Neuroscience
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Professional Pingju actors have been shown to exhibit practice-induced plastic changes in spontaneous regional brain activity; however, whether these changes are present in resting-state regional cerebral blood flow (CBF) remains largely unclear. Here, twenty professional Pingju opera actors and 20 age-, sex-, and handedness-matched untrained subjects were recruited, and resting-state CBF maps were obtained by using a three-dimensional pseudocontinuous arterial spin labelling sequence. Voxel-based comparisons of the CBF maps between the two groups were performed with two-sample t-tests, and correlation analyses between the CBF changes and years of training in the actor group were conducted. ⋯ Compared with untrained subjects, the actors showed significantly higher CBF in the right inferior temporal gyrus, right middle temporal gyrus, left temporal pole, and left inferior frontal gyrus, whereas significantly lower CBF was not found in the actor group (voxel-level uncorrected p < 0.001, cluster-level family-wise error corrected p < 0.05). Furthermore, there was no correlation between the mean CBF values from significantly different clusters and the years of training, and no significant alterations in CBF connectivity were found in the actor group. Overall, these results provided preliminary evidence that neural plastic changes in CBF are present in professional Pingju opera actors, which may correspond to specific experiences associated with Pingju opera training.
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Unilateral noise-induced hearing loss reduces the input to the central auditory pathway disrupting the excitatory and inhibitory inputs to the inferior colliculus (IC), an important binaural processing center. Little is known about the compensatory synaptic changes that occur in the IC as a consequence of unilateral noise-induced hearing loss. To address this issue, Sprague-Dawley rats underwent unilateral noise exposure resulting in severe unilateral hearing loss. ⋯ At 28-d post-exposure, the gene expression pattern was reversed with more than 85% of genes in the ipsilateral IC now downregulated. Most genes previously downregulated in the contralateral IC 2-d post-exposure had recovered; less than 15% remained downregulated. These time-dependent, asymmetric changes in synaptic plasticity gene expression could shed new light on the perceptual deficits associated with unilateral hearing loss and the dynamic structural and functional changes that occur in the IC days and months following unilateral noise-induced hearing loss.
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Aging occurs due to a combination of several factors, such as telomere attrition, cellular senescence, and stem cell exhaustion. The telomere attrition-dependent cellular senescence is regulated by increased levels of SMAD specific E3 ubiquitin protein ligase 2 (smurf2). With age smurf2 expression increases and Smurf2 protein interacts with several regulatory proteins including, Smad7, Ep300, Yy1, Sirt1, Mdm2, and Tp53, likely affecting its function related to cellular aging. ⋯ Also, the expression levels of its interacting partners defined by the STRING database, tp53, mdm2, ep300a, yy1a, smad7, and sirt1, were analyzed. Multivariate analysis indicated that smurf2, ep300a, and sirt1, whose proteins regulate ubiquitination, acetylation, and deacetylation of target proteins including Smad7 and Tp53, showed age- and brain region-dependent patterns. Our data suggest a likely balance between Smurf2- and Mdm2-mediated ubiquitination, and Ep300a-mediated acetylation/Sirt1-mediated deacetylation, which most possibly affects the functionality of other interacting partners in regulating cellular and synaptic aging and ultimately cognitive dysfunction.
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Myofascial pain syndrome (MPS) is a type of skeletal pain identified by myofascial trigger points (MTrPs). The formation of MTrPs is linked to muscle damage. The fibroblast growth factor receptor (FGFR1) has been found to cause pain sensitivity while repairing tissue damage. ⋯ PD173074 increased the mechanical pain threshold of the MTrPs group, and inhibited the expression of p-FGFR1, PI3K-p110γ, and p-AKT. Moreover, LY294002 increased the mechanical pain threshold of the MTrPs group. These findings suggest that FGFR1 may regulate myofascial pain in rats through the PI3K/AKT pathway.