INT38253

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Context Info
Confidence 0.63
First Reported 1986
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 35
Total Number 35
Disease Relevance 10.28
Pain Relevance 15.42

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

nucleolus (Trib3) nucleus (Trib3) enzyme binding (Trib3)
kinase activity (Trib3)
Anatomy Link Frequency
heart 5
plasma 3
dorsal root ganglion 3
vas deferens 2
afferent neurons 2
Trib3 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Kinase C 313 100.00 Very High Very High Very High
substance P 292 99.92 Very High Very High Very High
Calcitonin gene-related peptide 106 99.88 Very High Very High Very High
dorsal root ganglion 123 99.76 Very High Very High Very High
qutenza 52 99.74 Very High Very High Very High
Spinal cord 9 99.48 Very High Very High Very High
noradrenaline 18 99.08 Very High Very High Very High
Pain 5 98.76 Very High Very High Very High
ischemia 55 98.68 Very High Very High Very High
Inflammatory response 5 97.92 Very High Very High Very High
Disease Link Frequency Relevance Heat
Apoptosis 70 100.00 Very High Very High Very High
Heat Stress Disorders 5 99.84 Very High Very High Very High
Stress 9 99.82 Very High Very High Very High
Contracture 2 99.52 Very High Very High Very High
Phenylketonuria 1 99.40 Very High Very High Very High
Ganglion Cysts 125 99.28 Very High Very High Very High
Injury 37 99.12 Very High Very High Very High
Pain 5 98.76 Very High Very High Very High
Cv Unclassified Under Development 41 98.68 Very High Very High Very High
Cancer 10 98.08 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These results suggest that lead inhibits creatine kinase and pyruvate kinase activity by interaction with their thiol groups.
Localization (creatine) of kinase
1) Confidence 0.63 Published 2010 Journal Toxicol In Vitro Section Abstract Doc Link 19925858 Disease Relevance 0.19 Pain Relevance 0.09
Marcain, when added to the incubation medium, produced a large contracture and markedly increased release of creatine kinase.
Localization (release) of kinase associated with contracture
2) Confidence 0.53 Published 1986 Journal Nippon Seikeigeka Gakkai Zasshi Section Abstract Doc Link 3722966 Disease Relevance 0.27 Pain Relevance 0.07
In this study we investigated the in vitro effects of phenylalanine, the main metabolite known to accumulate in phenylketonuria, and/or alanine, on pyruvate kinase activity, glucose utilization, lactate release, and ADP concentration in brain cortex homogenates from 30-day-old Wistar rats.
Localization (release) of kinase in brain associated with phenylketonuria
3) Confidence 0.48 Published 2003 Journal Metab Brain Dis Section Abstract Doc Link 12603085 Disease Relevance 0.10 Pain Relevance 0
Pretreatment with rutaecarpine (100 or 300 microg/kg, i.v.) significantly reduced infarct size and creatine kinase release concomitantly with a significant increase in plasma concentrations of CGRP.
Localization (release) of kinase in plasma
4) Confidence 0.26 Published 2003 Journal Regul. Pept. Section Abstract Doc Link 12763639 Disease Relevance 0.29 Pain Relevance 0.49
The effects of agents that modulate intracellular release of calcium and protein kinase C (PKC) activation on noradrenaline (NA)-induced contractions of epididymal vas deferens in calcium-free/EGTA (1 mM) medium were investigated.
Localization (release) of kinase in vas deferens associated with kinase c and noradrenaline
5) Confidence 0.18 Published 1999 Journal Life Sci. Section Abstract Doc Link 10416820 Disease Relevance 0 Pain Relevance 0.48
Pharmacomechanical coupling in rat vas deferens: effects of agents that modulate intracellular release of calcium and protein kinase C activation.
Localization (release) of kinase in vas deferens associated with kinase c
6) Confidence 0.18 Published 1999 Journal Life Sci. Section Title Doc Link 10416820 Disease Relevance 0 Pain Relevance 0.61
Thirty minutes of global ischemia and 30 min of reperfusion caused a significant impairment of cardiac contractile function and an increased release of creatine kinase.
Localization (release) of kinase associated with ischemia
7) Confidence 0.16 Published 1999 Journal Eur. J. Pharmacol. Section Abstract Doc Link 10206178 Disease Relevance 0.10 Pain Relevance 0.46
Pretreatment with nitroglycerin at the concentration of 3x10(-7) or 10(-6) M for 5 min produced a significant improvement of cardiac function and a decrease in the release of creatine kinase.
Localization (release) of kinase
8) Confidence 0.16 Published 1999 Journal Eur. J. Pharmacol. Section Abstract Doc Link 10206178 Disease Relevance 0.09 Pain Relevance 0.55
Contractile dysfunction was associated with increases in tissue Na+ and Ca2+ levels, decreases in K+ and Mg2+ levels, and release of creatine kinase and purine nucleosides and bases (ATP metabolites) from the heart.
Localization (release) of kinase in heart
9) Confidence 0.14 Published 1995 Journal Eur. J. Pharmacol. Section Abstract Doc Link 7713159 Disease Relevance 0.39 Pain Relevance 0.72
Treatment of the perfused heart with either 10-100 microM of either mexiletine or lidocaine during pre-ischemia resulted in an enhancement of post-ischemic contractile recovery, a suppression of changes in tissue Na+, K+, Ca2+ and Mg2+ contents and an attenuation of the release of creatine kinase and ATP metabolites in an almost concentration-dependent manner.
Localization (release) of kinase in heart associated with ischemia, mexiletine and lidocaine
10) Confidence 0.14 Published 1995 Journal Eur. J. Pharmacol. Section Abstract Doc Link 7713159 Disease Relevance 0.39 Pain Relevance 0.68
Hypothermic ischemia for 4 h caused a decline in cardiac function, and an increase in the release of creatine kinase and in the content of TNF-alpha.
Localization (release) of kinase associated with ischemia
11) Confidence 0.13 Published 2001 Journal Eur. J. Pharmacol. Section Abstract Doc Link 11408036 Disease Relevance 0.26 Pain Relevance 0.40
Heart rate, coronary flow, left-ventricular pressure, and its first derivatives (+/-dp/dt(max)) were recorded, and plasma levels of NO and CGRP, the release of creatine kinase in coronary effluent and the content of TNF-alpha in myocardial tissues were measured.
Localization (release) of kinase in plasma associated with calcitonin gene-related peptide
12) Confidence 0.13 Published 2001 Journal Eur. J. Pharmacol. Section Abstract Doc Link 11408036 Disease Relevance 0.27 Pain Relevance 0.28
Pretreatment with monophosphoryl lipid A (500 microg/kg, i.p.) for 24 h improved the recovery of cardiac function and reduced the release of creatine kinase concomitantly with a decrease in the content of cardiac TNF-alpha.
Localization (release) of kinase
13) Confidence 0.13 Published 2001 Journal Eur. J. Pharmacol. Section Abstract Doc Link 11408036 Disease Relevance 0.24 Pain Relevance 0.42
Heart preparations from lean and obese Zucker rats treated with saline, subjected to low flow ischemia and reperfusion, showed at reperfusion: a) a low recovery of postischemic left ventricular developed pressure (LVDP), coupled to a substantial increase in coronary perfusion pressure, and b) a marked increase in creatine kinase released in the perfusates.
Localization (released) of kinase in Heart associated with ischemia and obesity
14) Confidence 0.11 Published 2000 Journal J. Endocrinol. Section Abstract Doc Link 10974647 Disease Relevance 0.94 Pain Relevance 0.05
However, ischemic preconditioning (three cycles of 5-min ischemia and 5-min reperfusion) or pretreatment with CGRP for 5 min dramatically improved the recovery of cardiac function, and reduced the release of cardiac creatine kinase and the TNF-alpha content.
Localization (release) of kinase associated with ischemia and calcitonin gene-related peptide
15) Confidence 0.11 Published 2000 Journal Eur. J. Pharmacol. Section Abstract Doc Link 11068026 Disease Relevance 0.51 Pain Relevance 0.62
Sixty minutes of left coronary artery occlusion and followed by 60 min of reperfusion caused a significant decrease in cardiac function and a significant increase in creatine kinase (CK) release and infarct size.
Localization (release) of kinase in left coronary artery
16) Confidence 0.11 Published 2008 Journal Regul. Pept. Section Abstract Doc Link 18166234 Disease Relevance 0.09 Pain Relevance 0.48
Thirty minutes of global ischemia and 40 min of reperfusion caused a dramatic decrease in myocardial function, and a significant increase in the release of cardiac creatine kinase in the coronary effluent and in the content of tumor necrosis factor-alpha (TNF-alpha) in myocardial tissues.
Localization (release) of kinase associated with necrosis, cancer and ischemia
17) Confidence 0.11 Published 2000 Journal Eur. J. Pharmacol. Section Abstract Doc Link 11068026 Disease Relevance 0.53 Pain Relevance 0.49
Reperfusion after 4 h of hypothermic ischemia caused a decline of cardiac function and an increase of creatine kinase (CK) release.
Localization (release) of kinase associated with ischemia
18) Confidence 0.11 Published 1999 Journal Regul. Pept. Section Abstract Doc Link 10100927 Disease Relevance 0.53 Pain Relevance 0.44
With combined pretreatment, early postischemic creatine kinase release was lower than control in hearts without pretreatment (0.48 +/- 0.11 vs 0.80 +/- 0.12 IU/5 minutes per heart; P =.001).
Localization (release) of kinase in hearts
19) Confidence 0.11 Published 2001 Journal J. Thorac. Cardiovasc. Surg. Section Body Doc Link 11689805 Disease Relevance 0 Pain Relevance 0
Pretreatment with preconditioning significantly reduced infarct size and the release of creatine kinase during reperfusion, and caused a significant increase in the expression of CGRP mRNA, concomitantly with an elevation in the plasma level of CGRP and NO.
Localization (release) of kinase in plasma associated with calcitonin gene-related peptide
20) Confidence 0.10 Published 2004 Journal Eur. J. Pharmacol. Section Abstract Doc Link 15464099 Disease Relevance 0.43 Pain Relevance 0.69

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