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Context Info
Confidence 0.28
First Reported 1985
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 3
Total Number 3
Disease Relevance 1.28
Pain Relevance 0.88

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

extracellular space (CSF2) extracellular region (CSF2)
Anatomy Link Frequency
plasma 2
neutrophil 2
CSF2 (Homo sapiens)
Pain Link Frequency Relevance Heat
Pain 13 99.44 Very High Very High Very High
gABA 86 98.84 Very High Very High Very High
Paresthesia 1 98.16 Very High Very High Very High
spinothalamic tract 1 86.40 High High
local anesthetic 8 81.84 Quite High
Dorsal column 1 54.00 Quite High
analgesia 7 50.00 Quite Low
Central nervous system 17 46.56 Quite Low
Peripheral nervous system 1 9.48 Low Low
central pain 20 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Pain 32 99.44 Very High Very High Very High
Neutrophil Disorders 22 98.90 Very High Very High Very High
Dysesthesia 1 98.16 Very High Very High Very High
Neutropenia 3 97.72 Very High Very High Very High
Disease 7 84.96 Quite High
Agranulocytosis 17 74.40 Quite High
Toxicity 4 50.00 Quite Low
Leukemia 2 17.12 Low Low
Lymphatic System Cancer 7 12.00 Low Low
INFLAMMATION 4 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
It does not increase the beta-endorphin level in CSF.
Neg (not) Positive_regulation (increase) of Negative_regulation (level) of CSF
1) Confidence 0.28 Published 1985 Journal Appl Neurophysiol Section Abstract Doc Link 3939284 Disease Relevance 0.37 Pain Relevance 0.39
In theory, SCN and CN are caused by an accumulation of neutrophil elastase, leading to an inactivation of G-CSF and a negative feedback on granulopoiesis, which causes neutropenia.
Positive_regulation (leading) of Negative_regulation (inactivation) of G-CSF in neutrophil associated with neutropenia and neutrophil disorders
2) Confidence 0.10 Published 2004 Journal BMC Blood Disord Section Body Doc Link PMC535939 Disease Relevance 0.91 Pain Relevance 0
Povl Krogsgaard-Larsen has discussed the potential development of amino acid analogs of GABA that would penetrate the BBB in the non-ionized form and increase drug CSF levels through ion trapping. 25 The decrease in buffer proteins, particularly hemoglobin, the increase in PCO2 from inequality of diffusion, and increased lactic acid production from glycolysis, produce a Gibbs Donnan equilibrium and pH gradient where the pH of CSF is approximately 0.09–0.10 pH units more acidic than the pH of the plasma.26 As a consequence of this pH gradient, ion trapping of selected GABA esters within the CSF likely occurs and is similar to the pH dependent ion trapping of local anesthetics across the placenta of a distressed acidotic fetus (a phenomena well recognized by obstetrical anesthesiologists).27 Also, ion trapping was an important consideration for the development of the proton pump inhibitors, since the highly acidic environment of the gastric parietal cells permitted intracellular trapping of medications like omeprazole.28 Because this trapping effect within the CSF is not well appreciated in the literature and is important for understanding the pharmacokinetics of GABA esters, an example follows: If the pKa value of a hypothetical GABA ester is 10, the pH of the CSF is 7.3 and the pH of plasma 7.4 then this effect may be approximated for comparison between the concentrations of protonated plasma ester [HB+plasma] and protonated CSF ester [HB+csf] as:

Therefore the CSF concentration of protonated GABA ester is approximately 1.26 × the plasma concentration from ion trapping effects secondary to pH differences between plasma and CSF.

Positive_regulation (increase) of Negative_regulation (decrease) of CSF in plasma associated with gaba and local anesthetic
3) Confidence 0.09 Published 2010 Journal Perspect Medicin Chem Section Body Doc Link PMC2918363 Disease Relevance 0 Pain Relevance 0.49

General Comments

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