INT123885

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Context Info
Confidence 0.57
First Reported 2005
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 23
Total Number 35
Disease Relevance 24.38
Pain Relevance 6.32

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

proteinaceous extracellular matrix (Lgals3) nucleus (Lgals3) extracellular matrix organization (Lgals3)
cytoplasm (Lgals3)
Anatomy Link Frequency
microglia 6
heart 5
plasma 3
corpus callosum 3
macrophages 2
Lgals3 (Mus musculus)
Pain Link Frequency Relevance Heat
chemokine 7 100.00 Very High Very High Very High
Nerve growth factor 624 99.92 Very High Very High Very High
fibrosis 345 99.40 Very High Very High Very High
Chronic pancreatitis 17 99.00 Very High Very High Very High
Spinal cord 65 98.36 Very High Very High Very High
Morphine 9 97.00 Very High Very High Very High
imagery 104 93.20 High High
anesthesia 29 92.92 High High
metalloproteinase 85 90.48 High High
Inflammatory response 27 89.36 High High
Disease Link Frequency Relevance Heat
Cirrhosis 15 99.92 Very High Very High Very High
Cancer 195 99.84 Very High Very High Very High
Acute Decompensated Heart Failure (ADHF) 60 99.84 Very High Very High Very High
Infection 83 99.68 Very High Very High Very High
Brain Injury 611 99.62 Very High Very High Very High
Fibrosis 300 99.40 Very High Very High Very High
Apoptosis 111 99.38 Very High Very High Very High
Metastasis 8 99.36 Very High Very High Very High
Myocardial Infarction 495 99.12 Very High Very High Very High
Pancreatitis 37 99.00 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The observation that galectin-3 is increased in decompensated heart failure has been published in a seminal paper by Sharma et al. [20].
Positive_regulation (increased) of galectin-3 in heart associated with acute decompensated heart failure (adhf)
1) Confidence 0.57 Published 2010 Journal Curr Heart Fail Rep Section Body Doc Link PMC2831188 Disease Relevance 0.42 Pain Relevance 0
Given the upregulation of galectin-3 well before the transition to overt heart failure, the authors concluded that galectin-3 may be a factor that should be considered as a novel target for intervention in heart failure.
Positive_regulation (upregulation) of galectin-3 in heart associated with myocardial infarction
2) Confidence 0.57 Published 2010 Journal Curr Heart Fail Rep Section Body Doc Link PMC2831188 Disease Relevance 0.78 Pain Relevance 0.03
The increased expression levels of galectin-3 are associated with the tendency to develop decompensated heart failure, and in clinical cohorts, increased plasma galectin-3 levels are linked with worse prognosis.
Positive_regulation (increased) of galectin-3 in heart associated with acute decompensated heart failure (adhf)
3) Confidence 0.57 Published 2010 Journal Curr Heart Fail Rep Section Body Doc Link PMC2831188 Disease Relevance 0.32 Pain Relevance 0.03
In animal models, upregulation of galectin-3 has been described for hepatic [31], renal [34, 35•, 36], and cardiac [20, 25, 26•] fibrosis.
Positive_regulation (upregulation) of galectin-3 associated with fibrosis
4) Confidence 0.57 Published 2010 Journal Curr Heart Fail Rep Section Body Doc Link PMC2831188 Disease Relevance 1.19 Pain Relevance 0.43
The increased expression levels of galectin-3 are associated with the tendency to develop decompensated heart failure, and in clinical cohorts, increased plasma galectin-3 levels are linked with worse prognosis.
Positive_regulation (increased) of galectin-3 in plasma associated with acute decompensated heart failure (adhf)
5) Confidence 0.57 Published 2010 Journal Curr Heart Fail Rep Section Body Doc Link PMC2831188 Disease Relevance 0.43 Pain Relevance 0.08
Besides typical changes for LV remodeling, such as hypertrophy, fibrosis, and apoptosis, the authors also describe an upregulation of galectin-3 in the LV [24].
Positive_regulation (upregulation) of galectin-3 associated with fibrosis, hypertrophy and apoptosis
6) Confidence 0.57 Published 2010 Journal Curr Heart Fail Rep Section Body Doc Link PMC2831188 Disease Relevance 0.67 Pain Relevance 0.08
Various fibrotic conditions are associated with upregulation of galectin-3: liver cirrhosis [30, 31], idiopathic lung fibrosis [32], and chronic pancreatitis [33].
Positive_regulation (upregulation) of galectin-3 in lung associated with fibrosis, cirrhosis, pulmonary fibrosis and chronic pancreatitis
7) Confidence 0.57 Published 2010 Journal Curr Heart Fail Rep Section Body Doc Link PMC2831188 Disease Relevance 1.20 Pain Relevance 0.43
Parallel to experiments described by Sharma et al. [20], we have observed that galectin-3 is upregulated in compensated and decompensated hypertrophy compared with healthy control rats; however, the difference is lesser than when comparing decompensated versus compensated rats (de Boer, unpublished data).
Positive_regulation (upregulated) of galectin-3 associated with hypertrophy
8) Confidence 0.57 Published 2010 Journal Curr Heart Fail Rep Section Body Doc Link PMC2831188 Disease Relevance 0.48 Pain Relevance 0.03
First, the fibrosis-related biomarkers including galectin-3 were increased compared with controls.
Positive_regulation (increased) of galectin-3 associated with fibrosis
9) Confidence 0.50 Published 2010 Journal Curr Heart Fail Rep Section Body Doc Link PMC2831188 Disease Relevance 0.89 Pain Relevance 0.19
In a different set of experiments, 20 ARO xenografted mice were injected with 100 µCi of 99mTc-labeled mAb to galectin-3 (30 µg protein) and 5 groups of 4 animals each were sacrificed at 3 hrs, 6 hrs, 9 hrs, 12 hrs and 24 hrs post-injection, respectively.
Positive_regulation (labeled) of galectin-3
10) Confidence 0.50 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2582451 Disease Relevance 0.41 Pain Relevance 0
To determine the in vivo expression of galectin-3 in tumor xenografts, some of the tumors were surgically excised and used for galectin-3 expression analysis as reported above.
Positive_regulation (used) of galectin-3 associated with cancer
11) Confidence 0.50 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2582451 Disease Relevance 0.73 Pain Relevance 0.13
Although the thyroid origin of ARO cells has been recently questioned [20], this galectin-3 positive cell line grows very efficiently in vivo and provides an useful model for setting experiments of galectin-3 immunotargeting with and without galectin-3 mRNA interference.
Positive_regulation (experiments) of galectin-3 in thyroid
12) Confidence 0.50 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2582451 Disease Relevance 0.63 Pain Relevance 0.08
Taken together from available clinical data, plasma and/or serum galectin-3 is increased in acute and chronic heart failure.
Positive_regulation (increased) of galectin-3 in plasma associated with myocardial infarction
13) Confidence 0.41 Published 2010 Journal Curr Heart Fail Rep Section Body Doc Link PMC2831188 Disease Relevance 0.62 Pain Relevance 0.04
In the failing or stressed heart, it has been shown that activated macrophages secrete galectin-3.
Positive_regulation (activated) of galectin-3 in macrophages
14) Confidence 0.41 Published 2010 Journal Curr Heart Fail Rep Section Body Doc Link PMC2831188 Disease Relevance 0.31 Pain Relevance 0.03
Sham animals had a significant increase in galectin-3/Mac-2 labelling compared to naïve animals that were not exposed to any type of surgical procedure (Figure 4).
Positive_regulation (increase) of galectin-3
15) Confidence 0.41 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2891720 Disease Relevance 0.83 Pain Relevance 0.20
Chronic upregulation of activated microglia immunoreactive for galectin-3/Mac-2 and nerve growth factor following diffuse axonal injury

Background

Positive_regulation (upregulation) of galectin-3 in microglia associated with nerve growth factor and diffuse axonal injury
16) Confidence 0.41 Published 2010 Journal J Neuroinflammation Section Title Doc Link PMC2891720 Disease Relevance 1.12 Pain Relevance 0.10
We report here that after TBI, there is chronic upregulation of galectin-3/Mac-2 immunoreactive microglia in the corpus callosum that persists at 28 days following injury.
Positive_regulation (upregulation) of Mac-2 immunoreactive microglia in corpus callosum associated with injury and brain injury
17) Confidence 0.41 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2891720 Disease Relevance 0.67 Pain Relevance 0.30
Chronic upregulation of galectin-3/Mac-2-ir microglia within the white matter after TBI
Positive_regulation (upregulation) of galectin-3/Mac-2-ir in white matter associated with brain injury
18) Confidence 0.41 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2891720 Disease Relevance 0.90 Pain Relevance 0
We report here that after TBI, there is chronic upregulation of galectin-3/Mac-2 immunoreactive microglia in the corpus callosum that persists at 28 days following injury.
Positive_regulation (upregulation) of galectin-3 in corpus callosum associated with injury and brain injury
19) Confidence 0.41 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2891720 Disease Relevance 0.67 Pain Relevance 0.30
Our studies find both an acute increase in galectin-3/Mac-2+/NGF+ microglia 1 day following injury as well as a relatively attenuated chronic upregulation of this population of microglia even 28 days following injury.
Positive_regulation (increase) of galectin-3 in microglia associated with nerve growth factor and injury
20) Confidence 0.41 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2891720 Disease Relevance 0.65 Pain Relevance 0.63

General Comments

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