Objectives: Speech comprehension under “cocktail party” scenarios deteriorates with age even in the absence of measurable hearing loss. Musical training is suggested to counteract the age-related decline in speech-in-noise (SIN) perception, yet which aspect of musical plasticity contributes to this compensation remains unclear. This study aimed to investigate the effects of musical experience and aging on SIN perception ability. We hypothesized a key mediation role of auditory working memory in ameliorating deficient SIN perception in older adults by musical training. Design: Forty-eight older musicians, 29 older nonmusicians, 48 young musicians, and 24 young nonmusicians all with (near) normal peripheral hearing were recruited. The SIN task was recognizing nonsense speech sentences either perceptually colocated or separated with a noise masker (energetic masking) or a two-talker speech masker (informational masking). Auditory working memory was measured by auditory digit span. Path analysis was used to examine the direct and indirect effects of musical expertise and age on SIN perception performance. Results: Older musicians outperformed older nonmusicians in auditory working memory and all SIN conditions (noise separation, noise colocation, speech separation, speech colocation), but such musician advantages were absent in young adults. Path analysis showed that age and musical training had opposite effects on auditory working memory, which played a significant mediation role in SIN perception. In addition, the type of musical training did not differentiate SIN perception regardless of age. Conclusions: These results provide evidence that musical training offsets age-related speech perception deficit at adverse listening conditions by preserving auditory working memory. Our findings highlight auditory working memory in supporting speech perception amid competing noise in older adults, and underline musical training as a means of “cognitive reserve” against declines in speech comprehension and cognition in aging populations.

Beta-adrenoceptor (β-AR) exerts critical regulation of cardiac function. MicroRNAs (miRNAs) are potentially involved in a variety of biological and pathological processes. This study aimed to investigate the role of miRNA let-7e in the up-regulation of β1-AR and arrhythmogenesis in acute myocardial infarction (AMI) in rats. β1-AR expression was significantly up-regulated and let-7a, c, d, e and i were markedly down-regulated in the infarcted heart after 6 and 24 hrs myocardial infarction. Forced expression of let-7e suppressed β1-AR expression at the protein level, without affecting β1-AR mRNA level, in neonatal rat ventricular cells (NRVCs). Silencing of let-7e by let-7e antisense inhibitor (AMO-let-7e) enhanced β1-AR expression at the protein level in NRVCs. Administration of the lentivirus vector containing precursor let-7e (len-pre-let-7e) significantly inhibited β1-AR expression in rats, whereas len-AMO-let-7e up-regulated β1-AR relative to the baseline control level, presumably as a result of depression of tonic inhibition of β1-AR by endogenous let-7e. Len-negative control (len-NC) did not produce significant influence on β1-AR expression. Len-pre-let-7e also profoundly reduced the up-regulation of β1-AR induced by AMI and this effect was abolished by len-AMO-let-7e. Importantly, len-pre-let-7e application significantly reduced arrhythmia incidence after AMI in rats and its anti-arrhythmic effect was cancelled by len-AMO-let-7e. Notably, anti-arrhythmic efficacy of len-pre-let-7e was similar to propranolol, a non-selective β-AR blocker and metoprolol, a selective β1-AR blocker. Down-regulation of let-7e contributes to the adverse increase in β1-AR expression in AMI and let-7e supplement may be a new therapeutic approach for preventing adverse β1-AR up-regulation and treating AMI-induced arrhythmia.

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Decreased ChAT-IR neurons and increased NOS-IR in the MP of colon ENS may contribute to the pathogenesis of colonic dysmotility in CP.

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