INT114363

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.67
First Reported 2003
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 50
Total Number 52
Disease Relevance 48.92
Pain Relevance 8.15

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

extracellular space (Hmgb1) extracellular region (Hmgb1) cell morphogenesis (Hmgb1)
nucleolus (Hmgb1) chromosome (Hmgb1) nucleus (Hmgb1)
Anatomy Link Frequency
macrophage 6
plasma 4
CLP 2
brain 2
lungs 2
Hmgb1 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammatory marker 5 99.98 Very High Very High Very High
ischemia 349 99.96 Very High Very High Very High
cytokine 962 99.78 Very High Very High Very High
Inflammatory response 511 99.70 Very High Very High Very High
chemokine 148 99.36 Very High Very High Very High
Inflammation 1093 99.22 Very High Very High Very High
cva 125 98.60 Very High Very High Very High
Multiple sclerosis 16 98.24 Very High Very High Very High
Nicotine 24 97.20 Very High Very High Very High
rheumatoid arthritis 57 97.04 Very High Very High Very High
Disease Link Frequency Relevance Heat
Sepsis 1770 100.00 Very High Very High Very High
Glioblastoma 300 100.00 Very High Very High Very High
Shock 58 100.00 Very High Very High Very High
Cv General 4 Under Development 36 99.96 Very High Very High Very High
INFLAMMATION 1825 99.84 Very High Very High Very High
Disease 327 99.78 Very High Very High Very High
Hypothermia 173 99.76 Very High Very High Very High
Cancer 2151 99.56 Very High Very High Very High
Adult Respiratory Distress Syndrome 122 99.52 Very High Very High Very High
Melanoma 80 99.52 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Intriguingly, we observed a time-dependent accumulation of exogenous HMGB1 clustering on macrophage cell surface within 2–6 hours of HMGB1 incubation, which correlates with the kinetics of HMGB1-induced release of proinflammatory cytokines [29].
Positive_regulation (accumulation) of HMGB1 in macrophage associated with cytokine
1) Confidence 0.67 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 0.27 Pain Relevance 0.28
Consequently, delayed administration of EGCG did not affect circulating levels of TNF at late stage of sepsis, but specifically attenuated systemic accumulation of HMGB1, as well as IL-6 and KC-two most reliable surrogate markers of lethal sepsis [34], [35].
Positive_regulation (accumulation) of HMGB1 associated with sepsis
2) Confidence 0.67 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 1.12 Pain Relevance 0.08
Our results show an increase in extracellular HMGB1 (approximately 30 kDa MW detected by western blot) released from Ad-TK + GCV treated GL26 tumor cells in vitro 48 h and 72 h after treatment (Figure 7A).
Positive_regulation (increase) of HMGB1 associated with cancer
3) Confidence 0.63 Published 2009 Journal PLoS Medicine Section Body Doc Link PMC2621261 Disease Relevance 1.01 Pain Relevance 0.03
HMGB1 was increased in the serum of tumor-bearing mice 7 d after treatment with Flt3L and TK (*p < 0.05; ?
Positive_regulation (increased) of HMGB1 associated with cancer
4) Confidence 0.63 Published 2009 Journal PLoS Medicine Section Body Doc Link PMC2621261 Disease Relevance 0.78 Pain Relevance 0.04
A marked increase in AST, ALT as well as HMGB1, MIF was observed after 9–10?
Positive_regulation (increase) of HMGB1
5) Confidence 0.61 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC3010695 Disease Relevance 0.78 Pain Relevance 0.28
At these time points, levels of HMGB-1 were also elevated and prompted us to further investigate the role of these factors in the development of cognitive dysfunction.
Positive_regulation (elevated) of HMGB-1 associated with cognitive disorder
6) Confidence 0.61 Published 2010 Journal Crit Care Section Body Doc Link PMC2911722 Disease Relevance 1.12 Pain Relevance 0.43
In a study using the cecal ligation and puncture (CLP) model of polymicrobial sepsis, HMGB-1 levels increased over the span of 1 to 2 days after CLP and remained elevated during the course of disease [17].
Positive_regulation (increased) of HMGB-1 in CLP associated with disease and sepsis
7) Confidence 0.55 Published 2007 Journal Crit Care Section Body Doc Link PMC2246216 Disease Relevance 0.82 Pain Relevance 0.14
An increase in HMGB1 levels were seen in plasma and epithelial lining fluids in lung injury [23].
Positive_regulation (increase) of HMGB1 in plasma associated with lung injury
8) Confidence 0.48 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2902015 Disease Relevance 1.01 Pain Relevance 0.56
To test the hypothesis that HMGB1 secreted from GBM-bearing mice after treatment with Flt3L plus TK (GCV) mediates TLR2 signaling and T cell-dependent brain tumor regression in vivo, we blocked circulating HMGB1 in vivo using glycyrrhizin or specific anti-HMGB1 immunoglobulins.
Positive_regulation (circulating) of HMGB1 in T cell associated with glioblastoma and brain tumor
9) Confidence 0.45 Published 2009 Journal PLoS Medicine Section Body Doc Link PMC2621261 Disease Relevance 0.76 Pain Relevance 0.03
Irradiation (Figure 9E–9H) and temozolomide (Figure 9I–9L) treatments also caused a significant increase (*, p < 0.05) in the levels of HMGB1 released from GL26 (?
Positive_regulation (caused) of HMGB1
10) Confidence 0.45 Published 2009 Journal PLoS Medicine Section Body Doc Link PMC2621261 Disease Relevance 0.86 Pain Relevance 0
Its beneficial effects in experimental sepsis were partly attributable to: 1) attenuation of systemic accumulation of proinflammatory mediator (e.g., HMGB1) and surrogate markers (e.g., IL-6 and KC) of lethal sepsis; and 2) suppression of HMGB1-mediated inflammatory responses by preventing accumulation of exogenous HMGB1 on macrophage cell surface.
Positive_regulation (accumulation) of HMGB1 in macrophage associated with inflammatory response and sepsis
11) Confidence 0.45 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 0.80 Pain Relevance 0.08
As expected, at 6 hours following HMGB1 incubation, levels of exogenous HMGB1 in macrophage whole-cell lysate or streptavidin-pulled-down fractions were increased in the presence of exogenous HMGB1 (“+rHMGB1”, Fig. 8C), but dramatically decreased in the presence of EGCG (“+rHMGB1+EGCG”, Fig. 8C).


Positive_regulation (increased) of HMGB1 in macrophage
12) Confidence 0.45 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 0 Pain Relevance 0.07
Its beneficial effects in experimental sepsis were partly attributable to: 1) attenuation of systemic accumulation of proinflammatory mediator (e.g., HMGB1) and surrogate markers (e.g., IL-6 and KC) of lethal sepsis; and 2) suppression of HMGB1-mediated inflammatory responses by preventing accumulation of exogenous HMGB1 on macrophage cell surface.
Positive_regulation (accumulation) of HMGB1 in macrophage associated with inflammatory response and sepsis
13) Confidence 0.45 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 0.78 Pain Relevance 0.07
In light of the late and prolonged kinetics of HMGB1 accumulation in experimental sepsis [11], we reasoned that it might be possible to rescue mice from lethal sepsis even if EGCG is administered after the onset of sepsis.
Positive_regulation (accumulation) of HMGB1 associated with sepsis
14) Confidence 0.45 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 1.30 Pain Relevance 0.04
Circulating HMGB1 levels are elevated in a delayed fashion (after 16–32 h) in endotoxemic and septic mice [7], [11], and in patients with sepsis [7], [14], [15].
Positive_regulation (elevated) of HMGB1 associated with sepsis
15) Confidence 0.45 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 1.39 Pain Relevance 0.11
Finally, while endotoxin (lipopolysaccharide, LPS) administration elevates IL-1 and TNF mRNA in various brain regions, HMGB1 mRNA is unchanged.
Neg (unchanged) Positive_regulation (unchanged) of HMGB1 in brain
16) Confidence 0.44 Published 2003 Journal Cytokine Section Abstract Doc Link 14609567 Disease Relevance 0.50 Pain Relevance 0.52
Activated Kupffer cells have been identified as a critical source of HMGB1 and MIF.
Positive_regulation (source) of HMGB1 in Kupffer cells
17) Confidence 0.44 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC3010695 Disease Relevance 0.75 Pain Relevance 0.22
Contrary to the cytokine changes, the LPS-induced elevation of HMGB-1 was not abrogated in the IL-1R-/- or IL-1Ra-treated animals (Figure 2c).


Positive_regulation (elevation) of HMGB-1 associated with cytokine
18) Confidence 0.44 Published 2010 Journal Crit Care Section Body Doc Link PMC2911722 Disease Relevance 0.20 Pain Relevance 0.25
Western blot analysis of cell culture supernatants revealed increased levels of HMGB1 following treatment with either Ad-TK (+GCV), radiation, or temozolomide (Figure 8).
Positive_regulation (increased) of HMGB1
19) Confidence 0.42 Published 2009 Journal PLoS Medicine Section Body Doc Link PMC2621261 Disease Relevance 0.73 Pain Relevance 0
Therapeutic efficacy of Ad-Flt3L and Ad-TK (+GCV) treatment was demonstrated in a second glioma model and in an intracranial melanoma model with concomitant increases in the levels of circulating HMGB1.


Positive_regulation (increases) of HMGB1 associated with melanoma and glioma
20) Confidence 0.42 Published 2009 Journal PLoS Medicine Section Abstract Doc Link PMC2621261 Disease Relevance 1.48 Pain Relevance 0

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox