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Purpose: The application of Chinese Mandarin electrolaryngeal (EL) speech for laryngectomees has been limited by its drawbacks such as single fundamental frequency, mechanical sound, and large radiation noise. To improve the intelligibility of Chinese Mandarin EL speech, a new perspective using the automatic speech recognition (ASR) system was proposed, which can convert EL speech into healthy speech, if combined with text-to-speech. Method: An ASR system was designed to recognize EL speech based on a deep learning model WaveNet and the connectionist temporal classification (WaveNet-CTC). This system mainly consists of 3 parts: the acoustic model, the language model, and the decoding model. The acoustic features are extracted during speech preprocessing, and 3,230 utterances of EL speech mixed with 10,000 utterances of healthy speech are used to train the ASR system. Comparative experiment was designed to evaluate the performance of the proposed method. Results: The results show that the proposed ASR system has higher stability and generalizability compared with the traditional methods, manifesting superiority in terms of Chinese characters, Chinese words, short sentences, and long sentences. Phoneme confusion occurs more easily in the stop and affricate of EL speech than the healthy speech. However, the highest accuracy of the ASR could reach 83.24% when 3,230 utterances of EL speech were used to train the ASR system. Conclusions: This study indicates that EL speech could be recognized effectively by the ASR based on WaveNet-CTC. This proposed method has a higher generalization performance and better stability than the traditional methods. A higher accuracy of the ASR system based on WaveNet-CTC can be obtained, which means that EL speech can be converted into healthy speech.

Schizophrenia (SCZ) is a complex neuropsychiatric disorder widely recognized for its impaired bioenergy utilization. The astrocyte‐neuron lactate shuttle (ANLS) plays a critical role in brain energy supply. Recent studies have revealed abnormal lactate metabolism in SCZ, which is associated with mitochondrial dysfunction, tissue hypoxia, gastric acid retention, oxidative stress, neuroinflammation, abnormal brain iron metabolism, cerebral white matter hypermetabolic activity, and genetic susceptibility. Furthermore, astrocytes, neurons, and glutamate abnormalities are prevalent in SCZ with abnormal lactate metabolism, which are essential components for maintaining ANLS in the brain. Therefore, an in‐depth study of the pathophysiological mechanisms of ANLS in SCZ with abnormal lactate metabolism will contribute to a better understanding of the pathogenesis of SCZ and provide new ideas and approaches for the diagnosis and treatment of SCZ. [ABSTRACT FROM AUTHOR]

Objective. This study investigated the nature of shared transcriptomic alterations in PBMs from periodontitis and atherosclerosis to unravel molecular mechanisms underpinning their association. Methods. Gene expression data from PBMs from patients with periodontitis and those with atherosclerosis were each downloaded from the GEO database. Differentially expressed genes (DEGs) in periodontitis and atherosclerosis were identified through differential gene expression analysis. The disease-related known genes related to periodontitis and atherosclerosis each were downloaded from the DisGeNET database. A Venn diagram was constructed to identify crosstalk genes from four categories: DEGs expressed in periodontitis, periodontitis-related known genes, DEGs expressed in atherosclerosis, and atherosclerosis-related known genes. A weighted gene coexpression network analysis (WGCNA) was performed to identify significant coexpression modules, and then, coexpressed gene interaction networks belonging to each significant module were constructed to identify the core crosstalk genes. Results. Functional enrichment analysis of significant modules obtained by WGCNA analysis showed that several pathways might play the critical crosstalk role in linking both diseases, including bacterial invasion of epithelial cells, platelet activation, and Mitogen-Activated Protein Kinases (MAPK) signaling. By constructing the gene interaction network of significant modules, the core crosstalk genes in each module were identified and included: for GSE23746 dataset, RASGRP2 in the blue module and VAMP7 and SNX3 in the green module, as well as HMGB1 and SUMO1 in the turquoise module were identified; for GSE61490 dataset, SEC61G, PSMB2, SELPLG, and FIBP in the turquoise module were identified. Conclusion. Exploration of available transcriptomic datasets revealed core crosstalk genes (RASGRP2, VAMP7, SNX3, HMGB1, SUMO1, SEC61G, PSMB2, SELPLG, and FIBP) and significant pathways (bacterial invasion of epithelial cells, platelet activation, and MAPK signaling) as top candidate molecular linkage mechanisms between atherosclerosis and periodontitis. [ABSTRACT FROM AUTHOR]

Pathogenic variants in GFPT1, encoding a key enzyme to synthesize UDP-N-acetylglucosamine (UDP-GlcNAc), cause congenital myasthenic syndrome (CMS). We made a knock-in (KI) mouse model carrying a frameshift variant in Gfpt1 exon 9, simulating that found in a patient with CMS. As Gfpt1 exon 9 is exclusively expressed in striated muscles, Gfpt1-KI mice were deficient for Gfpt1 only in skeletal muscles. In Gfpt1-KI mice, (1) UDP-HexNAc, CMP-NeuAc and protein O-GlcNAcylation were reduced in skeletal muscles; (2) aged Gfpt1-KI mice showed poor exercise performance and abnormal neuromuscular junction structures; and (3) markers of the unfolded protein response (UPR) were elevated in skeletal muscles. Denervation-mediated enhancement of endoplasmic reticulum (ER) stress in Gfpt1-KI mice facilitated protein folding, ubiquitin-proteasome degradation and apoptosis, whereas autophagy was not induced and protein aggregates were markedly increased. Lack of autophagy was accounted for by enhanced degradation of FoxO1 by increased Xbp1-s/u proteins. Similarly, in Gfpt1-silenced C2C12 myotubes, ER stress exacerbated protein aggregates and activated apoptosis, but autophagy was attenuated. In both skeletal muscles in Gfpt1-KI mice and Gfpt1-silenced C2C12 myotubes, maladaptive UPR failed to eliminate protein aggregates and provoked apoptosis., Competing Interests: Competing interests The authors declare no competing or financial interests., (© 2024. Published by The Company of Biologists Ltd.)

Mitochondrial damage is involved in many pathophysiological processes, such as tumor development, metabolism, and neurodegenerative diseases. The mitochondrial unfolded protein response (mtUPR) is the first stress-protective response initiated by mitochondrial damage, and it repairs or clears misfolded proteins to alleviate this damage. Studies have confirmed that the sirtuin family is essential for the mitochondrial stress response; in particular, SIRT1, SIRT3, and SIRT7 participate in the mtUPR in different axes. This article summarizes the associations of sirtuins with the mtUPR as well as specific molecular targets related to the mtUPR in different disease models, which will provide new inspiration for studies on mitochondrial stress, mitochondrial function protection, and mitochondria-related diseases, such as neurodegenerative diseases., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)