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Disease Info Card
Scalding Injury
Information about Scalding Injury: characteristics, related genes and pathways, plus antibodies you can use for research. This page is being enriched constantly, if you see some information you would like this page to include please send your suggestions to us.
Overview of Scalding Injury
Most recent studies have shown that Scalding Injury shares some biological mechanisms with burns-electric, chemical-burns, cicatrix, edema, hemorrhage, inflammation, multiple-organ-failure, pain, pseudomonas-infections, salmonella-infections, shock-traumatic, submersion, systemic-infection, thermal-injury, wound-infection.
Among the many pathways, these few ones have gauged particular interests from scientists studying Scalding Injury, and have been seen in publications frequently: Aging, Angiogenesis, Cell Death, Cell Proliferation, Coagulation, Cytokine Production, Excretion, Hypersensitivity, Immune Response, Inflammatory Response, Localization, Pathogenesis, Phagocytosis, Proteolysis, Regeneration, Secretion, Transport, Vasoconstriction, Virulence, Wound Healing
Quite a number of genes have been found to play important roles in Scalding Injury, such as ALB, CASP3, DAO, IFNG, IGF1, IL10, IL2, IL4, IL6, INS, MPO, PCNA, RANGAP1, SLC17A5, SOD1, TNF. See what Boster has to offer for the research of these genes by clicking the gene name links below and view a more detailed info card/product listing for that gene.
In a later update, we will include information such as current drugs and therapy solutions as well as on-going and past clinical trials for this disease. Plesae stay updated.