Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Tumor necrosis factor-alpha (TNF-α) is a pivotal mediator that triggers inflammatory process, oxidative stress, and multiple organ injury in sepsis.
|
28459157 |
2017 |
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Therefore, culture- and next-generation sequencing (NGS)-based fungal findings as well as corresponding plasma levels of β-d-glucan, interferon gamma (INF-γ), tumor necrosis factor alpha (TNF-α), interleukin (IL)-2, -4, -6, -10, -17A, and mid-regional proadrenomedullin (MR-proADM) were evaluated in 50 septic patients at six consecutive time points within 28 days after sepsis onset.
|
28820494 |
2017 |
Septicemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
<b>Conclusion</b> We uncovered an association between IL-10 1082 gene variation and sepsis in VLBW infants but did not identify associations between neonatal sepsis and TNF-α 308 or IL-6 gene variation.
|
27960200 |
2017 |
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
The progression of OPG levels paralleled the deterioration of kidney and endothelial functions from sepsis to sepsis-AKI, revealed as progressively increased levels of serum E-selectin (15.3%), endothelin-1 (ET-1) (19.6%), and decreased nitric oxide (NO) (29.7%), associated with elevations of TNF-α (25.5%) and TGF-β (18%).
|
28840836 |
2017 |
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
We investigated the effects of 24 h delayed normobaric oxygen (NBO<sub>2</sub>) and HBO<sub>2</sub> treatment on the endogenous production of the inflammatory markers interleukin (IL)-6, tumor necrosis factor (TNF)-α and IL-10, and on mortality in rats with cecal ligation and puncture (CLP) induced sepsis.
|
29204105 |
2017 |
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 |
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 |
We found a statistically significant reduction in brain tissue homogenate levels of TNF-α 59.5 ± 8.4/50.2 ± 6.2 (p = 0.007) and TOS 99.3 ± 16.9/82.3 ± 7.8 (p = 0.01) in rats treated with EE; although interleukin 6 levels were increased in the treatment group compared to the sepsis group, this was not statistically significant.
|
28859554 |
2017 |
Septicemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
However, no significant association was found between TNF-α -308G/A and -238G/A polymorphisms and sepsis-related mortality.
|
28294408 |
2017 |
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
In addition, rTM administered prior to or after LPS suppressed the level of pro-inflammatory cytokine TNF-α in sera at 1-3 h after LPS injection, whereas only the administration of rTM after LPS suppressed the levels of HMGB1 and nucleosome (late-phase mediators of sepsis) (9-12 h) in sera after the LPS injection.
|
28587368 |
2017 |
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 |
Blood urea nitrogen, creatinine, plasma neutrophil gelatinase-associated lipocalin, interleukin-6, interleukin-10, and tumor necrosis factor-α were markedly increased in the H d-gal group after establishment of the sepsis model (H d-gal vs control, <i>P</i><0.05 at 12 h and 24 h post-CLP).
|
28408808 |
2017 |
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 |
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 |
GeneticVariation
|
disease |
BEFREE |
This meta-analysis suggests that the -308G/A gene polymorphism in the TNF-α gene may contribute to risk of sepsis and septic shock, but not risk of mortality.
|
29212277 |
2017 |
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
In vivo Lipopolysaccharide Tolerance Recruits CD11b+ Macrophages to the Liver with Enhanced Bactericidal Activity and Low Tumor Necrosis Factor-Releasing Capability, Resulting in Drastic Resistance to Lethal Septicemia.
|
28675904 |
2017 |
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Increased levels of TNF-α in sepsis sera do not explain diminished keratinocyte migration.
|
28086962 |
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 |
GeneticVariation
|
disease |
BEFREE |
We found an association between the SNP LTA +252 with the development of sepsis [OR 1.29 (1.00-1.68)]; the SNP IL10 -1082 with sepsis severity [OR 0.53 (0.29-0.97)]; the TNF -308 with mortality [OR 0.33 (0.12-0.95)]; and the IL10 -592 and IL10 -1082 with admission to the intensive care unit (ICU) [OR 3.36 (1.57-7.18)] and [OR 0.18 (0.04-0.86)], respectively.
|
27592234 |
2016 |
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Tumor necrosis factor (TNF)-α is a pleiotropic cytokine with intense pro-inflammatory and immunomodulatory properties, and anti-TNF-α biologics are effective therapies for various inflammatory diseases such as inflammatory bowel disease (IBD) and sepsis.
|
27879679 |
2016 |
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
In the present study, a cell model of sepsis, comprising lipopolysaccharide (LPS)‑tolerant THP‑1 cells, was used to investigate whether the SirT1 activator, resveratrol, repressed the transcription of TNF‑α.
|
27878240 |
2016 |
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Furthermore, treating mice with a cGMP analog after the induction of sepsis increased TNFR shedding and decreased systemic inflammation.
|
25628461 |
2015 |
Septicemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
In the present study, we aim to investigate the association of promoter-region polymorphisms IL-6 (-174G/C) rs1800795 and TNF-α (-308G/A) rs1800629 with pneumonia-induced sepsis.
|
26025100 |
2015 |
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 |
GeneticVariation
|
disease |
BEFREE |
Tumor necrosis factor (TNF)-α variant is closely linked to sepsis syndrome and mortality after severe trauma.
|
26117649 |
2015 |