INT23251

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Context Info
Confidence 0.67
First Reported 1990
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 10
Total Number 10
Disease Relevance 2.98
Pain Relevance 1.59

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 (KLKB1) extracellular space (KLKB1) extracellular region (KLKB1)
plasma membrane (KLKB1)
Anatomy Link Frequency
plasma 9
vein 1
KLKB1 (Homo sapiens)
Pain Link Frequency Relevance Heat
lidocaine 4 99.12 Very High Very High Very High
bradykinin 20 98.92 Very High Very High Very High
Pain 14 97.60 Very High Very High Very High
antagonist 25 96.80 Very High Very High Very High
adenocard 1 89.72 High High
Restless leg syndrome 7 89.12 High High
b2 receptor 8 88.20 High High
addiction 21 5.00 Very Low Very Low Very Low
metalloproteinase 21 5.00 Very Low Very Low Very Low
ischemia 14 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Leukemia 14 99.84 Very High Very High Very High
Hypoxia 7 97.88 Very High Very High Very High
Pain 12 97.60 Very High Very High Very High
Hereditary Angioedema 91 95.12 Very High Very High Very High
Edema 51 92.80 High High
Peripheral Arterial Disease 126 90.40 High High
Atherosclerosis 28 89.12 High High
Adhesions 1 84.64 Quite High
Increased Venous Pressure Under Development 14 82.16 Quite High
Pressure And Volume Under Development 14 77.84 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The neutrophil count decreases to a lesser extent, but neutrophils also are stimulated to secrete lactoferrin and elastase concomitant with activation of plasma kallikrein.
Positive_regulation (activation) of plasma kallikrein in plasma
1) Confidence 0.67 Published 1990 Journal Ann. Thorac. Surg. Section Abstract Doc Link 2404474 Disease Relevance 0.08 Pain Relevance 0.14
These results suggest that the lipid solvent for propofol activates the plasma kallikrein-kinin system and produces bradykinin which modifies the injected local vein.
Positive_regulation (activates) of plasma kallikrein in vein associated with bradykinin
2) Confidence 0.67 Published 1999 Journal Br J Anaesth Section Abstract Doc Link 10655909 Disease Relevance 0.56 Pain Relevance 1.01
Replacement therapy with C1INH will inhibit both plasma kallikrein and activated factor XII.
Positive_regulation (activated) of plasma kallikrein in plasma
3) Confidence 0.06 Published 2010 Journal Allergy Asthma Clin Immunol Section Body Doc Link PMC2921104 Disease Relevance 1.07 Pain Relevance 0.30
In summary, a 15-h period of daytime activity could elevate plasma concentrations to 42 pM and 1.1 pM above control for free sVEGFR1 and VEGF respectively.
Positive_regulation (elevate) of plasma in plasma
4) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
This was due to a secondary “spill-over” of the elevated plasma free sVEGFR1 through increased extravasation into the distal compartment.
Positive_regulation (elevated) of plasma in plasma
5) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.15 Pain Relevance 0
This may suggest that hypoxia-induced secretion of sVEGFR1 (as opposed to lymphatic drainage of sVEFR1) is indeed the faster and major source of elevated plasma sVEGFR1 in exercise; but our simulations were unable to confirm the conclusion by Bailey et al. [49] that VEGF trapping by the surge of sVEGFR1 had caused the drop in plasma VEGF.
Positive_regulation (elevated) of plasma in plasma associated with hypoxia
6) Confidence 0.04 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.24 Pain Relevance 0
Hence we hypothesized that the physiological activity-dependent fluctuations in lymphatic drainage rates may contribute to the clinical heterogeneity observed in plasma measurements of VEGF and sVEGFR1.
Positive_regulation (measurements) of plasma in plasma
7) Confidence 0.04 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.40 Pain Relevance 0.09
This may suggest that hypoxia-induced secretion of sVEGFR1 (as opposed to lymphatic drainage of sVEFR1) is indeed the faster and major source of elevated plasma sVEGFR1 in exercise; but our simulations were unable to confirm the conclusion by Bailey et al. [49] that VEGF trapping by the surge of sVEGFR1 had caused the drop in plasma VEGF.
Positive_regulation (source) of plasma in plasma associated with hypoxia
8) Confidence 0.04 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.24 Pain Relevance 0
In plasma, steady-state concentrations of all soluble species were strongly dependent on transport rates, whereas in the interstitium, sVEGFR1 concentration was much more sensitive than VEGF to transport parameters.
Positive_regulation (dependent) of plasma in plasma
9) Confidence 0.04 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Possible candidates include: (a) human soluble VEGFR2 (160 kDa) – present in significant quantities in healthy human plasma (7–8 ng/mL) [140] and upregulated in acute myeloid leukemia [39]; (b) soluble NRP1 (90 kDa) – a VEGF165-specific antagonist, with documented renal expression in humans [141], [142]; and (c) cellular fibronectin (?
Positive_regulation (upregulated) of plasma in plasma associated with leukemia and antagonist
10) Confidence 0.04 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.24 Pain Relevance 0.05

General Comments

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