INT195145

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Context Info
Confidence 0.37
First Reported 2005
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 25
Total Number 27
Disease Relevance 7.20
Pain Relevance 6.59

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

cytosol (CA2) extracellular space (CA2) lyase activity (CA2)
response to stress (CA2) cytoplasm (CA2)
Anatomy Link Frequency
sensory neurons 3
macrophages 2
MCF-7 2
nose 2
blood 2
CA2 (Homo sapiens)
Pain Link Frequency Relevance Heat
Morphine 260 100.00 Very High Very High Very High
agonist 148 99.80 Very High Very High Very High
antagonist 56 99.76 Very High Very High Very High
imagery 37 99.70 Very High Very High Very High
Kinase C 8 99.52 Very High Very High Very High
narcan 40 99.48 Very High Very High Very High
dorsal root ganglion 116 99.32 Very High Very High Very High
conotoxin 14 99.30 Very High Very High Very High
Inflammation 193 98.56 Very High Very High Very High
addiction 27 97.92 Very High Very High Very High
Disease Link Frequency Relevance Heat
Death 51 100.00 Very High Very High Very High
Stress 171 99.64 Very High Very High Very High
Hyperplasia 6 99.60 Very High Very High Very High
Ganglion Cysts 135 99.32 Very High Very High Very High
INFLAMMATION 214 98.56 Very High Very High Very High
Embryonic Lethality 1 98.36 Very High Very High Very High
Cancer 116 97.98 Very High Very High Very High
Bacterial Infection 71 97.36 Very High Very High Very High
Aging 40 97.00 Very High Very High Very High
Starvation 6 96.44 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
This pattern is consistent with an earlier report in which serum inorganic phosphorus levels were found to be higher during the menstrual phase than in the other two phases.[11] The decrease in inorganic phosphorus levels with increased follicular Ca2+/Mg2+ ratios in the luteal phase as compared to the menstrual phase could be due to estrogen as reported earlier.[21] The present study also compares well with an earlier observation that high estrogen production can lead to a decrease in serum inorganic phosphorus levels.[24]

CONCLUSION

Positive_regulation (increased) of Gene_expression (ratios) of Ca2
1) Confidence 0.37 Published 2008 Journal Journal of Human Reproductive Sciences Section Body Doc Link PMC2700668 Disease Relevance 0.55 Pain Relevance 0.40
Further variations include increased expression of Ca2+-dependent protein kinase C isoforms in monocytes when compared to macrophages [56] and also that maturation into macrophages results in slower production of the cytokine, IL-1?
Positive_regulation (increased) of Gene_expression (expression) of Ca2 in macrophages associated with kinase c and cytokine
2) Confidence 0.32 Published 2008 Journal J Inflamm (Lond) Section Body Doc Link PMC2525633 Disease Relevance 0.08 Pain Relevance 0.24
Regulation of chemoattractant-induced NADPH oxidase by Ca2+ influx
Positive_regulation (induced) of Gene_expression (influx) of Ca2
3) Confidence 0.30 Published 2008 Journal J Leukoc Biol Section Body Doc Link PMC2567897 Disease Relevance 0 Pain Relevance 0.05
Interestingly, the present study also found enhanced CFTR and CAII expression in human hyperplasia tissues where inflammation was more prominent.
Positive_regulation (enhanced) of Gene_expression (expression) of CAII associated with inflammation and hyperplasia
4) Confidence 0.26 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2998414 Disease Relevance 1.05 Pain Relevance 0.51
At uniformly high Ca2+ loads, Pcat was activated in all the RBCs of each blood sample but to different extents, with a unimodal pattern of variation.
Positive_regulation (activated) of Gene_expression (loads) of Ca2 in blood
5) Confidence 0.24 Published 2007 Journal Blood Section Body Doc Link PMC1939906 Disease Relevance 0.33 Pain Relevance 0
The range of [Ca2+]i values over which Pcat activation increases in all the RBCs was far above physiological [Ca2+]i levels; at the [Ca2+]s levels of 50 ?
Positive_regulation (increases) of Gene_expression (was) of Ca2
6) Confidence 0.24 Published 2007 Journal Blood Section Body Doc Link PMC1939906 Disease Relevance 0 Pain Relevance 0
The range of [Ca2+]i values over which Pcat activation increases in all the RBCs was far above physiological [Ca2+]i levels; at the [Ca2+]s levels of 50 ?
Positive_regulation (increases) of Gene_expression (was) of Ca2
7) Confidence 0.24 Published 2007 Journal Blood Section Body Doc Link PMC1939906 Disease Relevance 0 Pain Relevance 0
Together with the demonstrated CFTR and CAII upregulation, therefore enhanced prostatic HCO3?
Positive_regulation (demonstrated) of Gene_expression (upregulation) of CAII
8) Confidence 0.23 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2998414 Disease Relevance 0.58 Pain Relevance 0.17
Together with the demonstrated CFTR and CAII upregulation, therefore enhanced prostatic HCO3?
Positive_regulation (enhanced) of Gene_expression (upregulation) of CAII
9) Confidence 0.23 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2998414 Disease Relevance 0.59 Pain Relevance 0.18
During OS, ROS/RNS usually activate Ca2+ channels and repress Ca2+ pumps (Ermak and Davies, 2002), resulting in elevation of [Ca2+]i and initiation of downstream events mentioned above.
Positive_regulation (activate) of Gene_expression (channels) of Ca2 associated with stress
10) Confidence 0.21 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2874397 Disease Relevance 0.61 Pain Relevance 0.04
Fig. 3C showed that after 48 h starvation, stimulation of MCF-7 cells with E2 (10 nM) for 24 h failed to affect both the number of cells responding to Icilin (48/205 in 0FCS vs. 66/299 in 0FCS+E2), and the amplitude of Ca2+ entry induced by Icilin (?
Positive_regulation (by) of Gene_expression (entry) of Ca2 in MCF-7 associated with starvation
11) Confidence 0.21 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2887400 Disease Relevance 0.16 Pain Relevance 0.03
Consistent with this view, the increase in Ca2+ levels in cells transfected with MOR1K was significantly higher than the increases observed in cells transfected with either MOR1 or empty vector, all morphine-dependent Ca2+ increases were sensitive to opioid-receptor blockage with naloxone and MOR1-dependent morphine-evoked increases in Ca2+ were not observed in COS1 cells that do not express endogenous MOR1K (Fig. 1B, 2B).
Positive_regulation (increase) of Gene_expression (levels) of Ca2 associated with narcan, opioid and morphine
12) Confidence 0.16 Published 2010 Journal Mol Pain Section Body Doc Link PMC2894766 Disease Relevance 0.15 Pain Relevance 1.02
A moderate increase in morphine-evoked Ca2+ levels was also observed in Be2C cells transfected with MOR1 or empty vector, however this was likely due to the high endogenous expression of MOR1K in this cell line (Fig.1B).
Positive_regulation (increase) of Gene_expression (levels) of Ca2 associated with morphine
13) Confidence 0.16 Published 2010 Journal Mol Pain Section Body Doc Link PMC2894766 Disease Relevance 0.17 Pain Relevance 0.85
We also tried to repeat these experiments in Ca2+ depleted H441 monolayers, unfortunately, the resistance and current levels post BAPTA_AM exposure were too low to detect due to impaired gap junctions and ion transport (data not shown).


Positive_regulation (experiments) of Gene_expression (depleted) of Ca2
14) Confidence 0.16 Published 2010 Journal Respir Res Section Body Doc Link PMC2889873 Disease Relevance 0.06 Pain Relevance 0
Without Ca2+, the basal secretion of morphine was not significantly changed compared to controls with Ca2+ (14±6 pg/106 neutrophils ±SD, n?
Neg (not) Positive_regulation (changed) of Gene_expression (controls) of Ca2 in neutrophils associated with morphine
15) Confidence 0.14 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2808358 Disease Relevance 0.06 Pain Relevance 0.75
Buytaert, et al. proposed that during PDT with hypericin occurs loss of the native SERCA2 protein levels and consequent endoplasmic reticulum Ca2+ depletion which causes disruption of Ca2+ homeostasis and cell death.
Positive_regulation (causes) of Gene_expression (depletion) of Ca2 in reticulum associated with cancer and death
16) Confidence 0.13 Published 2010 Journal International Journal of Molecular Sciences Section Body Doc Link PMC2852855 Disease Relevance 1.19 Pain Relevance 0
104 fold higher than that (1 nM) inducing TRPV1-dependent Ca2+-cytotoxicity in bona fide DRG sensory neurons [5] and ?
Positive_regulation (inducing) of Gene_expression (dependent) of Ca2 in sensory neurons
17) Confidence 0.13 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2566593 Disease Relevance 0.13 Pain Relevance 0.24
We validated here with different experimental means the previous hypothesis that TRPV1 mRNA expressed both in proliferating and in differentiated keratinocytes as well as in HaCaT cells does not confer agonist-mediated increase in [Ca2+]i and subsequent cell death, analogous to that observed during TRPV1+ sensory neuron depletion.
Positive_regulation (increase) of in sensory neuron Gene_expression (depletion) of Ca2 in keratinocytes associated with agonist and death
18) Confidence 0.13 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2566593 Disease Relevance 0.26 Pain Relevance 0.27
-conotoxin–sensitive) VDCCs that mediate the Ca2+ influx necessary for ?
Positive_regulation (necessary) of Gene_expression (influx) of Ca2 associated with conotoxin
19) Confidence 0.11 Published 2007 Journal PLoS Biology Section Body Doc Link PMC1868042 Disease Relevance 0.07 Pain Relevance 0.23
For determination of [Ca2+]i, neutrophils or FPR transfected HEK293 cells were placed on dishes coated with poly-L-lysine and then loaded with 1 or 2 µM Fura 2/AM (Molecular Probes-Invitrogen) for 30 min at 37°C as previously described [79].
Positive_regulation (transfected) of Gene_expression (transfected) of Ca2 in poly
20) Confidence 0.08 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2657213 Disease Relevance 0 Pain Relevance 0.18

General Comments

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