glutamic acid/نخر

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Tumor necrosis factor microsatellite polymorphism influences the development of insulin dependency in adult-onset diabetes patients with the DRB11502-DQB10601 allele and anti-glutamic acid decarboxylase antibodies.

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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 modulates the cytotoxic effect of tumor necrosis factor in the HL-60 cell line].

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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

Influence of L-glutamic acid on binding of interleukin-1beta, tumour necrosis factor-alpha and interleukin-6 to HL-60 cells.

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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

[Behavior of serum transaminase activity (glutamic acid-ox-alacetic acid transaminase) in allyl alcohol necrosis of rat liver].

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Administration of poly-D-glutamic acid induces proliferation of erythropoietin-producing peritubular cells in rat kidney.

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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

CD4(+) T cells from glutamic acid decarboxylase (GAD)65-specific T cell receptor transgenic mice are not diabetogenic and can delay diabetes transfer.

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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

[Effect of L-glutamic acid on the reception of cytokines by HL-60 cells].

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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

[Studying the neuroprotective effect of the novel glutamic acid derivative neiroglutam on focal cerebral ischemia in rats].

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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

Protective effects of dietary glycine and glutamic acid toward the toxic effects of oxidized mustard oil in rabbits.

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The protective role of glycine and glutamic acid against the toxic effects of oxidized oil was studied for the first time. Mustard seed oil was thermally oxidized and characterized for quality characteristics and polyphenolic composition using reversed phase HPLC-DAD. Significant changes in the

Serum titres of anti-glutamic acid decarboxylase-65 and anti-IA-2 autoantibodies are associated with different immunoregulatory milieu in newly diagnosed type 1 diabetes patients.

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Several studies correlated genetic background and pancreatic islet-cell autoantibody status (type and number) in type 1A diabetes mellitus (T1AD), but there are no data evaluating the relationship among these markers with serum cytokines, regulatory T cells and β cell function. This characterization

Modulation of gene expression related to Toll-like receptor signaling in dendritic cells by poly(gamma-glutamic acid) nanoparticles.

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Poly(gamma-glutamic acid) (gamma-PGA) nanoparticles (NPs) have previously been reported as an efficient antigen delivery system with adjuvant activity. In this study, the gene expression in murine bone marrow-derived dendritic cells (DCs) treated with gamma-PGA NPs was examined by oligonucleotide

Structural requirements of muramylpeptides for induction of necrosis at sites primed with Mycobacterium tuberculosis in guinea pigs.

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Intracutaneous injection of N-acetylmuramyl-L-alanyl-D-isoglutamine (MDP) in guinea pigs caused an extensive necrotic reaction in footpads prepared by injection of heat-killed Mycobacterium tuberculosis in water-in-mineral-oil emulsion. We examined a variety of analogs and derivatives of

L-glutamine and L-glutamic acid facilitate successful agrobacterium infection of recalcitrant tea cultivars.

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The first step in Agrobacterium tumefaciens infection of plants is the establishment of cell-cell contact between the two partners. However, failure to establish such contact makes many plants and explants recalcitrant to A. tumefaciens infection. Tea is one such example where even the popular

Poly-D-glutamic acid induces an acute lysosomal thesaurismosis of proximal tubules and a marked proliferation of interstitium in rat kidney.

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Renal damage caused by polycationic peptides is well documented, but renal damage caused by polyanionic peptides is not. During our attempts to inhibit the nephrotoxicity of aminoglycoside antibiotics by polyanionic peptides, we discovered that poly-D-glutamic acid (molecular weight, 20 kd; 250

Development and Characterization of a Potent Tumor Necrosis Factor-Alpha-Blocking Agent.

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Tumor necrosis factor-α (TNFα), one of the major proinflammatory cytokines, plays a key role in an effective immune response. However, the chronic presence of TNFα can lead to several inflammatory disorders, such as rheumatoid arthritis, psoriasis, Crohn's disease, etc. Inhibition of TNFα by

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glutamic acid/نخر

Tumor necrosis factor microsatellite polymorphism influences the development of insulin dependency in adult-onset diabetes patients with the DRB1*1502-DQB1*0601 allele and anti-glutamic acid decarboxylase antibodies.

[L-Glutamic acid modulates the cytotoxic effect of tumor necrosis factor in the HL-60 cell line].

Influence of L-glutamic acid on binding of interleukin-1beta, tumour necrosis factor-alpha and interleukin-6 to HL-60 cells.

[Behavior of serum transaminase activity (glutamic acid-ox-alacetic acid transaminase) in allyl alcohol necrosis of rat liver].

Administration of poly-D-glutamic acid induces proliferation of erythropoietin-producing peritubular cells in rat kidney.

CD4(+) T cells from glutamic acid decarboxylase (GAD)65-specific T cell receptor transgenic mice are not diabetogenic and can delay diabetes transfer.

[Effect of L-glutamic acid on the reception of cytokines by HL-60 cells].

[Studying the neuroprotective effect of the novel glutamic acid derivative neiroglutam on focal cerebral ischemia in rats].

Protective effects of dietary glycine and glutamic acid toward the toxic effects of oxidized mustard oil in rabbits.

Serum titres of anti-glutamic acid decarboxylase-65 and anti-IA-2 autoantibodies are associated with different immunoregulatory milieu in newly diagnosed type 1 diabetes patients.

Modulation of gene expression related to Toll-like receptor signaling in dendritic cells by poly(gamma-glutamic acid) nanoparticles.

Structural requirements of muramylpeptides for induction of necrosis at sites primed with Mycobacterium tuberculosis in guinea pigs.

L-glutamine and L-glutamic acid facilitate successful agrobacterium infection of recalcitrant tea cultivars.

Poly-D-glutamic acid induces an acute lysosomal thesaurismosis of proximal tubules and a marked proliferation of interstitium in rat kidney.

Development and Characterization of a Potent Tumor Necrosis Factor-Alpha-Blocking Agent.

قاعدة بيانات الأعشاب الطبية الأكثر اكتمالا التي يدعمها العلم

Tumor necrosis factor microsatellite polymorphism influences the development of insulin dependency in adult-onset diabetes patients with the DRB11502-DQB10601 allele and anti-glutamic acid decarboxylase antibodies.