INT48994

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Context Info
Confidence 0.46
First Reported 1995
Last Reported 2010
Negated 1
Speculated 0
Reported most in Abstract
Documents 17
Total Number 17
Disease Relevance 3.29
Pain Relevance 4.69

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

transport (Slc4a8)
Anatomy Link Frequency
duodenum 2
sensory neuron 1
proximal 1
afferent neurons 1
14.2 1
Slc4a8 (Mus musculus)
Pain Link Frequency Relevance Heat
gABA 7 100.00 Very High Very High Very High
narcan 6 99.84 Very High Very High Very High
fibrosis 32 99.56 Very High Very High Very High
qutenza 27 99.00 Very High Very High Very High
Ventral tegmentum 8 99.00 Very High Very High Very High
Morphine 10 98.96 Very High Very High Very High
adenocard 8 98.92 Very High Very High Very High
withdrawal 4 98.60 Very High Very High Very High
Versed 5 90.08 High High
anesthesia 5 87.44 High High
Disease Link Frequency Relevance Heat
Targeted Disruption 12 99.84 Very High Very High Very High
Cystic Fibrosis 32 99.56 Very High Very High Very High
Tremor 1 75.84 Quite High
Drug Dependence 1 72.32 Quite High
Opiate Addiction 1 46.04 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Luminal acidification increased the mucosal level of PGE2 as well as 6-keto-PGF1alpha, yet stimulated HCO3- secretion in both WT and IP (-/-) mice, in an indomethacin-inhibitable and sensory neuron-dependent manners.
Localization (secretion) of HCO3 in sensory neuron
1) Confidence 0.46 Published 2004 Journal Digestion Section Body Doc Link 15308871 Disease Relevance 0.07 Pain Relevance 0
CONCLUSION: The presence of IP receptors is not essential for acid-induced HCO3- secretion and mucosal defense against acid injury in the duodenum, although activation of IP receptors results in stimulation of HCO3- secretion.
Localization (secretion) of HCO3 in duodenum
2) Confidence 0.41 Published 2004 Journal Digestion Section Body Doc Link 15308871 Disease Relevance 0.05 Pain Relevance 0
CONCLUSION: The presence of IP receptors is not essential for acid-induced HCO3- secretion and mucosal defense against acid injury in the duodenum, although activation of IP receptors results in stimulation of HCO3- secretion.
Localization (secretion) of HCO3 in duodenum
3) Confidence 0.41 Published 2004 Journal Digestion Section Body Doc Link 15308871 Disease Relevance 0 Pain Relevance 0
BACKGROUND/AIM: We investigated the role of prostacyclin (PGI2) IP receptors in the acid-induced secretion of HCO3- using IP receptor knockout [IP (-/-)] mice, in comparison with capsaicin-induced secretion.
Localization (secretion) of HCO3 associated with targeted disruption and qutenza
4) Confidence 0.41 Published 2004 Journal Digestion Section Abstract Doc Link 15308871 Disease Relevance 0.10 Pain Relevance 0.17
No role for prostacyclin IP receptors in duodenal HCO3- secretion induced by mucosal acidification in mice--comparison with capsaicin-induced response.
Localization (secretion) of HCO3 associated with qutenza
5) Confidence 0.41 Published 2004 Journal Digestion Section Title Doc Link 15308871 Disease Relevance 0 Pain Relevance 0.29
RESULTS: PGE2 stimulated HCO3- secretion in both WT and IP (-/-) mice, while cicaprost increased it in WT but not IP (-/-) mice.
Localization (secretion) of HCO3
6) Confidence 0.41 Published 2004 Journal Digestion Section Body Doc Link 15308871 Disease Relevance 0.08 Pain Relevance 0
Capsaicin increased duodenal HCO3- secretion in WT mice, in an indomethacin-sensitive manner, yet no such response was observed in the animals lacking IP receptors.
Localization (secretion) of HCO3
7) Confidence 0.41 Published 2004 Journal Digestion Section Body Doc Link 15308871 Disease Relevance 0.06 Pain Relevance 0
Under urethane anesthesia, a proximal duodenal loop was perfused with saline, and the secretion of HCO3- was measured at pH 7.0 using a pH-stat method and by adding 2 mM HCl.
Localization (secretion) of HCO3 in proximal
8) Confidence 0.41 Published 2004 Journal Digestion Section Body Doc Link 15308871 Disease Relevance 0.09 Pain Relevance 0
Although duodenal HCO3- secretion induced by both acid and capsaicin depends on afferent neurons, it seems that the mode of interaction with the afferent neurons differs regarding dependency on the PGI2/IP receptors.


Localization (secretion) of HCO3 in afferent neurons
9) Confidence 0.41 Published 2004 Journal Digestion Section Body Doc Link 15308871 Disease Relevance 0 Pain Relevance 0
Basal HCO3- secretion was diminished significantly (P < 0.01) in CFTR(-/-)vs. normal CFTR(+/+) mice (2.8 +/- 0.5 vs. 5.3 +/- 0.4 micromol x cm(-1) x h(-1)).
Localization (secretion) of HCO3
10) Confidence 0.06 Published 1997 Journal Am. J. Physiol. Section Abstract Doc Link 9142920 Disease Relevance 0.14 Pain Relevance 0.24
Either forskolin (10(-6)-10(-4) M) or carbachol (10(-6)-10(-3) M) was perfused intraluminally to activate adenosine 3',5'-cyclic monophosphate (cAMP)- and Ca2+-mediated HCO3- secretion, respectively.
Localization (secretion) of HCO3 associated with adenocard
11) Confidence 0.06 Published 1997 Journal Am. J. Physiol. Section Abstract Doc Link 9142920 Disease Relevance 0.15 Pain Relevance 0.26
CFTR mediates cAMP- and Ca2+-activated duodenal epithelial HCO3- secretion.
Localization (secretion) of HCO3
12) Confidence 0.06 Published 1997 Journal Am. J. Physiol. Section Title Doc Link 9142920 Disease Relevance 0.19 Pain Relevance 0.25
The aims of this series of experiments were to determine if CFTR mediates basal and stimulated duodenal epithelial HCO3- secretion.
Localization (secretion) of HCO3
13) Confidence 0.06 Published 1997 Journal Am. J. Physiol. Section Abstract Doc Link 9142920 Disease Relevance 0.19 Pain Relevance 0.26
Moreover, in CFTR(-/-) mice, both forskolin- and carbachol-stimulated peak HCO3- secretions were fourfold less compared with those in CFTR(+/+) littermates (3.7 +/- 0.2 vs. 15.6 +/- 2.1 and 4.7 +/- 0.3 vs. 14.2 +/- 2.5 micromol x cm(-1) x h(-1), respectively; P < 0.01).
Localization (secretions) of HCO3 in 14.2
14) Confidence 0.06 Published 1997 Journal Am. J. Physiol. Section Abstract Doc Link 9142920 Disease Relevance 0.13 Pain Relevance 0.22
In contrast, CF jejuna spontaneously secreted neither Cl- nor HCO3-, which may indicate that CF jejuna have a defect in the ability to secrete both of these anions.
Neg (neither) Localization (secreted) of HCO3 associated with fibrosis
15) Confidence 0.03 Published 1995 Journal Am. J. Physiol. Section Abstract Doc Link 7534995 Disease Relevance 0.92 Pain Relevance 0.55
Ion substitution studies revealed basal Isc in normal jejuna to be due primarily to Cl- secretion but these tissues appeared to be capable of HCO3- secretion as well.
Localization (secretion) of HCO3
16) Confidence 0.03 Published 1995 Journal Am. J. Physiol. Section Abstract Doc Link 7534995 Disease Relevance 0.91 Pain Relevance 0.54
Importantly, treatment with the cAMP activity inhibitor rp-cAMPS [(R)-adenosine, cyclic 3',5'-(hydrogenphosphorothioate) triethylammonium] (50 ng/0.5 microl), directly to the VTA, attenuated somatic withdrawal signs to systemic morphine produced by intra-VTA NLX (500 ng/0.5 microl), directly tying enhanced cAMP-driven GABA release to naloxone-precipitated morphine withdrawal in the VTA.
Localization (release) of cAMP-driven associated with ventral tegmentum, gaba, adenocard, narcan, withdrawal and morphine
17) Confidence 0.01 Published 2010 Journal J. Neurosci. Section Abstract Doc Link 20203187 Disease Relevance 0.20 Pain Relevance 1.92

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