|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Antibodies to ubiquitin were able to (1) significantly increase (2- to 5-fold) the TNF-alpha response to endotoxin in whole blood from trauma and sepsis patients, (2) completely neutralize the inhibitory effect of trauma patients' serum on healthy donors' TNF-alpha production, and (3) partially neutralize the inhibitory effect of sepsis patients' serum on healthy donors' TNF-alpha production.
|
12406900 |
2003 |
|
Septicemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Association between Tumor Necrosis Factor-α Promoter -308 G/A Polymorphism and Early Onset Sepsis in Preterm Infants.
|
31006736 |
2019 |
|
Septicemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Association of TNF-α-308 G/A polymorphism with sepsis remains controversial.
|
24944154 |
2014 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Based on LPS induced sepsis model for the measurement of TNF-α inhibition in Swiss Albino mice and neutrophilia inhibition for asthma and COPD in Sprague Dawley rats with the potential molecules, compound 4 m would be great promise as a hit inhibitor in the future study.
|
30131242 |
2018 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Basophil-derived tumor necrosis factor can enhance survival in a sepsis model in mice.
|
30664762 |
2019 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Because TNF-α is a major mediator of the pathophysiology of sepsis and blocking inflammation is a possible line of therapy in such circumstances, we tested the efficacy of rPPE18 in reducing symptoms of sepsis in a mouse model of <i>Escherichia coli-</i>induced septic peritonitis. rPPE18 significantly decreased levels of serum TNF-α, IL-1β, IL-6, and IL-12 and reduced organ damage in mice injected i.p. with high doses of <i>E. coli</i> Peritoneal cells isolated from rPPE18-treated mice had characteristics of M2 macrophages which are protective in excessive inflammation.
|
29669785 |
2018 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Because the nuclear factor-κB (NF-κB) coupled pathway is believed to amplify inflammation prevailing in sepsis, the authors tested the hypotheses that the insertion-deletion polymorphism (-94ins/delATTG) (1) alters nuclear translocation of nuclear factor-κB and activator protein-1 (NF-κB1) in monocytes after lipopolysaccharide stimulation; (2) affects lipopolysaccharide-induced NF-κB1 messenger RNA expression, tumor necrosis factor α concentrations, and tissue factor activity; and (3) may be associated with increased 30-day mortality in patients with sepsis.
|
23249930 |
2013 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Bezafibrate treatment led to a reduction in leukocyte adherence, improved functional capillary density (FCD), and a reduction in interleukin-1α (IL-1α), tumour necrosis factor α (TNF-α) and granulocyte macrophage colony stimulating factors (GM-CSF) plasma levels in experimental sepsis.
|
29859746 |
2018 |
|
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 |
GeneticVariation
|
disease |
BEFREE |
Both rs187084 and rs352162 were significantly associated with TNF-α production by peripheral blood leucocytes in response to bacterial DNA stimulation and a higher sepsis morbidity rate in patients with major trauma.
|
21633947 |
2011 |
|
Septicemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Both serovars significantly increased the production of cytokines associated with acute sepsis (tumor necrosis factor alpha [TNF-α], interleukin β [IL-β], and IL-6), but temporal differences occurred between these serovars and between different <i>S</i> Choleraesuis strains.
|
30037797 |
2018 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
BTED for 6 hours significantly reduced the mRNA expression levels of tumor necrosis factor alpha (TNF-α) and IL-1β (all p < 0.05 vs. sepsis group), whereas mRNA expression of TNF-α and IL-1β in the intestine was increased after 6 hours' septic bile infusion compared with normal bile infusion group (all p < 0.05).
|
29847538 |
2018 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
By combining phenotypic analysis of exhaustion markers with functional analysis of cytokine production, we found that PD-1+ CD4+ cells in cancer hosts failed to make any cytokines following CLP, while the 2B4+ PD-1lo cells in cancer mice secreted increased TNF during sepsis.
|
29338031 |
2018 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Change in DNA methylation pattern, histone modification, and microRNA regulation has been shown in sepsis models to silence or activate pro-inflammatory genes such as TNF-α and interleukins, anti-oxidant enzymes, and many signaling pathways.
|
30179122 |
2018 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Circulating levels of the cytokines IL-6, IL-8, IL-10, MCP-1, IP-10, and TNF were additionally measured using bead-based multiplex assay and found to peak at <12 hours and be significantly increased in patients with sepsis at all three time points (<12 hours, 4 days, and 14 days after sepsis) compared to healthy subjects.
|
30300408 |
2018 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Compared with healthy children, children with sepsis demonstrated lower LPS-induced TNF-α production (P < 0.0001) and lower phytohemagglutinin-induced IFN-γ production (P < 0.0001).
|
29470918 |
2018 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
CONCLUSIONS The levels of plasma BNP and cTnI are associated with the severity of sepsis in pediatric patients, and were positively correlated with CRP and TNF-alpha levels, which provides a novel strategy for the early diagnosis and evaluation of sepsis in pediatric patients.
|
30956276 |
2019 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Concomitant with a delayed increase of plasma TNF-α in ethanol-treated mice, plasma PTX3 was also suppressed in the early phase of sepsis.
|
28965650 |
2017 |
|
Septicemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Considering combinations of genotypes, the TNF-alpha high and IL-10 low producer genotype combination was associated with a approximately 6-fold increased risk of death compared to the TNF-alpha-low and IL-10 intermediate/high producer genotype combination, after adjustment for either APACHE II (P=0.004), MOF score (P=0.004) or sepsis (P=0.006).
|
15036247 |
2004 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Diabetes exacerbates serum tumor necrosis factor (TNF) levels in sepsis by increasing splenic TNF production.
|
29780390 |
2018 |
|
Septicemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Distribution of TNF-α(308) genotypes is associated with outcome, IL-10(1082) with type of microorganism and underlying cause of sepsis, and CD14(159) with type of microorganism.
|
20163933 |
2010 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Elevated levels of PCT, IL-6, IL-8, IL-10, and TNFα were observed in most patients with sepsis and DIC.
|
30991817 |
2019 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Forced expression of CRBN in macrophage of KO mice suppressed activation of 5' adenosine monophosphate-activated protein kinase (AMPK) and HO-1 and augmented expression of TNF-α and HMGB1 as inhibition of AMPK by compound C. These studies demonstrate the contribution of CRBN expression to the pathogenesis of CLP-induced sepsis and peritoneal macrophage responses and suggest a novel therapeutic modality for polymicrobial sepsis.
|
29170136 |
2018 |
|
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 |
AlteredExpression
|
disease |
BEFREE |
Gene transcripts of TNFα were lower among patients with severe sepsis/shock than among patients with sepsis; that was not the case for TREM-1.
|
21855288 |
2012 |