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1. Full Text Cerebral ischemia-reperfusion injury in rats-A 3 T MRI study on biphasic blood-brain barrier opening and the dynamics of edema formation
by Pillai, Deepu R and Dittmar, Michael S and Baldaranov, Dobri and Heidemann, Robin M and Henning, Erica C and Schuierer, Gerhard and Bogdahn, Ulrich and Schlachetzki, Felix
Journal of Cerebral Blood Flow & Metabolism, ISSN 0271-678X, 11/2009, Volume 29, Issue 11, pp. 1846 - 1855
Serial magnetic resonance imaging (MRI) was performed to investigate the temporal and spatial relationship between the biphasic nature of blood–brain barrier... 
Stroke | Blood-brain barrier | Magnetic resonance imaging | Cerebral edema | blood-brain barrier | magnetic resonance imaging | ARTERY OCCLUSION | PERMEABILITY | cerebral edema | FOCAL ISCHEMIA | stroke | TIGHT JUNCTION | NEUROSCIENCES | INFARCTION | DISRUPTION | ENDOCRINOLOGY & METABOLISM | ALBUMIN | PROTEINS | HEMATOLOGY | WATER | Brain Ischemia - complications | Brain Edema - etiology | Reperfusion Injury - pathology | Brain Edema - pathology | Rats | Male | Blood-Brain Barrier - pathology | Magnetic Resonance Imaging | Animals | Time Factors | Brain Ischemia - pathology | Reperfusion Injury - complications | Disease Models, Animal | Index Medicus
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2. Full Text Cardiac arrest-induced regional blood–brain barrier breakdown, edema formation and brain pathology: a light and electron microscopic study on a new model for neurodegeneration and neuroprotection in porcine brain
by Sharma, Hari Shanker and Miclescu, Adriana and Wiklund, Lars and Medicinska fakulteten and Anestesiologi och intensivvård and Medicinska och farmaceutiska vetenskapsområdet and Uppsala universitet and Institutionen för kirurgiska vetenskaper
Journal of Neural Transmission, ISSN 0300-9564, 1/2011, Volume 118, Issue 1, pp. 87 - 114
Brief cardiac arrest and survival is often associated with marked neurological alterations related to cognitive and sensory motor functions. However, detail... 
Edema | Neurosciences | Neuronal damage | Astrocytes | Myelin | Cardiac arrest | Perivascular edema | Luxol fast blue | Glial changes | Myelin basic protein | Endothelial cells | Nissl stain | GFAP | Neurology | Pig brain | Medicine & Public Health | Ultrastructure | Pharmacology/Toxicology | Psychiatry | METHYLENE-BLUE | METHAMPHETAMINE INTOXICATION | CLINICAL NEUROLOGY | PROTEIN IMMUNOREACTIVITY | CEREBROSPINAL FLUID BARRIER | CENTRAL-NERVOUS-SYSTEM | SPINAL-CORD-INJURY | QUALITY-OF-LIFE | DARK NEURONS | NEUROSCIENCES | EXTRACELLULAR-SPACE | HUMAN CEREBRAL-CORTEX | Immunohistochemistry | Microscopy, Electron, Transmission | Neurons - pathology | Brain Edema - etiology | Myelin Sheath - pathology | Albumins - metabolism | Neuroglia - pathology | Brain Edema - pathology | Electrolytes - metabolism | Extracellular Space | Nerve Degeneration - pathology | Blood-Brain Barrier - pathology | Animals | Neuroprotective Agents - pharmacology | Models, Biological | Swine | Brain - pathology | Methylene Blue | Brain Chemistry | Heart Arrest - complications | Heart Arrest - pathology | Medical research | Brain | Neurons | Albumin | Antioxidants | Dropsy | Analysis | Medicine, Experimental | Brain damage | Intermediate filament proteins | Myelin proteins | Index Medicus | Heart | Leakage | neuropil | Neuroprotection | Brain stem | Glial fibrillary acidic protein | Cognitive ability | Cortex | Neuronal-glial interactions | Fibers | Methylene blue | Blood-brain barrier | Thalamus | Medical and Health Sciences | Medicin och hälsovetenskap | MEDICINE | Myelin basi | MEDICIN
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3. Full Text Mast Cells Increase Vascular Permeability by Heparin-Initiated Bradykinin Formation In Vivo
by Oschatz, Chris and Maas, Coen and Lecher, Bernd and Jansen, Thomas and Björkqvist, Jenny and Tradler, Thomas and Sedlmeier, Reinhard and Burfeind, Peter and Cichon, Sven and Hammerschmidt, Sven and Müller-Esterl, Werner and Wuillemin, Walter A and Nilsson, Gunnar and Renné, Thomas
Immunity, ISSN 1074-7613, 02/2011, Volume 34, Issue 2, pp. 258 - 268
Activated mast cells trigger edema in allergic and inflammatory disease. We report a paracrine mechanism by which mast cell-released heparin increases vascular... 
COAGULATION-FACTOR-XII | CONTACT SYSTEM | ACTIVATION | ENZYME | HEREDITARY ANGIOEDEMA | CHONDROITIN SULFATE-E | ADVERSE CLINICAL EVENTS | ALLERGIC REACTIONS | RECEPTOR | MECHANISMS | IMMUNOLOGY | Capillary Permeability - physiology | Plasma | Capillary Leak Syndrome - physiopathology | Kallikrein-Kinin System - physiology | Complement C1 Inhibitor Protein - physiology | Heparin - secretion | Male | Leukocytes - physiology | Factor XII - physiology | Paracrine Communication - physiology | Immunoglobulin E - immunology | Heparin - physiology | Hypotension - physiopathology | Passive Cutaneous Anaphylaxis - physiology | Hypotension - etiology | Bradykinin - biosynthesis | Capillary Leak Syndrome - etiology | Rats | Cell Adhesion | Skin - blood supply | Edema - etiology | Animals | Mast Cells - secretion | Signal Transduction - physiology | Edema - physiopathology | Mice | Enzyme Activation | Endothelial Cells - pathology | Bradykinin - genetics | Heparan sulfate | Rodents | Blood pressure | Permeability | Pressure transducers | Veins & arteries | Index Medicus
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4. Full Text Hdac3 regulates lymphovenous and lymphatic valve formation
by Janardhan, Harish P and Milstone, Zachary J and Shin, Masahiro and Lawson, Nathan D and Keaney, John F and Trivedi, Chinmay M
Journal of Clinical Investigation, ISSN 0021-9738, 11/2017, Volume 127, Issue 11, pp. 4193 - 4206
Lymphedema, the most common lymphatic anomaly, involves defective lymphatic valve development; yet the epigenetic modifiers underlying lymphatic valve... 
MEDICINE, RESEARCH & EXPERIMENTAL | HISTONE DEACETYLASE 3 | CARDIAC MYOCYTE PROLIFERATION | EMBERGER SYNDROME | PRIMARY LYMPHEDEMA | IN-VIVO | VASCULAR INTEGRITY | LINEAGE ANALYSIS | GATA2 DEFICIENCY | MONOMAC SYNDROME | TRANSGENIC MICE | Epigenesis, Genetic | Humans | Mice, Transgenic | E1A-Associated p300 Protein - metabolism | Lymphatic System - enzymology | Animals | Enhancer Elements, Genetic | Gene Expression Regulation, Developmental | Base Sequence | Lymphatic Vessels - enzymology | GATA2 Transcription Factor - metabolism | HEK293 Cells | Histone Deacetylases - physiology | Lymphangiogenesis | Binding Sites | GATA2 Transcription Factor - genetics | Histones | Care and treatment | Diagnosis | Research | Lymphedema | Endothelium | ETS protein | Edema | Histone deacetylase | Enzymes | Lymphatic system | Transcription factors | Ets-1 protein | Leukemia | Genomics | Genomes | Lethality | Roles | Gene expression | Histone acetyltransferase | Blood | Morphogenesis | Blood platelets | Rodents | Epigenetics | Mutation | Mechanical stimuli | Index Medicus | Abridged Index Medicus
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5. Full Text Dimethyl fumarate attenuates cerebral edema formation by protecting the blood–brain barrier integrity
by Kunze, Reiner and Urrutia, Andrés and Hoffmann, Angelika and Liu, Hui and Helluy, Xavier and Pham, Mirko and Reischl, Stefan and Korff, Thomas and Marti, Hugo H
Experimental Neurology, ISSN 0014-4886, 04/2015, Volume 266, pp. 99 - 111
Brain edema is a hallmark of various neuropathologies, but the underlying mechanisms are poorly understood. We aim to characterize how tissue hypoxia, together... 
Edema | Stroke | Ischemia | Nrf2 | Dimethyl fumarate | Blood–brain barrier | Blood-brain barrier | ARTERY OCCLUSION | PLACEBO-CONTROLLED PHASE-3 | NEUROSCIENCES | VASCULAR LEAKAGE | MULTIPLE-SCLEROSIS | IN-VITRO MODEL | NRF2-MEDIATED ANTIOXIDANT RESPONSE | TIGHT JUNCTION PROTEINS | TNF-ALPHA | ENDOTHELIAL GROWTH-FACTOR | ACID ESTERS | Animals, Newborn | RNA, Small Interfering - genetics | Brain Edema - pathology | Mice, Inbred C57BL | Male | Infarction, Middle Cerebral Artery - pathology | Blood-Brain Barrier - drug effects | Brain Edema - prevention & control | Stroke - pathology | Cell Movement - drug effects | Animals | Fumarates - pharmacology | Brain Ischemia - pathology | Mice | Matrix Metalloproteinases - metabolism | Dimethyl Fumarate | Immunosuppressive Agents - pharmacology | Tight Junctions - pathology | Tight Junctions - drug effects | Stroke (Disease) | Proteins | Dimethylformamide | Psoriasis | Cerebral edema | Analysis | Index Medicus
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6. Full Text Brain Alanine Formation as an Ammonia-Scavenging Pathway during Hyperammonemia: Effects of Glutamine Synthetase Inhibition in Rats and Astrocyte—Neuron Co-Cultures
by Dadsetan, Sherry and Kukolj, Eva and Bak, Lasse K and SØrensen, Michael and Ott, Peter and Vilstrup, Hendrik and Schousboe, Arne and Keiding, Susanne and Waagepetersen, Helle S
Journal of Cerebral Blood Flow & Metabolism, ISSN 0271-678X, 8/2013, Volume 33, Issue 8, pp. 1235 - 1241
Hyperammonemia is a major etiological toxic factor in the development of hepatic encephalopathy. Brain ammonia detoxification occurs primarily in astrocytes by... 
hyperammonemia | methionine sulfoximine | alanine | hepatic encephalopathy | ACUTE LIVER-FAILURE | NEUROSCIENCES | CEREBRAL-CORTEX | DEHYDROGENASE | METABOLISM | SPECTROSCOPY | AMINO-ACIDS | EDEMA | ENDOCRINOLOGY & METABOLISM | MAGNETIC-RESONANCE | ACCUMULATION | HEMATOLOGY | HEPATIC-ENCEPHALOPATHY | Astrocytes - drug effects | Gas Chromatography-Mass Spectrometry | Hyperammonemia - metabolism | Rats, Wistar | Ammonia - metabolism | Glutamate-Ammonia Ligase - antagonists & inhibitors | Coculture Techniques | Enzyme Inhibitors - pharmacology | Rats | Alanine - metabolism | Methionine Sulfoximine - pharmacology | Chromatography, High Pressure Liquid | Enzyme Inhibitors - therapeutic use | Brain Chemistry - physiology | gamma-Aminobutyric Acid - physiology | Amino Acids - metabolism | Animals | Female | Neurons - drug effects | Index Medicus | Original
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7. Full Text L‐PGDS‐derived PGD2 attenuates acute lung injury by enhancing endothelial barrier formation
by Horikami, Daiki and Toya, Naoki and Kobayashi, Koji and Omori, Keisuke and Nagata, Nanae and Murata, Takahisa
The Journal of Pathology, ISSN 0022-3417, 07/2019, Volume 248, Issue 3, pp. 280 - 290
Acute lung injury (ALI) is caused by various stimuli such as acid aspiration and infection, resulting in severe clinical outcomes with high mortality.... 
lipocalin‐type prostaglandin D synthase | epithelial cell | vascular permeability | acute lung injury | endothelial cell | Acute respiratory distress syndrome | Prostaglandins | Permeability | Analysis | Mortality | Endothelium | Plasma | Edema | Epithelial cells | Lung | Lipocalin | Neutrophils | Endotoxins | Lipids | Leukocytes (neutrophilic) | Inflammation | Prostaglandin D2 | Macrophages | Endothelial cells | Hemopoiesis | Lungs | Bioaccumulation | Bone marrow | Infiltration | Inhibition | Trachea
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8. Full Text Selective inhibition of tumor necrosis factor-α prevents nucleus pulposus-induced thrombus formation, intraneural edema, and reduction of nerve conduction velocity: Possible implications for future pharmacologic treatment strategies of sciatica
by Olmarker, Kjell and Rydevik, Björn
Spine, ISSN 0362-2436, 04/2001, Volume 26, Issue 8, pp. 863 - 869
Study Design. The possibility to prevent nucleus pulposus-induced functional and structural nerve root injury by selective tumor necrosis factor-alpha... 
Spinal nerve roots | TNF-α | Spine | Intervertebral disc | Cytokine | Herniated disc | Nerve fiber | Sciatica | cytokine | intervertebral disc | LOW-BACK-PAIN | CROHNS-DISEASE | TNF-alpha | ROOT INJURY | CHEMICALLY-MODIFIED TETRACYCLINES | spine | EXPERIMENTAL NEUROPATHY | PORCINE CAUDA-EQUINA | CLINICAL NEUROLOGY | spinal nerve roots | sciatica | CYCLOSPORINE-A | nerve fiber | FUNCTIONAL-CHANGES | VASCULAR ENDOTHELIAL-CELLS | ORTHOPEDICS | herniated disc | Cauda Equina - pathology | Intervertebral Disc Displacement - complications | Intervertebral Disc - innervation | Sciatica - drug therapy | Nerve Fibers - physiology | Spinal Nerve Roots - physiopathology | Etanercept | Infliximab | Swine | Immunoglobulin G - pharmacology | Neural Conduction - drug effects | Antirheumatic Agents - pharmacology | Thrombosis - prevention & control | Intervertebral Disc - pathology | Intervertebral Disc Displacement - drug therapy | Edema - prevention & control | Nerve Fibers - pathology | Sciatica - pathology | Antibodies, Monoclonal - pharmacology | Intervertebral Disc Displacement - pathology | Sciatica - etiology | Cauda Equina - physiopathology | Enoxaparin - pharmacology | Edema - etiology | Thrombosis - pathology | Animals | Receptors, Tumor Necrosis Factor | Thrombosis - etiology | Anticoagulants - pharmacology | Intervertebral Disc - blood supply | Spinal Nerve Roots - pathology | Edema - pathology | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Index Medicus
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9. Full Text Inhibition of HIF prolyl-4-hydroxylases by FG-4497 reduces brain tissue injury and edema formation during ischemic stroke
by Reischl, Stefan and Li, Lexiao and Walkinshaw, Gail and Flippin, Lee A and Marti, Hugo H and Kunze, Reiner
PLoS ONE, ISSN 1932-6203, 01/2014, Volume 9, Issue 1, pp. e84767 - e84767
Ischemic stroke results in disruption of the blood-brain barrier (BBB), edema formation and neuronal cell loss. Some neuroprotective factors such as vascular... 
MOUSE-BRAIN | NERVOUS-SYSTEM | HYPOXIA-INDUCIBLE FACTOR-1-ALPHA | ALZHEIMERS-DISEASE | VEGF | MULTIDISCIPLINARY SCIENCES | FOCAL CEREBRAL-ISCHEMIA | PROLYL HYDROXYLASES | NEUROPROTECTION | ENDOTHELIAL GROWTH-FACTOR | VASCULAR LEAKAGE | Neurons - pathology | Brain Injuries - drug therapy | Brain Infarction - metabolism | Brain Infarction - pathology | Male | Hypoxia-Inducible Factor-Proline Dioxygenases - antagonists & inhibitors | Brain Injuries - metabolism | Stroke - pathology | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Neurons - metabolism | Neurons - drug effects | Brain Infarction - drug therapy | Tight Junction Proteins - metabolism | Astrocytes - drug effects | Endothelial Cells - metabolism | Edema - drug therapy | Stroke - drug therapy | Protein Transport | Edema - metabolism | Stroke - metabolism | Animals | Signal Transduction - drug effects | Intracellular Space - metabolism | Mice | Brain Injuries - pathology | Astrocytes - metabolism | Endothelial Cells - drug effects | Brain | Dropsy | Edema | Ischemia | Neurons | Glycoproteins | DNA binding proteins | Hydroxylases | Vascular endothelial growth factor | Endothelium | Neuroprotection | Diabetic retinopathy | Transcription factors | Phosphorylation | Erythropoietin | Damage prevention | Proteins | Prevention | Angiogenesis | Signal transduction | Blood-brain barrier | Neurodegeneration | Rodents | Physiology | Prolyl hydroxylase | Inhibition | Leakage | Deprivation | Stroke | Cell survival | Astrocytes | Hydroxylase | Permeability | Zonula occludens-1 protein | Endothelial cells | Signaling | Injury prevention | Hypoxia | Brain injury | Veins & arteries | Index Medicus
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10. Full Text Blood–brain barrier disruption induced by hemoglobin in vivo: Involvement of up-regulation of nitric oxide synthase and peroxynitrite formation
by Ding, Rui and Chen, Yizhao and Yang, Shuo and Deng, Xinqing and Fu, Zhenghao and Feng, Liang and Cai, Yingqian and Du, Mouxuan and Zhou, Yuxi and Tang, Yanping
Brain Research, ISSN 0006-8993, 2014, Volume 1571, pp. 25 - 38
Abstract Accumulating evidence has demonstrated that up-regulation of nitric oxide synthase (NOS) and subsequent peroxynitrite (ONOO− ) formation exert a... 
Neurology | Hemoglobin | Nitric oxide synthase | Peroxynitrite | Brain edema | Intracerebral hemorrhage | Blood–brain barrier | Blood-brain barrier | CELLS | HEMORRHAGE | INJURY | NEUROSCIENCES | PATHOPHYSIOLOGY | INHIBITION | MATRIX-METALLOPROTEINASE ACTIVATION | NITROTYROSINE | DYSFUNCTION | CEREBRAL-ISCHEMIA | EXPRESSION | Cerebral Hemorrhage - chemically induced | Nitric Oxide - blood | Brain Edema - metabolism | Enzyme-Linked Immunosorbent Assay | Blood-Brain Barrier - physiopathology | Claudin-5 - metabolism | Motor Activity - drug effects | Rats | Male | Blood-Brain Barrier - drug effects | Rats, Sprague-Dawley | Tyrosine - analogs & derivatives | Up-Regulation - drug effects | Tyrosine - metabolism | Animals | Analysis of Variance | Time Factors | Peroxynitrous Acid - metabolism | Nitric Oxide Synthase - metabolism | Zonula Occludens-1 Protein - metabolism | Cerebral Hemorrhage - pathology | Hemoglobins - toxicity | Disease Models, Animal | Medical colleges | Brain | Nitric oxide | Analysis | Injuries | Index Medicus
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11. Full Text Inhibition of protein kinase Cβ reverses increased blood-brain barrier permeability during hyperglycemic stroke and prevents edema formation in vivo
by Cipolla, Marilyn J and Huang, Quillan and Sweet, Julie G
Stroke, ISSN 0039-2499, 11/2011, Volume 42, Issue 11, pp. 3252 - 3257
Background and Purpose-We investigated the effect of circulating factors and protein kinase C beta on blood-brain barrier permeability and edema during... 
blood- brain barrier | hyperglycemia | reperfusion injury | vasogenic edema | protein kinase C | blood-brain barrier | protein kinase C beta vasogenic edema | ACTIVATION | GLUCOSE | ACUTE ISCHEMIC-STROKE | PERIPHERAL VASCULAR DISEASE | STRESS | CLINICAL NEUROLOGY | Capillary Permeability - physiology | Protein Kinase C beta | Phthalimides - therapeutic use | Protein Kinase C - physiology | Rats, Wistar | Capillary Permeability - drug effects | Rats | Male | Protein Kinase C - antagonists & inhibitors | Stroke - drug therapy | Blood-Brain Barrier - drug effects | Hyperglycemia - drug therapy | Brain Edema - enzymology | Stroke - enzymology | Brain Edema - prevention & control | Phthalimides - pharmacology | Animals | Blood-Brain Barrier - enzymology | Protein Kinase Inhibitors - therapeutic use | Hyperglycemia - enzymology | Protein Kinase Inhibitors - pharmacology | Index Medicus
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