INT22661

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Context Info
Confidence 0.67
First Reported 1990
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 3
Disease Relevance 1.32
Pain Relevance 0.29

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

cytosol (Aldh3a1) oxidoreductase activity (Aldh3a1) endoplasmic reticulum (Aldh3a1)
cytoplasm (Aldh3a1)
Anatomy Link Frequency
CPA 2
Aldh3a1 (Mus musculus)
Pain Link Frequency Relevance Heat
Enkephalin 2 99.68 Very High Very High Very High
alcohol 3 84.56 Quite High
anesthesia 4 5.00 Very Low Very Low Very Low
ketamine 2 5.00 Very Low Very Low Very Low
isoflurane 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Residual Neoplasm 20 98.68 Very High Very High Very High
Colorectal Cancer 64 97.52 Very High Very High Very High
Sprains And Strains 3 89.20 High High
Cancer 340 88.44 High High
Lung Cancer 2 58.12 Quite High
Solid Tumor 12 48.76 Quite Low
Genetic Translocation 2 44.88 Quite Low
Acute Promyelocytic Leukemia 2 43.08 Quite Low
Disease 16 35.12 Quite Low
Hematologic Neoplasms 2 31.04 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The Leu-enkephalin administration induced T-ALDH from saline control.
Positive_regulation (induced) of ALDH associated with enkephalin
1) Confidence 0.67 Published 1990 Journal Pharmacol. Biochem. Behav. Section Abstract Doc Link 2315366 Disease Relevance 0.25 Pain Relevance 0.29
When considered in conjunction with the 10-fold higher proficiency of ALDH1 versus ALDH3 and SSDH at inactivating CPA intermediates [24], one might interpret these results to suggest that CoCSC resistance to CPA might be predominantly mediated by ALDH1 enzymatic activity.


Positive_regulation (proficiency) of ALDH3 in CPA
2) Confidence 0.47 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2413402 Disease Relevance 0.44 Pain Relevance 0
These observations are supported by qRT-PCR using TG or NTG cells isolated by FACS, which show that ALDH1A1 is the predominant cytoplasmic ALDH enzyme in colorectal tumors and its expression is further increased in residual tumor cells following therapy with CPA; consistent with the phenotypic increase in ALDH+ cells among the CoCSC phenotype.
Positive_regulation (increase) of ALDH in CPA associated with colorectal cancer and residual neoplasm
3) Confidence 0.38 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2413402 Disease Relevance 0.64 Pain Relevance 0

General Comments

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