INT32852

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Context Info
Confidence 0.57
First Reported 1985
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 18
Total Number 19
Disease Relevance 10.59
Pain Relevance 3.08

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

generation of precursor metabolites and energy (FECH) mitochondrion (FECH) small molecule metabolic process (FECH)
Anatomy Link Frequency
bone marrow 1
FECH (Homo sapiens)
Pain Link Frequency Relevance Heat
tetrodotoxin 2 99.76 Very High Very High Very High
Pain 288 99.44 Very High Very High Very High
Osteoarthritis 56 94.08 High High
anesthesia 1 91.52 High High
isoflurane 6 76.56 Quite High
Calcium channel 2 63.40 Quite High
Chronic low back pain 2 59.44 Quite High
pruritus 1 57.20 Quite High
abdominal pain 1 53.12 Quite High
burning pain 2 44.84 Quite Low
Disease Link Frequency Relevance Heat
Erythropoietic Protoporphyria 312 100.00 Very High Very High Very High
Porphyria 52 99.78 Very High Very High Very High
Pain 239 99.44 Very High Very High Very High
Liver Failure 8 98.48 Very High Very High Very High
Blister 12 98.06 Very High Very High Very High
Anaemia 39 97.84 Very High Very High Very High
Sunburn 98 96.56 Very High Very High Very High
Pressure And Volume Under Development 20 95.80 Very High Very High Very High
Erythema 7 95.40 Very High Very High Very High
Low Back Pain 58 94.84 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Tetrodotoxin reversibly blocked the stimulus evoked EpP but hardly influenced the amplitude-frequency histogram of spontaneous EpPs in 10(-8)-10(-6) M concentration.
Negative_regulation (blocked) of EpP associated with tetrodotoxin
1) Confidence 0.57 Published 1985 Journal Acta Physiol Hung Section Abstract Doc Link 2986414 Disease Relevance 0 Pain Relevance 0.10
In addition, as the basic enzymatic defect in EPP is at the level of the bone marrow stem cells, which are the target cells of choice in the development of retroviral-mediated gene transfer, definitive treatment of EPP by gene therapy is a distinct hope for the future.
Negative_regulation (defect) of EPP in bone marrow associated with erythropoietic protoporphyria
2) Confidence 0.55 Published 1994 Journal Br. J. Dermatol. Section Abstract Doc Link 7857832 Disease Relevance 0.78 Pain Relevance 0.05
In EPP, deficient ferrochelatase activity leads to the excessive production and biliary excretion of protoporphyrin (PP).
Negative_regulation (deficient) of ferrochelatase associated with erythropoietic protoporphyria
3) Confidence 0.53 Published 2010 Journal Korean J Hepatol Section Abstract Doc Link 20375647 Disease Relevance 1.26 Pain Relevance 0.05
It represents an inherited disorder of heme metabolism that is due to a reduced ferrochelatase enzyme activity.
Negative_regulation (reduced) of ferrochelatase associated with porphyria
4) Confidence 0.44 Published 2010 Journal Photodermatol Photoimmunol Photomed Section Abstract Doc Link 20070832 Disease Relevance 0.74 Pain Relevance 0.09
Erythropoietic protoporphyria (EPP, MIM 177000) is an inherited disorder caused by a partial deficiency of ferrochelatase (FECH) which catalyses the chelation of iron into protoporphyrin to form haem.
Spec (partial) Negative_regulation (deficiency) of ferrochelatase associated with erythropoietic protoporphyria
5) Confidence 0.43 Published 2000 Journal Eur. J. Pediatr. Section Abstract Doc Link 11039124 Disease Relevance 0.26 Pain Relevance 0.09
Erythropoietic Protoporphyria (EPP) is an inherited deficiency of ferrochelatase, the last enzyme of the heme pathway.
Negative_regulation (deficiency) of EPP associated with erythropoietic protoporphyria
6) Confidence 0.42 Published 2009 Journal Cell. Mol. Biol. (Noisy-le-grand) Section Abstract Doc Link 19268000 Disease Relevance 0.52 Pain Relevance 0.20
Erythropoietic protoporphyria (EPP) is an inherited inborn error of porphyrin metabolism caused by decreased activity of the enzyme ferrochelatase, the terminal enzyme of the haem biosynthetic pathway, which catalyses the insertion of iron into protoporphyrin to form haem.
Negative_regulation (decreased) of ferrochelatase associated with erythropoietic protoporphyria
7) Confidence 0.40 Published 1994 Journal Br. J. Dermatol. Section Abstract Doc Link 7857832 Disease Relevance 0.52 Pain Relevance 0
S cluster biogenesis severely diminishes FECH protein levels (69), there might be some cases of EPP in human patients caused by deficient Fe?
Negative_regulation (diminishes) of FECH associated with erythropoietic protoporphyria
8) Confidence 0.39 Published 2010 Journal Biochemistry Section Body Doc Link PMC2885827 Disease Relevance 0.71 Pain Relevance 0.10
Erythropoietic protoporphyria (EPP) is an inherited disorder of haem biosynthesis caused by decreased activity of the enzyme ferrochelatase (FECH), which catalyses the insertion of iron into protoporphyrin, the last step in haem biosynthesis.
Negative_regulation (decreased) of enzyme ferrochelatase associated with porphyria and erythropoietic protoporphyria
9) Confidence 0.37 Published 2007 Journal Br. J. Dermatol. Section Abstract Doc Link 17711525 Disease Relevance 0.74 Pain Relevance 0.09
Because most subjects reported their maximum pain intensity on the first day following the FCE, Table 3 reflects the status 24 h following the FCE.
Negative_regulation (following) of FCE associated with pain
10) Confidence 0.34 Published 2008 Journal J Occup Rehabil Section Body Doc Link PMC2522381 Disease Relevance 1.15 Pain Relevance 1.15
The normative data in the current study is therefore additional to the question whether the FCE can be administered safely.
Negative_regulation (administered) of FCE
11) Confidence 0.34 Published 2008 Journal J Occup Rehabil Section Body Doc Link PMC2522381 Disease Relevance 0.78 Pain Relevance 0.78
Erythropoietic protoporphyria is an autosomal dominant or autosomal recessive photodermatosis characterized by a deficiency of the enzyme ferrochelatase.
Negative_regulation (deficiency) of ferrochelatase associated with erythropoietic protoporphyria
12) Confidence 0.32 Published 1995 Journal Dermatology (Basel) Section Abstract Doc Link 7655119 Disease Relevance 0.36 Pain Relevance 0.09
Thus, it appears that the contribution of SE to the prediction of FCE performances is moderate at best (in one instance), but insignificant in most instances.
Negative_regulation (prediction) of FCE
13) Confidence 0.31 Published 2008 Journal J Occup Rehabil Section Body Doc Link PMC2668547 Disease Relevance 0.07 Pain Relevance 0.07
Our study indicates a potential preventive use of FCE.
Negative_regulation (preventive) of FCE
14) Confidence 0.29 Published 2010 Journal Int Arch Occup Environ Health Section Body Doc Link PMC2980625 Disease Relevance 0.23 Pain Relevance 0.09
Erythropoietic protoporphyria (EPP) is a painful photodermatosis without blisters caused by inborn errors of the haem biosynthetic pathway due, in the majority of patients, to a deficient activity of the enzyme ferrochelatase (ferrohaemprotolyase, haem synthetase, ferrohaem-protolyase, EC4.99.1.1, FECH (EPP), (MIM 177000) or caused, in about 2% of patients, by a gain of activity of the erythroid specific aminolevulinic acid synthase 2 (ALAS; EC 2.3.1.27).
Negative_regulation (deficient) of EPP associated with pain, erythropoietic protoporphyria and blister
15) Confidence 0.08 Published 2009 Journal Orphanet J Rare Dis Section Body Doc Link PMC2747912 Disease Relevance 0.75 Pain Relevance 0.10
FECH deficiency in EPP appears to lead to a steady state in which decreased erythropoiesis is matched by reduced iron absorption and supply.
Negative_regulation (deficiency) of EPP associated with erythropoietic protoporphyria
16) Confidence 0.07 Published 2009 Journal Orphanet J Rare Dis Section Body Doc Link PMC2747912 Disease Relevance 0.56 Pain Relevance 0
Erythropoiesis was impaired in most patients with dominant EPP from UK and France [18,19].
Negative_regulation (impaired) of EPP associated with erythropoietic protoporphyria
17) Confidence 0.07 Published 2009 Journal Orphanet J Rare Dis Section Body Doc Link PMC2747912 Disease Relevance 0.64 Pain Relevance 0
It has been reported that certain types of neoplastic cells have not only reduced ferrochelatase activity, but also enhanced porphobilinogen deaminase (PBGD) activity.3,9,26 Low ferrochelatase activity may be of lesser important to deficiencies in mitochondrial energy generation because tumour cells typically have low activities of mitochondrial cytochrome oxidase and utilise glycolysis rather than oxidative phosphorylation.17 In addition, certain malignant cells have low iron stores, a characteristic of proliferating cells, leading both to increased expression of transferrin receptors and, importantly, to decreased conversion of PpIX into haem.27,28 Porphobilinogen deaminase is considered to have the lowest activity in the haem biosynthetic pathway29,30 and the reason for its up-regulation in certain tumour cells has not yet been elucidated.9 It is generally considered to be rate-limiting in the ALA-induced synthesis of PpIX in neoplastic cells.31 Notwithstanding this, other reports have failed to find a clear relationship connection between high PBGD and/or low ferrochelatase activity and PpIX accumulation.32–34

Clinical administration of ALA

Negative_regulation (reduced) of ferrochelatase associated with malignant neoplastic disease and cancer
18) Confidence 0.03 Published 2007 Journal Perspectives in Medicinal Chemistry Section Body Doc Link PMC2754918 Disease Relevance 0.53 Pain Relevance 0
Both of these postsynaptic changes would be likely to lead to the prolongation of the falling phase of the EPP.
Negative_regulation (prolongation) of EPP
19) Confidence 0.02 Published 2008 Journal The Journal of Physiology Section Body Doc Link PMC2538785 Disease Relevance 0 Pain Relevance 0.03

General Comments

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