Search

We propose a multi-singer emotional singing voice synthesizer, Muse-SVS, that expresses emotion at various intensity levels by controlling subtle changes in pitch, energy, and phoneme duration while accurately following the score. To control multiple style attributes while avoiding loss of fidelity and expressiveness due to interference between the attributes, Muse-SVS represents all attributes and their relations together by a joint embedding in a unified embedding space. Muse-SVS can express emotional intensity levels not included in the training data through embedding interpolation and extrapolation. We also propose a statistical pitch predictor to express pitch variation according to emotional intensity, and a context-aware residual duration predictor to prevent the accumulation of phoneme-level duration prediction errors, which is crucial for synchronization with instrumental parts. In addition, we propose a novel ASPP-Transformer, which combines atrous spatial pyramid pooling (ASPP) and Transformer, to improve fidelity and expressiveness by referring to broad contexts. In experiments, Muse-SVS exhibited improved fidelity, expressiveness, and synchronization performance compared with baseline models. The visualization results show that Muse-SVS effectively express the variation in pitch, energy, and phoneme duration according to emotional intensity. To the best of our knowledge, Muse-SVS is the first neural SVS capable of controlling emotional intensity.

Bcl-2 is an intracellular membrane-associated protein that prevents cell death induced by a variety of apoptotic stimuli. A mechanism by which Bcl-2 exerts an anti-cell death effect is, however, not fully understood. In the present study, Bcl-2 suppressed cell death of N18TG neuroglioma cells caused by various apoptotic stresses, including etoposide, staurosporine, anisomycin, and ultraviolet irradiation. Concomitantly, Bcl-2 disrupted a signaling cascade to the c-Jun N-terminal kinase activation induced by the apoptotic stresses. Bcl-2 also prevented the etoposide-induced stimulation of MEKK1. Furthermore, overexpression of c-Jun N-terminal kinase antagonized the death-protective function of Bcl-2. These data suggest that suppression of the c-Jun N-terminal kinase signaling pathway may be critical for Bcl-2 action.

During the hair follicle (HF) cycle, HR protein expression is not concordant with the presence of the Hr mRNA transcript, suggesting an elaborate regulation of Hr gene expression. Here we present evidence that the 5′ untranslated region (UTR) of the Hr gene has internal ribosome entry site (IRES) activity and this activity is regulated by the binding of poly (rC) binding protein 2 (PCBP2) to Hr mRNA. Overexpression and knockdown of PCBP2 resulted in a decrease in Hr 5′ UTR IRES activity and an increase in HR protein expression without changing mRNA levels. We also found that this regulation was disrupted in a mutant Hr 5′ UTR that has a mutation responsible for Marie Unna hereditary hypotrichosis (MUHH) in both mice and humans. These findings suggest that Hr mRNA expression is regulated at the post-transcriptional level via IRES-mediated translation control through interaction with PCPB2, but not in MUHH.