Green- and Blue-Emitting Tb3+-Activated Linde Type A Zeolite-Derived Boro-Aluminosilicate Glass for Deep UV Detection/Imaging.

Tb3+-activated LTA zeolite-derived boro-aluminosilicate glass samples with a composition of xTb2O3-68(Na2O-Al2O3-SiO2)-32B2O3 (x = 0.2, 1.0 and 10 extra wt%) were prepared using the melt-quenching method. The emission spectra recorded upon ultraviolet (UV) excitation with two different wavelengths of 193 and 378 nm showed blue light (5D3 to 7FJ=6,5,4 and 5D4 to 7F6 transitions of Tb3+) and green light (5D4 to 7F5 transition of Tb3+) emissions with comparable intensities up to a Tb3+ concentration of 10 extra wt%. Of note, the mean decay times of the green luminescence of the glass samples were relatively fast (<20 µs). The synthesized glass has potential in applications concerning UV imaging, UV detection, and plasma display panels.

Spider venom-derived peptide JZTX-14 prevents migration and invasion of breast cancer cells via inhibition of sodium channels.

Nav1.5 channel is crucial for the proliferation and migration of breast cancer cells. In this study, we investigated the anticancer effect of JZTX-14, a natural peptide considered an effective antagonist of Nav1.5. First, we successfully isolated and purified the 31 amino acid peptide JZTX-14 containing three pairs of disulfide bonds from spider venom and synthesised JZTX-14 by solid phase synthesis. We then predicted their physiochemical properties and structures in the peptide database. Further, we investigated the effects of natural and synthetic JZTX-14 on the proliferation and migration of MDA-MB-231 breast cancer cells via modulation of sodium current through the Nav1.5 channel. The results showed that both synthetic and natural JZTX-14 inhibited Nav1.5 currents, indicating the successful synthesis of JZTX-14. However, JZTX-14 did not affect MDA-MB-231 cell proliferation but inhibited its migration. Transcriptome analysis revealed that JZTX-14 downregulated S100A4 and FBXO2 and upregulated SERPINB2 in MDA-MB-231 cells. Western blot analysis demonstrated an increased level of the epithelial marker, E-cadherin, and decreased levels of the mesenchymal markers, N-cadherin and vimentin, and matrix metalloproteinase (MMP2), indicating the possible underlying mechanism of the inhibition of MDA-MB-231 cell migration by JZTX-14. This study provides a new target for inhibiting breast cancer metastasis and identifies a potent natural peptide for treating Triple-negative breast cancer.

Rapid, convenient, and ultrasensitive point-of-care sensing of histamine from fish: A Portable chromatographic platform based on derivatization reaction.

Food poisoning caused by histamine ingestion is one of the prevalent allergies associated with fish consumption in the world. Reliable detection of histamine from fish by a portable platform was of urgent importance to food safety. A portable technology for on-site monitoring of histamine in tuna was established through combined azo-derivatized thin-layer chromatography (TLC) with surface-enhanced Raman scattering (SERS) spectroscopy. The real tuna meat sample was directly applied onto the portable sensor for the separation of histamine and azo-derivatizing of histamine was reacted on the TLC plate. The colorless histamine was visualized by azo-derivatization after spraying Pauly reagent onto the diatomite TLC plate. The molecule information and concentration of the histamine was measured and calculated by SERS spectra. Diatomite TLC plate was capable of separating histamine with 1.32 × 10-7 M of Au colloid for the SERS enhancement. Accordingly, the limit of detection of histamine from mixture sample could achieve 2.8 × 10-4 ppm. These results indicated that the portable azo-derivatized TLC-SERS sensor not only visualizes the histamine but also improves the intensity of the Raman spectra. The azo-derivatized TLC-SERS sensor could be applied for rapid, convenient, and ultrasensitive point-of-care sensing of histamine in fish.

Pyruvate dehydrogenase B regulates myogenic differentiation via the FoxP1-Arih2 axis.

BACKGROUND: Sarcopenia, the age-related decline in skeletal muscle mass and function, diminishes life quality in elderly people. Improving the capacity of skeletal muscle differentiation is expected to counteract sarcopenia. However, the mechanisms underlying skeletal muscle differentiation are complex, and effective therapeutic targets are largely unknown. METHODS: The human Gene Expression Omnibus database, aged mice and primary skeletal muscle cells were used to assess the expression level of pyruvate dehydrogenase B (PDHB) in human and mouse aged state. d-Galactose (d-gal)-induced sarcopenia mouse model and two classic cell models (C2C12 and HSkMC) were used to assess the myogenic effect of PDHB and the underlying mechanisms via immunocytochemistry, western blotting, quantitative real-time polymerase chain reaction, RNA interference or overexpression, dual-luciferase reporter assay, RNA sequencing and untargeted metabolomics. RESULTS: We identified that a novel target PDHB promoted myogenic differentiation. PDHB expression decreased in aged mouse muscle relative to the young state (-50% of mRNA level, P < 0.01) and increased during mouse and primary human muscle cell differentiation (+3.97-fold, P < 0.001 and +3.79-fold, P < 0.001). Knockdown or overexpression of PDHB modulated the expression of genes related to muscle differentiation, namely, myogenic factor 5 (Myf5) (-46%, P < 0.01 and -27%, P < 0.05; +1.8-fold, P < 0.01), myogenic differentiation (MyoD) (-55%, P < 0.001 and -34%, P < 0.01; +2.27-fold, P < 0.001), myogenin (MyoG) (-60%, P < 0.001 and -70%, P < 0.001; +5.46-fold, P < 0.001) and myosin heavy chain (MyHC) (-70%, P < 0.001 and -69%, P < 0.001; +3.44-fold, P < 0.001) in both C2C12 cells and HSkMC. Metabolomic and transcriptomic analyses revealed that PDHB knockdown suppressed pyruvate metabolism (P < 0.001) and up-regulated ariadne RBR E3 ubiquitin protein ligase 2 (Arih2) (+7.23-fold, P < 0.001) in cellular catabolic pathways. The role of forkhead box P1 (FoxP1) (+4.18-fold, P < 0.001)-mediated Arih2 transcription was the key downstream regulator of PDHB in muscle differentiation. PDHB overexpression improved d-gal-induced muscle atrophy in mice, which was characterized by significant increases in grip strength, muscle mass and mean muscle cross-sectional area (1.19-fold to 1.5-fold, P < 0.01, P < 0.05 and P < 0.001). CONCLUSIONS: The comprehensive results show that PDHB plays a sarcoprotective role by suppressing the FoxP1-Arih2 axis and may serve as a therapeutic target in sarcopenia.

Apol9a regulates myogenic differentiation via the ERK1/2 pathway in C2C12 cells.

Background: The rising prevalence of obesity and its complications is a big challenge for the global public health. Obesity is accompanied by biological dysfunction of skeletal muscle and the development of muscle atrophy. The deep knowledge of key molecular mechanisms underlying myogenic differentiation is crucial for discovering novel targets for the treatment of obesity and obesity-related muscle atrophy. However, no effective target is currently known for obesity-induced skeletal muscle atrophy. Methods: Transcriptomic analyses were performed to identify genes associated with the regulation of myogenic differentiation and their potential mechanisms of action. C2C12 cells were used to assess the myogenic effect of Apol9a through immunocytochemistry, western blotting, quantitative polymerase chain reaction, RNA interference or overexpression, and lipidomics. Results: RNA-seq of differentiated and undifferentiated C2C12 cells revealed that Apol9a expression significantly increased following myogenic differentiation and decreased during obesity-induced muscle atrophy. Apol9a silencing in these C2C12 cells suppressed the expression of myogenesis-related genes and reduced the accumulation of intracellular triglycerides. Furthermore, RNA-seq and western blot results suggest that Apol9a regulates myogenic differentiation through the activation of extracellular signal-regulated kinase 1/2 (ERK1/2). This assumption was subsequently confirmed by intervention with PD98059. Conclusion: In this study, we found that Apol9a regulates myogenic differentiation via the ERK1/2 pathway. These results broaden the putative function of Apol9a during myogenic differentiation and provide a promising therapeutic target for intervention in obesity and obesity-induced muscle atrophy.

Slc2a6 regulates myoblast differentiation by targeting LDHB.

BACKGROUND: Type 2 diabetes mellitus is a global health problem. It often leads to a decline in the differentiation capacity of myoblasts and progressive loss of muscle mass, which in turn results in deterioration of skeletal muscle function. However, effective therapies against skeletal muscle diseases are unavailable. METHODS: Skeletal muscle mass and differentiation ability were determined in db/+ and db/db mice. Transcriptomics and metabolomics approaches were used to explore the genetic mechanism regulating myoblast differentiation in C2C12 myoblasts. RESULTS: In this study, the relatively uncharacterized solute carrier family gene Slc2a6 was found significantly up-regulated during myogenic differentiation and down-regulated during diabetes-induced muscle atrophy. Moreover, RNAi of Slc2a6 impaired the differentiation and myotube formation of C2C12 myoblasts. Both metabolomics and RNA-seq analyses showed that the significantly differentially expressed genes (e.g., LDHB) and metabolites (e.g., Lactate) during the myogenic differentiation of C2C12 myoblasts post-Slc2a6-RNAi were enriched in the glycolysis pathway. Furthermore, we show that Slc2a6 regulates the myogenic differentiation of C2C12 myoblasts partly through the glycolysis pathway by targeting LDHB, which affects lactic acid accumulation. CONCLUSION: Our study broadens the understanding of myogenic differentiation and offers the Slc2a6-LDHB axis as a potential therapeutic target for the treatment of diabetes-associated muscle atrophy. Video abstract.

Entrepreneurial Leadership and Entrepreneurial Performance in Start-Ups: A Moderated Serial Mediation Model.

The purpose of this study is to explore the impact of entrepreneurial leadership on entrepreneurial performance in start-ups. Specifically, a moderated serial mediation model was developed to investigate the mediating role of tacit knowledge sharing and job embeddedness and the moderating effect of career growth opportunities. Data was collected from 376 start-up employees via an online survey platform. Using hierarchical multiple regression and Hayes' PROCESS Macro by SPSS 21.0, and structural equation modeling by AMOS 23.0, support was found for both mediation and moderation effects. Results showed that entrepreneurial leadership significantly positively affects entrepreneurial performance by mediating with tacit knowledge sharing and job embeddedness. Moreover, career growth opportunities moderate the serial mediating effect of tacit knowledge sharing and job embeddedness between entrepreneurial leadership and entrepreneurial performance. This study provides theoretical guidance for entrepreneurial leadership to improve entrepreneurial performance.

Slc25a5 regulates adipogenesis by modulating ERK signaling in OP9 cells.

BACKGROUND: A comprehensive understanding of the molecular mechanisms of adipogenesis is a critically important strategy for identifying new targets for obesity intervention. METHODS: Transcriptomic and lipidomic approaches were used to explore the functional genes regulating adipogenic differentiation and their potential mechanism of action in OP9 cells and adipose-derived stem cells. Oil Red O staining was used to detect oil droplets in adipocytes. RESULTS: RNA sequencing (RNA-seq) showed that Slc25a5 expression was significantly upregulated in adipogenic differentiation. Depletion of Slc25a5 led to the suppressed expression of adipogenesis-related genes, reduced the accumulation of triglycerides, and inhibited PPARγ protein expression. Moreover, the knockdown of Slc25a5 resulted in significant reduction of oxidative phosphorylation (OXPHOS) protein expression (ATP5A1, CQCRC2, and MTCO1) and ATP production. The RNA-seq and real-time quantitative polymerase chain reaction (RT-qPCR) results suggested that adipogenic differentiation is possibly mediated by ERK1/2 phosphorylation, and this hypothesis was confirmed by intervention with PD98059 (an ERK 1/2 inhibitor). CONCLUSIONS: This study indicates that Slc25a5 inhibits adipogenesis and might be a new therapeutic target for the treatment of obesity.

The Effect of Entrepreneurial Leadership on Employees' Tacit Knowledge Sharing in Start-Ups: A Moderated Mediation Model.

BACKGROUND: This study explores the causal relationship between entrepreneurial leadership and employees' tacit knowledge sharing in start-ups. Construct a moderated mediation model to test the mediating role of affective commitment and the moderating role of career growth opportunities. METHODS: A questionnaire was used to collect data, and 485 samples of employees in Chinese start-ups were collected. Regression analysis and structural equation model were used to analyze data and verify hypotheses. RESULTS: The study shows that entrepreneurial leadership has a significant positive effect on employees' affective commitment and tacit knowledge sharing. Affective commitment plays a mediating effect between entrepreneurial leadership and employees' tacit knowledge sharing. Career growth opportunities play a positive moderating role in the impact of entrepreneurial leadership on affective commitment and tacit knowledge sharing, and positively moderate the indirect effect of entrepreneurial leadership on tacit knowledge sharing through affective commitment. CONCLUSION: The research illustrates that the managers of start-ups can improve employees' affective commitment by giving full play to entrepreneurial leadership and combining the career growth opportunities provided by the organization. Employees' tacit knowledge sharing behavior is stimulated, providing guiding value for knowledge management and the human resource management of start-ups.

Classification of sleep apnea based on EEG sub-band signal characteristics.

Sleep apnea syndrome (SAS) is a disorder in which respiratory airflow frequently stops during sleep. Alterations in electroencephalogram (EEG) signal are one of the physiological changes that occur during apnea, and can be used to diagnose and monitor sleep apnea events. Herein, we proposed a method to automatically distinguish sleep apnea events using characteristics of EEG signals in order to categorize obstructive sleep apnea (OSA) events, central sleep apnea (CSA) events and normal breathing events. Through the use of an Infinite Impulse Response Butterworth Band pass filter, we divided the EEG signals of C3-A2 and C4-A1 into five sub-bands. Next, we extracted sample entropy and variance of each sub-band. The neighbor composition analysis (NCA) method was utilized for feature selection, and the results are used as input coefficients for classification using random forest, K-nearest neighbor, and support vector machine classifiers. After a 10-fold cross-validation, we found that the average accuracy rate was 88.99%. Specifically, the accuracy of each category, including OSA, CSA and normal breathing were 80.43%, 84.85%, and 95.24%, respectively. The proposed method has great potential in the automatic classification of patients' respiratory events during clinical examinations, and provides a novel idea for the development of an automatic classification system for sleep apnea and normal events without the need for expert intervention.

Stereogenic phosphorus-induced diastereoselective formation of chiral carbon during nucleophilic addition of chiral H-P species to aldehydes or ketones.

P,C-stereogenic α-hydroxyl phosphinates or phosphine oxides were prepared from the additions of (RP)-phosphinate to ketones or (RP)-phosphine oxide to aldehydes, respectively, catalyzed by bases at room temperature in up to >99:1 diasteromeric ratio (d.r.P/d.r.C) and 99 % yields. The diastereoselectivity was induced by reversible equilibrium and different stabilities between two diastereomers of adduct, which was caused by the spatial interaction between menthoxyl or menthyl to alkyl groups of aldehydes or ketones.