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lauric acid/nekrosis

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Recombinant human tumor necrosis factor (rh TNF) when administered intravenously together with the phospholipase C inhibitor tricyclodecan-9-yl-xanthogenate (D609) and lauric acid (C12), leads to the partial regression of various human tumor transplants in athymic mice. Extensive necrosis occurred
The study was designed to investigate the neuro-protection of lauric acid (LA) on haloperidol (HPD) induced Parkinson's disease (PkD) rat model. Rats were divided into group A (normal), group B (diseased, by HPD 1mg/kg i.p. for 14 days), group C (standard treatment, levodopa 30 mg/kg), group D

Cholesteatoma debris as an activator of human monocytes. Potentiation of the production of tumor necrosis factor.

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Tumor necrosis factor (TNF) is a cytokine which stimulates osteoclastic bone resorption and inhibits collagen synthesis in vitro. In this study the effect of human cholesteatoma debris and its constituents on the production of TNF-alpha by human monocytes in vitro was studied. Cultured human

Experimental treatment of equine sarcoid using a xanthate compound and recombinant human tumour necrosis factor alpha.

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A xanthate compound with antiviral and antitumoural activities, tricyclodecan-9-yl-xanthogenate (D609) in combination with the potassium salt of the lauric acid (KC12) and, in a further investigation, the above-mentioned substances together with recombinant human TNF alpha (rh-TNF alpha), were

Intracellular ATP in balance of pro- and anti-inflammatory cytokines in adipose tissue with and without tissue expansion.

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To understand the mechanism of white fat expansion in the presence of inflammation, we examined the balance of pro- and anti-inflammatory cytokines in epididymal fat during weight gain in diet-induced obese mice. The pro- and anti-inflammatory cytokines were examined in white fat of diet-induced

Disappearance of gender-related difference in the toxicity of benzotriazole ultraviolet absorber in juvenile rats.

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2-(2'-hydroxy-3',5'-di-tert-butylphenyl)benzotriazole (HDBB) is an ultraviolet absorber used in plastic resin products, such as building materials and automobile components. In oral repeated dose toxicity studies using 5- or 6-week-old rats, this chemical induced hepatic histopathological changes,
Objective: To compare the circular pathological changes of chronic hepatitis B (CHB) patients according to the tongue diagnosis. Methods: Totally 41 CHB patients with typical
LPS is a fundamental constituent of the outer membrane of all Gram-negative bacteria, and the lipid A domain plays a central role in the induction of inflammatory responses. We identified genes of the Neisseria gonorrhoeae lipid A biosynthetic pathway by searching the complete gonococcal genome

Segmental small intestinal allografts in the dog. I. Morphological and functional indices of rejection.

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Fourteen dogs received an orthotopically vascularized allograft of a 100-cm length of terminal ileum as a Thiry-Vella segment. Absorption, motility, myoelectrical activity and morphology of the allograft were studied to determine the most reliable indices of rejection. The earliest histological

[Human monocytes show chemotaxis in response to cholesteatoma debris].

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Using a microchamber technique, we tested cholesteatoma debris and certain of its constituents for effects on the migration of human peripheral blood monocytes and polymorphonuclear leukocytes. Cholesteatoma debris induced significant migration of monocytes. When the individual constituents of
Genetically engineered mesenchymal stem cells (MSCs), as non-viral gene delivery platforms, are rapidly evolving in tumor therapy due to their low immunogenicity and natural tumor-homing capacity. Methods: In this paper, we selected reconstituted high-density lipoprotein (rHDL), a

Ranking the toxicity of fatty acids on Jurkat and Raji cells by flow cytometric analysis.

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The fatty acids have an important role in the control of leukocyte metabolism and function. Higher concentrations of certain fatty acids, particularly polyunsaturated fatty acids (PUFAs) and volatile fatty acids, can cause cell death via apoptosis or, when concentrations are greater, necrosis. In
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