Music intervention (MI) has been applied as an effective adjunctive treatment for pain control in various clinical settings. However, no meta-analysis has yet been published on the analgesic effects of MI in infants and children. We performed a systematic review of PubMed, EMBASE, Web of Science, and Cochrane Library databases to identify randomized controlled trials (RCTs) with the keywords “pain” AND “music therapy” from inception to January 2022. Primary outcomes were pain intensity and vital signs. Standardized mean difference (SMD) values and the corresponding 95% confidence intervals (CIs) were computed using a random effect model. Subgroup analyses with age groups, types of pain, and music styles were conducted. A total of 38 RCTs involving 5601 participants met the selection criteria. MI significantly decreased the pain levels (SMD = −0.57, p < 0.001), both in the newborn group (p = 0.007) and in the infant/children group (p < 0.001). MI significantly reduced heart rate (SMD = −0.50, p < 0.001) and respiratory rate (SMD = −0.60, p = 0.002) and increased peripheral capillary oxygen saturation (SMD = 0.44, p < 0.001). In subgroup analyses of types of pain, MI had significant effects on prick pain (p = 0.003), chronic and procedural pain (p < 0.001), and postoperative pain (p = 0.018). As for music styles, significant analgesic effects were observed for classical music (p < 0.001), kids’ music (p < 0.001), and pop music (p = 0.001), but not for world music (p = 0.196), special composition (p = 0.092), and multiple music combinations (p = 0.420). In conclusion, our analysis provides supportive evidence about the efficacy of MI, especially classical, kids’, and pop music, in controlling prick, procedural, and postoperative pain in the pediatric population.

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We attempted to examine the alterations elicited by opioids via coexpressed μ-opioid (MOP) and nociceptin/orphanin FQ (NOP) receptors for receptor localization and Erk1/2 (p44/42 MAPK) in human embryonic kidney (HEK) 293 cells. Through two-photon microscopy, the proximity of MOP and NOP receptors was verified by fluorescence resonance energy transfer (FRET), and morphine but not buprenorphine facilitated the process of MOP-NOP heterodimerization. Single-particle tracking (SPT) further revealed that morphine or buprenorphine hindered the movement of the MOP-NOP heterodimers. After exposure to morphine or buprenorphine, receptor localization on lipid rafts was detected by immunocytochemistry, and phosphorylation of Erk1/2 was determined by immunoblotting in HEK 293 cells expressing MOP, NOP, or MOP+NOP receptors. Colocalization of MOP and NOP on lipid rafts was enhanced by morphine but not buprenorphine. Morphine stimulated the phosphorylation of Erk1/2 with a similar potency in HEK 293 cells expressing MOP and MOP+NOP receptors, but buprenorphine appeared to activate Erk1/2 solely through NOP receptors. Our results suggest that opioids can fine-tune the cellular localization of opioid receptors and phosphorylation of Erk1/2 in MOP+NOP-expressing cells.

Background and Objectives: Nicotinamide adenine dinucleotide (NAD) is an important coenzyme in various physiological processes, including sirtuins (SIRTs) and kynurenine pathway (KP). Previous studies have shown that lower NAD levels can be indicative of increased risks of cancer and psychiatric disorders. However, there has been no prior study exploring the link between NAD homeostasis and psychiatric disorders from a genetic perspective. Therefore, we aimed to investigate the association of genetic polymorphism in the pathways of NAD biosynthesis with major depressive disorder (MDD). Methods: A total of 317 patients were included in the case group and were compared with sex-matched control group of 1268 participants (1:4 ratio) from Taiwan Biobank (TWB). All subjects in the control group were over 65 years old, which is well past the average age of onset of MDD. Genomic DNA extracted from patients’ blood buffy coat was analyzed using the Affymetrix TWB array. Full-model tests were conducted for the analysis of single nucleotide polymorphism (SNPs) in all candidate genes. We focused on genes within the NAD-related candidate pathways, including 15 in KP, 12 in nicotinate metabolism, 7 in SIRTs, and 19 in aldehyde dehydrogenases (ALDHs). A total of 508 SNPs were analyzed in this study. After significant SNPs were determined, 5000 genome-wide max(T) permutations were performed in Plink. Finally, we built a predictive model with logistic regression and assessed the interactions of SNPs with the haplotype association tests. Results: We found three SNPs that were significantly associated with MDD in our NAD-related candidate pathways, one within the KP (rs12622574 in ACMSD) and two within the nicotinate metabolism (rs28532698 in BST1 and rs3733593 in CD38). The observed association with MDD was significant in the dominant model of inheritance with marital status, education level, and body mass index (BMI) adjusted as covariates. Lastly, in haplotype analysis, the three associated SNPs consisted of one haploblock in ACMSD, four haploblocks in BST1, and two haploblocks in CD38. Conclusions: This study provides the first evidence that genetic variations involved in NAD homeostasis in the KP and nicotinate metabolism may be associated with the occurrence of MDD.

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