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dimethyl sulfoxide/akuutti patologinen solukuolema
Linkki tallennetaan leikepöydälle
Sivu 1 alkaen 241 tuloksia
Protection against adriamycin-induced skin necrosis in the rat by dimethyl sulfoxide and alpha-tocopherol.
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Extravasation of Adriamycin during i.v. infusion can cause serious local complications. We have used a rat skin model to study the protection afforded by dimethyl sulfoxide and alpha-tocopherol (vitamin E) against Adriamycin-induced skin necrosis. Topical daily application of 1 ml dimethyl sulfoxide
Dimethyl sulfoxide activates tumor necrosis factorα-p53 mediated apoptosis and down regulates D-fructose-6-phosphate-2-kinase and lactate dehydrogenase-5 in Dalton's lymphoma in vivo.
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Dimethyl sulfoxide (DMSO) is evident to induce apoptosis in certain tumor cells in vitro. However, its apoptotic mechanism remains unexplored in in vivo tumors. This article describes that DMSO, being non-toxic to the normal lymphocytes, up regulated TNFα and p53, declined Bcl-2/Bax ratio, activated
Inhibitory effect of dimethyl sulfoxide (DMSO) on necrosis and oxidative stress caused by D-galactosamine in the rat liver.
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D-Galactosamine (D-Galn: 300 mg/kg) was intraperitoneally administered to rats. After 6 h the activity of plasma GOT and GPT was significantly higher than that of the control group and plasma GOT and GPT activities increased thereafter. These results indicated that the necrotic process was initiated
Effect of Biochanin A on Retina Levels of Vascular Endothelial Growth Factor, Tumor Necrosis Factor-Alpha and Interleukin-1Beta in Rats With Streptozotocin-Induced Diabetes.
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OBJECTIVE
Without proper medication for the treatment of diabetic retinopathy, retinal cells become malnourished and degenerate, which results in damage to vision cells and can lead to blindness. Flavonoids such as biochanin A (BCA) can directly target various facets of angiogenesis. We assessed the
Reduced mitochondrial formation of H(2)O(2) is responsible for resistance of dimethyl sulfoxide differentiated U937 cells to peroxynitrite.
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Previous studies performed in our laboratory indicated that non-toxic concentrations of peroxynitrite nevertheless commit U937 cells to a rapid necrosis that is however prevented by a survival signaling driven by cytosolic phospholipase A(2)-released arachidonic acid. Toxicity was mediated by
Effect of dimethyl sulfoxide and glycerol on acute bowel ischemia in the rat.
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After a 30 minute period of superior mesenteric artery occlusion in adult rats, there was a significant decrease in peritoneal inflammatory reaction, ileus, peritoneal adhesion formation, and histologically proved bowel wall necrosis in animals given intravenous dimethyl sulfoxide at the end of the
The effect of dimethyl sulfoxide on gray matter injury in experimental spinal cord trauma.
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The possible effect of dimethyl sulfoxide upon the development of lesions in the gray matter after experimental spinal cord trauma has been investigated with the use of cytochrome oxidase assay and quantitative histologic measurement of total liquefaction necrosis. Observations were made in 17
Binding of G-CSF, GM-CSF, tumor necrosis factor-alpha, and gamma-interferon to cell surface receptors on human myeloid leukemia cells triggers rapid tyrosine and serine phosphorylation of a 75-Kd protein.
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Granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF), gamma-interferon (gamma-IFN), or tumor necrosis factor-alpha (TNF-alpha) triggered the rapid, stable phosphorylation of a 75-Kd protein (p75) when incubated with permeabilized HL60 human myeloid
Bacterial lipopolysaccharide enhances aflatoxin B1 hepatotoxicity in rats by a mechanism that depends on tumor necrosis factor alpha.
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Exposure to a nontoxic dose of bacterial endotoxin (lipopolysaccharide [LPS]) potentiates the hepatotoxicity of aflatoxin B(1) (AFB(1)). Because some of the pathophysiologic effects associated with LPS are mediated through tumor necrosis factor alpha (TNF-alpha), this study was conducted to explore
Dimethyl sulfoxide therapy in the treatment of vesicant extravasation: two case presentations.
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The prevention and treatment of vesicant extravasation presents unique nursing challenges. In two case studies, the authors describe the clinical response of patients to dimethyl sulfoxide after multivesicant extravasation. The patients studied did not experience deep tissue necrosis or resultant
Modulation of lens-induced uveitis by dimethyl sulfoxide.
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Experimental lens-induced uveitis was produced in Lewis rats by sensitization with bovine lens protein prior to disruption of the lens capsule. Treatment of these animals by intraperitoneal injection of dimethyl sulfoxide resulted in reduction in retinal vasculitis, hemorrhage and necrosis.
The protective effect of dimethyl sulfoxide in experimental ischemia of the intestine.
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Experiments with two models of intestinal ischemia were performed in order to examine the protective effect of dimethyl sulfoxide (DMSO). Segmental ischemia of the small intestine for 150 minutes caused necrosis of the affected bowel in 90% of the animals. Intravenous administration of DMSO or
Dimethyl sulfoxide increases the survival of primarily ischemic island skin flaps.
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There is ample evidence of the involvement of free radicals in mediating skin flap necrosis. Dimethyl sulfoxide (DMSO) is a well-tolerated, safe drug that is a powerful scavenger of the hydroxyl free radical. The current study investigated the effect of DMSO on the survival of 9 x 4 cm skin flaps
Protective effect of doxorubicin in vitamin C or dimethyl sulfoxide against skin ulceration in the pig.
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BACKGROUND
Accidental extravasation of doxorubicin leads to skin necrosis and significant morbidity. Based on our previous work in the rat, we hypothesized that the free radical scavengers dimethyl sulfoxide (DMSO) and vitamin C prevent doxorubicin-induced skin ulcers in white swine.
METHODS
Fifteen
Dimethyl sulfoxide potentiates death receptor-mediated apoptosis in the human myeloid leukemia U937 cell line through enhancement of mitochondrial membrane depolarization.
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Dimethyl sulfoxide (DMSO) is a widely used prototypical chemical inducer of cell differentiation. In the present study, the effects of DMSO on susceptibility of human myeloid leukemia U937 cells towards ligation of distinct death receptors (DRs) were investigated. DMSO sensitized cells towards
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