ライフサイエンスコーパス: pancreatic enzyme

1 share only 36-44% sequence identity with the pancreatic enzyme.

2 f liver transaminases, serum creatinine, and pancreatic enzymes.

3 each substrate are similar in the liver and pancreatic enzymes.

4 trients; an equivalent function to digestive pancreatic enzymes.

5 es developed in 10.6%; 50.4% reported taking pancreatic enzymes; 54.6% reported needing antacids.

6 Pancreatic enzyme activities related to either CEL or PT

7 Models using pancreatic enzyme activity showed good prediction power.

8 of activated CD4(+) T cells specific for the pancreatic enzyme amylase can induce pancreatitis in the

9 Pancreatic enzyme and bile acid delivery to the duodenum

10 dysfunction are associated with elevation of pancreatic enzymes and even pancreatitis.

11 as cholecystokinin 8-stimulated secretion of pancreatic enzymes and secretin-induced gastrointestinal

12 We have found that abnormal pancreatic enzymes are useful prognostic marker of death

13 e-associated pancreatitis (abdominal pain or pancreatic enzymes at least three times the ULN or both

14 ed by at least two criteria: abdominal pain, pancreatic enzymes at least three times the upper limit

15 fection includes expression of mRNA for some pancreatic enzymes by intestinal epithelial cells and th

16 is, inflammation, and circulatory release of pancreatic enzymes, clinical signs resembling those of h

17 res overlap with those of sepsis, imply that pancreatic enzymes contribute to tissue damage in fatal

18 Insufficient pancreatic enzyme dosing is common for treatment of panc

19 pport recommendations that the daily dose of pancreatic enzymes for most patients should remain below

20 died the prognostic significance of abnormal pancreatic enzymes for survival.

21 tabilized preferentially the wild-type human pancreatic enzyme in MIN6 beta-cells, and SUMOylation in

22 Therefore, we tested the benefits of pancreatic enzymes in an aggressive mouse model of PDA (

23 agic shock (T/HS) or sham shock, the role of pancreatic enzymes in gut injury was tested by diversion

24 ere, necrotizing pancreatitis, with elevated pancreatic enzymes in the blood and necrotic acinar cell

25 cterize health benefits and risks of dietary pancreatic enzymes in three mouse models of PDA-KC, KCR8

26 heir resisting digestion by gastric acid and pancreatic enzymes in vivo.

27 Finally, pancreatic enzyme-induced gut and lung injury seems to i

28 used with saline containing a broadly acting pancreatic enzyme inhibitor (6-amidino-2-naphthyl p-guan

29 osis after 4 weeks of alcohol treatment; the pancreatic enzymes lipase and amylase were not elevated.

30 ized by suppressed expression of a cohort of pancreatic enzymes not previously reported in DCs, which

31 32 elected enzyme treatment, which included pancreatic enzymes, nutritional supplements, detoxificat

32 sters are hydrolyzed in the intestine by the pancreatic enzyme, pancreatic triglyceride lipase, and i

33 riggers for investigation were elevations in pancreatic enzymes, re-admissions for abdominal pain, an

34 Oral pancreatic enzyme replacement therapy (PERT) with pancre

35 Mean dose of pancreatic enzyme replacement was similar in both groups

36 Approximately half of the patients required pancreatic enzyme replacement, while only 11% developed

37 A deficiency because of steatorrhea, despite pancreatic enzyme replacement.

38 rug Administration required manufacturers of pancreatic enzymes replacement therapy (PERT) to have ap

39 ic and surgical intervention, and the use of pancreatic enzyme-replacement therapy.

40 d that chronic decerebration decreased basal pancreatic enzyme secretion from 318 +/- 12 to 233 +/- 9

41 ate vagal mucosal afferent fibers to mediate pancreatic enzyme secretion via a common cholinergic pat

42 nin (CCK) at physiological levels stimulates pancreatic enzyme secretion via gastroduodenal mucosal v

43 CCK, non-CCK-mediated luminal stimuli evoke pancreatic enzyme secretion via stimulation of a vagal a

44 ution infusion (which stimulates 50% maximal pancreatic enzyme secretion).

45 ulates apical acinar cell Ca(2+) signals and pancreatic enzyme secretion.

46 However, dietary pancreatic enzymes stimulated tumor growth in the termin

47 Alterations in the activity of pancreatic enzymes, such as chymotrypsin and trypsin, wh

48 tigate the relation between dose and type of pancreatic-enzyme supplement and fibrosing colonopathy.

49 The mean dose of pancreatic-enzyme supplement was 50,046 units of lipase

50 Pancreatic enzyme supplementation does not completely co

51 this effect was reversed by dietary porcine pancreatic enzyme supplementation.

52 Median survival improved with dietary pancreatic enzyme supplements and was extended further w

53 Dietary pancreatic enzyme supplements reversed these symptoms in

54 who were treated with routine vitamin D and pancreatic enzyme supplements with the vitamin D status

55 and zinc measurements, the proper dosing of pancreatic enzyme supplements, and treatment of pancreat

56 strong relation between high daily doses of pancreatic-enzyme supplements and the development of fib

57 sis, the majority of whom take high-strength pancreatic-enzyme supplements to control intestinal mala

58 The CF group also took pancreatic enzymes that provided > or = 80000 U lipase.

59 malnutrition, which was unresponsive to oral pancreatic enzyme therapy or a gluten-free diet.

60 cystic fibrosis (CF), even with replacement pancreatic enzyme therapy, is often associated with decr

61 erventions that included high-calorie diets, pancreatic-enzyme therapy, and fat-soluble vitamin suppl

62 as new upper abdominal pain, an elevation in pancreatic enzymes to at least three times the upper lim

63 rker revealed by the microarray: a cohort of pancreatic enzymes (trypsin, carboxypeptidase, elastase,

64 Suppressed expression of one of the pancreatic enzymes, trypsin, in these DC impeded their a

65 mes in gut injury was tested by diversion of pancreatic enzymes via pancreatic duct exteriorization w

66 A large increase in pancreatic enzymes was noticed shortly after the DSA pro

67 and the laboratory tests, including that for pancreatic enzymes, were unremarkable.

68 y low levels of activators in the absence of pancreatic enzymes, whereas in the presence of enzymes,

69 e stomach and changes in admixture of gastro-pancreatic enzymes, which could have a major impact on p

70 he enzyme is approximately twice that of the pancreatic enzyme, while K(m) values for each substrate