INT275993

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Context Info
Confidence 0.36
First Reported 2009
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 2
Disease Relevance 0.53
Pain Relevance 0.03

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

signal transduction (Pde1b) nucleus (Pde1b) cytoplasm (Pde1b)
Pde1b (Mus musculus)
Pain Link Frequency Relevance Heat
Bioavailability 1 50.24 Quite High
gABA 11 5.00 Very Low Very Low Very Low
depression 9 5.00 Very Low Very Low Very Low
imagery 5 5.00 Very Low Very Low Very Low
long-term potentiation 4 5.00 Very Low Very Low Very Low
headache 3 5.00 Very Low Very Low Very Low
Central nervous system 2 5.00 Very Low Very Low Very Low
cva 2 5.00 Very Low Very Low Very Low
Calcium channel 2 5.00 Very Low Very Low Very Low
antagonist 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Pulmonary Hypertension 66 99.40 Very High Very High Very High
Disease 17 96.16 Very High Very High Very High
Apoptosis 2 77.52 Quite High
Hypoxia 4 45.32 Quite Low
Renal Insufficiency 1 25.28 Quite Low
Cirrhosis 1 12.48 Low Low
Increased Venous Pressure Under Development 5 6.36 Low Low
Cv General 4 Under Development 22 5.00 Very Low Very Low Very Low
Depression 9 5.00 Very Low Very Low Very Low
Hypertension 6 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Thus, the [Ca2+]i threshold required for the sustained CaMKII activation was markedly lowered by PDE1 reduction.
Negative_regulation (lowered) of Gene_expression (reduction) of PDE1
1) Confidence 0.36 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
One study comparing sildenafil to inhaled NO (iNO) demonstrated comparable reductions in PA pressures and pulmonary vascular resistance (PVR), but increased cardiac index (CI) was seen only with sildenafil treatment, consistent with an inotropic effect.24 However, other investigators, examining load-independent measures of myocardial performance, found no changes in systolic or diastolic function with sildenafil treatment.25 Circulating endothelial progenitor cells are reduced in idiopathic PAH and congenital PAH, and treatment with sildenafil has been shown to increase these cells to levels consistently higher than other PAH therapies.26 Sildenafil also inhibits PDE-1, which is expressed in low levels in the pulmonary circulation under baseline conditions but is upregulated in the disease state.27 The clinical significance of these findings remains uncertain.
Negative_regulation (inhibits) of Gene_expression (expressed) of PDE-1 associated with pulmonary hypertension and disease
2) Confidence 0.09 Published 2010 Journal Drug design, development and therapy Section Body Doc Link PMC2880338 Disease Relevance 0.53 Pain Relevance 0.03

General Comments

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