INT35467
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Similar effects were produced by the selective D-2 antagonists, sulpiride and metoclopramide, which had no effect on hyperpolarizations evoked by norepinephrine. | |||||||||||||||
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The possibility of a defect in d-2-hydroxyglutarate dehydrogenation prompted us to employ E. coli d-2-hydroxyacid dehydrogenase cDNA to search the human expressed sequence tags database. | |||||||||||||||
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Group D 2 1,000 mL of 10% of glucose in water, 40 units of fast acting insulin in the same rate as Group B. | |||||||||||||||
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There was a significantly higher peak pain rating after D2 compared to C2 during MVBF or MVJO (P<0.022), whereas no significant difference in peak pain ratings was found between A2 and B2 (P>0.084). | |||||||||||||||
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Without D2 activation, acceleration of contraction is blocked, movement acceleration cannot occur, and stepping fails. | |||||||||||||||
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Urinary concentrations of tumor necrosis factor, prostaglandins E2, D2 and F2 alpha, and thromboxane B2 were not different among either patient groups or controls. | |||||||||||||||
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As dopamine release is acutely impaired, synaptic concentration cannot achieve a level necessary for micromolar D2 activation. | |||||||||||||||
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In the present study, the density of striatal DA terminals and DA receptors and the expression of D-1, D-2, and D-3 receptors, preproenkephalin (PPE-A), preprotachykinin (PPT), and nitric oxide synthase (NOS) mRNAs in the striatum and nucleus accumbens and nigral TH mRNA expression were examined. | |||||||||||||||
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It is well accepted that, in humans, most circulating T3 is derived from extrathyroidal deiodination of T4 via D2 [3]; thus, it makes sense to hypothesize that defects in D2 expression/activity could interfere with the efficacy of L-T4 monotherapy. | |||||||||||||||
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Role of dopamine agonists in proliferation of D2 receptors | |||||||||||||||
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Because the D2 reductions are associated with decreased activity in the anterior cingulate gyrus and in the orbitofrontal cortex they postulate that this is one of the mechanisms by which DA disruption leads to compulsive drug administration and the lack of control over drug intake in the drug-addicted individual. | |||||||||||||||
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Venlafaxine probably inhibits serotonin uptake only in low doses, whereas both serotonin and noradrenaline uptake are inhibited following high doses.115 The drug does not possess significant affinity for 5HT1A, 5HT2A, D2, muscarinic, or ? | |||||||||||||||
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In the dopamine receptor network, many ligands are preferably predicted for dopamine receptor D2, and small number of ligands like perphenazine hydrochloride (D04965) is common among all dopamine receptors (D1, D2 and D3). | |||||||||||||||
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Repeated measures ANOVA for factors GROUP and SESSION revealed no significant interaction for d1 of the right hand (F(3,60)= 0.060, p = 0.981) and left d2 (F(3,60) =0.387, p = 0.763), but for fingers d2 (F(3,60) =7.519, p ? | |||||||||||||||
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Repeated measures ANOVA for factors GROUP and SESSION revealed no significant interaction for d1 of the right hand (F(3,60)= 0.060, p = 0.981) and left d2 (F(3,60) =0.387, p = 0.763), but for fingers d2 (F(3,60) =7.519, p ? | |||||||||||||||
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By contrast, we show that the D2 and D3 receptor subtypes are expressed in the lumbar spinal cord as in the rat where the D2 [58], [59] and D3 [60] receptor subtypes are highly expressed. | |||||||||||||||
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Overall, D2, D3 and D5 receptor subtypes were expressed in the lumbar spinal cord sections. | |||||||||||||||
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As D2 receptors are more highly expressed in the dorsal horn, their stimulation might contribute to modulating the somesthetic processes and spinal reflexes [13]. | |||||||||||||||
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The detection of D2 labeling in spinal cord sections showed that D2 receptors were intensely expressed in the dorsal horns mainly within the laminae I to VI, as illustrated in Figure 2C. | |||||||||||||||
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Levels in D2 were higher than S2 or controls for MCP-1 and M-CSF. | |||||||||||||||
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General Comments
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