INT246315

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Context Info
Confidence 0.15
First Reported 2008
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 22
Total Number 22
Disease Relevance 2.73
Pain Relevance 4.64

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 (Ednra) plasma membrane (Ednra) signal transducer activity (Ednra)
Anatomy Link Frequency
glial cells 2
granule cells 2
nerve 1
muscle 1
nucleus 1
Ednra (Mus musculus)
Pain Link Frequency Relevance Heat
Glutamate 931 100.00 Very High Very High Very High
antagonist 21 99.96 Very High Very High Very High
Neurotransmitter 171 99.52 Very High Very High Very High
gABA 114 99.48 Very High Very High Very High
tetrodotoxin 40 98.24 Very High Very High Very High
GABAergic 228 96.20 Very High Very High Very High
Action potential 136 94.20 High High
Glutamate receptor 19 87.92 High High
Calcium channel 4 80.32 Quite High
Pain 5 74.92 Quite High
Disease Link Frequency Relevance Heat
Hypertension 62 100.00 Very High Very High Very High
Blister 38 99.26 Very High Very High Very High
Diarrhoea 19 98.04 Very High Very High Very High
Renal Disease 19 97.48 Very High Very High Very High
Sickle Cell Anemia 27 96.08 Very High Very High Very High
Death 87 94.88 High High
Shock 38 92.36 High High
Infection 19 91.92 High High
Poisoning 44 86.56 High High
Increased Venous Pressure Under Development 51 82.24 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Therapies specifically targeted at PH pathology include vasodilatory agents, such as phosphodiesterase-5 inhibitors and prostanoids, as well as endothelin receptor antagonists and arginine supplementation.
Localization (targeted) of endothelin receptor associated with antagonist and hypertension
1) Confidence 0.15 Published 2010 Journal F1000 Med Rep Section Body Doc Link PMC2948405 Disease Relevance 1.28 Pain Relevance 0.20
Subsequent application of ET (still in the presence of bicuculline) led to a further potentiation of the sEPSC frequency by a factor ?
Localization (application) of ET
2) Confidence 0.10 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2948003 Disease Relevance 0 Pain Relevance 0.20
Subsequent application of ET (10?
Localization (application) of ET
3) Confidence 0.10 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2948003 Disease Relevance 0 Pain Relevance 0.32
Moreover no blebs were observed on the cultured cells submitted to ET 10?
Localization (submitted) of ET associated with blister
4) Confidence 0.10 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2948003 Disease Relevance 0.16 Pain Relevance 0.12
6 M for at least 15 min) prior to application of ET.
Localization (application) of ET
5) Confidence 0.10 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2948003 Disease Relevance 0 Pain Relevance 0.30
6 M, for 10 min, not illustrated) or a mixture of the 3 drugs (see a typical recording from a series of 8 in Fig. 5E) did not prevent the depolarizing effect of ET on granule cells (Fig. 5F).
Localization (granule cells) of ET in granule cells
6) Confidence 0.10 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2948003 Disease Relevance 0 Pain Relevance 0.13
We did not observe any pyknotic nucleus indicating that ET (10?
Localization (indicating) of ET in nucleus
7) Confidence 0.10 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2948003 Disease Relevance 0.09 Pain Relevance 0.03
Subsequent application of ET (10?
Localization (application) of ET
8) Confidence 0.10 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2948003 Disease Relevance 0 Pain Relevance 0.15
Given the kinetic of the membranes changes caused by ET, we could not construct the I?
Localization (caused) of ET
9) Confidence 0.10 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2948003 Disease Relevance 0 Pain Relevance 0
This indicates that the cells constituting this layer (i.e. the inhibitory GABAergic neurons and the astrocyte related Bergmann's glial cells), as well as neuronal processes, corresponding to parallel fibers from granule cells and dendritic trees of Purkinje cells, are not targeted by ET.
Neg (not) Localization (targeted) of ET in glial cells associated with gabaergic
10) Confidence 0.10 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2948003 Disease Relevance 0 Pain Relevance 0.15
Overall these data confirm that the granule cell can be targeted and affected by ET, leading to [Ca2+]i rise likely due to Ca2+ influx, glutamate release and membrane severing.
Localization (targeted) of ET in granule cell associated with glutamate
11) Confidence 0.10 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2948003 Disease Relevance 0.15 Pain Relevance 0.15
Although one of the most prominent effects of ET in nerve tissue is the stimulation of glutamate release (see electrophysiological data in Fig. 4), no experimental evidence supports the possibility that ET directly acts on nerve ending.
Localization (release) of ET in nerve associated with glutamate
12) Confidence 0.10 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2948003 Disease Relevance 0.08 Pain Relevance 0.23
7 M ET of Ca2+-intracellular rise as well as glutamate release.
Localization (release) of ET associated with glutamate
13) Confidence 0.10 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2948003 Disease Relevance 0 Pain Relevance 0.35
The lactate des-hydrogenase released by ET treated cells was quantified using the Cytotoxicity Detection Kitplus (LDH) (Roche) on 96-well plates, following the manufacturer instructions.
Localization (released) of ET
14) Confidence 0.09 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2948003 Disease Relevance 0.16 Pain Relevance 0.22
ET-induced release of glutamate may involve two distinct effects of ET: i) stimulation of the neurotransmitter release machinery, and ii) leakage from severed cells.
Localization (release) of ET associated with neurotransmitter and glutamate
15) Confidence 0.09 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2948003 Disease Relevance 0.08 Pain Relevance 0.56
ET is secreted in the gut lumen as a proto-toxin and following its activation by endoproteases the toxin compromises the intestinal barrier [2].
Localization (secreted) of ET in gut
16) Confidence 0.09 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2948003 Disease Relevance 0.29 Pain Relevance 0
We could not completely exclude the possibility that the ET-induced depolarization of the granule cell soma was indirect, mediated by an ET-induced release of excitatory neuroactive molecules from neighboring glial cells (as the oligodendrocytes that are targeted by ET).
Localization (release) of ET in glial cells
17) Confidence 0.09 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2948003 Disease Relevance 0 Pain Relevance 0.11
ET-induced release of glutamate may involve two distinct effects of ET: i) stimulation of the neurotransmitter release machinery, and ii) leakage from severed cells.
Localization (release) of ET associated with neurotransmitter and glutamate
18) Confidence 0.09 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2948003 Disease Relevance 0.08 Pain Relevance 0.56
This possibility is supported by our observations that LDH, which is a cytosolic protein, is released upon application of high ET concentration (10?
Localization (released) of ET
19) Confidence 0.09 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2948003 Disease Relevance 0.06 Pain Relevance 0.48
Our observations that ET stimulates glutamate release in cerebellar primary and cultured slices are fully consistent with the several previous studies, which have shown ET-induced release of various neurotransmitters, including glutamate [19]–[21].
Localization (release) of ET associated with neurotransmitter and glutamate
20) Confidence 0.09 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2948003 Disease Relevance 0.09 Pain Relevance 0.35

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