INT261007

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Context Info
Confidence 0.75
First Reported 2009
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 7
Total Number 12
Disease Relevance 4.25
Pain Relevance 0.06

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

Gclm (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Inflammatory response 7 71.68 Quite High
Inflammation 48 58.24 Quite High
Glutamate 26 5.00 Very Low Very Low Very Low
ischemia 20 5.00 Very Low Very Low Very Low
cytokine 16 5.00 Very Low Very Low Very Low
Dopamine 12 5.00 Very Low Very Low Very Low
anesthesia 11 5.00 Very Low Very Low Very Low
imagery 10 5.00 Very Low Very Low Very Low
Inflammatory mediators 5 5.00 Very Low Very Low Very Low
isoflurane 5 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Pancreatitis 400 98.88 Very High Very High Very High
Coronary Artery Disease 108 98.66 Very High Very High Very High
Neurodegenerative Disease 5 88.32 High High
Targeted Disruption 12 82.76 Quite High
INFLAMMATION 54 71.68 Quite High
Sprains And Strains 40 63.40 Quite High
Stress 92 54.24 Quite High
Colitis 5 53.36 Quite High
Disease 23 45.56 Quite Low
Injury 16 31.52 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Therefore, we speculate that increased microglial expression of Srxn1, Blvrb, and Gclm is also mediated by activation of Nrf2.
Gene_expression (expression) of Gclm
1) Confidence 0.75 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819254 Disease Relevance 0.22 Pain Relevance 0.06
The increase in GCLm mRNA expression was less pronounced in the AP and placebo groups when compared to sham operated animals (3.07 vs.
Gene_expression (expression) of GCLm mRNA associated with pancreatitis
2) Confidence 0.51 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2639703 Disease Relevance 0.44 Pain Relevance 0
Levels of GCLC and GCLM mRNA were quantified using the comparative threshold cycle method, normalized to18S rRNA expression and expressed as ratio to controls (a.u.).


Gene_expression (Levels) of GCLM mRNA
3) Confidence 0.44 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2639703 Disease Relevance 0 Pain Relevance 0
Because GCL is composed of both a catalytic and modulatory subunit [37], the increase in GCL activity in this study could be due to enhanced expression of either GCLm and/or GCLc.
Gene_expression (expression) of GCLm
4) Confidence 0.44 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2639703 Disease Relevance 0.34 Pain Relevance 0
On the other hand, we found enhanced GCL activity and expression of the GCL subunits GCLc and GCLm in probiotic-treated animals leading to a significant increase in GSH contents.
Gene_expression (expression) of GCLm
5) Confidence 0.38 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2639703 Disease Relevance 0.23 Pain Relevance 0
Similarly, levels of GCLm mRNA after probiotic pre-treatment (10.3 (2.56) a.u) were 2.7 fold higher than average values seen in placebo treated rats (3.88 (0.75) a.u).
Gene_expression (levels) of GCLm mRNA
6) Confidence 0.34 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2639703 Disease Relevance 0.35 Pain Relevance 0
However, we did not detect E-cadherin in null-IZ-transfected hormone-producing cells (Fig. 1I).


Gene_expression (producing) of null-IZ
7) Confidence 0.01 Published 2010 Journal Acta Histochemica et Cytochemica Section Body Doc Link PMC2875860 Disease Relevance 0.43 Pain Relevance 0
In contrast, the mean signal intensity of prolactin mRNA signals in rE-cad-IZ-transfected cells did not differ from that of intact cells and null-IZ-transfected cells.


Gene_expression (transfected) of null-IZ associated with coronary artery disease
8) Confidence 0.01 Published 2010 Journal Acta Histochemica et Cytochemica Section Body Doc Link PMC2875860 Disease Relevance 0.46 Pain Relevance 0
In contrast, we detected only N-cadherin in null-IZ-transfected cells (Fig. 1C, 1E, and 1G).
Gene_expression (transfected) of null-IZ
9) Confidence 0.01 Published 2010 Journal Acta Histochemica et Cytochemica Section Body Doc Link PMC2875860 Disease Relevance 0.45 Pain Relevance 0
However, we did not detect E-cadherin in null-IZ-transfected hormone-producing cells (Fig. 1I).


Neg (not) Gene_expression (transfected) of null-IZ
10) Confidence 0.01 Published 2010 Journal Acta Histochemica et Cytochemica Section Body Doc Link PMC2875860 Disease Relevance 0.43 Pain Relevance 0
The mean signal intensity of prolactin protein in rE-cad-IZ-transfected cells was approximately 25% of that of intact cells and null-IZ-transfected cells.
Gene_expression (transfected) of null-IZ associated with coronary artery disease
11) Confidence 0.01 Published 2010 Journal Acta Histochemica et Cytochemica Section Body Doc Link PMC2875860 Disease Relevance 0.47 Pain Relevance 0
In null-IZ-transfected cells (indicated by the arrowheads in Fig. 2), prolactin immunoreactivity and mRNA signals (Fig. 2C, 2E and 2G) were identical to those detected in intact cells.
Gene_expression (transfected) of null-IZ
12) Confidence 0.01 Published 2010 Journal Acta Histochemica et Cytochemica Section Body Doc Link PMC2875860 Disease Relevance 0.41 Pain Relevance 0

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