INT215077

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Context Info
Confidence 0.42
First Reported 2007
Last Reported 2008
Negated 1
Speculated 0
Reported most in Body
Documents 3
Total Number 7
Disease Relevance 5.09
Pain Relevance 1.05

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 2
vagus nerve 2
Hmgb1 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammatory response 147 99.92 Very High Very High Very High
Inflammation 196 97.88 Very High Very High Very High
Nicotine 7 97.62 Very High Very High Very High
agonist 5 97.44 Very High Very High Very High
Neuropeptide 15 96.76 Very High Very High Very High
vagus nerve 30 94.82 High High
cytokine 179 92.92 High High
Inflammatory mediators 75 92.16 High High
Neurotransmitter 10 81.08 Quite High
antagonist 10 63.20 Quite High
Disease Link Frequency Relevance Heat
INFLAMMATION 441 99.72 Very High Very High Very High
Sepsis 599 99.68 Very High Very High Very High
Disease 76 86.36 High High
Hemorrhagic Shock 5 81.96 Quite High
Pancreatitis 5 80.56 Quite High
Adult Respiratory Distress Syndrome 20 79.04 Quite High
Lung Injury 10 76.36 Quite High
Injury 74 73.08 Quite High
Myocardial Infarction 5 66.56 Quite High
Endotoxemia 31 57.24 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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].
Neg (not) Negative_regulation (attenuated) of Positive_regulation (accumulation) of HMGB1 associated with sepsis
1) Confidence 0.42 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 1.13 Pain Relevance 0.08
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.
Negative_regulation (preventing) of Positive_regulation (accumulation) of HMGB1 in macrophage associated with inflammatory response and sepsis
2) Confidence 0.42 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 0.80 Pain Relevance 0.08
Indeed, stimulation of the vagus nerve by physical methods (e.g. electrical or
         mechanical) (Refs 125, 126) or chemical agents (such as the cholinergic agonists nicotine
         and GTS-21) (Refs 127, 128) conferred protection against lethal endotoxaemia and sepsis
         partly by attenuating systemic HMGB1 accumulation.


Negative_regulation (attenuating) of Positive_regulation (accumulation) of HMGB1 in vagus nerve associated with nicotine, agonist, vagus nerve and sepsis
3) Confidence 0.38 Published 2008 Journal Expert Reviews in Molecular Medicine Section Body Doc Link PMC2586610 Disease Relevance 0.45 Pain Relevance 0.35
In animal models of sepsis induced by
           CLP or bacteraemia, administration of VIP attenuated systemic HMGB1 accumulation, and
           consequently reduced animal lethality (Ref. 118). 
Negative_regulation (attenuated) of Positive_regulation (accumulation) of HMGB1 associated with sepsis
4) Confidence 0.38 Published 2008 Journal Expert Reviews in Molecular Medicine Section Body Doc Link PMC2586610 Disease Relevance 0.41 Pain Relevance 0.11
As discussed below, several agents have been proven protective
       against experimental sepsis partly through attenuating systemic HMGB1 accumulation (Table 2). 
Negative_regulation (attenuating) of Positive_regulation (accumulation) of HMGB1 associated with sepsis
5) Confidence 0.38 Published 2008 Journal Expert Reviews in Molecular Medicine Section Body Doc Link PMC2586610 Disease Relevance 0.62 Pain Relevance 0.04
In animal
           models of sepsis induced by CLP or bacteraemia, administration of urocortin attenuated
           systemic HMGB1 accumulation and reduced animal lethality (Ref. 118), supporting a therapeutic potential for neuropeptides in
           experimental sepsis.


Negative_regulation (attenuated) of Positive_regulation (accumulation) of HMGB1 associated with neuropeptide and sepsis
6) Confidence 0.38 Published 2008 Journal Expert Reviews in Molecular Medicine Section Body Doc Link PMC2586610 Disease Relevance 0.44 Pain Relevance 0.13
It is thus important to pharmacologically modulate, rather than abrogate, systemic HMGB1
           accumulation to facilitate resolution of a potentially injurious inflammatory
         response.


Negative_regulation (abrogate) of Positive_regulation (accumulation) of HMGB1 associated with inflammation
7) Confidence 0.38 Published 2008 Journal Expert Reviews in Molecular Medicine Section Body Doc Link PMC2586610 Disease Relevance 1.25 Pain Relevance 0.26

General Comments

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