INT160210

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Context Info
Confidence 0.36
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 7
Total Number 7
Disease Relevance 3.96
Pain Relevance 0.27

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

Anatomy Link Frequency
skeletal muscle 2
ras (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 59 100.00 Very High Very High Very High
cINOD 2 50.00 Quite Low
beta blocker 11 28.48 Quite Low
Calcium channel 12 24.36 Low Low
cva 4 13.16 Low Low
headache 11 10.16 Low Low
antagonist 50 5.00 Very Low Very Low Very Low
tolerance 6 5.00 Very Low Very Low Very Low
Onset of action 6 5.00 Very Low Very Low Very Low
Bioavailability 5 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Vasculitis 17 100.00 Very High Very High Very High
INFLAMMATION 49 95.52 Very High Very High Very High
Inflammatory Breast Neoplasms 1 94.80 High High
Increased Venous Pressure Under Development 10 93.52 High High
Acute Coronary Syndrome 1 93.16 High High
Breast Cancer 46 93.12 High High
Metastasis 9 92.44 High High
Pressure And Volume Under Development 21 91.60 High High
Insulin Resistance 8 90.60 High High
Adhesions 6 88.84 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Another potential cause of reduced insulin sensitivity through RAS activation may be a result of vasoconstrictive effects, thereby reducing blood flow to skeletal muscle (Furuhashi et al 2003).
Negative_regulation (reduced) of Gene_expression (activation) of RAS in skeletal muscle
1) Confidence 0.36 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2350139 Disease Relevance 1.07 Pain Relevance 0.03
Several compounds in preclinical and clinical trials have targeted various stages of the Ras signaling cascade, including inhibition of Ras expression via antisense oligo-deoxynucleotides, interference via farnesyltransferase inhibitors, and inhibition of Ras downstream effectors via MEK, PI3K inhibitors, and others.
Negative_regulation (inhibition) of Gene_expression (expression) of Ras
2) Confidence 0.18 Published 2010 Journal Breast Cancer Res Section Body Doc Link PMC2972555 Disease Relevance 0.90 Pain Relevance 0.05
CONCLUSIONS: The prescribing of H(2)RAs decreased, whereas the prescribing of PPIs increased, between 1997 and 2006 in this population of concession beneficiaries in Australia.
Negative_regulation (decreased) of Gene_expression (prescribing) of RAs
3) Confidence 0.15 Published 2009 Journal Clin Ther Section Body Doc Link 19446158 Disease Relevance 0 Pain Relevance 0
Reducing vascular inflammation via antagonism of the RAS
Negative_regulation (Reducing) of Gene_expression (antagonism) of RAS associated with inflammation and vasculitis
4) Confidence 0.12 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2350124 Disease Relevance 1.00 Pain Relevance 0.19
Blockade of the RAS in such high-renin conditions prevents the angiotensin II-dependent BP maintenance (Brunner et al 1988) and thus enhances the effect of the diuretic (Neutel et al 1999b).
Negative_regulation (Blockade) of Gene_expression (conditions) of RAS
5) Confidence 0.04 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2293961 Disease Relevance 0.18 Pain Relevance 0
Recent studies show that olmesartan medoxomil produces almost complete 24 h blockade of the RAS.
Negative_regulation (blockade) of Gene_expression (produces) of RAS
6) Confidence 0.03 Published 2006 Journal Vascular Health and Risk Management Section Body Doc Link PMC1994016 Disease Relevance 0.52 Pain Relevance 0
This shows that using a higher dose of olmesartan medoxomil can produce an almost complete 24 h RAS blockade.
Negative_regulation (blockade) of Gene_expression (produce) of RAS
7) Confidence 0.03 Published 2006 Journal Vascular Health and Risk Management Section Body Doc Link PMC1994016 Disease Relevance 0.21 Pain Relevance 0

General Comments

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