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Recently, several studies have demonstrated that tumor necrosis factor microsatellite polymorphism (TNFalpha) contributes to the susceptibility of type 1 diabetes. This study investigates the influence of TNFalpha on the predisposition to insulin dependency in adult-onset diabetic patients with type
L-Glutamic acid was shown to increase the stability of cells of the HL-60 line of human promyelocyte leukemia to the cytotoxic action of tumor necrosis factor alpha (TNF-alpha) due to the inhibition of apoptotic and NF-kappaB-activating cascades induced by this cytokine. At the same time, L-glutamic
Rabbits were poisoned by the intraperitoneal injection of plasmocid dihydroiodide at a dosage of 80 mg. per kg. body weight. Animals were euthanatized 1, 2, 5, 7, 9, 12, 24 and 48 hours after plasmocid injection and serum and diaphragmatic muscle collected. The serum was examined for its serum
To elucidate the mechanism of differentiating activity on L-Glu to HL-60 cells, its influence on binding of human recombinant interleukine-1beta (rHuIL-1beta), tumour necrosis factor-alpha (rHuTNF-alpha) and interleukine-6 (IL-6) by HL-60 cells was studied. It was established, that L-Glu converted
Erythropoietin (EPO), a 34-kDa glycoprotein, is produced predominantly by peritubular interstitial cells (PIC) in the renal cortex and is physiologically released when ambient oxygen pressure falls. However, the exact nature of EPO-producing cells in the kidney is not well understood. We discovered
Glutamic acid decarboxylase (GAD)65 is an early and important antigen in both human diabetes mellitus and the nonobese diabetic (NOD) mouse. However, the exact role of GAD65-specific T cells in diabetes pathogenesis is unclear. T cell responses to GAD65 occur early in diabetes pathogenesis, yet only
L-Glutamic acid at a concentration of 0.1 microM was found to induce differentiation of the cell line of HL-60 promyelocytic leukemia into granulocytes or neutrophils. The HL-60 cells have no specific glutamate-binding sites, but L-glutamic acid influences the reception of several cytokines by these
Experimental infectious mouse hepatitis is associated with an increase in glutamic-oxaloacetic transaminase activity of the serum (SGO-T). A relationship appears to exist between the rise in SGO-T activity and (a) the size of the virus inoculum, (b) the blood virus titer, and (c) the degree of liver
We have studied the neuroprotective effect of the novel glutamic acid derivative neiroglutam on reversible focal cerebral ischemia in rats. The neuroprotective drug action was assessed by the ability to reduce the severity of neurological deficit (1, 2, 3, 5 and 7 days), forelimb fine-motor