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American Journal of Pathology, The, ISSN 0002-9440, 2017, Volume 187, Issue 6, pp. 1327 - 1342
Alkali burns to the eye constitute a leading cause of worldwide blindness. In recent case series, corneal transplantation revealed unexpected damage to the... 
Pathology | EMERGENCY | TUMOR-NECROSIS-FACTOR | IN-VITRO | CYTOKINES | THERAPY | PROTECTION | BOSTON KERATOPROSTHESIS | ENDOTOXIN | EYE BURNS | PATHOLOGY | GLAUCOMA | Neuroprotective Agents - therapeutic use | Tumor Necrosis Factor-alpha - metabolism | Eye Burns - drug therapy | Retina - metabolism | Apoptosis - drug effects | Burns, Chemical - metabolism | Cornea - immunology | Retina - immunology | Infliximab - therapeutic use | Uveitis, Anterior - pathology | Infliximab - pharmacology | Burns, Chemical - etiology | Corneal Injuries - metabolism | Retinal Ganglion Cells - pathology | Receptors, Tumor Necrosis Factor, Type I - deficiency | Eye Burns - pathology | Corneal Injuries - etiology | Neuroprotective Agents - pharmacology | Uvea - metabolism | Disease Models, Animal | Uveitis, Anterior - prevention & control | Alkalies | Drug Evaluation, Preclinical - methods | Rabbits | Corneal Injuries - pathology | Oxidation-Reduction | Mice, Inbred C57BL | Eye Burns - etiology | Receptors, Tumor Necrosis Factor, Type I - genetics | Uveitis, Anterior - chemically induced | Receptors, Tumor Necrosis Factor, Type II - genetics | Mice, Knockout | Receptors, Tumor Necrosis Factor, Type II - deficiency | Animals | Uveitis, Anterior - metabolism | Burns, Chemical - drug therapy | Burns, Chemical - pathology | Eye Burns - metabolism | Apoptosis - physiology | Corneal Injuries - drug therapy | Retina - pathology | Sodium Hydroxide | Retina - injuries | Retinal Ganglion Cells - drug effects | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Hydrogen-Ion Concentration | Index Medicus | Abridged Index Medicus | Regular
Journal Article
Carbohydrate Polymers, ISSN 0144-8617, 01/2016, Volume 135, pp. 308 - 315
Journal Article
Journal Article
Investigative Ophthalmology and Visual Science, ISSN 0146-0404, 01/2017, Volume 58, Issue 1, pp. 96 - 105
PURPOSE. Tumor necrosis factor (TNF)-alpha is upregulated in eyes following corneal alkali injury and contributes to corneal and also retinal damage. Prompt... 
Burn | Corneal wound healing | Tumor necrosis factor alpha | Antibody therapy | Retinal protection | Drug delivery system | Polydimethylsiloxane | burn | SAFETY | polydimethylsiloxane | TRANSPLANTATION | corneal wound healing | PERIPHERAL ULCERATIVE KERATITIS | TOPICAL INFLIXIMAB | tumor necrosis factor alpha | retinal protection | IN-VIVO | OPHTHALMOLOGY | drug delivery system | GLAUCOMA | antibody therapy | Retina - drug effects | Retinal Diseases - prevention & control | Tumor Necrosis Factor-alpha - metabolism | Eye Burns - drug therapy | Retina - metabolism | Burns, Chemical - diagnosis | Follow-Up Studies | Antirheumatic Agents - administration & dosage | Drug Implants | Infliximab - administration & dosage | Corneal Injuries - diagnosis | Cornea - drug effects | Eye Burns - chemically induced | Retinal Diseases - etiology | Female | Cornea - pathology | Eye Burns - diagnosis | Corneal Neovascularization - etiology | Disease Models, Animal | Rabbits | Retinal Diseases - diagnosis | Conjunctiva | Corneal Neovascularization - prevention & control | Cornea - metabolism | Animals | Corneal Neovascularization - diagnosis | Burns, Chemical - drug therapy | Corneal Injuries - drug therapy | Delayed-Action Preparations | Retina - pathology | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Index Medicus | Cornea
Journal Article
Scientific Reports, ISSN 2045-2322, 12/2017, Volume 7, Issue 1, pp. 17763 - 11
We investigated the effect of a peroxisome proliferator-activated receptor alpha (PPAR?alpha) agonist ophthalmic solution in wound healing using a rat corneal... 
GAMMA | PPAR-ALPHA | CELLS | LIPID-METABOLISM | COLLAGEN | TIE2 | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | FACTOR-KAPPA-B | EXPRESSION | BASEMENT-MEMBRANE | Eye Burns - drug therapy | Ophthalmic Solutions - pharmacology | Burns, Chemical - metabolism | Corneal Neovascularization - drug therapy | Collagen Type III - metabolism | Male | Angiopoietin-1 - metabolism | RNA, Messenger - metabolism | Angiopoietin-2 - metabolism | Corneal Injuries - metabolism | Myofibroblasts - metabolism | Cicatrix - metabolism | Fenofibrate - pharmacology | Cornea - drug effects | Alkalies - pharmacology | Neutrophils - metabolism | Wound Healing - drug effects | Disease Models, Animal | Endothelial Cells - metabolism | Neutrophils - drug effects | Rats | Myofibroblasts - drug effects | Up-Regulation - drug effects | Cornea - metabolism | Cicatrix - drug therapy | Macrophages - metabolism | Animals | Corneal Neovascularization - metabolism | Neovascularization, Pathologic - drug therapy | Burns, Chemical - drug therapy | Eye Burns - metabolism | Macrophages - drug effects | PPAR alpha - agonists | Vascular Endothelial Growth Factors - metabolism | Neovascularization, Pathologic - metabolism | Corneal Injuries - drug therapy | Cornea | Wound healing | Angiopoietin | Stroma | Collagen (type III) | Leukocytes (neutrophilic) | Inflammation | Gene expression | Macrophages | Endothelial cells | Vascularization | Fenofibrate | Rodents | Vascular endothelial growth factor | Index Medicus
Journal Article
Journal Article
Microvascular Research, ISSN 0026-2862, 09/2018, Volume 119, pp. 29 - 37
Journal Article
Journal of Cellular Physiology, ISSN 0021-9541, 11/2016, Volume 231, Issue 11, pp. 2506 - 2516
Journal Article
International Immunopharmacology, ISSN 1567-5769, 07/2017, Volume 48, pp. 126 - 134
Cornea is an avascular transparent tissue. Ocular trauma caused by a corneal alkali burn induces corneal neovascularization (CNV), inflammation, and fibrosis,... 
Zerumbone | Cornea | Alkali-burned injury | CCL2/MCP-1 | STAT3 | TROPICAL GINGER SESQUITERPENE | APOPTOSIS | GENETIC ABLATION | FACTOR EXPRESSION | IMMUNOLOGY | CANCER | EPITHELIAL-CELLS | INHIBITS ANGIOGENESIS | PHARMACOLOGY & PHARMACY | NEOVASCULARIZATION | NF-KAPPA-B | HERPETIC STROMAL KERATITIS | Eye Burns - drug therapy | Burns, Chemical - metabolism | Corneal Neovascularization - drug therapy | Humans | Sesquiterpenes - therapeutic use | Corneal Injuries - metabolism | Eye Burns - pathology | Cornea - drug effects | Eye Burns - chemically induced | Female | Chemokine CCL2 - metabolism | Cornea - pathology | Macrophages, Peritoneal - drug effects | Wound Healing - drug effects | STAT3 Transcription Factor - metabolism | Fibroblasts - metabolism | Alkalies | Cell Line | Corneal Injuries - pathology | Cells, Cultured | Chemokine CCL2 - genetics | Corneal Neovascularization - chemically induced | Corneal Injuries - chemically induced | Cornea - metabolism | Animals | Corneal Neovascularization - metabolism | Fibroblasts - drug effects | Burns, Chemical - drug therapy | Burns, Chemical - pathology | Eye Burns - metabolism | Mice, Inbred BALB C | Sesquiterpenes - pharmacology | Chemokine CCL2 - antagonists & inhibitors | Corneal Injuries - drug therapy | Macrophages, Peritoneal - metabolism | STAT3 Transcription Factor - antagonists & inhibitors | Corneal Neovascularization - pathology | Wound healing | Neovascularization | Endothelial growth factors | RNA | Health aspects | Analysis | Medical research | Care and treatment | Medicine, Experimental | Muscle proteins | Biosafety | Wounds and injuries | CC chemokine receptors | Transcription | Transforming growth factor | Smooth muscle | Matrix metalloproteinase | Macrophages | Vascularization | Angiogenesis | Cell activation | Immunology | CCR2 protein | Actin | Rodents | Fibroblasts | Metalloproteinase | Inhibition | Vascular endothelial growth factor | Burns (injuries) | Activation analysis | Stat3 protein | Trauma | Monocyte chemoattractant protein | Fibrosis | Healing | Mice | Infiltration | Organic chemicals | Burns | Monocyte chemoattractant protein 1 | Peritoneum | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 06/2017, Volume 12, Issue 6, pp. e0179982 - e0179982
Epidemiological studies have indicated that smoking is a pivotal risk factor for the progression of several chronic diseases. Nicotine, the addictive component... 
FIBROSIS | CELLS | GROWTH-FACTOR-BETA | PROTEIN | MULTIDISCIPLINARY SCIENCES | ALPHA | CIGARETTE-SMOKE | PROLIFERATION | NEOVASCULARIZATION | PROGRESSION | KERATOCYTES | Eye Burns - drug therapy | Burns, Chemical - metabolism | Humans | Actins - metabolism | Vascular Endothelial Growth Factor A - metabolism | Corneal Injuries - metabolism | Nicotine - pharmacology | Eye Burns - pathology | Cornea - blood supply | Cornea - drug effects | Eye Burns - chemically induced | Protective Agents - pharmacology | Female | Cornea - pathology | Cotinine | Wound Healing - drug effects | Disease Models, Animal | Fibroblasts - metabolism | Cell Line | Receptors, Nicotinic - metabolism | Collagen Type I - metabolism | Corneal Injuries - pathology | Random Allocation | Fibroblasts - pathology | Corneal Injuries - chemically induced | Cornea - metabolism | Animals | Fibroblasts - drug effects | Burns, Chemical - drug therapy | Burns, Chemical - pathology | Eye Burns - metabolism | Mice, Inbred BALB C | Wound Healing - physiology | Corneal Injuries - drug therapy | Sodium Hydroxide | Transforming Growth Factor beta - metabolism | Eye | Care and treatment | Wound healing | Physiological aspects | Genetic aspects | Research | Injuries | Nicotine | Cell proliferation | Drinking water | Veterinary colleges | Cornea | Shape memory alloys | Transcription | Transforming growth factor-b | Smooth muscle | Combustion | Matrix metalloproteinase | Kinases | Assaying | Epidemiology | Risk factors | Cell adhesion & migration | Angiogenesis | Pathways | Actin | Eye injuries | Metalloproteinase | Inhibition | Vascular endothelial growth factor | Injury analysis | Chronic illnesses | Eyes | Alkali metals | Filter paper | Gene expression | Cigarette smoking | Cigarettes | Gelatinase B | 1-Phosphatidylinositol 3-kinase | Diseases | Inhibitors | Collagen | Fibrosis | Healing | Acetylcholine receptors (nicotinic) | Acetylcholine | Mice | In vitro methods and tests | Smoking | Index Medicus
Journal Article
International Journal of Molecular Medicine, ISSN 1107-3756, 07/2016, Volume 38, Issue 1, pp. 75 - 82
Chemical burns are a major cause of corneal injury. Oxidative stress, inflammatory responses and neovascularization after the chemical burn aggravate corneal... 
inflammation | oxidative stress | NADPH oxidase | neovascularization | corneal injury | alkali burn | Oxidative stress | Alkali burn | Corneal injury | Inflammation | Neovascularization | MEDICINE, RESEARCH & EXPERIMENTAL | RAT | FACTOR-KAPPA-B | NAD(P)H OXIDASE | NOX FAMILY | ENDOTHELIAL-CELLS | SMOOTH-MUSCLE-CELLS | GROWTH-FACTOR | STROMAL CELLS | EXPRESSION | Eye Burns - drug therapy | Inflammation - pathology | Corneal Neovascularization - drug therapy | Humans | NADPH Oxidases - metabolism | Burns, Chemical - complications | Corneal Injuries - complications | Eye Burns - complications | Eye Burns - pathology | Acetophenones - pharmacology | Corneal Neovascularization - enzymology | Corneal Neovascularization - complications | Corneal Injuries - enzymology | Eye Burns - enzymology | Alkalies | Corneal Injuries - pathology | Mice, Inbred C57BL | Enzyme Inhibitors - pharmacology | Onium Compounds - pharmacology | Enzyme Inhibitors - therapeutic use | Animals | Burns, Chemical - drug therapy | Burns, Chemical - pathology | Burns, Chemical - enzymology | Oxidative Stress - drug effects | Corneal Injuries - drug therapy | Corneal Neovascularization - pathology | Oxidases | Complications and side effects | Cornea | Gene expression | Burns, Chemical | Health aspects | Injuries | Enzymes | Angiogenesis | Cytokines | Rodents | Burns | Laboratory animals | Vascular endothelial growth factor | Experiments
Journal Article