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In recent years, with rising concerns over food quality and safety, computer vision technology has gradually attracted attention and begun to be widely used in the field of food quality evaluation. Machine learning technologies such as artificial neural networks (ANN), convolutional neural networks (CNN), and support vector machines (SVM) allow automatic assessment and monitoring of food quality by training on large amounts of food images and related data. Particularly, with the development of deep learning, the computer is now able to more accurately recognize food features such as appearance, shape, and color, thereby allowing food classification, prediction and quality monitoring. In addition to its conventional application in food quality assessment, learning technologies also find application in more complex tasks such as defect detection, foreign object detection, and freshness assessment. These technologies not only improve the efficiency of food production and processing but also reduce errors caused by human factors, thereby ensuring food quality and safety. However, despite the significant progress in the application of learning technologies in food quality assessment, there are still challenges that need to be overcome. For instance, the high cost of acquiring and annotating food image datasets, as well as insufficient data quality and quantity, may affect the performance and generalization ability of models. Furthermore, the interpretability and transparency of models are important issues, especially when explaining or making decisions on food quality assessment results. Therefore, further research is needed to explore how to improve the quality and scale of datasets, optimize the robustness and interpretability of models, and develop more efficient and sustainable food quality assessment systems.

In this work, an Ag–Ti2SnC composite was fabricated by the hot-pressing sintering method, and the erosion behavior of Ag–Ti2SnC with volume percentages of 10–40% was studied at a load voltage of 10 kV. The arc life and breakdown current were observed at about 31–36 ms and 39 A, respectively. The cathode spot traveled the fastest on the surface of the Ag–40 vol% Ti2SnC composite. Due to emission center model, the temperature of the minor protrusions on the cathode surface increased, resulting in Ag ions, Ti ions, and Sn ions being generated. Combining with the ionized oxygen, Ag2O, AgO, TiO2, and SnO2 were formed on the eroded Ag–Ti2SnC surface after arc erosion. The research results will broaden the application range of Ag–Ti2SnC electrical contact material and enrich the arc erosion mechanism.

Antimicrobial peptides (AMPs), ancient scavengers of bacteria, are very poorly induced in macrophages infected by Mycobacterium tuberculosis (M. tuberculosis), but the underlying mechanism remains unknown. Here, we report that L-alanine interacts with PRSS1 and unfreezes the inhibitory effect of PRSS1 on the activation of NF-κB pathway to induce the expression of AMPs, but mycobacterial alanine dehydrogenase (Ald) Rv2780 hydrolyzes L-alanine and reduces the level of L-alanine in macrophages, thereby suppressing the expression of AMPs to facilitate survival of mycobacteria. Mechanistically, PRSS1 associates with TAK1 and disruptes the formation of TAK1/TAB1 complex to inhibit TAK1-mediated activation of NF-κB pathway, but interaction of L-alanine with PRSS1, disables PRSS1-mediated impairment on TAK1/TAB1 complex formation, thereby triggering the activation of NF-κB pathway to induce expression of AMPs. Moreover, deletion of antimicrobial peptide gene β-defensin 4 (Defb4) impairs the virulence by Rv2780 during infection in mice. Both L-alanine and the Rv2780 inhibitor, GWP-042, exhibits excellent inhibitory activity against M. tuberculosis infection in vivo. Our findings identify a previously unrecognized mechanism that M. tuberculosis uses its own alanine dehydrogenase to suppress host immunity, and provide insights relevant to the development of effective immunomodulators that target M. tuberculosis. In this work, authors mechanistically investigate the reduced induction of antimicrobial peptides in Mycobacterium tuberculosis infected macrophages. [ABSTRACT FROM AUTHOR]

Studying the hydro-liquefaction kinetics of lignite contributes to optimizing the mild liquefaction process for lignite. In this paper, the direct liquefaction performance of Shengli lignite (SL) was investigated using a H2/THN system with 4 MPa of initial pressure, and reaction kinetic models were established for the heating-up stage and the isothermal stage. The result showed that the liquefaction performance of the SL was excellent, with a conversion of 62.18% and an oil and gas (O + G) yield of 29.88% at 698.15 K. After one hour of reaction, the conversion and O + G yield were 94.61% and 76.78%, respectively. During the heating-up stage, the easily reactive part of the SL was 50.07%, and it was converted directly into oil, gas, asphaltene (AS), and preasphaltene (PA) simultaneously. There was no significant secondary hydrogenation conversion of the AS and PA products. During the isothermal stage, the hard-to-react part was predominantly converted into AS and PA, while the remaining easily reactive part continue to react completely. The conversion of AS and PA into oil and gas was a rate-controlling step during this stage. The amount of unreacted coal estimated using the model calculated in the isothermal stage was 2.98%, which was significantly consistent with the experimental value of 2.81%. [ABSTRACT FROM AUTHOR]

Internal N6-methyladenosine (m6A) modifications are among the most abundant modifications of messenger RNA, playing a critical role in diverse biological and pathological processes. However, the functional role and regulatory mechanism of m6A modifications in the immune response to Mycobacterium tuberculosis infection remains unknown. Here, we report that methyltransferase-like 14 (METTL14)-dependent m6A methylation of NAPDH oxidase 2 (Nox2) mRNA was crucial for the host immune defense against M. tuberculosis infection and that M. tuberculosis-secreted antigen EsxB (Rv3874) inhibited METTL14-dependent m6A methylation of Nox2 mRNA. Mechanistically, EsxB interacted with p38 MAP kinase and disrupted the association of TAB1 with p38, thus inhibiting the TAB1-mediated autophosphorylation of p38. Interaction of EsxB with p38 also impeded the binding of p38 with METTL14, thereby inhibiting the p38-mediated phosphorylation of METTL14 at Thr72. Inhibition of p38 by EsxB restrained liquid–liquid phase separation (LLPS) of METTL14 and its subsequent interaction with METTL3, preventing the m6A modification of Nox2 mRNA and its association with the m6A-binding protein IGF2BP1 to destabilize Nox2 mRNA, reduce ROS levels, and increase intracellular survival of M. tuberculosis. Moreover, deletion or mutation of the phosphorylation site on METTL14 impaired the inhibition of ROS level by EsxB and increased bacterial burden or histological damage in the lungs during infection in mice. These findings identify a previously unknown mechanism that M. tuberculosis employs to suppress host immunity, providing insights that may empower the development of effective immunomodulators that target M. tuberculosis. [ABSTRACT FROM AUTHOR]

Objective: This study aims to investigate the prevalence of NTM in household water in China and assess its potential role as a source of infection for NTM pulmonary disease, a crucial step for understanding and controlling the spread of this increasingly prevalent disease., Methods: To examine the prevalence of mycobacteria in household water, 500 mL water samples and swabs were collected from all taps of 19 patients' homes. The amplification of mycobacterial 16SrRNA with bacteriological identification was as a protocol to discriminate mycobacterial isolations from non- mycobacterial isolations. The 570bp 16SrRNA amplicon was sequenced and used to define mycobacterial species., Results: The mycobacteria isolated from clinical samples from 19 patients included M. intracellulare, M. avium, M. abscessus, and M. kansasii. NTM isolated from household water of patients included M. avium (1 case), M. abscessus (2 cases), M. kansasii (8 cases), M. gordonae (1 case), M. gilvum (1 case), M. fortuitum (1 case), M. porcinum (1 case). M. abscessus, M. kansasii, and M. avium causing human disease were isolated from household water. Though M. intracellulare was the predominant species isolated from patients with NTM pulmonary disease, it was not found in household water. In addition, our results revealed that NTM preferentially colonize in biofilm/sediment (75% of positive growths were from tap swab samples), indicating the significance of finding specific NTM species in household water in relation to the patients' conditions, or the lack of correlation between M. intracellulare in patients and its absence in household water., Conclusions: The isolation of pathogenic NTM species from household water underscores the critical role of water hygiene in preventing NTM pulmonary disease and highlights the need for targeted public health strategies.

Internal N 6 -methyladenosine (m 6 A) modifications are among the most abundant modifications of messenger RNA, playing a critical role in diverse biological and pathological processes. However, the functional role and regulatory mechanism of m 6 A modifications in the immune response to Mycobacterium tuberculosis infection remains unknown. Here, we report that methyltransferase-like 14 (METTL14)-dependent m 6 A methylation of NAPDH oxidase 2 (Nox2) mRNA was crucial for the host immune defense against M. tuberculosis infection and that M. tuberculosis-secreted antigen EsxB (Rv3874) inhibited METTL14-dependent m 6 A methylation of Nox2 mRNA. Mechanistically, EsxB interacted with p38 MAP kinase and disrupted the association of TAB1 with p38, thus inhibiting the TAB1-mediated autophosphorylation of p38. Interaction of EsxB with p38 also impeded the binding of p38 with METTL14, thereby inhibiting the p38-mediated phosphorylation of METTL14 at Thr72. Inhibition of p38 by EsxB restrained liquid-liquid phase separation (LLPS) of METTL14 and its subsequent interaction with METTL3, preventing the m 6 A modification of Nox2 mRNA and its association with the m 6 A-binding protein IGF2BP1 to destabilize Nox2 mRNA, reduce ROS levels, and increase intracellular survival of M. tuberculosis. Moreover, deletion or mutation of the phosphorylation site on METTL14 impaired the inhibition of ROS level by EsxB and increased bacterial burden or histological damage in the lungs during infection in mice. These findings identify a previously unknown mechanism that M. tuberculosis employs to suppress host immunity, providing insights that may empower the development of effective immunomodulators that target M. tuberculosis., (© 2024. The Author(s).)