ライフサイエンスコーパス: hyperinflammation

1 er frequently associated with a nonresolving hyperinflammation.

2 leading to an increased bacterial burden and hyperinflammation.

3 (FHL4), a life-threatening disease of severe hyperinflammation.

4 cases by infectious agents, leads to severe hyperinflammation.

5 y characterized by initial cytokine-mediated hyperinflammation.

6 (MOF) may result from overwhelming systemic hyperinflammation.

7 g in response to TLR4 activation, leading to hyperinflammation, a hallmark of cystic fibrosis (CF) di

8 and plant fibers can dramatically reduce the hyperinflammation and also the infiltration by neutrophi

9 d by immune dysregulation with granulomatous hyperinflammation and autoimmunity, with relatively norm

10 hreatening syndrome, characterized by severe hyperinflammation and immunopathological manifestations

11 Both hyperinflammation and immunosuppression are implicated a

12 Fatal H7N9 infections are characterized by hyperinflammation and increased cellular infiltrates in

13 remia leads to Toll-like receptor 4-mediated hyperinflammation and lethality.

14 rmia and hyperoxia would attenuate postshock hyperinflammation and thereby organ dysfunction.

15 ugh hyperoxia alone attenuated the postshock hyperinflammation and thereby tended to improve visceral

16 kely to result from increased mucus density, hyperinflammation, and defective bacterial killing could

17 rized by defective cellular cytotoxicity and hyperinflammation, and the only cure known to date is he

18 bility of many pathogenic antigens to induce hyperinflammation, and the previously identified role of

19 thal hemorrhagic shock, hyperoxia attenuated hyperinflammation, and thereby showed a favorable trend

20 ulated immune reaction involving features of hyperinflammation, as well as protracted immune suppress

21 Conversely, in systemic infection, hyperinflammation associated with M1-mediated pyroptosis

22 In sepsis, M1 macrophages can compensate for hyperinflammation by acquiring an M2-like immunosuppress

23 us as reflected in increased mortality after hyperinflammation caused by acute endotoxemia.

24 e inflammation caused by excess lipoxins and hyperinflammation driven by excess leukotriene B(4).

25 ell migration to initiate the suppression of hyperinflammation during endotoxemia.

26 ard macrophages, is critical for suppressing hyperinflammation during the first 3 h of endotoxemia.

27 However, the CF hyperinflammation expressed in short-term (6-11-day-old)

28 llular signaling pathway that contributes to hyperinflammation in CGD and in septic patients.

29 eoxygenase (IDO), was proposed as a cause of hyperinflammation in CGD and this pathway has been consi

30 stays, we speculate that this SNP results in hyperinflammation in diseases such as sepsis.

31 R engagement and pulmonary lymphocytosis and hyperinflammation in Mtb-infected mice.

32 Hyperinflammation is also a significant clinical manifes

33 Some alpha-VEGF -/R rats showed a hyperinflammation leading to increased pro-inflammatory

34 or repression activity of Miz1, resulted in hyperinflammation, lung injury and greater mortality in

35 wever, in CF airways, the Ca(2+)(i)-mediated hyperinflammation may be ineffective in promoting the er

36 c deaths to examine whether death was due to hyperinflammation or immunosuppression.

37 ryopyrin, a protein implicated in hereditary hyperinflammation syndromes, and was termed PAN2 for PAA

38 ive care units, and patients who survive the hyperinflammation that develops early during sepsis late

39 initial insult and coincides with a stage of hyperinflammation that is followed by a condition of inn

40 e targets for mitigating the cytokine-driven hyperinflammation that occurs in HLH.

41 s equipped with mechanisms that downregulate hyperinflammation to avoid collateral damage.

42 ry response syndrome transition implies that hyperinflammation triggers acute sepsis mortality, where

43 rrhagic shock-induced tissue hypoxia induces hyperinflammation, ultimately causing multiple organ fai

44 embolisms and in the alpha-VEGF (-/R) group, hyperinflammation was the main cause of death.

45 atory response that turned to an exaggerated hyperinflammation with the onset of severe pneumonia.