INT21246

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Context Info
Confidence 0.10
First Reported 1990
Last Reported 2008
Negated 0
Speculated 1
Reported most in Body
Documents 3
Total Number 4
Disease Relevance 3.30
Pain Relevance 0.79

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

plasma membrane (ATP1A4) transmembrane transport (ATP1A4)
Anatomy Link Frequency
tubules 1
heart 1
ATP1A4 (Homo sapiens)
Pain Link Frequency Relevance Heat
sodium channel 13 100.00 Very High Very High Very High
agonist 61 94.80 High High
Dopamine 12 89.08 High High
dopamine receptor 1 81.84 Quite High
Inflammation 28 77.36 Quite High
Percutaneous transluminal coronary angioplasty 4 75.00 Quite High
Angina 1 67.92 Quite High
adenocard 2 59.36 Quite High
cytokine 11 57.76 Quite High
ischemia 8 55.12 Quite High
Disease Link Frequency Relevance Heat
Hypoxia 33 99.98 Very High Very High Very High
Pressure And Volume Under Development 46 99.46 Very High Very High Very High
Hypertension 5 98.56 Very High Very High Very High
Adult Respiratory Distress Syndrome 120 98.54 Very High Very High Very High
Chronic Renal Failure 23 96.12 Very High Very High Very High
Heart Disease 1 95.92 Very High Very High Very High
Injury 259 93.88 High High
Heart Rate Under Development 2 93.48 High High
Lung Injury 25 88.96 High High
Diuresis 1 82.08 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Despite the fact that numerous studies have been published regarding the possible presence in plasma of an endogenous Na-K pump inhibitor with a digitalis-like structure in essential hypertension, very little is known about this factor in heart disease in general, and in situations characterized by low cardiac output.
Spec (possible) Negative_regulation (inhibitor) of Na-K in heart associated with heart rate under development, heart disease and hypertension
1) Confidence 0.10 Published 1990 Journal Life Sci. Section Abstract Doc Link 2168510 Disease Relevance 0.50 Pain Relevance 0.18
Furosemide may increase the urine flow rate to decrease intratubular obstruction and will inhibit Na-K-ATPase, which will limit oxygen consumption in already damaged tubules with a low oxygen supply.
Negative_regulation (inhibit) of Na-K-ATPase in tubules
2) Confidence 0.06 Published 2008 Journal Pediatr Nephrol Section Body Doc Link PMC2756346 Disease Relevance 0.86 Pain Relevance 0.25
Hypoxia, a common feature of ALI/ARDS, may in addition contribute to impaired edema clearance because hypoxia decreases expression of subunits of the sodium channel and of the Na,K-ATPase pump [24].
Negative_regulation (decreases) of Na,K-ATPase associated with pressure and volume under development, hypoxia, sodium channel and adult respiratory distress syndrome
3) Confidence 0.04 Published 2004 Journal Crit Care Section Body Doc Link PMC522843 Disease Relevance 1.11 Pain Relevance 0.24
OA may also promote ALI by increasing the ratio between angiotensin-converting enzymes I and II [47], upregulating inducible nitric-oxide synthase (iNOS), and inhibiting alveolar epithelial Na,K-ATPase activity [48].
Negative_regulation (inhibiting) of Na,K-ATPase associated with adult respiratory distress syndrome
4) Confidence 0.03 Published 2008 Journal Crit Care Section Body Doc Link PMC2646309 Disease Relevance 0.83 Pain Relevance 0.12

General Comments

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