|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Inhibition of the cytokine tumor necrosis factor alpha (TNFα), originally considered as a mediator in sepsis, has led to frustrating results.
|
30343600 |
2018 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Inhibition of this late-phase pathway reduced the extent of TNF-α production by mouse macrophages exposed to the TLR4 ligand lipopolysaccharide (LPS) and ameliorated LPS-induced sepsis in mice.
|
24084649 |
2013 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
It has been shown that Fas, Fas-L, TNF and TNFR-1 display high serum concentrations in subjects with sepsis.
|
28144786 |
2017 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
CTD_human |
Ketamine inhibits the proinflammatory cytokine-induced reduction of cardiac intracellular cAMP accumulation.
|
9806674 |
1998 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Key mediators of pathologic sequelae of sepsis in the brain include cytokines, including TNF-α, and sphingolipids, which are biologically active components of cellular membranes that possess diverse functions.
|
28670310 |
2017 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Lethality from sepsis is believed to be mediated by a proinflammatory cytokine cascade, yet blocking the proinflammatory cytokines tumor necrosis factor alpha (TNF-alpha) and interleukin-1 (IL-1) fails to prevent mortality in human disease and a mouse model of sepsis induced by cecal ligation and puncture (CLP).
|
12117955 |
2002 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Liberation of TNF receptors (TNFRs) from cell surfaces can dampen the cellular response to TNF, a cytokine that is critical in the innate immune response and promotes programmed cell death but can also promote sepsis.
|
26535007 |
2015 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Lipopolysaccharide stimulates the production and the release of numerous endogenous mediators of sepsis: tumor necrosis factor alpha, interleukin-1, and interleukin-6 that induce fever production.
|
10085413 |
1999 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
lncRNA ITSN1-2 was highly expressed in sepsis patients compared to healthy controls and could differentiate sepsis patients from healthy controls with area under the curve (AUC) 0.777 (95% CI: 0.740-0.813). lncRNA ITSN1-2 expression was positively correlated with APACHE II score, C-reactive protein (CRP), TNF-α, IL-6, and IL-8 levels, but negatively correlated with IL-10 level.
|
30803045 |
2019 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Low TNF-α concentrations 300 min after sepsis induction could be interpreted as considerable immunosuppression during CLI sepsis.
|
21296198 |
2011 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Macrophages play an important role in the early stage of sepsis as they are tasked with eliminating invading microbes and also attracting other immune cells by the release of proinflammatory cytokines such as interleukin-1β, interleukin-6, and tumor necrosis factor-α.
|
31658116 |
2019 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
MALAT1 knockdown significantly increased LVSP and +dp/dsmax, decreased LVEDP and -dp/dsmax of sepsis as well as levels of cTn-I, CK, CK-MB, TNF-α, IL-1β, IL-6, IL-10, IL-17, IFN-γ, C5 and C5a.
|
29227823 |
2018 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Methane suppressed the expression of the toll-like receptor 4/nuclear factor-kappa B (NF-κB) signaling pathway and stimulated the expression of peroxisome proliferator-activated receptor-γ (PPAR-γ) during sepsis, which inhibited the activation of NF-κB and decreased the level of inflammatory cytokines, such as tumor necrosis factor-α, interleukin-6, and interleukin-1β.
|
30601406 |
2019 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Monocytes were isolated from 47 patients when they developed sepsis and stimulated by bacterial endotoxin for the production of TNFα and of interleukin-6 (IL-6).
|
22609212 |
2012 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Moreover, pretreatment with clonidine attenuated the plasma tumor necrosis factor α (TNF-α) induced by sepsis.Clonidine administered i.t. or i.p. increased p-AMPKα1 and p-AMPKα2, but decreased p-Tyk2 and p-mTOR levels in both control and sepsis groups, suggesting that the up-regulations of p-AMPKα1 and p-AMPKα2, or down-regulations of p-mTOR and p-Tyk2 may play critical roles for the protective effect of clonidine against sepsis-induced mortality.
|
28883754 |
2017 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Moreover, significant lower levels of TNF-<i>α</i>, IL-6, bacterial loads, MPO, and ROS were discovered in the KO-CLP sepsis group in contrast to the WT-CLP sepsis group.
|
28694565 |
2017 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Moreover, the model confirms the low production of TNFα and increased levels of C-C motif ligand 2 when monocytes exhibit a tolerant state similar to that of patients with sepsis.
|
28824640 |
2017 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Most common serious adverse events were sepsis and thrombotic events observed in 8 and 4 patients, respectively.Treatment with anti-TNFs may be associated with a higher survival rate compared with historic cohorts of AA amyloidosis, especially when started early with a lower serum creatinine level at baseline.
|
28834898 |
2017 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Nfe2l2(-/-) mice in sepsis also generated higher hepatic TNF-α mRNA levels, lower NRF-1 and PGC-1α mRNA levels, and no enhancement of anti-inflammatory Il10, Socs3, or bcl-x(L) gene expression.
|
21454555 |
2011 |
|
Septicemia
|
0.400 |
PosttranslationalModification
|
disease |
BEFREE |
Our data suggest that nucleosome repositioning controls both the induction and epigenetic silencing phases of TNFalpha transcription associated with sepsis.
|
19901031 |
2010 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Our findings suggest that TNF-alpha-mediated up-regulation of PDE2 may destabilize endothelial barrier function in sepsis.
|
15650061 |
2005 |
|
Septicemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Our results suggest that the G/A genotype of <i>TNF-α</i> rs1800629 and rs361525 increases sepsis risk in an Asian population.
|
29340067 |
2017 |
|
Septicemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Patients with IL-10 (-1082A/A) genotypes were found significantly higher in post traumatic sepsis patients and had a significantly higher risk to developed sepsis complication (p < 0.05, OR = 0.86, C.I = 0.08-8.8).In case of TNF-α (-308) position, GA and GG genotype patients have a significantly lower risk of poor outcome (p < 0.05, OR = 0.25, C.I = 0.01-1.3) and (p < 0.05, OR = 0.22, C.I = 0.01-0.5) in comparison to AA genotype.
|
26561011 |
2015 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
CTD_human |
Pentoxifylline reduces plasma tumour necrosis factor-alpha concentration in premature infants with sepsis.
|
8741040 |
1996 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Phospholipase D1 is a regulator of tumor necrosis factor-α expression and release upon LPS-induced sepsis and following myocardial infarction (MI).
|
30555342 |
2018 |