[Characterization of bacterial swarming motility: a review].

Swarming motility is a typical synergistic motion, in which bacteria use flagella and Type Ⅳ Pili together to move collectively on semi-solid surfaces. Swarming motility is a hot topic of research in the field of microbiology because of its close relationship with biofilm formation, fruiting bodies formation, pathogen invasion and microbial dispersal and symbiosis. A large number of studies have been conducted on bacterial swarming motility, including changes in the expression of key proteins, changes in chemical communications between bacteria as well as mechanical changes. The expression of flagellin and the level of intracellular c-di-GMP complicatedly regulates the collective behavior of bacteria in colonies, which consequently impacts the swarming motility. The unique physical properties of swarmer cells are conducive to the expansion of the whole colony. Factors such as nutrient and water content in the surrounding growth environment of bacteria also affect the ability of bacteria to swarm to different degrees. It is challenging to construct a universal model of swarming motility based on the molecular mechanisms of swarming in the future.

Enhancement of rice husks saccharification through hydrolase preparation assisted by lytic polysaccharide monooxygenase.

Rice husk is an abundant agricultural waste generated from rice production, but its application is limited. Considering its complex components, the rice husk was hydrolyzed by different enzymes to enhance its saccharification. In this study, saccharification of the rice husk by cellulase, xylosidase, and xylanase was first investigated. The synergistic effect of LPMO on the above hydrolases and different enzyme combinations in the saccharification process was then explored. Thereafter, the formulation of the enzyme cocktail and the degradation conditions were optimized to obtain the highest saccharification efficiency. The results showed that the optimum enzyme cocktail consists of Celluclast 1.5 L (83.3 mg/g substrate), the key enzymes in the saccharification process, worked with BpXyl (20 mg/g substrate), BpXyn11 (24 mg/g substrate), and R17L/N25G (4 mg/g substrate). The highest reducing sugar concentration (1.19 mg/mL) was obtained at pH 6.0 and 60 â„ƒ for 24 h. Fourier transform infrared spectroscopy and scanning electron microscopy were employed to characterize the structural changes in the rice husk after degradation. The results showed that the key chemical bonds in cellulose and hemicellulose were broken. This study illuminated the concept of saccharifying lignocellulose from rice husk using LPMO synergistically assisted combined-hydrolase including cellulase, xylosidase, and xylanase, and provided a theoretical basis for lignocellulose biodegradation.

TFEB coordinates autophagy and pyroptosis as hepatotoxicity responses to ZnO nanoparticles.

Zinc oxide nanoparticles (ZnO NPs) have drawn serious concerns about their biotoxicity due to their extensive applications in biological medicine, clinical therapeutic, daily chemical production, food and agricultural additives. In our present study, we clarified hepatotoxic mechanism of ZnO NPs through investigating the crosstalk between autophagy and pyroptosis, a remaining enigma in hepatocyte stimulated by ZnO NPs. Based on the effects of autophagy intervention by Rapamycin (Rap) and 3-Methyladenine (3-MA), and the observation of pyroptosis morphology and related indexes, the autophagy and pyroptosis simultaneously initiated by ZnO NPs were interrelated and the autophagy characterized by autophagosome production and increased expression of autophagy proteins was identified as a protective response of ZnO NPs against pyroptosis. According to the analysis of protein expression and fluorescence localization, the NLRP3 inflammasome assemble and the classical Caspase-1/GSDMD-dependent pyroptosis induced by ZnO NPs was modulated by autophagy. In this process, the adjustment of TFEB expression and nuclear translocation by gene knockout and gene overexpression, further altered the tendency of ZnO NPs-induced pyroptosis via the regulation of autophagy and lysosomal biogenesis. The knockout of TFEB gene exacerbated the pyroptosis via autophagy elimination and lysosome inhibition. While the alleviation of NLRP3 generation and pyroptosis activation was observed after treatment of TFEB gene overexpression. Additionally, the siRNA interference confirmed that TRAF-6 was involved in the TFEB-mediated global regulation of autophagy-lysosome-pyroptosis in response to ZnO NPs. Accordingly, pyroptosis induced by ZnO NPs in hepatocyte could be significantly avoided by TFEB-regulated autophagy and lysosome, further providing new insights for the risk assessment and therapeutic strategy.

Milk protein hydrolysates obtained with immobilized alcalase and neutrase on magnetite nanoparticles: Characterization and antigenicity study.

Enzymatic hydrolysis is the most commonly used method to reduce the antigenicity of milk protein, but free protease is unstable and difficult to recycle after application. In this study, alcalase and neutrase were selected for immobilization on the modified magnetic Fe3 O4 nanoparticles. The reusability of the immobilized enzyme was 68.23% of the total starting activity after 5 recycling batches. The optimal hydrolysis conditions were an enzyme to substrate ratio of 6000 U/g and reaction at 50℃ and pH 8.5 for 3 h. Under these conditions, 22.76% hydrolysis of hydrolysate was achieved, and the antigenicity reduction rates of ß-lactoglobulin and casein were 21.34% and 30.89%, respectively. In addition, 82.75% of the hydrolysate had a molecular weight less than 1 kDa, and free amino acids represented 13.65% of the sample. This result showed that the hydrolysis with immobilized enzyme was similar to that with free enzyme and the immobilized enzyme could be applied to produce hypoallergenic hydrolysate. PRACTICAL APPLICATION: Reduces milk protein allergenicity.

Food-Origin Mycotoxin-Induced Neurotoxicity: Intend to Break the Rules of Neuroglia Cells.

Mycotoxins are key risk factors in human food and animal feed. Most of food-origin mycotoxins could easily enter the organism and evoke systemic toxic effects, such as aflatoxin B1 (AFB1), ochratoxin A (OTA), T-2 toxin, deoxynivalenol (DON), zearalenone (ZEN), fumonisin B1 (FB1), and 3-nitropropionic acid (3-NPA). For the last decade, the researches have provided much evidences in vivo and in vitro that the brain is an important target organ on mycotoxin-mediated neurotoxic phenomenon and neurodegenerative diseases. As is known to all, glial cells are the best regulator and defender of neurons, and a few evaluations about the effects of mycotoxins on glial cells such as astrocytes or microglia have been conducted. The fact that mycotoxin contamination may be a key factor in neurotoxicity and glial dysfunction is exactly the reason why we reviewed the activation, oxidative stress, and mitochondrial function changes of glial cells under mycotoxin infection and summarized the mycotoxin-mediated glial cell proliferation disorders, death pathways, and inflammatory responses. The purpose of this paper is to analyze various pathways in which common food-derived mycotoxins can induce glial toxicity and provide a novel perspective for future research on the neurodegenerative diseases.

Baicalin inhibits the TGF-ß1/p-Smad3 pathway to suppress epithelial-mesenchymal transition-induced metastasis in breast cancer.

TGF-ß1 is an epithelial-mesenchymal transition (EMT)-inducing factor that is critical in tumor progression. However, whether the effect of TGF-ß1 on breast cancer is through the EMT pathway remains to be determined, and drug development based on this mechanism needs to be improved. Results of this study showed that TGF-ß1 dysregulation significantly correlated with the expression levels of EMT-associated markers and transcriptional factors. Exogenous expression of TGF-ß1 promoted breast cancer cell metastasis and EMT progression. In addition, direct binding of baicalin to TGF-ß1 caused its inactivation, which subsequently blocked signal transduction and inhibited breast cancer cell metastasis. In vivo experiment results further invalidated the inhibitory effect of baicalin on TGF-ß1-induced tumor metastasis. These results suggest that baicalin, an active ingredient used in traditional Chinese medicine, exhibits a potential therapeutic effect on breast cancer metastasis by regulating TGF-ß1-dependent EMT progression.