INT1150

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Context Info
Confidence 0.59
First Reported 1975
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 42
Total Number 45
Disease Relevance 29.38
Pain Relevance 7.73

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
lung 2
spinal cord 2
macrophages 1
aortic arch 1
hippocampus 1
ecs (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 447 100.00 Very High Very High Very High
Endocannabinoid 126 100.00 Very High Very High Very High
Cannabinoid receptor 13 99.84 Very High Very High Very High
anesthesia 23 99.56 Very High Very High Very High
antidepressant 68 99.44 Very High Very High Very High
ischemia 260 99.32 Very High Very High Very High
metalloproteinase 25 98.98 Very High Very High Very High
Pain 28 98.72 Very High Very High Very High
Neuropathic pain 35 98.70 Very High Very High Very High
Spinal cord 174 98.24 Very High Very High Very High
Disease Link Frequency Relevance Heat
INFLAMMATION 487 100.00 Very High Very High Very High
Shock 94 100.00 Very High Very High Very High
Mouth Cancer 19 99.84 Very High Very High Very High
Cancer 1024 99.66 Very High Very High Very High
Hemorrhagic Shock 96 99.58 Very High Very High Very High
Colorectal Cancer 4 99.48 Very High Very High Very High
Metastasis 119 99.40 Very High Very High Very High
Cv Unclassified Under Development 263 99.32 Very High Very High Very High
Apoptosis 237 98.78 Very High Very High Very High
Pain 25 98.72 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Control animals received the same drug treatments but no ECS.
Neg (no) Gene_expression (received) of ECS associated with shock
1) Confidence 0.59 Published 1975 Journal J. Neural Transm. Section Abstract Doc Link 164522 Disease Relevance 1.11 Pain Relevance 0.40
A dose of bicuculline (0.1 mg/kg i.p.) which was slightly proconvulsant in the flurothyl test did not significantly alter the postictal rise in S.T. produced by ECS.
Gene_expression (produced) of ECS associated with shock
2) Confidence 0.56 Published 1982 Journal Life Sci. Section Abstract Doc Link 7162340 Disease Relevance 0.53 Pain Relevance 0.30
Levels of ECs are tightly controlled by enzymatic biosynthesis and degradation in vivo.
Gene_expression (Levels) of ECs associated with endocannabinoid
3) Confidence 0.48 Published 2010 Journal J Mass Spectrom Section Abstract Doc Link 19950120 Disease Relevance 0.10 Pain Relevance 0.24
Perimeters changed only with ECS.
Gene_expression (changed) of ECS
4) Confidence 0.36 Published 2009 Journal Int Angiol Section Body Doc Link 19506542 Disease Relevance 0.07 Pain Relevance 0
Moreover, NAC attenuated the ECS-related overexpression of proapoptotic genes and normalized the levels of proapoptotic proteins in rat lung.
Gene_expression (overexpression) of ECS in lung
5) Confidence 0.34 Published 2005 Journal Mutat. Res. Section Abstract Doc Link 16137721 Disease Relevance 1.02 Pain Relevance 0.07
Three alternate-day ECSs produced comparable downregulation for a comparable period as six daily ECSs; this suggests that ECS produces time-dependent effects.
Gene_expression (produces) of ECS associated with shock
6) Confidence 0.22 Published 2000 Journal J ECT Section Abstract Doc Link 11005049 Disease Relevance 0.62 Pain Relevance 0.13
Here we present quantitative analyses of ictal expression and post-ictal suppression following ECS, MST, and anesthesia-alone sham in the same model to test whether differential neurophysiological characteristics of the seizures could be identified.
Gene_expression (suppression) of ECS associated with anesthesia, convulsion and shock
7) Confidence 0.21 Published 2008 Journal Clin EEG Neurosci Section Abstract Doc Link 18751564 Disease Relevance 1.10 Pain Relevance 0.18
Transmission electron microscopy (TEM) analysis of the superficial vascular plexus in sEng-expressing mice revealed structural alterations in tight junctions between microvascular ECs (Figure 3C).
Gene_expression (expressing) of ECs
8) Confidence 0.20 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2659748 Disease Relevance 0 Pain Relevance 0.04
ECs also express the TGF?
Gene_expression (express) of ECs
9) Confidence 0.20 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2659748 Disease Relevance 0.21 Pain Relevance 0
Nuclear condensation associated with apoptosis was apparent in some, but not all pericytes (Figure 7C) and ECs (Figure D), and, consistent with our findings of non-perfusion and impaired NO formation in sEng expressing mice, many vessels appeared completely or partially collapsed (Figures 7E and 7F).


Gene_expression (expressing) of ECs in vessels associated with apoptosis
10) Confidence 0.20 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2659748 Disease Relevance 0.50 Pain Relevance 0
Higher ictal expression with ECS was associated with slowed completion time for an orientation task given immediately after the treatments.
Gene_expression (expression) of ECS associated with shock
11) Confidence 0.15 Published 2009 Journal J ECT Section Abstract Doc Link 19300292 Disease Relevance 1.26 Pain Relevance 0.08
The data suggest that TMS produces in rats some responses that are regarded as predictive for antidepressant activity, similar to those produced by ECS, but less adverse effects.
Gene_expression (produced) of ECS associated with antidepressant, transcranial magnetic stimulation and shock
12) Confidence 0.13 Published 1997 Journal Biol. Psychiatry Section Abstract Doc Link 9359978 Disease Relevance 0.64 Pain Relevance 0.63
There was increased expression of Fos-like immunoreactivity after ECS- compared to non-ECS-treated controls in all age groups.
Gene_expression (expression) of ECS associated with shock
13) Confidence 0.12 Published 1991 Journal Brain Res. Section Abstract Doc Link 1687805 Disease Relevance 0.71 Pain Relevance 0.30
It is possible that IQGAP1 expressed in inflammatory cells and/or ECs may regulate cross-talk between these cells, as reported for the role of neutrophil NADPH oxidase in activation of redox signaling in ECs [40] or endothelial IQGAP1 in lymphocyte transendothelial migration [41].
Gene_expression (expressed) of ECs in neutrophil associated with inflammation
14) Confidence 0.10 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2955540 Disease Relevance 0.58 Pain Relevance 0.13
For example, 8 of the 10 human HOXB genes were found expressed in cultured umbilical vein ECs and this expression could be modulated by vascular signaling molecules including tissue plasminogen activator (TPA), and vascular endothelial growth factor (VEGF) [8].
Gene_expression (expressed) of ECs in umbilical vein
15) Confidence 0.09 Published 2008 Journal BMC Dev Biol Section Body Doc Link PMC2570687 Disease Relevance 0.13 Pain Relevance 0
Furthermore, while Hoxa3-lacZ expression in the endothelial layer was difficult to discern by X-Gal staining as exemplified in Figure 6A, endogenous Hoxa3 protein expression in both ECs and VSMCs of the aortic arch was confirmed by immunolabeling (Fig. 6B,C).
Gene_expression (expression) of ECs in aortic arch
16) Confidence 0.09 Published 2008 Journal BMC Dev Biol Section Body Doc Link PMC2570687 Disease Relevance 0.07 Pain Relevance 0
BM transplantation revealed that IQGAP1 expressed in both BM-derived cells and tissue resident cells, such as ECs, is required for post-ischemic neovascularization.
Gene_expression (expressed) of ECs
17) Confidence 0.09 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2955540 Disease Relevance 0.55 Pain Relevance 0.11
Since IQGAP1 is expressed in both macrophages and capillary-like ECs (Figure 2), which are major sources of ROS in ischemic tissue [11], we next examined the role of IQGAP1 in ROS production induced by hindlimb ischemia.
Gene_expression (expressed) of ECs in macrophages associated with ischemia
18) Confidence 0.09 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2955540 Disease Relevance 0.75 Pain Relevance 0.40
We have shown that IQGAP1 translocates to the leading edge where it binds to VEGFR2 and NADPH oxidase2, a major source of ROS in ECs, thereby promoting ROS production and directional EC migration [18], [20].
Gene_expression (source) of ECs in edge
19) Confidence 0.09 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2955540 Disease Relevance 0.46 Pain Relevance 0.12
We previously reported that reactive oxygen species (ROS) derived from NADPH oxidase expressed in inflammatory cells and ECs play a critical role in ischemia-induced neovascularization [11].
Gene_expression (expressed) of ECs associated with inflammation and ischemia
20) Confidence 0.09 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2955540 Disease Relevance 0.82 Pain Relevance 0.34

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