Pain
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The attentional demand of pain has primarily been investigated within an intrapersonal context. Little is known about observers' attentional processing of another's pain. The present study investigated, within a sample of parents (n=65; 51 mothers, 14 fathers) of school children, parental selective attention to children's facial display of pain and the moderating role of child's facial expressiveness of pain and parental catastrophizing about their child's pain. ⋯ This interference effect was particularly pronounced for high-catastrophizing parents, suggesting that being confronted with increasing child pain displays becomes particularly demanding for high-catastrophizing parents. Finally, parents with higher levels of catastrophizing increasingly attended away from low pain expressions, whereas selective attention to high-pain expressions did not differ between high-catastrophizing and low-catastrophizing parents. Theoretical implications and further research directions are discussed.
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Existing microarray gene expression profiling studies of tonic/chronic pain were subjected to meta-analysis to identify genes found to be regulated by these pain states in multiple, independent experiments. Twenty studies published from 2002 to 2008 were identified, describing the statistically significant regulation of 2254 genes. Of those, a total of 79 genes were found to be statistically significant "hits" in 4 or more independent microarray experiments, corresponding to a conservative P<0.01 overall. ⋯ We independently confirmed the regulation of 43 of these genes in the rat-CCI-DRG condition; the genetic correlates in all other conditions were largely and, in some cases, strikingly, independent. However, a handful of genes were identified whose regulation bridged etiology, anatomical locus, and/or species. Most notable among these were Reg3b (regenerating islet-derived 3 beta; pancreatitis-associated protein) and Ccl2 (chemokine [C-C motif] ligand 2), which were significantly upregulated in every condition in the rat.
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Randomized Controlled Trial Multicenter Study
Efficacy of acupuncture for migraine prophylaxis: a single-blinded, double-dummy, randomized controlled trial.
Insufficient clinical trial data were available to prove the efficacy of acupuncture for migraine prophylaxis. A multicenter, double-dummy, single-blinded, randomized controlled clinical trial was conducted at the outpatient departments of acupuncture at 5 hospitals in China to evaluate the effectiveness of acupuncture. A total of 140 patients with migraine without aura were recruited and assigned randomly to 2 different groups: the acupuncture group treated with verum acupuncture plus placebo and the control group treated with sham acupuncture plus flunarizine. ⋯ The secondary outcome measures included the number of migraine days, visual analogue scale (VAS, 0 to 10 cm) for pain, as well as the physical and mental component summary scores of the 36-item short-form health survey (SF-36). The patients in the acupuncture group had better responder rates and fewer migraine days compared with the control group (P<.05), whereas there were no significant differences between the 2 groups in VAS scores and SF-36 physical and mental component summary scores (P>.05). The results suggested that acupuncture was more effective than flunarizine in decreasing days of migraine attacks, whereas no significantly differences were found between acupuncture and flunarizine in reduction of pain intensity and improvement of the quality of life.
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Gout is characterized by the deposition of monosodium urate (MSU) crystals. Despite being one of the most painful forms of arthritis, gout and the mechanisms responsible for its acute attacks are poorly understood. In the present study, we found that MSU caused dose-related nociception (ED(50) [ie, the necessary dose of MSU to elicit 50% of the response relative to the control value]=0.04 [95% confidence interval 0.01-0.11]mg/paw) and edema (ED(50)=0.08 [95% confidence interval 0.04-0.16]mg/paw) when injected into the hind paw of rats. ⋯ Furthermore, the antagonism of histaminergic H1 and serotoninergic receptors decreased the edema, but not the nociception of MSU. Finally, the prevention of the tryptase activity was capable of largely reducing both MSU-induced nociception and edema. Collectively, the present findings demonstrate that MSU produces nociceptive and edematogenic responses mediated by TRPV1 receptor activation and mast cell degranulation.