INT70801

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Context Info
Confidence 0.42
First Reported 1997
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 12
Total Number 14
Disease Relevance 3.08
Pain Relevance 4.10

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

oxidoreductase activity (Hmgcr) aging (Hmgcr) endoplasmic reticulum (Hmgcr)
embryo development (Hmgcr)
Anatomy Link Frequency
liver 4
plasma 1
brain 1
bowel 1
urine 1
Hmgcr (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Morphine 32 98.70 Very High Very High Very High
Inflammation 23 98.34 Very High Very High Very High
opiate 12 95.48 Very High Very High Very High
imagery 6 94.20 High High
withdrawal 6 91.52 High High
narcan 6 90.56 High High
Neurotransmitter 1 81.52 Quite High
Serotonin 2 81.04 Quite High
Nicotine 2 78.48 Quite High
addiction 6 75.00 Quite High
Disease Link Frequency Relevance Heat
Inflammatory Bowel Disease 9 98.62 Very High Very High Very High
Hepatocellular Cancer 3 93.76 High High
Disorder Of Lipid Metabolism 216 91.40 High High
Ileitis 1 79.24 Quite High
Morphine Dependence 6 75.00 Quite High
Increased Venous Pressure Under Development 6 74.76 Quite High
Diabetes Mellitus 36 69.36 Quite High
Hypertension 21 68.84 Quite High
Dyslipidemia /

Combined Dyslipidemia

48 65.08 Quite High
Body Weight 12 62.48 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Nor does mevalonate, the direct product of HMG-CoA reductase, affect the stimulated release by 50 ?
Gene_expression (product) of HMG-CoA reductase
1) Confidence 0.42 Published 2003 Journal Lipids Health Dis Section Body Doc Link PMC153527 Disease Relevance 0 Pain Relevance 0
Morphine was present in plasma, urine, and brain at 24 and 48 h, whereas M3G was detected in plasma and urine only.
Gene_expression (detected) of M3G in plasma associated with morphine
2) Confidence 0.37 Published 1997 Journal Pharmacol. Biochem. Behav. Section Abstract Doc Link 9259009 Disease Relevance 0.13 Pain Relevance 1.13
Figure 2 presented that the gene expression of HMG-CoA reductase, the key enzyme of cholesterol synthesis, suppressed significantly in the cholesterol-fed rats as compared with the control rats, which suggested that the hepatic cholesterol biosynthesis was inhibited by the high dietary cholesterol.
Gene_expression (expression) of HMG-CoA reductase associated with disorder of lipid metabolism
3) Confidence 0.36 Published 2010 Journal Lipids Health Dis Section Body Doc Link PMC2820024 Disease Relevance 0.21 Pain Relevance 0.04
With regard to the cholesterol homeostasis, the activity of phosphatidate phophatase (PAP) and the mRNA expression of HMG-CoA reductase, acyl-CoA: cholesterol acyltransferase (ACAT) and cholesterol 7?
Gene_expression (expression) of HMG-CoA reductase
4) Confidence 0.36 Published 2010 Journal Lipids Health Dis Section Body Doc Link PMC2820024 Disease Relevance 0.19 Pain Relevance 0
Assays-on-Demand, Gene Expression Products [Mm00662319_m1 for FAS, Mm00486279_m1 for ACAT, and Hs99999901_s1 for 18SRNA, Applied Biosystems, Tokyo, Japan) and TaqMan MGB Gene Expression Kits for HMG-CoA reductase (forward primer,5'-AGTGATTGTGTCAGTATTATTGTGGAAG-3';reverse primer,5'-GGTA CTGGCTGAAAAGTCACAAGAG-3'; and TaqMan MGB probe, 5'-FAM-TTGCTGTTGTATGTAAAG\T-MGB-3') were used for the quantitative real-time reverse transcribed polymerase chain reaction(RT-PCR) analysis of FAS, ACAT, 18SRNA, and HMG-CoA reductase expression in the liver.
Gene_expression (expression) of HMG-CoA reductase in liver
5) Confidence 0.36 Published 2010 Journal Lipids Health Dis Section Body Doc Link PMC2820024 Disease Relevance 0 Pain Relevance 0
Mevalonate, the product of HMG-CoA reductase, did not reduce the stimulation observed in the presence of simvastatin indicating that HMG-CoA reductase activity is not involved.
Gene_expression (product) of HMG-CoA reductase
6) Confidence 0.32 Published 2003 Journal Lipids Health Dis Section Abstract Doc Link PMC153527 Disease Relevance 0.07 Pain Relevance 0
Mevalonate, the product of HMG-CoA reductase, does not suppress simvastatin's stimulated AA release.
Gene_expression (product) of HMG-CoA reductase
7) Confidence 0.32 Published 2003 Journal Lipids Health Dis Section Body Doc Link PMC153527 Disease Relevance 0 Pain Relevance 0
Morphine was present in plasma, urine, and brain at 24 and 48 h, whereas M3G was detected in plasma and urine only.
Gene_expression (detected) of M3G in urine associated with morphine
8) Confidence 0.13 Published 1997 Journal Pharmacol. Biochem. Behav. Section Abstract Doc Link 9259009 Disease Relevance 0.13 Pain Relevance 1.13
Morphine was present in plasma, urine, and brain at 24 and 48 h, whereas M3G was detected in plasma and urine only.
Gene_expression (detected) of M3G in brain associated with morphine
9) Confidence 0.13 Published 1997 Journal Pharmacol. Biochem. Behav. Section Abstract Doc Link 9259009 Disease Relevance 0.13 Pain Relevance 1.13
In one study, the IC50 of pitavastatin for HMG-CoA reductase inhibition in rat liver microsomes was 6.8 nM, being 2.4-fold higher than that of simvastatin and 6.8-fold higher than that of pravastatin.13 Pitavastatin inhibits HMG-CoA reductase and synthesis of cholesterol in the liver like other statins, however, the IC50 for the inhibition of cholesterol synthesis from [14C] acetic acid in the cultured human hepatoma cell line HepG2 was found to be 5.8 nM, being 2.9-fold higher than that of simvastatin and 5.7-fold higher than that of atorvastatin.14 Since these results might simply indicate stronger inhibition of HMG-CoA reductase by pitavastatin, the effects of the drugs on induction of the LDL receptor was compared at the standardized concentration determined by the inhibitory action of the drugs on cholesterol synthesis.
Gene_expression (synthesis) of HMG-CoA reductase in liver associated with hepatocellular cancer
10) Confidence 0.09 Published 2009 Journal Vascular Health and Risk Management Section Body Doc Link PMC2788597 Disease Relevance 0.38 Pain Relevance 0.04
In one study, the IC50 of pitavastatin for HMG-CoA reductase inhibition in rat liver microsomes was 6.8 nM, being 2.4-fold higher than that of simvastatin and 6.8-fold higher than that of pravastatin.13 Pitavastatin inhibits HMG-CoA reductase and synthesis of cholesterol in the liver like other statins, however, the IC50 for the inhibition of cholesterol synthesis from [14C] acetic acid in the cultured human hepatoma cell line HepG2 was found to be 5.8 nM, being 2.9-fold higher than that of simvastatin and 5.7-fold higher than that of atorvastatin.14 Since these results might simply indicate stronger inhibition of HMG-CoA reductase by pitavastatin, the effects of the drugs on induction of the LDL receptor was compared at the standardized concentration determined by the inhibitory action of the drugs on cholesterol synthesis.
Gene_expression (inhibition) of HMG-CoA reductase in liver associated with hepatocellular cancer
11) Confidence 0.09 Published 2009 Journal Vascular Health and Risk Management Section Body Doc Link PMC2788597 Disease Relevance 0.46 Pain Relevance 0.05
In one study, the IC50 of pitavastatin for HMG-CoA reductase inhibition in rat liver microsomes was 6.8 nM, being 2.4-fold higher than that of simvastatin and 6.8-fold higher than that of pravastatin.13 Pitavastatin inhibits HMG-CoA reductase and synthesis of cholesterol in the liver like other statins, however, the IC50 for the inhibition of cholesterol synthesis from [14C] acetic acid in the cultured human hepatoma cell line HepG2 was found to be 5.8 nM, being 2.9-fold higher than that of simvastatin and 5.7-fold higher than that of atorvastatin.14 Since these results might simply indicate stronger inhibition of HMG-CoA reductase by pitavastatin, the effects of the drugs on induction of the LDL receptor was compared at the standardized concentration determined by the inhibitory action of the drugs on cholesterol synthesis.
Neg (inhibits) Gene_expression (inhibits) of HMG-CoA reductase in liver associated with hepatocellular cancer
12) Confidence 0.09 Published 2009 Journal Vascular Health and Risk Management Section Body Doc Link PMC2788597 Disease Relevance 0.38 Pain Relevance 0.04
The following parameters were measured in patients with inflammatory bowel disease and in individuals with differing hemispheric dominance: (1) plasma HMG CoA reductase, digoxin, dolichol, ubiquinone, and magnesium levels; (2) tryptophan/tyrosine catabolic patterns; (3) free-radical metabolism; (4) glycoconjugate metabolism; and (5) membrane composition and RBC membrane Na+-K+ ATPase activity.
Gene_expression (metabolism) of HMG CoA reductase in bowel associated with inflammation
13) Confidence 0.09 Published 2003 Journal Int. J. Neurosci. Section Abstract Doc Link 12959741 Disease Relevance 0.64 Pain Relevance 0.28
HMG CoA reductase activity, serum digoxin, RBC membrane Na(+)-K+ ATPase activity, serum magnesium, and tyrosine/tryptophan catabolic patterns were assessed in spiritual/atheistic individuals and in those differing hemispheric dominance.
Gene_expression (assessed) of HMG CoA reductase
14) Confidence 0.05 Published 2003 Journal Int. J. Neurosci. Section Abstract Doc Link 12803140 Disease Relevance 0 Pain Relevance 0.25

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