Music is used in healthcare to promote physical and psychological well-being. As clinical applications of music continue to expand, there is a growing need to understand the biological mechanisms by which music influences health. Here we explore the neurochemistry and social flow of group singing. Four participants from a vocal jazz ensemble were conveniently sampled to sing together in two separate performances: pre-composed and improvised. Concentrations of plasma oxytocin and adrenocorticotropic hormone (ACTH) were measured before and after each singing condition to assess levels of social affiliation, engagement and arousal. A validated assessment of flow state was administered after each singing condition to assess participants' absorption in the task. The feasibility of the research methods were assessed and initial neurochemical data was generated on group singing. Mean scores of the flow state scale indicated that participants experienced flow in both the pre-composed (M = 37.06) and improvised singing conditions (M = 34.25), with no significant difference between conditions. ACTH concentrations decreased in both conditions, significantly so in the pre-composed singing condition, which may have contributed to the social flow experience. Mean plasma oxytocin levels increased only in response to improvised singing, with no significant difference between improvised and pre-composed singing conditions observed. The results indicate that group singing reduces stress and arousal, as measured by ACTH, and induces social flow in participants. The effects of pre-composed and improvised group singing on oxytocin are less clear. Higher levels of plasma oxytocin in the improvised condition may perhaps be attributed to the social effects of improvising musically with others. Further research with a larger sample size is warranted.

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A novel tantalum pentoxide nanoparticle-electrochemically reduced graphene oxide nanocomposite-modified glassy carbon electrode (Ta2O5-ErGO/GCE) was developed for the detection of oxytetracycline in milk. The composition, structure and morphology of GO, Ta2O5, and Ta2O5-ErGO were characterized by X-ray diffraction (XRD) and scanning electron microscopy (SEM). Oxytetracycline electrochemical behavior on the bare GCE, GO/GCE, ErGO/GCE, and Ta2O5-ErGO/GCE was studied by cyclic voltammetry. The voltammetric conditions (including scan rate, pH, deposition potential, and deposition time) were systematically optimized. With the spacious electrochemical active area, the Ta2O5-ErGO/GCE showed a great magnification of the oxidation signal of oxytetracycline, while that of the other electrodes (GCE, GO/GCE, ErGO/GCE) could not reach the same level. Under the optimum conditions, the currents were proportional to the oxytetracycline concentration in the range from 0.2 to 10 μM, and a low detection limit of 0.095 μM (S/N = 3) was detectable. Moreover, the proposed Ta2O5-ErGO/GCE performed practically with satisfactory results. The preparation of Ta2O5-ErGO/GCE in the current work provides a minor outlook of detecting trace oxytetracycline in milk.

Glial cell line-derived neurotrophic factor (GDNF) has been identified as a potent survival factor for both central and peripheral neurons. GDNF has been shown to be a potent survival factor for motor neurons during programmed cell death and continuous treatment with GDNF maintains hyperinnervation of skeletal muscle in adulthood. However, little is known about factors regulating normal production of endogenous GDNF in skeletal muscle. This study aimed to examine the role that motor neurons play in regulating GDNF secretion by skeletal muscle. A co-culture of skeletal muscle cells (C2C12) and cholinergic neurons, glioma × neuroblastoma hybrid cells (NG108-15) were used to create nerve muscle interactions in vitro. Acetylcholine receptors (AChRs) on nerve-myotube co-cultures were blocked with alpha bungarotoxin (α-BTX). GDNF protein content in cells and in culture medium was analyzed by enzyme-linked immunosorbant assay (ELISA) and western blotting. GDNF localization was examined by immunocytochemistry. The nerve-muscle co-culture study indicated that the addition of motor neurons to skeletal muscle cells reduced the secretion of GDNF by skeletal muscle. The results also showed that blocking AChRs with α-BTX reversed the action of neural cells on GDNF secretion by skeletal muscle. Although ELISA results showed no GDNF in differentiated NG108-15 cells grown alone, immunocytochemical analysis showed that GDNF was localized in NG108-15 cells co-cultured with C2C12 myotubes. These results suggest that motor neurons may be regulating their own supply of GDNF secreted by skeletal muscle and that activation of AChRs may be involved in this process.

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