INT255665

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Context Info
Confidence 0.63
First Reported 2008
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 5
Total Number 10
Disease Relevance 7.65
Pain Relevance 0.51

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

cell differentiation (Flt1) endosome (Flt1) Golgi apparatus (Flt1)
plasma membrane (Flt1) nucleus (Flt1) kinase activity (Flt1)
Anatomy Link Frequency
macrophages 4
cochlea 1
endothelial cells 1
hearts 1
Flt1 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 30 91.92 High High
agonist 54 90.24 High High
ischemia 3 83.04 Quite High
aspirin 30 64.04 Quite High
anesthesia 9 5.00 Very Low Very Low Very Low
bradykinin 5 5.00 Very Low Very Low Very Low
nud 3 5.00 Very Low Very Low Very Low
headache 3 5.00 Very Low Very Low Very Low
Versed 3 5.00 Very Low Very Low Very Low
corticosteroid 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Hypertrophy 25 99.68 Very High Very High Very High
Pre-eclampsia 768 98.50 Very High Very High Very High
Hypoxia 60 98.04 Very High Very High Very High
Diabetes Mellitus 72 94.60 High High
Hypertension 98 93.88 High High
Thrombosis 10 93.16 High High
Left Ventricular Hypertrophy 1 92.28 High High
Injury 42 91.92 High High
INFLAMMATION 30 91.92 High High
Albuminuria 20 90.24 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The odds for developing preeclampsia were significantly increased 2 to 3 fold for each 2-fold elevation in the concentration of sFlt1, sEng and the ratio of combined angiogenic factors (sFlt1+ sEng/PlGF) at study entry among women with multifetal gestations who later developed preeclampsia (Table 2).
Localization (concentration) of sFlt1 associated with pre-eclampsia
1) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2952583 Disease Relevance 1.21 Pain Relevance 0.06
The odds for developing preeclampsia were significantly increased 2 to 3 fold for each 2-fold elevation in the concentration of sFlt1, sEng and the ratio of combined angiogenic factors (sFlt1+ sEng/PlGF) at study entry among women with multifetal gestations who later developed preeclampsia (Table 2).
Localization (concentration) of sFlt1 associated with pre-eclampsia
2) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2952583 Disease Relevance 1.13 Pain Relevance 0.06
In conclusion, we have observed that the maternal concentration of the angiogenic factors sFlt1, sEng and PlGF are significantly higher among women with multifetal gestations compared with other high-risk groups including: pre-existing diabetes, chronic hypertension and previous preeclampsia.
Localization (sEng) of sFlt1 associated with diabetes mellitus, hypertension and pre-eclampsia
3) Confidence 0.55 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2952583 Disease Relevance 0.88 Pain Relevance 0.03
We also examined the localization of EP2, VEGF, Flt-1, and Flk-1 in the cochlea by immunohistochemistry.


Spec (examined) Localization (localization) of Flt-1 in cochlea
4) Confidence 0.39 Published 2010 Journal BMC Neurosci Section Abstract Doc Link PMC2847564 Disease Relevance 0.23 Pain Relevance 0.19
and VEGFR-1 are preserved during hypertrophy, which results in increased expression of VEGFR-1 in hearts that are both hypoxic and hypertrophied.
Localization (preserved) of VEGFR-1 in hearts associated with hypertrophy and hypoxia
5) Confidence 0.26 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2603310 Disease Relevance 1.31 Pain Relevance 0.04
Other authors also demonstrated that statins decreased the release of sFlt-1 from endothelial cells and normal –term placental villous explants [36].
Localization (release) of sFlt-1 in endothelial cells
6) Confidence 0.11 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965104 Disease Relevance 0.66 Pain Relevance 0
We previously demonstrated that pravastatin inhibited the release of sFlt-1 from macrophages [6].
Localization (release) of sFlt-1 in macrophages
7) Confidence 0.11 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965104 Disease Relevance 0.76 Pain Relevance 0
Previous results from our laboratory showed that pravastatin prevents sFlt-1 release from macrophages and thus rescue pregnancies [6].
Localization (release) of sFlt-1 in macrophages
8) Confidence 0.11 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965104 Disease Relevance 0.19 Pain Relevance 0
Pravastatin restores VEGF levels in the CBA/J x DBA/2 model by a dual mechanism: inhibition of sFlt-1 release from macrophages [6] and stimulation of VEGF release from trophoblasts.


Localization (release) of sFlt-1 in macrophages
9) Confidence 0.11 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965104 Disease Relevance 0.40 Pain Relevance 0
We demonstrated that complement activation induces tissue factor expression on macrophages stimulating sFlt-1 release and causing placental angiogenesis failure and abnormal pregnancies.
Localization (release) of sFlt-1 in macrophages
10) Confidence 0.11 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965104 Disease Relevance 0.88 Pain Relevance 0.13

General Comments

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