INT164366

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Context Info
Confidence 0.71
First Reported 2002
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 26
Total Number 26
Disease Relevance 5.90
Pain Relevance 16.54

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

cytosol (NLRP1) nucleus (NLRP1) intracellular (NLRP1)
enzyme binding (NLRP1) cytoplasm (NLRP1)
Anatomy Link Frequency
NAc 4
brain 2
urine 2
neuronal 2
embryo 1
NLRP1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Dopamine 1211 100.00 Very High Very High Very High
Nucleus accumbens 301 100.00 Very High Very High Very High
Glutamate 106 99.98 Very High Very High Very High
Ventral tegmentum 163 99.94 Very High Very High Very High
amygdala 45 99.60 Very High Very High Very High
Neurotransmitter 109 99.56 Very High Very High Very High
tolerance 69 99.52 Very High Very High Very High
agonist 146 99.46 Very High Very High Very High
Opioid 375 99.32 Very High Very High Very High
gABA 75 98.90 Very High Very High Very High
Disease Link Frequency Relevance Heat
Sepsis 34 99.80 Very High Very High Very High
Attention Deficit Hyperactivity Disorder 150 98.86 Very High Very High Very High
Syndrome 186 97.12 Very High Very High Very High
Substance Withdrawal Syndrome 40 96.20 Very High Very High Very High
Drug Dependence 139 95.40 Very High Very High Very High
Suicidal Behaviour 19 93.84 High High
Diarrhoea 6 92.28 High High
Cramps 5 91.72 High High
Anxiety Disorder 62 91.12 High High
Opiate Addiction 140 90.64 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Using western blotting technique, we aimed to detect the presence of Nalp1 and Nalp3 proteins in the HCE-T cells.
Localization (presence) of Nalp1 in T cells
1) Confidence 0.71 Published 2008 Journal Molecular Vision Section Body Doc Link PMC2526096 Disease Relevance 0 Pain Relevance 0
It is important to note that NAC itself is also efficiently cleared by the kidney and excreted into urine in high concentrations (Borgstrom et al. 1986; Rodenstein et al. 1978).
Localization (excreted) of NAC in urine
2) Confidence 0.47 Published 2008 Journal Environ Health Perspect Section Body Doc Link PMC2199271 Disease Relevance 0 Pain Relevance 0.03
In addition, our results demonstrate that the amount of MeHg excreted into urine after NAC challenge is proportional to the MeHg body burden, indicating that NAC may be useful as a bio-monitoring agent.
Localization (excreted) of NAC in urine
3) Confidence 0.47 Published 2008 Journal Environ Health Perspect Section Body Doc Link PMC2199271 Disease Relevance 0.07 Pain Relevance 0
In humans the half-life of NAC in blood plasma is only 2 hr; this short half-life is due largely to NAC’s rapid urinary excretion (Borgstrom et al. 1986; Rodenstein et al. 1978).
Localization (excretion) of NAC in blood
4) Confidence 0.47 Published 2008 Journal Environ Health Perspect Section Body Doc Link PMC2199271 Disease Relevance 0 Pain Relevance 0.04
We also examined whether NAC is effective at accelerating urinary excretion of MeHg in rats of both sexes and at different ages, and whether it can diminish MeHg levels in the developing embryo.
Localization (excretion) of NAC in embryo
5) Confidence 0.47 Published 2008 Journal Environ Health Perspect Section Body Doc Link PMC2199271 Disease Relevance 0.24 Pain Relevance 0
Moreover, dopamine release in the VTA is linked to polymorphisms of the DRD2 gene and even attention-deficit hyperactivity disorder (ADHD), whereby carriers of the DRD2 A1 allele show a reduced NAc release of dopamine (DA).
Localization (release) of NAc in NAc associated with nucleus accumbens, ventral tegmentum, dopamine and attention deficit hyperactivity disorder
6) Confidence 0.46 Published 2010 Journal Med. Hypotheses Section Abstract Doc Link 19914781 Disease Relevance 0.48 Pain Relevance 0.94
If music causes a powerful activation in spite of the DRD2 A1 allele due to a strong DA neuronal release which subsequently impinges on existing D2 receptors, then it is reasonable to assume that music is a strong indirect D2 agonist (by virtue of DA neuronal release in the NAc) and may have important therapeutic applicability in Reward Deficiency Syndrome (RDS) related behaviors including Substance Use Disorder (SUD).
Localization (release) of NAc in NAc associated with drug dependence, nucleus accumbens, dopamine, syndrome and agonist
7) Confidence 0.43 Published 2010 Journal Med. Hypotheses Section Abstract Doc Link 19914781 Disease Relevance 0.56 Pain Relevance 0.78
Furthermore, in patients with sepsis who were administered NAC, Paterson and coworkers [18] found decreased nuclear factor-?
Localization (administered) of NAC associated with sepsis
8) Confidence 0.30 Published 2004 Journal Crit Care Section Body Doc Link PMC522835 Disease Relevance 1.00 Pain Relevance 0.23
Neuroimaging studies in humans have shown that rewarding stimuli activate dopaminergic cells in the VTA [64-66] eliciting an increase of dopamine release in the NAc [67].
Localization (release) of NAc associated with nucleus accumbens, ventral tegmentum and dopamine
9) Confidence 0.24 Published 2008 Journal Ann Gen Psychiatry Section Body Doc Link PMC2515304 Disease Relevance 0.32 Pain Relevance 0.41
Our solution is to stimulate DA release at the NAc naturally, not via powerful DA agonists that could ultimately lead to DA down-regulation.
Localization (release) of NAc associated with nucleus accumbens, dopamine and agonist
10) Confidence 0.14 Published 2008 Journal Theor Biol Med Model Section Body Doc Link PMC2615745 Disease Relevance 0 Pain Relevance 0.79
While dopamine (DA) is critical to maintain normalization of natural rewards, the neuronal release of DA into NAc synaptic sites is somewhat complex.
Localization (release) of NAc in neuronal associated with nucleus accumbens and dopamine
11) Confidence 0.14 Published 2008 Journal Theor Biol Med Model Section Body Doc Link PMC2615745 Disease Relevance 0.16 Pain Relevance 0.40
The disinhibition of dopamine-containing neurons in the ventral tegmental area (VTA) allows them to release dopamine in the NAc and (via amygdala) in certain parts of the hippocampus, permitting the completion of the cascade and the development of the reward sensation [23].
Localization (release) of NAc in hippocampus associated with nucleus accumbens, ventral tegmentum, dopamine, hippocampus and amygdala
12) Confidence 0.14 Published 2008 Journal Theor Biol Med Model Section Body Doc Link PMC2615745 Disease Relevance 0.08 Pain Relevance 1.01
This release of DA into the NAc causes feelings of pleasure.
Localization (release) of NAc in NAc associated with nucleus accumbens and dopamine
13) Confidence 0.13 Published 2002 Journal Sci Pract Perspect Section Body Doc Link PMC2851054 Disease Relevance 0.17 Pain Relevance 1.30
For example, opioid tolerance that reduces the VTA’s release of DA into the NAc may prevent the patient from obtaining pleasure from normally rewarding activities such as eating.
Localization (release) of NAc associated with nucleus accumbens, ventral tegmentum, dopamine, tolerance and opioid
14) Confidence 0.13 Published 2002 Journal Sci Pract Perspect Section Body Doc Link PMC2851054 Disease Relevance 0.70 Pain Relevance 1.52
Use of these substances and engaging in these aforementioned behaviors commonly induces the release of neuronal DA into the synapse at the NAc, the reward center of the brain [3].
Localization (release) of NAc in brain associated with nucleus accumbens and dopamine
15) Confidence 0.13 Published 2008 Journal Theor Biol Med Model Section Body Doc Link PMC2615745 Disease Relevance 0.15 Pain Relevance 0.52
For example, more opioid is needed to stimulate the VTA brain cells of the mesolimbic reward system to release the same amount of DA in the NAc.
Localization (release) of NAc in brain associated with nucleus accumbens, ventral tegmentum, dopamine and opioid
16) Confidence 0.12 Published 2002 Journal Sci Pract Perspect Section Body Doc Link PMC2851054 Disease Relevance 0.63 Pain Relevance 2.05
One variant, by Koob and LeMoal (2001), is based on the idea that neurons of the mesolimbic reward pathways are naturally “set” to release enough DA in the NAc to produce a normal level of pleasure.
Localization (release) of NAc in neurons associated with nucleus accumbens and dopamine
17) Confidence 0.12 Published 2002 Journal Sci Pract Perspect Section Body Doc Link PMC2851054 Disease Relevance 0.37 Pain Relevance 1.23
The result of utilizing this natural dopaminergic activating approach over time should lead to neuronal DA release at the NAc, potentiating a proliferation of D2 receptors [28,29].
Localization (release) of NAc in neuronal associated with nucleus accumbens and dopamine
18) Confidence 0.12 Published 2008 Journal Theor Biol Med Model Section Body Doc Link PMC2615745 Disease Relevance 0.35 Pain Relevance 0.26
Thus, acute treatment should consist of preferential blocking of postsynaptic Nucleus Accumbens (NAc) dopamine receptors (D1-D5), whereas long term activation of the mesolimbic dopaminergic system should involve activation and/or release of Dopamine (DA) at the NAc site.
Localization (release) of NAc in Nucleus associated with dopamine and dopamine receptor
19) Confidence 0.12 Published 2008 Journal Theor Biol Med Model Section Abstract Doc Link PMC2615745 Disease Relevance 0.24 Pain Relevance 0.50
The chemical messages include serotonin, enkephalins, GABA and dopamine, all working in concert to provide a net release of DA at the NAc (a region in the mesolimbic system).
Localization (release) of NAc associated with nucleus accumbens, dopamine, gaba, enkephalin and serotonin
20) Confidence 0.12 Published 2008 Journal Theor Biol Med Model Section Body Doc Link PMC2615745 Disease Relevance 0.05 Pain Relevance 0.52

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