INT169475

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Context Info
Confidence 0.73
First Reported 2005
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 14
Total Number 14
Disease Relevance 9.02
Pain Relevance 3.90

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

cytosol (HRAS) signal transduction (HRAS) Golgi apparatus (HRAS)
plasma membrane (HRAS) nucleus (HRAS) GTPase activity (HRAS)
Anatomy Link Frequency
joints 2
cartilage 1
pore 1
fibroblasts 1
osteoclast 1
HRAS (Homo sapiens)
Pain Link Frequency Relevance Heat
Osteoarthritis 221 97.96 Very High Very High Very High
cytokine 17 97.12 Very High Very High Very High
Pain 120 96.44 Very High Very High Very High
Inflammation 38 95.80 Very High Very High Very High
tolerance 3 94.84 High High
antagonist 13 94.20 High High
headache 5 91.76 High High
fibrosis 7 88.20 High High
Chronic pancreatitis 5 86.48 High High
Analgesic 8 68.52 Quite High
Disease Link Frequency Relevance Heat
Adenocarcinoma 5 99.60 Very High Very High Very High
Renal Disease 2 99.56 Very High Very High Very High
Necrosis 4 98.60 Very High Very High Very High
Cancer 140 98.24 Very High Very High Very High
Osteoarthritis 213 97.96 Very High Very High Very High
Head Trauma 2 97.96 Very High Very High Very High
Thrombocytopenia 2 97.16 Very High Very High Very High
Pain 118 96.44 Very High Very High Very High
Renal Failure 2 96.20 Very High Very High Very High
INFLAMMATION 47 95.80 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Furthermore, expression of epidermal growth factor receptor (EGFR) and its ligands; serine protease inhibitor Kazal type 3 (Spink3) and transforming growth factor alpha (TGF alpha) and activation of K-Ras (GTP-Ras formation), which are frequently observed in human PDA, were indeed observed in parallel with TCs formation.
Localization (observed) of K-Ras associated with adenocarcinoma
1) Confidence 0.73 Published 2010 Journal Exp. Anim. Section Abstract Doc Link 20660988 Disease Relevance 0.88 Pain Relevance 0.43
All H2RAs are eliminated renally to some extent, and their clearance is therefore appreciably reduced in patients with renal failure, mandating dose adjustment in such patients [35].
Localization (eliminated) of H2RAs associated with renal failure
2) Confidence 0.13 Published 2005 Journal Crit Care Section Body Doc Link PMC1065099 Disease Relevance 1.02 Pain Relevance 0.26
In addition, H2RAs do not inhibit vagally induced acid secretion, making them less efficacious in neurosurgical or head trauma patients with hyperacidity.
Localization (secretion) of H2RAs in head associated with head trauma
3) Confidence 0.12 Published 2005 Journal Crit Care Section Body Doc Link PMC1065099 Disease Relevance 1.03 Pain Relevance 0.22
HA, a polymer of alternating glucuronic acid and GlcN-Ac units is being synthesized at the inside of the cell at the plasma membrane, and then released into the extracellular matrix [27].
Localization (released) of HA in extracellular matrix
4) Confidence 0.05 Published 2008 Journal BMC Musculoskelet Disord Section Body Doc Link PMC2553787 Disease Relevance 0.57 Pain Relevance 0.23
Intra-articular injection of HA or its derivates into the hip joint is safe and well tolerated.
Localization (injection) of HA in articular
5) Confidence 0.04 Published 2010 Journal BMC Musculoskelet Disord Section Body Doc Link PMC2998460 Disease Relevance 0.74 Pain Relevance 0.50
This study had a small patient population (32 hips LMW HA and 24 hips HMW HA) and they did not use a power calculation to prove that they included enough patients.
Localization (population) of HA in hips
6) Confidence 0.04 Published 2010 Journal BMC Musculoskelet Disord Section Body Doc Link PMC2998460 Disease Relevance 0.49 Pain Relevance 0.28
Since GlcN is an important building block of HA and HA is found in high amounts in articular joints, increasing HA production through the administration of GlcN might be a way to explain the pain relieving effect of GlcN.
Localization (found) of HA in joints associated with pain
7) Confidence 0.04 Published 2008 Journal BMC Musculoskelet Disord Section Body Doc Link PMC2553787 Disease Relevance 0.97 Pain Relevance 0.80
Type B synoviocytes and fibroblasts synthesize HA and secrete it into the joint space.
Localization (secrete) of HA in fibroblasts
8) Confidence 0.02 Published 2009 Journal Journal of pain research Section Body Doc Link PMC3004631 Disease Relevance 0.26 Pain Relevance 0.20
On the other hand, PH-20 may be also responsible for the release of aggrecan ternary complexes made of aggrecans, link protein, and HA from cartilage matrix upon stimulation with retinoic acid, a process that persists when cartilage explants are bathed with AG3340 at concentrations that completely inhibit the collagenolytic activity present in explants as well as the enzymatic activity of both aggrecanase-1 and aggrecanase-2 [54].
Localization (release) of HA in cartilage
9) Confidence 0.02 Published 2005 Journal Arthritis Res Ther Section Body Doc Link PMC1175024 Disease Relevance 0.33 Pain Relevance 0.09
These differences were related to the presence of HA as opposed to alterations in the microarchitecture, as mineralized and non-mineralized control scaffolds exhibited similar wall thicknesses (mineralized scaffolds: 58±27 µm, non-mineralized scaffolds: 50±30 µm) and pore diameters (mineralized scaffolds: 432±106 µm, non-mineralized scaffolds: 451±123 µm) (Fig. 1C,D).


Localization (presence) of HA in pore
10) Confidence 0.02 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2809751 Disease Relevance 0.52 Pain Relevance 0
Since GlcN is an important building block of HA and HA is found in high amounts in articular joints, increasing HA production through the administration of GlcN might be a way to explain the pain relieving effect of GlcN.
Localization (found) of HA in joints associated with pain
11) Confidence 0.02 Published 2008 Journal BMC Musculoskelet Disord Section Body Doc Link PMC2553787 Disease Relevance 0.97 Pain Relevance 0.80
It has been found that (i) coatings with silica content lower than 60 wt% are more susceptible to corrosion and precipitate carbonated HA on their surface during in vitro tests; however (ii) these coatings have a higher thermal expansion than the metal, (iii), after 2 month in simulated body fluid, crack grows in the coating, reaches the glass/metal interface and initiates delamination, and (iv) glasses with silica content higher than 60wt% are more resistant to corrosion and have lower thermal expansion, and these coatings do not crack, but such glasses with silica do not precipitate apatite even after two months in simulated body fluid [151].
Localization (precipitate) of HA in body
12) Confidence 0.01 Published 2010 Journal International Journal of Molecular Sciences Section Body Doc Link PMC2871132 Disease Relevance 0.29 Pain Relevance 0
While VEGF, PTHrP, and IL-11, all of which are critical regulators of tumor angiogenesis [26], [38] and osteoclast resorption [2], [11]–[13], [36], were not affected by the presence of HA, IL-8 secretion increased under these conditions.
Localization (secretion) of HA in osteoclast associated with cancer
13) Confidence 0.01 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2809751 Disease Relevance 0.96 Pain Relevance 0.09
The MMC, established as described above, were maintained in culture for 3 days in the presence of PPS, HA, dextran sulfate (DS) or heparin at concentrations of 0.0, 0.1, 0.5, 1.0, 2.5, 5.0, 10.0 and 20.0 ?
Localization (presence) of HA
14) Confidence 0.01 Published 2010 Journal Arthritis Res Ther Section Body Doc Link PMC2875662 Disease Relevance 0 Pain Relevance 0

General Comments

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