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guanidine/nekroza

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Stran 1 iz 71 rezultatov

Dynamic equilibrium unfolding pathway of human tumor necrosis factor-alpha induced by guanidine hydrochloride.

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Prijava / prijava
The dynamic equilibrium unfolding pathway of human tumor necrosis factor-alpha (TNF-alpha) during denaturation at different guanidine hydrochloride (GdnHCl) concentrations (0-4.2 M) was investigated by steady-state fluorescence spectroscopy, potassium iodide (KI) fluorescence quenching, far-UV
Acute myocardial infarction is a highly prevalent cardiovascular disease in Taiwan. Among several etiological risk factors, obesity and inflammation are strongly associated with the frequency of hypertension, cardiovascular disease, diabetes, and myocardial infarction. To discriminate obesity- and

Formation of an alpha-helix in human tumor necrosis factor-alpha by guanidine hydrochloride-induced unfolding.

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Prijava / prijava
Human tumor necrosis factor-alpha (TNF-alpha) is a trimeric protein consisting primarily of beta-sheet. GdnHCl-induced unfolding of TNF-alpha was investigated at room temperature by circular dichroism (CD) and size exclusion chromatography. The secondary and tertiary structure of TNF-alpha persisted

Inhibition of tobacco necrosis virus by guanidine carbonate.

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Prijava / prijava
Serum factors, including mannose binding lectins (MBL), influence innate responses to microbes. Little is known about the effects of serum factors or MBL on the interaction of Blastomyces dermatitidis, a pulmonary fungal pathogen, with macrophages or on tumor necrosis factor alpha (TNF-alpha)

In vitro study of the potential role of guanidines in leukocyte functions related to atherogenesis and infection.

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BACKGROUND The blunted immune response upon stimulation in chronic renal failure (CRF) is often coupled to a baseline inflammatory status which has been related to atherogenesis. Uremic biologic fluids and several specific uremic retention solutes alter cell-mediated immune responses, as well as the
1. The incubation of mouse isolated diaphragm with guanidine for 60 min produced ultrastructural changes in the neuromuscular junction, the intramuscular fascicles of the phrenic nerve and the skeletal muscle fibers. 2. The main morphological characteristics of both the end terminals and the nerve

Tumor necrosis factor-alpha induces pial arteriolar dilation in newborn pigs.

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Prijava / prijava
The present study in piglets was designed to examine cerebrovascular effects of tumor necrosis factor-alpha (TNF alpha) and potential mechanisms involved. Anesthetized new-born pigs with closed cranial windows implanted were used. Effects of nitric oxide synthase (NOS) inhibitors,
LIGHT is a membrane-bound protein that belongs to the tumor necrosis factor (TNF) superfamily ligands. In this study, we established an effective strategy for producing a bioactive soluble form of LIGHT (sLIGHT), an extracellular region (Ile⁸⁴-Val²⁴⁰) of human LIGHT. Because sLIGHT was expressed as
In pigs, induction of embryonic degeneration, by exogenous oestrogens given early in gestation, has been long recognised. However, the underlying mechanisms responsible for this degeneration remain unclear. The present study was conducted to determine whether oestrogen-induced early porcine

Tumor necrosis factor-alpha gene polymorphism in reflux nephropathy.

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Prijava / prijava
OBJECTIVE Interstitial scarring contributes to the progression of renal failure in reflux nephropathy. The proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) has been implicated in the disease susceptibility and pathogenesis of several inflammatory diseases promoting interstitial

The anti-inflammatory and antinociceptive effects of NF-kappaB inhibitory guanidine derivative ME10092.

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The guanidine compound ME10092 (1-(3,4-dimethoxy-2-chlorobenzylideneamino)-guanidine) is known to possess anti-radical and anti-ischemic activity but its molecular targets have not been identified. This study investigated whether ME10092 regulates the nuclear factor kappa B (NF-kappaB)-mediated
End-stage-renal disease (ESRD) is a final result of various etiologies. Prognostic indicators leading to ESRD in chronic kidney diseases have been studied extensively, of which, genetic factors remain a subject of great concern. Interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) are
OBJECTIVE In coronary arteries, hyperhomocysteinemia (HHcy, a known risk factor for coronary heart disease) impairs flow-induced dilations, which can be reversed by superoxide dismutase (SOD). To evidence increased O2*- generation and elucidate its source, we characterized changes in activity
p38 mitogen-activated protein kinase (MAPK) signaling is known to be increased in chronic obstructive pulmonary disease (COPD) macrophages. We have studied the effects of the p38 MAPK inhibitor
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