INT24684

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Context Info
Confidence 0.78
First Reported 1988
Last Reported 2010
Negated 3
Speculated 0
Reported most in Body
Documents 30
Total Number 42
Disease Relevance 26.21
Pain Relevance 13.56

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

peptidase activity (PLAT) protein modification process (PLAT) extracellular space (PLAT)
extracellular region (PLAT) cytoplasm (PLAT)
Anatomy Link Frequency
endothelium 8
vascular endothelium 4
endothelial cells 4
forearm 3
platelet 2
PLAT (Homo sapiens)
Pain Link Frequency Relevance Heat
Migraine 1004 99.64 Very High Very High Very High
bradykinin 75 99.56 Very High Very High Very High
substance P 210 99.54 Very High Very High Very High
anesthesia 2 99.32 Very High Very High Very High
Inflammation 207 98.80 Very High Very High Very High
Inflammatory response 22 98.80 Very High Very High Very High
narcan 1 97.96 Very High Very High Very High
ischemia 31 97.88 Very High Very High Very High
cva 75 95.84 Very High Very High Very High
Morphine 1 95.04 Very High Very High Very High
Disease Link Frequency Relevance Heat
Atherosclerosis 95 100.00 Very High Very High Very High
Headache 991 99.64 Very High Very High Very High
Increased Venous Pressure Under Development 300 99.34 Very High Very High Very High
Stress 86 99.08 Very High Very High Very High
INFLAMMATION 235 98.80 Very High Very High Very High
Thrombosis 89 98.80 Very High Very High Very High
Cv Unclassified Under Development 61 97.88 Very High Very High Very High
Aseptic Necrosis Of Bone 6 97.60 Very High Very High Very High
Epilepsy 195 96.88 Very High Very High Very High
Hemorrhage 50 95.84 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
by stimulating the release of plasminogen activator inhibitor type 1 and by reducing the release of t-PA through the extrinsic route [30], the release of TNF-?
Localization (release) of t-PA
1) Confidence 0.78 Published 2010 Journal BMC Neurol Section Body Doc Link PMC2891694 Disease Relevance 0.38 Pain Relevance 0.19
In ischemia the impairment of endothelial cell integrity might predominate, leading to impaired synthesis and/or the release of endothelial substances such as t-PA.
Localization (release) of t-PA in endothelial cell associated with ischemia
2) Confidence 0.75 Published 2002 Journal BMC Cardiovasc Disord Section Body Doc Link PMC117121 Disease Relevance 0.24 Pain Relevance 0.09
In three of the four patients with high PAI and with osteonecrosis present 0.3, 2, and 6 years prior to Stanozolol Rx, there was no clinical improvement after 14-156 weeks of Rx despite normalization of stimulated tPA-Fx and PAI-Fx.
Localization (normalization) of tPA associated with aseptic necrosis of bone
3) Confidence 0.73 Published 1995 Journal Am. J. Hematol. Section Abstract Doc Link 7717367 Disease Relevance 0.58 Pain Relevance 0.27
If CRHBP does not function appropriately it may prevent the inactivation of CRH, causing the release of tPA and the activation of stress related response.
Localization (release) of tPA associated with stress
4) Confidence 0.56 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2553267 Disease Relevance 0.50 Pain Relevance 0.11
CRH is released by several cell types, including but not limited to neuronal cells, the gastrointestinal tracts, placenta, and fetal membranes; tPA is released in response to CRH and acts downstream of CRH receptor 1 (CRHR1), a necessary step for the activation of stress related response [37], a major etiologic factor associated with PTB.
Localization (released) of tPA in placenta associated with stress
5) Confidence 0.56 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2553267 Disease Relevance 0.39 Pain Relevance 0.04
Third, endothelial fibrinolytic capacity depends on the balance between endothelial release of t-PA and plasminogen activator inhibitor type 1 (PAI-1) [21].
Localization (release) of t-PA
6) Confidence 0.53 Published 2010 Journal BMC Neurol Section Body Doc Link PMC3017034 Disease Relevance 0.77 Pain Relevance 0.47
In conclusion, the absence of differences in endothelium-dependent vasodilation, basal endothelial nitric oxide production and stimulated t-PA release between migraine patients and healthy control subjects argues against the presence of endothelial dysfunction in forearm resistance vessels of migraine patients.


Localization (release) of t-PA in forearm associated with migraine and increased venous pressure under development
7) Confidence 0.53 Published 2010 Journal BMC Neurol Section Body Doc Link PMC3017034 Disease Relevance 0.76 Pain Relevance 0.45
As an estimate of local t-PA release, the product of the arteriovenous plasma concentration gradient and forearm plasma flow was calculated: release = (Cv-Ca) × FBF × [(101-hematocrit)/100], where Cv and Ca are the venous and arterial plasma concentrations, respectively [21].
Localization (release) of t-PA in forearm
8) Confidence 0.53 Published 2010 Journal BMC Neurol Section Body Doc Link PMC3017034 Disease Relevance 0.05 Pain Relevance 0.10
No difference was observed in the forearm t-PA release between migraine patients and control subjects, suggesting that endothelial fibrinolytic capacity is normal in migraine patients during a headache-free interval.
Localization (release) of t-PA in forearm associated with migraine and headache
9) Confidence 0.53 Published 2010 Journal BMC Neurol Section Body Doc Link PMC3017034 Disease Relevance 1.17 Pain Relevance 0.69
The endogenous fibrinolytic system and, in particular, the acute release of t-PA from the endothelium protects the circulation from intravascular thrombosis.
Localization (release) of t-PA in endothelium associated with thrombosis
10) Confidence 0.53 Published 2010 Journal BMC Neurol Section Body Doc Link PMC3017034 Disease Relevance 1.26 Pain Relevance 0.63
Beta-adrenergic receptor mediated release of tissue plasminogen activator in anaesthetized dogs.
Localization (release) of tissue plasminogen activator associated with anesthesia
11) Confidence 0.51 Published 1988 Journal Thromb. Res. Section Title Doc Link 2840752 Disease Relevance 0 Pain Relevance 0.13
CRH is released by several cell types, including but not limited to neuronal cells, the gastrointestinal tracts, placenta, and fetal membranes; tPA is released in response to CRH and acts downstream of CRH receptor 1 (CRHR1), a necessary step for the activation of stress related response [37], a major etiologic factor associated with PTB.
Localization (released) of tPA in placenta associated with stress
12) Confidence 0.49 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2553267 Disease Relevance 0.38 Pain Relevance 0.04
The primary reason for clots seems to reside in the inflammatory process that leads to platelet aggregation and decrease in release of tissue plasminogen activator.
Localization (release) of tissue plasminogen activator in platelet associated with inflammation
13) Confidence 0.47 Published 2008 Journal The Open Cardiovascular Medicine Journal Section Body Doc Link PMC2627529 Disease Relevance 1.94 Pain Relevance 0.18
FBF responses and t-PA release were comparable between migraine patients and control subjects.


Localization (release) of t-PA associated with migraine
14) Confidence 0.46 Published 2010 Journal BMC Neurol Section Abstract Doc Link PMC3017034 Disease Relevance 0.91 Pain Relevance 0.79
To this end, endothelial function was assessed in vivo in the human forearm resistance vasculature by measuring: (1) stimulated endothelial NO release, (2) basal endothelial NO release and (3) stimulated endothelial t-PA release.


Localization (release) of t-PA in vasculature
15) Confidence 0.46 Published 2010 Journal BMC Neurol Section Body Doc Link PMC3017034 Disease Relevance 1.45 Pain Relevance 0.71
Our findings indicate that several markers of endothelial function, including the stimulated and basal endothelial NO release and stimulated endothelial t-PA release, are not altered in migraine patients in between migraine attacks.
Localization (release) of t-PA associated with migraine
16) Confidence 0.46 Published 2010 Journal BMC Neurol Section Body Doc Link PMC3017034 Disease Relevance 0.96 Pain Relevance 0.83
In response to specific stimuli, endothelial cells secrete local vaso-active mediators, including the vasodilator nitric oxide (NO) and vasoconstrictor endothelin-1 (ET-1) and tissue-type plasminogen activator (t-PA), which contributes to the fibrinolytic pathway.
Localization (secrete) of t-PA in endothelial cells
17) Confidence 0.46 Published 2010 Journal BMC Neurol Section Body Doc Link PMC3017034 Disease Relevance 1.41 Pain Relevance 0.93
The basal and stimulated t-PA release were comparable (P = 0.69 and P = 0.87, respectively) between migraine patients (-0.6 ± 1.1 ng.dL-1.min-1 and 7.4 ± 5.5 ng.dL-1.min-1) and controls (-0.6 ± 2.1 ng.dL-1.min-1 and 7.1 ± 5.5 ng.dL-1.min-1).
Localization (release) of t-PA associated with migraine
18) Confidence 0.46 Published 2010 Journal BMC Neurol Section Body Doc Link PMC3017034 Disease Relevance 1.00 Pain Relevance 1.13
In both groups, substance P caused an increase in t-PA release (P < 0.001).
Localization (release) of t-PA associated with substance p
19) Confidence 0.46 Published 2010 Journal BMC Neurol Section Abstract Doc Link PMC3017034 Disease Relevance 0.91 Pain Relevance 0.79
In addition, we compared the acute t-PA release in response to substance P in both groups.
Localization (release) of t-PA associated with substance p
20) Confidence 0.46 Published 2010 Journal BMC Neurol Section Body Doc Link PMC3017034 Disease Relevance 1.00 Pain Relevance 0.87

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