INT32783

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Context Info
Confidence 0.60
First Reported 1985
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 33
Total Number 34
Disease Relevance 30.55
Pain Relevance 6.86

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
pulmonary artery 3
muscle 1
brain 1
cerebellum 1
medial 1
Pah (Rattus norvegicus)
Pain Link Frequency Relevance Heat
fluoxetine 55 99.72 Very High Very High Very High
sSRI 16 99.72 Very High Very High Very High
Enkephalin 22 99.64 Very High Very High Very High
withdrawal 23 99.28 Very High Very High Very High
tolerance 23 99.24 Very High Very High Very High
Serotonin 75 99.04 Very High Very High Very High
Arthritis 2 98.52 Very High Very High Very High
midbrain 2 96.56 Very High Very High Very High
antagonist 255 96.48 Very High Very High Very High
Substantia nigra 2 96.00 Very High Very High Very High
Disease Link Frequency Relevance Heat
Pulmonary Hypertension 3518 100.00 Very High Very High Very High
Disease 263 100.00 Very High Very High Very High
Congenital Anomalies 32 99.92 Very High Very High Very High
Hypertrophy 376 99.80 Very High Very High Very High
Peripheral Arterial Disease 45 99.68 Very High Very High Very High
Hypoxia 147 99.48 Very High Very High Very High
Apoptosis 52 99.24 Very High Very High Very High
Adhesions 20 98.72 Very High Very High Very High
Right Ventricular Dysfunction 13 98.64 Very High Very High Very High
Systemic Sclerosis 145 98.58 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
However, it has not been shown whether quantification of the pulmonary artery flow deceleration (PAD) is useful for detecting PAH or measuring its severity.
Gene_expression (detecting) of PAH in pulmonary artery associated with pulmonary hypertension and peripheral arterial disease
1) Confidence 0.60 Published 2010 Journal Int J Cardiovasc Imaging Section Body Doc Link PMC2868165 Disease Relevance 0.87 Pain Relevance 0.04
Depletion of cofactors required for the PAH activity, physiologically by hypoxia or pharmacologically by intracellular iron chelation, increases the HIF-1?
Gene_expression (activity) of PAH associated with hypoxia
2) Confidence 0.58 Published 2007 Journal The Open Biochemistry Journal Section Body Doc Link PMC2570544 Disease Relevance 0.38 Pain Relevance 0.10
After 12 weeks treatment, it was found that even through fluoxetine treatment resulted in complete reversal of PAH, PAH recurred after fluoxetine withdrawal.
Gene_expression (recurred) of PAH associated with pulmonary hypertension, withdrawal and fluoxetine
3) Confidence 0.55 Published 2009 Journal Clin. Exp. Pharmacol. Physiol. Section Abstract Doc Link 19473340 Disease Relevance 0.86 Pain Relevance 0.85
Furthermore, observer related variability of the invasive and noninvasive parameters of PAH in rats is relatively unknown.Fig. 1Progression of PAH demonstrated by echocardiography at baseline, and 21 and 35 days after MCT induction.
Gene_expression (1Progression) of PAH associated with pulmonary hypertension
4) Confidence 0.52 Published 2010 Journal Int J Cardiovasc Imaging Section Body Doc Link PMC2868165 Disease Relevance 0.81 Pain Relevance 0.04
The antagonism of the ETA receptor was shown to be essential for the protection from MCT-induced PAH, irrespective of the presence of the ETB receptors, although a protective role of ETB receptor-mediated action in the pathogenesis of this disease model could not be ruled out [18].
Gene_expression (protection) of PAH associated with pulmonary hypertension and disease
5) Confidence 0.50 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2843902 Disease Relevance 0.87 Pain Relevance 0.15
Nitric oxide (NO) inhalation is currently among the first line treatments for post-operative pediatric pulmonary hypertension or in the child with acute severe new presentation of PAH being managed on the intensive care unit,36,37 as it reduces PA pressure rapidly.38 Inhaled NO therapy is also used acutely in persistent pulmonary hypertension of the newborn.39 The mode of action of NO is via the stimulation of guanylyl cyclase and hence increased production of cyclic guanylate monophosphate (cGMP) in pulmonary smooth muscle cells; this causes uptake of calcium into the sarcoplasmic reticulum, which then leads to muscle relaxation, reduced PA pressure and PVR, and hence increased oxygenation.
Gene_expression (presentation) of PAH in muscle associated with pulmonary hypertension
6) Confidence 0.47 Published 2009 Journal Vascular Health and Risk Management Section Body Doc Link PMC2697585 Disease Relevance 0.81 Pain Relevance 0
It has been shown to be effective in improving hemodynamic parameters, exercise tolerance and quality of life in patients with PAH.101,102

Novel therapies

Gene_expression (therapies) of PAH associated with pulmonary hypertension and tolerance
7) Confidence 0.47 Published 2009 Journal Vascular Health and Risk Management Section Body Doc Link PMC2697585 Disease Relevance 0.54 Pain Relevance 0.11
Limited research has suggested that modulation of the process of apoptosis (programmed cell death) involved in the process of vascular remodelling in PAH could be one possible therapeutic opportunity.112,113 For example, survivin (also known as Birc5), is one of a family of genes known to inhibit apoptosis; the use of molecular antagonists of survivin to increase cell death and prevent vascular remodelling may, in the future, hold therapeutic potential.114 Similarly, preliminary research has suggested that the use of the 3-hydroxy-3-methyl-glutaryl-CoA (HMG CoA) reductase inhibitor, pravastatin, and the Cox-2 inhibitor, celecoxib, prevent the development of monocrotaline-induced PAH in rats.115,116 Simvastatin has been found to be ineffective in this respect in vitro.117

Serotonin pathways

Gene_expression (remodelling) of PAH associated with pulmonary hypertension, antagonist, apoptosis, serotonin and death
8) Confidence 0.47 Published 2009 Journal Vascular Health and Risk Management Section Body Doc Link PMC2697585 Disease Relevance 1.12 Pain Relevance 0.17
Intratracheal transfer of the human prostacyclin synthase (PGIS) gene to rats with MCT-induced PAH augmented pulmonary prostacyclin synthesis, ameliorated MCT-induced PAH, and improved survival in MCT rats [56].
Gene_expression (transfer) of PAH associated with pulmonary hypertension
9) Confidence 0.44 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2843902 Disease Relevance 0.76 Pain Relevance 0.04
Furthermore, a selective serotonin reuptake inhibitor, sertraline, protects against MCT-induced PAH by decreasing pulmonary artery pressure, RV hypertrophy index, and pulmonary artery remodeling, probably related to a reduction in serotonin transporter mRNA [23].
Gene_expression (protects) of PAH in pulmonary artery associated with hypertrophy, pulmonary hypertension, serotonin and ssri
10) Confidence 0.44 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2843902 Disease Relevance 1.15 Pain Relevance 0.66
Delayed administration of EPCs 3 weeks after MCT prevented the further progression of PAH 2 weeks later; whereas animals receiving EPCs transfected with the human eNOS gene exhibited significant regression of established disease at day 35 compared with day 21.
Gene_expression (progression) of PAH associated with pulmonary hypertension and disease
11) Confidence 0.44 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2843902 Disease Relevance 0.52 Pain Relevance 0
Progression of PAH is associated with increased proliferation and migration of pulmonary vascular SMCs.
Gene_expression (Progression) of PAH in SMCs associated with pulmonary hypertension
12) Confidence 0.44 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2843902 Disease Relevance 0.99 Pain Relevance 0.04
Intramuscular injection of a plasmid encoding a 7-terminal deleted dominant negative inhibitor of MCP-1 in rats simultaneously injected with MCT inhibited the progression of MCT-induced PAH, RV hypertrophy, medial hypertrophy of pulmonary arterioles, and mononuclear cell infiltration into the lungs [55].

2.2.3.

Gene_expression (progression) of PAH in medial associated with hypertrophy and pulmonary hypertension
13) Confidence 0.44 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2843902 Disease Relevance 0.74 Pain Relevance 0.05
Progression of PAH is associated with increased serine elastase activity and deposition of extracellular matrix (ECM) protein tenascin-C in lung parenchyme.
Gene_expression (Progression) of PAH in ECM associated with pulmonary hypertension
14) Confidence 0.44 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2843902 Disease Relevance 1.28 Pain Relevance 0.04
Progression of PAH is associated with increased pulmonary expression of the serotonin transporter (5-HTT), which leads to hyperplasia of the pulmonary artery SMCs (PA-SMCs).
Gene_expression (Progression) of PAH in pulmonary artery associated with pulmonary hypertension, serotonin and hyperplasia
15) Confidence 0.44 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2843902 Disease Relevance 0.93 Pain Relevance 0.36
If cell-based gene transfer using VEGF-expressing PA-SMCs was delayed till PAH had developed, also a significant decrease in the progression of PAH and RV hypertrophy was documented [62].
Gene_expression (progression) of PAH associated with hypertrophy and pulmonary hypertension
16) Confidence 0.44 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2843902 Disease Relevance 0.71 Pain Relevance 0
Long-term inhibition of Rho-kinase, an effector of the small GTPase Rho, ameliorated MCT-induced PAH in rats and hypoxia-induced PAH in mice.
Gene_expression (ameliorated) of PAH associated with pulmonary hypertension and hypoxia
17) Confidence 0.44 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2843902 Disease Relevance 1.23 Pain Relevance 0
In patients with idiopathic or familial PAH who present in WHO class IV with evidence of right ventricular dysfunction, the authors and others recommend that intravenous epoprostenol be considered as first line therapy (Galie 2004).
Gene_expression (present) of PAH associated with pulmonary hypertension and right ventricular dysfunction
18) Confidence 0.42 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2350123 Disease Relevance 0.61 Pain Relevance 0
One of the most important abnormalities in PAH is an over expression of endothelin-1 (ET-1).
Gene_expression (expression) of PAH associated with pulmonary hypertension and congenital anomalies
19) Confidence 0.36 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2350123 Disease Relevance 1.88 Pain Relevance 0.12
Pathogenesis and rationale for PAH therapies
Gene_expression (therapies) of PAH associated with pulmonary hypertension
20) Confidence 0.36 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2350123 Disease Relevance 1.21 Pain Relevance 0.06

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