ライフサイエンスコーパス: severe pancreatitis

1 ome and might be used to treat patients with severe pancreatitis.

2 of benefit in the treatment of patients with severe pancreatitis.

3 ce in mediating the progression from mild to severe pancreatitis.

4 extravascular (migrated) neutrophils only in severe pancreatitis.

5 ncreatitis, but lung fMLFK only increased in severe pancreatitis.

6 the time of drainage were considered to have severe pancreatitis.

7 ain strains of mice, Coxsackievirus causes a severe pancreatitis.

8 n patients had mild pancreatitis, and 23 had severe pancreatitis.

9 e radicals, which potentiate organ injury in severe pancreatitis.

10 as-ligand double-deficient mice die early of severe pancreatitis.

11 in those patients having CT scan findings of severe pancreatitis.

12 t, and 1 patient died because of concomitant severe pancreatitis.

13 .94%) moderate pancreatitis, and 12 (14.12%) severe pancreatitis.

14 ns in the treatment of moderately severe and severe pancreatitis.

15 sk of bias) included patients with predicted severe pancreatitis.

16 nce in the incidence of moderately severe or severe pancreatitis (22.1% in the aggressive-resuscitati

17 Loss of TRMs led to exacerbation of severe pancreatitis and death, due to impaired acinar ce

18 Coxsackievirus infection causes severe pancreatitis and myocarditis in humans, often lea

19 itical steps in the progression from mild to severe pancreatitis and responsible for many of its syst

20 WON is a common consequence of severe pancreatitis and typically occurs 3 to 5 weeks af

21 went biliopancreatic duct ligation to induce severe pancreatitis, and rPAF-AH administration was begu

22 replicated to high titers in vivo and caused severe pancreatitis but minimal myocarditis.

23 all significantly increased in both mild and severe pancreatitis, but lung fMLFK only increased in se

24 ients with mild versus moderately severe and severe pancreatitis, but we found no correlation between

25 n of oxidative stress to the pathogenesis of severe pancreatitis by examining the prevalence of funct

26 caused by caerulein and more prominently in severe pancreatitis caused by feeding a choline-deficien

27 Moderate-to-severe pancreatitis developed in 13 patients (4.4%) in t

28 diet administered by nasogastric tube during severe pancreatitis does not worsen outcome compared wit

29 enetic deletion of CD73 would result in more severe pancreatitis due to decreased generation of extra

30 was the development of moderately severe or severe pancreatitis during the hospitalization.

31 IL-33R, T1/ST2, significantly developed more severe pancreatitis, had greater weight loss, and contai

32 Earlier animal studies of moderate and severe pancreatitis have shown that blockade of this pow

33 t admission predicted the development of the severe pancreatitis in different groups of the patients.

34 ECLS is useful in treating severe pancreatitis-induced ARDS.

35 During severe pancreatitis, interleukin (IL)-1beta and tumor ne

36 Among patients with severe pancreatitis, limited evidence revealed no statis

37 Mild and severe pancreatitis models in the rat.

38 evalence of PPCF was higher in patients with severe pancreatitis (n = 16 [70%]) than in those with mi

39 ateral exocytosis in part explained the less severe pancreatitis observed in Munc18c(+/-) mice after

40 Severe pancreatitis occurs in 20%-30% of all patients wi

41 given ethanol or fatty acids developed more severe pancreatitis than mice not given ethanol or fatty

42 hanol to animals maintained on an LPD caused severe pancreatitis that was ameliorated by phosphate re

43 In mice with severe pancreatitis, we found systemic inflammatory resp

44 Moderate and severe pancreatitis were characterized by much greater l

45 Infection with CVB4-V results in an early, severe pancreatitis, which can lead to mortality or prog

46 IER3 expression was induced by both mild and severe pancreatitis, which promoted PanIN formation and

47 9-9 expression in mice resulted in rapid and severe pancreatitis with hyperactivation of epidermal gr