Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
For instance, NO potentiates the hepatic oxidative injury in warm ischemia/reperfusion, while iNOS expression protects against hepatic apoptotic cell death seen in models of sepsis and hepatitis.
|
14527083 |
2003 |
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
These results suggest that TXA2 has a protective role against the development of vascular hyporesponsiveness via its inhibitory action on the iNOS-NO system under pathological conditions such as sepsis.
|
14557367 |
2003 |
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Little is known about transcriptional regulation of the human iNOS gene in vivo under basal conditions or in sepsis.
|
15507544 |
2005 |
Septicemia
|
0.400 |
Biomarker
|
disease |
CTD_human |
Down-regulation of CXCR2 on neutrophils in severe sepsis is mediated by inducible nitric oxide synthase-derived nitric oxide.
|
17138957 |
2007 |
Septicemia
|
0.400 |
Biomarker
|
disease |
CTD_human |
Essential role of nitric oxide in sepsis-induced impairment of endothelium-derived hyperpolarizing factor-mediated relaxation in rat pulmonary artery.
|
20035746 |
2010 |
Septicemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
In this study, we assessed whether SNPs within NOS2 gene were associated with severity of sepsis in Chinese populations.
|
23192595 |
2013 |
Septicemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Sepsis independently associated with HF, increased NOx, peripheral neutrophils, and fibrinogen levels, decreased prothrombin and the presence of the NOS3 (E298D) and NOS2A (exon 22) SNPs.
|
25239655 |
2014 |
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Sepsis increased NOS2 expression in the heart, increased plasma nitrite + nitrate levels, and reduced isoproterenol-induced isolated ventricle contraction, whole heart tension development, and β-adrenergic receptor density.
|
28526706 |
2017 |
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
NOS isoform activation is related to liver failure during sepsis, but the mechanisms driving mitochondrial impairment remain unclear.
|
28110436 |
2017 |
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
This study clearly highlights the NOS2-dependent and -independent responses in this mouse model of peritonitis induced sepsis.
|
29309892 |
2018 |
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Pretreatment with ZSCLE (100, 200, and 300 mg/kg) restored the normal heart rate (HR); decreased the elevated levels of malondialdehyde; the activity of myeloperoxidase, nitric oxide (NO), and inducible NO synthase; and the expression of nuclear factor kappa B (NF-κB), but increased the content of glutathione and antioxidant enzyme activities in mice with sepsis.
|
29549730 |
2018 |
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
In vivo investigation showed that γ-GC reduced sepsis lethality and attenuated systemic inflammatory responses in mice, as well as inhibited lipopolysaccharide (LPS)-stimulated production of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), high-mobility group box 1 (HMGB1), and nitric oxide (NO) and the expression of inducible NO synthase and cyclooxygenase 2 in RAW264.7 cells.
|
30326393 |
2019 |