INT2883

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Context Info
Confidence 0.59
First Reported 1977
Last Reported 2008
Negated 0
Speculated 0
Reported most in Abstract
Documents 9
Total Number 9
Disease Relevance 3.25
Pain Relevance 3.08

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

signal transduction (CCK) extracellular space (CCK) extracellular region (CCK)
Anatomy Link Frequency
plasma 6
CCK (Homo sapiens)
Pain Link Frequency Relevance Heat
Cholecystokinin 58 100.00 Very High Very High Very High
Bile 16 100.00 Very High Very High Very High
tetrodotoxin 1 99.84 Very High Very High Very High
Somatostatin 1 99.74 Very High Very High Very High
antagonist 1 97.88 Very High Very High Very High
Chronic pancreatitis 8 96.48 Very High Very High Very High
agonist 4 50.00 Quite Low
opiate 3 50.00 Quite Low
nud 35 38.52 Quite Low
visual analogue scale 9 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Exocrine Pancreatic Insufficiency 16 99.88 Very High Very High Very High
Gallstones 3 99.54 Very High Very High Very High
Pancreatitis 8 96.48 Very High Very High Very High
Systemic Sclerosis 102 96.12 Very High Very High Very High
Steatorrhea 16 91.60 High High
Enteropathy 1 88.04 High High
Diabetes Mellitus 2 73.84 Quite High
Gastric Motility Disorder 8 73.68 Quite High
Diabetic Nephropathy 12 59.92 Quite High
Functional Bowel Disorder 1 52.40 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
A failure of cholecystokinin (CCK) release after a meal has been shown among patients with exocrine pancreatic insufficiency.
Negative_regulation (failure) of Localization (release) of CCK associated with exocrine pancreatic insufficiency and cholecystokinin
1) Confidence 0.59 Published 1997 Journal Pancreas Section Abstract Doc Link 8981511 Disease Relevance 0.28 Pain Relevance 0.20
To test the hypothesis, based on studies in healthy man and dog, that patients with impaired digestion due to severe pancreatic insufficiency have impaired postprandial cholecystokinin (CCK) secretion that can be improved by the addition of pancreatic enzymes, we have studied plasma CCK responses to a test meal with and without addition of pancreatic enzymes in 10 patients with pancreatic insufficiency and steatorrhea, in 8 patients with chronic pancreatitis without steatorrhea, and in 6 healthy subjects.
Negative_regulation (impaired) of Localization (secretion) of CCK in plasma associated with steatorrhea, exocrine pancreatic insufficiency, chronic pancreatitis and cholecystokinin
2) Confidence 0.59 Published 1989 Journal Regul. Pept. Section Abstract Doc Link 2772268 Disease Relevance 0.73 Pain Relevance 0.39
This effect is not mediated by inhibition of CCK release, as loperamide even enhances basal CCK plasma levels.
Negative_regulation (inhibition) of Localization (release) of CCK in plasma
3) Confidence 0.43 Published 2005 Journal Neurogastroenterol. Motil. Section Body Doc Link 16185316 Disease Relevance 0 Pain Relevance 0
A failure of cholecystokinin (CCK) release after a meal has been shown among patients with exocrine pancreatic insufficiency.
Negative_regulation (failure) of Localization (release) of cholecystokinin associated with exocrine pancreatic insufficiency and cholecystokinin
4) Confidence 0.43 Published 1997 Journal Pancreas Section Abstract Doc Link 8981511 Disease Relevance 0.28 Pain Relevance 0.20
To test the hypothesis, based on studies in healthy man and dog, that patients with impaired digestion due to severe pancreatic insufficiency have impaired postprandial cholecystokinin (CCK) secretion that can be improved by the addition of pancreatic enzymes, we have studied plasma CCK responses to a test meal with and without addition of pancreatic enzymes in 10 patients with pancreatic insufficiency and steatorrhea, in 8 patients with chronic pancreatitis without steatorrhea, and in 6 healthy subjects.
Negative_regulation (impaired) of Localization (secretion) of cholecystokinin in plasma associated with steatorrhea, exocrine pancreatic insufficiency, chronic pancreatitis and cholecystokinin
5) Confidence 0.43 Published 1989 Journal Regul. Pept. Section Abstract Doc Link 2772268 Disease Relevance 0.73 Pain Relevance 0.39
However, also taking into account the altered gallbladder refilling noticed in SSc patients, this therapeutic option should be considered with caution, since the long-acting octreotide formulation has been shown to greatly increase the risk of gallstone formation probably by suppression of endogenous cholecystokinin release [71].
Negative_regulation (suppression) of Localization (release) of cholecystokinin associated with gallstones, systemic sclerosis and cholecystokinin
6) Confidence 0.41 Published 2008 Journal BMC Gastroenterol Section Body Doc Link PMC2276219 Disease Relevance 1.14 Pain Relevance 0.05
Somatostatin was able to abolish the stimulated CCK release.
Negative_regulation (abolish) of Localization (release) of CCK associated with bile and somatostatin
7) Confidence 0.37 Published 1977 Journal Clin. Chim. Acta Section Abstract Doc Link 562241 Disease Relevance 0.10 Pain Relevance 0.84
CCK-8 (10 nM-10 microM) stimulated [3H]acetylcholine release from pancreatic lobules that was blocked by tetrodotoxin, a calcium-free medium, and the CCK antagonist L364,718.
Negative_regulation (blocked) of Localization (release) of CCK associated with tetrodotoxin, antagonist and cholecystokinin
8) Confidence 0.37 Published 1992 Journal Am. J. Physiol. Section Abstract Doc Link 1636705 Disease Relevance 0 Pain Relevance 0.84
It is concluded that loperamide inhibits basal and amino acid-stimulated gallbladder motility and intraduodenal output of bilirubin and amylase, despite an enhanced postprandial cholecystokinin release.
Negative_regulation (inhibits) of Localization (release) of cholecystokinin associated with cholecystokinin
9) Confidence 0.33 Published 1997 Journal Hepatology Section Abstract Doc Link 9252131 Disease Relevance 0 Pain Relevance 0.17

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