INT2463

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Context Info
Confidence 0.81
First Reported 1977
Last Reported 2011
Negated 0
Speculated 0
Reported most in Abstract
Documents 101
Total Number 101
Disease Relevance 37.54
Pain Relevance 47.59

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 15
respiratory 6
small intestine 5
central nervous system 3
duodenum 3
CCK (Homo sapiens)
Pain Link Frequency Relevance Heat
Cholecystokinin 1817 100.00 Very High Very High Very High
Neuropeptide 57 100.00 Very High Very High Very High
Bile 43 100.00 Very High Very High Very High
Enkephalin 23 100.00 Very High Very High Very High
Neurotransmitter 16 100.00 Very High Very High Very High
Somatostatin 12 100.00 Very High Very High Very High
Calcitonin gene-related peptide 10 100.00 Very High Very High Very High
substance P 9 100.00 Very High Very High Very High
Dynorphin 6 100.00 Very High Very High Very High
vagus nerve 9 99.84 Very High Very High Very High
Disease Link Frequency Relevance Heat
Critical Illness 660 99.92 Very High Very High Very High
Disease 48 99.60 Very High Very High Very High
Attention Deficit Hyperactivity Disorder 9 99.54 Very High Very High Very High
Exocrine Pancreatic Insufficiency 81 99.44 Very High Very High Very High
Pancreatitis 195 99.34 Very High Very High Very High
Irritable Bowel Syndrome /

Irritable Bowel Syndrome Super

115 99.20 Very High Very High Very High
Pain 119 99.12 Very High Very High Very High
Steatorrhea 91 99.10 Very High Very High Very High
Gallstones 7 99.02 Very High Very High Very High
Peripheral Primitive Neuroectodermal Tumors 6 98.76 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Effects of ethanol on meal-stimulated secretion of pancreatic polypeptide and cholecystokinin: comparison of healthy volunteers, heavy drinkers, and patients with chronic pancreatitis.
Localization (secretion) of cholecystokinin associated with chronic pancreatitis and cholecystokinin
1) Confidence 0.81 Published 1996 Journal J. Gastroenterol. Section Title Doc Link 8808434 Disease Relevance 0.56 Pain Relevance 0.50
In the present study, the validity of this hypothesis was investigated in humans by studying the effects of atropine, cisapride, and ethanol on the meal-stimulated secretion of pancreatic polypeptide (PP) and cholecystokinin (CCK) in healthy volunteers, heavy drinkers, and CP patients.
Localization (secretion) of cholecystokinin associated with chronic pancreatitis and cholecystokinin
2) Confidence 0.81 Published 1996 Journal J. Gastroenterol. Section Abstract Doc Link 8808434 Disease Relevance 0.59 Pain Relevance 0.59
In the present study, the validity of this hypothesis was investigated in humans by studying the effects of atropine, cisapride, and ethanol on the meal-stimulated secretion of pancreatic polypeptide (PP) and cholecystokinin (CCK) in healthy volunteers, heavy drinkers, and CP patients.
Localization (secretion) of CCK associated with chronic pancreatitis and cholecystokinin
3) Confidence 0.81 Published 1996 Journal J. Gastroenterol. Section Abstract Doc Link 8808434 Disease Relevance 0.59 Pain Relevance 0.59
In humans, free fatty acids rather than triglycerides, when present in the duodenum, stimulate CCK release and gallbladder contraction.
Localization (release) of CCK in duodenum associated with cholecystokinin
4) Confidence 0.81 Published 1997 Journal Pancreas Section Abstract Doc Link 8981511 Disease Relevance 0.33 Pain Relevance 0.17
A failure of cholecystokinin (CCK) release after a meal has been shown among patients with exocrine pancreatic insufficiency.
Localization (release) of CCK associated with exocrine pancreatic insufficiency and cholecystokinin
5) Confidence 0.81 Published 1997 Journal Pancreas Section Abstract Doc Link 8981511 Disease Relevance 0.28 Pain Relevance 0.20
A failure of cholecystokinin (CCK) release after a meal has been shown among patients with exocrine pancreatic insufficiency.
Localization (release) of cholecystokinin associated with exocrine pancreatic insufficiency and cholecystokinin
6) Confidence 0.81 Published 1997 Journal Pancreas Section Abstract Doc Link 8981511 Disease Relevance 0.28 Pain Relevance 0.20
Previous studies have suggested that intraduodenal protease suppression of pancreatic exocrine secretion may be mediated through cholecystokinin (CCK) release.
Localization (release) of CCK associated with cholecystokinin
7) Confidence 0.81 Published 1985 Journal J. Lab. Clin. Med. Section Abstract Doc Link 3973464 Disease Relevance 0.17 Pain Relevance 0.42
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.
Localization (secretion) of cholecystokinin in plasma associated with steatorrhea, exocrine pancreatic insufficiency, chronic pancreatitis and cholecystokinin
8) Confidence 0.81 Published 1989 Journal Regul. Pept. Section Abstract Doc Link 2772268 Disease Relevance 0.73 Pain Relevance 0.39
Integrated CCK secretion in the three groups during bombesin infusion was similar (patients with steatorrhea 134 +/- 23 pM.20 min, patients without steatorrhea 131 +/- 33 pM.20 min, and healthy subjects 146 +/- 28 pM.20 min), indicating a normal capacity to secrete CCK in response to a humoral stimulus.
Localization (secrete) of CCK associated with steatorrhea and cholecystokinin
9) Confidence 0.81 Published 1989 Journal Regul. Pept. Section Abstract Doc Link 2772268 Disease Relevance 0.88 Pain Relevance 0.44
These data are in agreement with the suggestions from previous studies that digestion of nutrients by pancreatic enzymes plays an important role in the regulation of plasma CCK secretion after feeding.
Localization (secretion) of CCK in plasma associated with cholecystokinin
10) Confidence 0.81 Published 1989 Journal Regul. Pept. Section Abstract Doc Link 2772268 Disease Relevance 0.68 Pain Relevance 0.38
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.
Localization (secretion) of CCK in plasma associated with steatorrhea, exocrine pancreatic insufficiency, chronic pancreatitis and cholecystokinin
11) Confidence 0.81 Published 1989 Journal Regul. Pept. Section Abstract Doc Link 2772268 Disease Relevance 0.73 Pain Relevance 0.39
Integrated CCK secretion in the three groups during bombesin infusion was similar (patients with steatorrhea 134 +/- 23 pM.20 min, patients without steatorrhea 131 +/- 33 pM.20 min, and healthy subjects 146 +/- 28 pM.20 min), indicating a normal capacity to secrete CCK in response to a humoral stimulus.
Localization (secretion) of CCK associated with steatorrhea and cholecystokinin
12) Confidence 0.81 Published 1989 Journal Regul. Pept. Section Abstract Doc Link 2772268 Disease Relevance 1.02 Pain Relevance 0.53
A randomised, double-blind, cross-over study in ten right-handed volunteers was performed evaluating the influence of cholecystokinin (CCK)-excretion on the perception of pain in a standardised model.
Localization (excretion) of cholecystokinin associated with pain and cholecystokinin
13) Confidence 0.81 Published 2003 Journal Pain Section Abstract Doc Link 12927624 Disease Relevance 0.70 Pain Relevance 1.00
A randomised, double-blind, cross-over study in ten right-handed volunteers was performed evaluating the influence of cholecystokinin (CCK)-excretion on the perception of pain in a standardised model.
Localization (excretion) of CCK associated with pain and cholecystokinin
14) Confidence 0.81 Published 2003 Journal Pain Section Abstract Doc Link 12927624 Disease Relevance 0.70 Pain Relevance 1.00
CONCLUSIONS: Although it significantly increases cholecystokinin secretion, the intraduodenal infusion of long-chain triglycerides does not affect small-bowel transit time, whereas the infusion of medium-chain triglycerides accelerates small-bowel transit time, independent of cholecystokinin.


Localization (secretion) of cholecystokinin in bowel
15) Confidence 0.81 Published 1995 Journal JPEN J Parenter Enteral Nutr Section Body Doc Link 7658601 Disease Relevance 0 Pain Relevance 0
In 5 human subjects, 95% pure cholecystokinin (CCK) given as a background infusion in doses of 42, 84, or 168 pmol kg-1 h-1 did not significantly alter acid secretion in response to graded doses (11-300 pmol kg-1 h-1) of synthetic human gastrin-17-I.
Localization (secretion) of CCK associated with cholecystokinin
16) Confidence 0.81 Published 1979 Journal Gastroenterology Section Abstract Doc Link 447032 Disease Relevance 0.13 Pain Relevance 0.38
Currently, there are no data on the impact of insulin on the release of CCK or PYY in humans.
Localization (release) of CCK associated with cholecystokinin
17) Confidence 0.80 Published 2007 Journal Crit Care Section Body Doc Link PMC2246231 Disease Relevance 0.27 Pain Relevance 0.27
This observation is at variance with recent findings that suggest that critically ill patients with feed intolerance have higher plasma CCK and PYY release in response to duodenal nutrients than patients who tolerated feeds [28,29].
Localization (release) of CCK in plasma associated with critical illness and cholecystokinin
18) Confidence 0.80 Published 2007 Journal Crit Care Section Body Doc Link PMC2246231 Disease Relevance 0.27 Pain Relevance 0.20
Consistent with our recent study [29], the postprandial release of PYY is related to the release of CCK, which supports the concept that CCK is an important proximal mediator for the release of PYY [9,10].
Localization (release) of CCK in proximal associated with cholecystokinin
19) Confidence 0.80 Published 2007 Journal Crit Care Section Body Doc Link PMC2246231 Disease Relevance 0.16 Pain Relevance 0.21
For example, in response to duodenal nutrient, there is a greater degree of antral hypo-motility, pyloric hyperactivity [27], and exaggerated release of both CCK and PYY in critically ill patients [28,29].
Localization (release) of CCK associated with critical illness, attention deficit hyperactivity disorder and cholecystokinin
20) Confidence 0.80 Published 2007 Journal Crit Care Section Body Doc Link PMC2246231 Disease Relevance 0.58 Pain Relevance 0.32

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