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Puslapis 1 nuo 71 rezultatus
Dynamic equilibrium unfolding pathway of human tumor necrosis factor-alpha induced by guanidine hydrochloride.
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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
The -308G/A of Tumor Necrosis Factor (TNF)-α and 825C/T of Guanidine Nucleotide Binding Protein 3 (GNB3) are associated with the onset of acute myocardial infarction and obesity in Taiwan.
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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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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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Evasion of innate immune responses: evidence for mannose binding lectin inhibition of tumor necrosis factor alpha production by macrophages in response to Blastomyces dermatitidis.
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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
In vitro studies of the ultrastructural changes induced by guanidine in the nerves, muscle fibers and neuromuscular junction of the mouse diaphragm.
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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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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,
L-cysteine-enhanced renaturation of bioactive soluble tumor necrosis factor ligand family member LIGHT from inclusion bodies in Escherichia coli.
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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
Elevation in tumour necrosis factor-alpha (TNF-alpha) messenger RNA levels in the uterus of pregnant gilts after oestrogen treatment.
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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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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
Interleukin 1 receptor antagonist and tumor necrosis factor-alpha gene polymorphism in patients with end-stage renal failure.
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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
Increased superoxide production in coronary arteries in hyperhomocysteinemia: role of tumor necrosis factor-alpha, NAD(P)H oxidase, and inducible nitric oxide synthase.
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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
Inhibition of lipopolysaccharide-stimulated chronic obstructive pulmonary disease macrophage inflammatory gene expression by dexamethasone and the p38 mitogen-activated protein kinase inhibitor N-cyano-N'-(2-{[8-(2,6-difluorophenyl)-4-(4-fluoro-2-methylphenyl)-7-oxo-7,8-dihydropyrido[2,3-d] pyrimidin-2-yl]amino}ethyl)guanidine (SB706504).
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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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