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1 share only 36-44% sequence identity with the pancreatic enzyme.
2  IL-23 and IL-22 and decreased production of pancreatic enzymes.
3 f liver transaminases, serum creatinine, and pancreatic enzymes.
4 ent pancreas biopsy, mainly due to a rise in pancreatic enzymes.
5  each substrate are similar in the liver and pancreatic enzymes.
6 trients; an equivalent function to digestive pancreatic enzymes.
7 sures the afferent transport of the bile and pancreatic enzymes.
8 infant digestion with or without gastric and pancreatic enzymes.
9 e B/C, endocrine dysfunction, and the use of pancreatic enzymes.
10 nbiotics (2 studies), antibiotics (1 study), pancreatic enzymes (1 study), and psychosocial stimulati
11 es developed in 10.6%; 50.4% reported taking pancreatic enzymes; 54.6% reported needing antacids.
12                        Our data suggest that pancreatic enzymes act as the primary metabolic barrier
13                                              Pancreatic enzyme activities related to either CEL or PT
14                                 Models using pancreatic enzyme activity showed good prediction power.
15 the alimentary tract and potentially augment pancreatic enzyme activity, the effect of ivacaftor on r
16 of activated CD4(+) T cells specific for the pancreatic enzyme amylase can induce pancreatitis in the
17 its isomer FAG were digested with individual pancreatic enzymes (amylase, trypsin or lipase), FAG rem
18                                              Pancreatic enzyme and bile acid delivery to the duodenum
19                                   A trial of pancreatic enzymes and antioxidants (a combination of mu
20 dysfunction are associated with elevation of pancreatic enzymes and even pancreatitis.
21 as cholecystokinin 8-stimulated secretion of pancreatic enzymes and secretin-induced gastrointestinal
22 ligation, all animals were supplemented with pancreatic enzymes and vitamins resulting in blood conce
23                  We have found that abnormal pancreatic enzymes are useful prognostic marker of death
24 e-associated pancreatitis (abdominal pain or pancreatic enzymes at least three times the ULN or both
25 ed by at least two criteria: abdominal pain, pancreatic enzymes at least three times the upper limit
26 fection includes expression of mRNA for some pancreatic enzymes by intestinal epithelial cells and th
27 is, inflammation, and circulatory release of pancreatic enzymes, clinical signs resembling those of h
28 res overlap with those of sepsis, imply that pancreatic enzymes contribute to tissue damage in fatal
29                                 Insufficient pancreatic enzyme dosing is common for treatment of panc
30 ity at 160 mg daily was asymptomatic grade 3 pancreatic enzyme elevation without symptomatic pancreat
31 ts (two with acute pancreatitis and two with pancreatic enzyme elevation), of which three events led
32  well tolerated, with self-limiting rash and pancreatic enzyme elevations as notable grade 3/4 advers
33 pport recommendations that the daily dose of pancreatic enzymes for most patients should remain below
34 died the prognostic significance of abnormal pancreatic enzymes for survival.
35 tabilized preferentially the wild-type human pancreatic enzyme in MIN6 beta-cells, and SUMOylation in
36  dysfunction in 91 patients (11%) and use of pancreatic enzymes in 108 (12%).
37         Therefore, we tested the benefits of pancreatic enzymes in an aggressive mouse model of PDA (
38 to hydrochloric acid, pepsin, bile salts and pancreatic enzymes in gastric contents damages esophagea
39 agic shock (T/HS) or sham shock, the role of pancreatic enzymes in gut injury was tested by diversion
40 rrence of pain or alters the blood levels of pancreatic enzymes in patients with predicted mild acute
41 ere, necrotizing pancreatitis, with elevated pancreatic enzymes in the blood and necrotic acinar cell
42                The physiological activity of pancreatic enzymes in the ileum has been studied in heal
43 cterize health benefits and risks of dietary pancreatic enzymes in three mouse models of PDA-KC, KCR8
44 heir resisting digestion by gastric acid and pancreatic enzymes in vivo.
45 diation was performed 5 months after initial pancreatic enzymes increase, resulting in a decrease of
46                                     Finally, pancreatic enzyme-induced gut and lung injury seems to i
47 used with saline containing a broadly acting pancreatic enzyme inhibitor (6-amidino-2-naphthyl p-guan
48 osis after 4 weeks of alcohol treatment; the pancreatic enzymes lipase and amylase were not elevated.
49 ized by suppressed expression of a cohort of pancreatic enzymes not previously reported in DCs, which
50  32 elected enzyme treatment, which included pancreatic enzymes, nutritional supplements, detoxificat
51 sters are hydrolyzed in the intestine by the pancreatic enzyme, pancreatic triglyceride lipase, and i
52 riggers for investigation were elevations in pancreatic enzymes, re-admissions for abdominal pain, an
53 ed malnutrition through the use of effective pancreatic enzyme replacement and a high-energy, high-pr
54  allows the study of digestive processes and pancreatic enzyme replacement therapies.
55                                         Oral pancreatic enzyme replacement therapy (PERT) with pancre
56 ative chemotherapy, palliative chemotherapy, pancreatic enzyme replacement therapy (PERT), referral t
57 n, presence of comorbidities, and the use of pancreatic enzyme replacement therapy (PERT).
58 thin 8 weeks after surgery without requiring pancreatic enzyme replacement therapy.
59                                 Mean dose of pancreatic enzyme replacement was similar in both groups
60  Approximately half of the patients required pancreatic enzyme replacement, while only 11% developed
61  in nutrient malabsorption and requires oral pancreatic enzyme replacement.
62 A deficiency because of steatorrhea, despite pancreatic enzyme replacement.
63 rug Administration required manufacturers of pancreatic enzymes replacement therapy (PERT) to have ap
64 ic and surgical intervention, and the use of pancreatic enzyme-replacement therapy.
65 IL-22 in early life has a negative impact on pancreatic enzyme secretion and food absorption.
66 d that chronic decerebration decreased basal pancreatic enzyme secretion from 318 +/- 12 to 233 +/- 9
67 ate vagal mucosal afferent fibers to mediate pancreatic enzyme secretion via a common cholinergic pat
68 nin (CCK) at physiological levels stimulates pancreatic enzyme secretion via gastroduodenal mucosal v
69  CCK, non-CCK-mediated luminal stimuli evoke pancreatic enzyme secretion via stimulation of a vagal a
70 ution infusion (which stimulates 50% maximal pancreatic enzyme secretion).
71 ulates apical acinar cell Ca(2+) signals and pancreatic enzyme secretion.
72                             However, dietary pancreatic enzymes stimulated tumor growth in the termin
73               Alterations in the activity of pancreatic enzymes, such as chymotrypsin and trypsin, wh
74 tigate the relation between dose and type of pancreatic-enzyme supplement and fibrosing colonopathy.
75                             The mean dose of pancreatic-enzyme supplement was 50,046 units of lipase
76                                              Pancreatic enzyme supplementation does not completely co
77                 Compared with standard care, pancreatic enzyme supplementation reduced inpatient mort
78  this effect was reversed by dietary porcine pancreatic enzyme supplementation.
79        Median survival improved with dietary pancreatic enzyme supplements and was extended further w
80                                      Dietary pancreatic enzyme supplements reversed these symptoms in
81  who were treated with routine vitamin D and pancreatic enzyme supplements with the vitamin D status
82  and zinc measurements, the proper dosing of pancreatic enzyme supplements, and treatment of pancreat
83  strong relation between high daily doses of pancreatic-enzyme supplements and the development of fib
84 sis, the majority of whom take high-strength pancreatic-enzyme supplements to control intestinal mala
85                       The CF group also took pancreatic enzymes that provided > or = 80000 U lipase.
86 malnutrition, which was unresponsive to oral pancreatic enzyme therapy or a gluten-free diet.
87  cystic fibrosis (CF), even with replacement pancreatic enzyme therapy, is often associated with decr
88 erventions that included high-calorie diets, pancreatic-enzyme therapy, and fat-soluble vitamin suppl
89 as new upper abdominal pain, an elevation in pancreatic enzymes to at least three times the upper lim
90 rker revealed by the microarray: a cohort of pancreatic enzymes (trypsin, carboxypeptidase, elastase,
91          Suppressed expression of one of the pancreatic enzymes, trypsin, in these DC impeded their a
92 mes in gut injury was tested by diversion of pancreatic enzymes via pancreatic duct exteriorization w
93                          A large increase in pancreatic enzymes was noticed shortly after the DSA pro
94 and the laboratory tests, including that for pancreatic enzymes, were unremarkable.
95 y low levels of activators in the absence of pancreatic enzymes, whereas in the presence of enzymes,
96 e stomach and changes in admixture of gastro-pancreatic enzymes, which could have a major impact on p
97 he enzyme is approximately twice that of the pancreatic enzyme, while K(m) values for each substrate
98  (EPI) stems from a deficiency of functional pancreatic enzymes with consequent maldigestion and maln