INT56658

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Context Info
Confidence 0.58
First Reported 1993
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 7
Total Number 11
Disease Relevance 5.60
Pain Relevance 2.22

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

cytoplasm (Spnb4)
Anatomy Link Frequency
clock neurons 3
dorsal 1
finger 1
ventral 1
Spnb4 (Mus musculus)
Pain Link Frequency Relevance Heat
Morphine 5 98.96 Very High Very High Very High
Eae 90 98.68 Very High Very High Very High
Dynorphin 3 98.30 Very High Very High Very High
narcan 2 96.56 Very High Very High Very High
antagonist 5 96.38 Very High Very High Very High
Opioid 4 96.14 Very High Very High Very High
anesthesia 70 91.92 High High
nalbuphine 2 91.04 High High
imagery 10 86.96 High High
tail-flick 1 86.12 High High
Disease Link Frequency Relevance Heat
Disease 510 100.00 Very High Very High Very High
Dystonia 240 100.00 Very High Very High Very High
Injury 65 100.00 Very High Very High Very High
Stuttering 10 98.08 Very High Very High Very High
Attention Deficit Hyperactivity Disorder 40 92.16 High High
Syndrome 40 90.40 High High
Hyperuricemia 95 90.28 High High
Cognitive Disorder 180 86.76 High High
Metabolic Disorder 5 80.40 Quite High
Aggression 10 74.36 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Additional pharmacological tests were used as criteria for Dyn A release: a) Small doses of the opioid antagonists naloxone and norbinaltorphimine administered IT inhibited the antagonistic action; b) dynorphin antiserum given IT blocked the action of Dyn A; c) desensitization to the effect of Dyn A was produced by 3-h pretreatment with morphine, 10 mg/kg SC, or by pretreatment with the agents themselves.
Gene_expression (produced) of Dyn associated with dynorphin, antagonist, narcan, opioid and morphine
1) Confidence 0.58 Published 1993 Journal Pharmacol. Biochem. Behav. Section Abstract Doc Link 8101007 Disease Relevance 0 Pain Relevance 1.71
The third caveat is that corticospinal motor signs do no seem to show graded severity across the patient groups, since they are equally frequent and severe in both classic and variant LND (Fig. 6).
Gene_expression (classic) of LND associated with disease
2) Confidence 0.34 Published 2010 Journal Brain Section Body Doc Link PMC2842514 Disease Relevance 0.83 Pain Relevance 0.09
The third caveat is that corticospinal motor signs do no seem to show graded severity across the patient groups, since they are equally frequent and severe in both classic and variant LND (Fig. 6).
Gene_expression (variant) of LND associated with disease
3) Confidence 0.34 Published 2010 Journal Brain Section Body Doc Link PMC2842514 Disease Relevance 0.82 Pain Relevance 0.09
Collectively, these patients are labelled LND variants.
Gene_expression (variants) of LND associated with disease
4) Confidence 0.30 Published 2010 Journal Brain Section Body Doc Link PMC2842514 Disease Relevance 0.95 Pain Relevance 0
For example, the hyperlordotic postures seen in some variants may reflect milder expressions of the more severe truncal dystonia and opisthotonic postures common in classic LND (Jinnah et al., 2006).
Gene_expression (expressions) of LND associated with dystonia and disease
5) Confidence 0.30 Published 2010 Journal Brain Section Body Doc Link PMC2842514 Disease Relevance 1.74 Pain Relevance 0
It is tempting to speculate that this onychophagia is a forme fruste of more serious finger biting, which is the commonest expression of self-injury in classic LND (Anderson and Ernst, 1994; Schretlen et al., 2005).
Gene_expression (expression) of LND in finger associated with injury and disease
6) Confidence 0.27 Published 2010 Journal Brain Section Body Doc Link PMC2842514 Disease Relevance 1.20 Pain Relevance 0
Under LD conditions, increasing Shaw levels in all clock neurons (LNv, LNd, DN1, DN2 and DN3), or in subsets of clock neurons (LNd and DNs or DNs alone) increases locomotor activity at night.
Gene_expression (levels) of LNd in clock neurons associated with eae
7) Confidence 0.01 Published 2008 Journal PLoS ONE Section Abstract Doc Link PMC2386553 Disease Relevance 0 Pain Relevance 0.12
cry-GAL4/UAS-Shaw flies, which express in fewer clock neurons compared to tim-GAL4 (LNv, LNd, 4 DN1 and 2 DN3's) maintain rhythmic behavior (Figure 3C).
Gene_expression (flies) of LNd in clock neurons
8) Confidence 0.01 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2386553 Disease Relevance 0.06 Pain Relevance 0
Under LD conditions, increasing Shaw levels in all clock neurons (LNv, LNd, DN1, DN2 and DN3), or in subsets of clock neurons (LNd and DNs or DNs alone) increases locomotor activity at night.
Gene_expression (levels) of LNd in clock neurons associated with eae
9) Confidence 0.01 Published 2008 Journal PLoS ONE Section Abstract Doc Link PMC2386553 Disease Relevance 0 Pain Relevance 0.12
Clock neurons can be visualized and genetically accessed by using GAL4 drivers [37] that are controlled by clock-cell specific promoters such as those from the timeless (Figure 1A, C and E–G) and Pdf (Figure 1D) genes [26]–[27]. tim-GAL4 is expressed strongly in all clock neurons including the DN1, DN2, and DN3 groups and in the well characterized dorsal and ventral lateral neurons (LNd and LNv).
Gene_expression (groups) of LNd in ventral
10) Confidence 0.01 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2386553 Disease Relevance 0 Pain Relevance 0.04
Clock neurons can be visualized and genetically accessed by using GAL4 drivers [37] that are controlled by clock-cell specific promoters such as those from the timeless (Figure 1A, C and E–G) and Pdf (Figure 1D) genes [26]–[27]. tim-GAL4 is expressed strongly in all clock neurons including the DN1, DN2, and DN3 groups and in the well characterized dorsal and ventral lateral neurons (LNd and LNv).
Gene_expression (groups) of LNd in dorsal
11) Confidence 0.00 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2386553 Disease Relevance 0 Pain Relevance 0.04

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