-Dawley | Hydrogen Peroxide - metabolism | Thrombosis - pathology | Intercellular Adhesion Molecule-1 - metabolism | Lung Injury - physiopathology | Animals | Reperfusion Injury - physiopathology | Cytosol - metabolism | Lung Injury - complications | Hemodynamics | Vascular Cell Adhesion Molecule-1 - metabolism | Mesenchymal Stem Cell Transplantation | Apoptosis | Mitogen-Activated Protein Kinases - metabolism | Peroxidase - metabolism | Pulmonary Embolism - physiopathology | Care and treatment | Stem cells | Physiological aspects | Research | Properties | Reperfusion injury | Risk factors | Cytochrome | Reactive oxygen species | Transplants & implants | Bcl-2 protein | Mesenchyme | Embolisms | Membrane permeability | Prostaglandin E2 | Stem cell transplantation | Critical care | Angiogenesis | Mitochondria | Reperfusion | Allografts | Pathways | Ischemia | Rodents | Bone marrow | Thromboembolism | Alveoli | Drug dosages | Injuries | Glutathione | Edema | NF-κB protein | Cytokines | Internal medicine | Rats | MAP kinase | Inflammation | Permeability | Thrombosis | Embolism | Medicine | Cytochrome c | Signaling | Lungs | Skin & tissue grafts | Interleukin 10 | Ventilation | Hypoxia | Clinical medicine | Laboratory animals | Preconditioning | Cell migration
Journal Article
Journal Article