INT190208

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Context Info
Confidence 0.23
First Reported 2005
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 15
Total Number 15
Disease Relevance 14.10
Pain Relevance 3.37

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

extracellular region (MMRN1) cell adhesion (MMRN1)
Anatomy Link Frequency
fibroblasts 2
endothelial cells 1
pancreas 1
cheek 1
basement membranes 1
MMRN1 (Homo sapiens)
Pain Link Frequency Relevance Heat
metalloproteinase 184 99.92 Very High Very High Very High
Inflammation 234 99.00 Very High Very High Very High
fibrosis 83 98.16 Very High Very High Very High
cytokine 145 96.16 Very High Very High Very High
chemokine 40 96.04 Very High Very High Very High
Chronic pancreatitis 132 95.96 Very High Very High Very High
Pain 18 87.64 High High
Kinase C 3 82.76 Quite High
Inflammatory mediators 11 79.48 Quite High
Osteoarthritis 5 74.16 Quite High
Disease Link Frequency Relevance Heat
Primary Sclerosing Cholangitis 308 100.00 Very High Very High Very High
Apoptosis 71 99.56 Very High Very High Very High
INFLAMMATION 271 99.00 Very High Very High Very High
Airway Remodeling 5 98.68 Very High Very High Very High
Uterine Fibroids 360 98.32 Very High Very High Very High
Fibrosis 142 98.16 Very High Very High Very High
Emphysema 65 97.12 Very High Very High Very High
Pulmonary Disease 214 96.76 Very High Very High Very High
Disease 68 96.70 Very High Very High Very High
Keloid Scars 105 96.40 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
A potential influence of late changes in mRNA transcription (24 hours) on the increase of ECM proteins in coculture and the contributing source of these proteins (PSC and/or PBMC) was examined using quantitative RT-PCR.
Positive_regulation (increase) of ECM associated with primary sclerosing cholangitis
1) Confidence 0.23 Published 2007 Journal J Transl Med Section Body Doc Link PMC2234395 Disease Relevance 0.84 Pain Relevance 0.41
Moreover, this site specific variance in ECM deposition can be due to the following reasons: 1) The packed immune clusters are actually forming in expanded perivascular spaces as hinted by the presence of central CD31 positive endothelial cells; 2) In vitro, the matrix degradation enzyme MMP-1 was increased together with an increase in ECM proteins collagen1 and fibronectin; 3) High amounts of TNFalpha exert cytotoxic effects on PSC [20] which is probably represented in vivo as a function of their density.
Positive_regulation (increase) of ECM in endothelial cells associated with primary sclerosing cholangitis
2) Confidence 0.20 Published 2007 Journal J Transl Med Section Body Doc Link PMC2234395 Disease Relevance 0.59 Pain Relevance 0.03
Thus, anti-fibrogenic therapies aim to reduce the activity of PSC in order to inhibit the accumulation of ECM proteins and also to prevent digestion of the basement membranes, which allows PSC to enter inflammatory areas and to excessively deposit ECM.
Positive_regulation (accumulation) of ECM in basement membranes associated with inflammation and primary sclerosing cholangitis
3) Confidence 0.16 Published 2007 Journal J Transl Med Section Body Doc Link PMC2234395 Disease Relevance 1.82 Pain Relevance 0.62
However, our findings may also be due to several other factors: first, we used PBMC, which have only been in direct contact with the inflamed pancreas to a very minor extent; second, upregulation of PSC-produced ECM proteins seems to be a function of PBMC in general, not particularly of PBMC which are derived from CP patients; and third, our study addresses interactions of PBMC and PSC in an artificial set-up which may reflect the experimental processing of both PSC and PBMC.
Positive_regulation (upregulation) of ECM in pancreas associated with primary sclerosing cholangitis and chronic pancreatitis
4) Confidence 0.14 Published 2007 Journal J Transl Med Section Body Doc Link PMC2234395 Disease Relevance 1.15 Pain Relevance 0.23
We further hypothesize that both these pathways may play a synergistic role in inducing the abnormal ECM remodelling in leiomyogenesis and could potentially play a significant role clinically as combinational therapy for treatment for leiomyomas.
Positive_regulation (inducing) of ECM associated with uterine fibroids
5) Confidence 0.13 Published 2008 Journal Clinical Endocrinology Section Body Doc Link PMC2610401 Disease Relevance 0.52 Pain Relevance 0.03
It is known as an inducer of ECM proteins and its role in the pathogenesis of fibrosis is well established.
Positive_regulation (inducer) of ECM associated with fibrosis
6) Confidence 0.13 Published 2008 Journal Clinical Endocrinology Section Body Doc Link PMC2610401 Disease Relevance 0.56 Pain Relevance 0.15
To further increase the ECM characteristics of these matrices, peptides such as laminin and human teasing-C may be covalently attached to them (Ahmed et al., 2006; Birbaumer et al., 2008; Koh et al., 2008; Bhardwaj and Kundu, 2010).
Positive_regulation (increase) of ECM
7) Confidence 0.09 Published 2010 Journal Frontiers in Neuroengineering Section Body Doc Link PMC2972680 Disease Relevance 0.06 Pain Relevance 0
Overproduction of MMP-12 causes pathological ECM protein breakdown and excessive airway remodeling, which has been implicated in a range of respiratory diseases, including asthma and chronic obstructive pulmonary disease (COPD).
Positive_regulation (causes) of ECM in respiratory associated with asthma, pulmonary disease, metalloproteinase, respiratory disease and airway remodeling
8) Confidence 0.09 Published 2005 Journal Respir Res Section Body Doc Link PMC1363355 Disease Relevance 1.33 Pain Relevance 0.90
3 plays an important role in ECM accumulation.
Positive_regulation (accumulation) of ECM
9) Confidence 0.09 Published 2008 Journal Clinical Endocrinology Section Body Doc Link PMC2610401 Disease Relevance 0.56 Pain Relevance 0.15
This analysis revealed the upregulation of ECM-related genes and apoptosis genes, and the downregulation of anti-inflammatory genes in COPD tissues (Wang et al 2008).
Positive_regulation (upregulation) of ECM-related associated with pulmonary disease, inflammation and apoptosis
10) Confidence 0.04 Published 2008 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2629979 Disease Relevance 1.26 Pain Relevance 0.07
As such, the genes identified from the bovine array may be indicative of those genes required to generate a more 'hydrogel'-like ECM, rather than the more fibrous NP tissue found in adult aged human discs.
Positive_regulation (generate) of ECM
11) Confidence 0.04 Published 2010 Journal Arthritis Res Ther Section Body Doc Link PMC2875656 Disease Relevance 0.14 Pain Relevance 0.07
This analysis revealed the upregulation of many ECM-related proteins and the downregulation of immune-function and cell signaling-related genes in severe vs mild emphysema (Spira et al 2004).
Positive_regulation (upregulation) of ECM-related associated with emphysema
12) Confidence 0.03 Published 2008 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2629979 Disease Relevance 0.93 Pain Relevance 0.10
Although hypertrophic scarring or keloid formation are regarded as different disease entities based on their patho-histological data (Figures 3 and 4), they still share some common characteristics, including increased fibroblast function, excessive accumulation of ECM, and the common initial inflammatory phase.
Positive_regulation (accumulation) of ECM in fibroblast associated with inflammation, disease and keloid scars
13) Confidence 0.01 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2910481 Disease Relevance 1.88 Pain Relevance 0.23
This will proceed for 2 to 3 days and then the proliferative phase, signified by an abundance of fibroblasts and an accumulation of ECM, fades in and lasts for 3–6 weeks.
Positive_regulation (accumulation) of ECM in fibroblasts
14) Confidence 0.01 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2910481 Disease Relevance 1.44 Pain Relevance 0.18
This increase in ECM deposition indicates that the hamster cheek-pouch model is suitable to assess the anti-fibrotic potential of SAP as it pertains to radiation-induced fibrosis.


Positive_regulation (increase) of ECM in cheek associated with fibrosis
15) Confidence 0.01 Published 2010 Journal Fibrogenesis Tissue Repair Section Body Doc Link PMC2905325 Disease Relevance 1.02 Pain Relevance 0.18

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