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ZnO is a promising high‐temperature thermoelectric (TE) material due to its superior stability and earth abundance. However, the coupling relation between Seebeck coefficient and electrical conductivity on carrier concentration limits the optimum TE performance for most TE materials, especially ZnO. Herein, enhancement of TE performance is achieved via a stepwise optimization strategy composed of carrier concentration optimization and carrier filtering effect for fabricating robust ZnO‐based composite ceramics through a self‐developed specific high‐pressure synthesis followed by spark plasma sintering. Specifically, doping SnO2 provide substantial electrons to surge the carrier concentration. The subsequent compositing Si3N4 nanoparticles results in the unique reaction‐generated Zn2SiO4 nanoprecipitates with a larger bandgap and intrinsically low thermal conductivity, which introduce an excellent carrier filtering effect to increase the Seebeck coefficient by 57.7% at 300 K without compromising electrical conductivity much and enhance phonon scattering to cause an ultralow lattice thermal conductivity of 1.39 W m−1 K−1 achieving amorphous limits of ZnO (1.4±0.1 W m−1 K−1). Consequently, a high peak ZT (figure of merit) of 0.691 at 873 K is obtained, which is higher than that of previously reported ZnO‐based TE materials. This work demonstrates a feasible and effective strategy to fabricate high‐performance TE materials, especially those with inferior electrical conductivity. [ABSTRACT FROM AUTHOR]

SUMMARY: Effectors play important roles in facilitating the infection of plant pathogenic fungi. However, the gene expression regulatory mechanism of effector genes, in particular at the post‐transcriptional level, is largely unknown. In this study, we uncovered the post‐transcriptional regulation of an effector gene VmSP1 by a miRNA‐like RNA (Vm‐milR16) facilitating the infection of the apple tree Valsa canker pathogen Valsa mali. Genetic and molecular biological assays indicated that the expression of VmSP1 could be suppressed by Vm‐milR16‐mediated mRNA cleavage in a sequence‐specific manner. During V. mali infection, Vm‐milR16 was downregulated, whereas VmSP1 was upregulated, which further indicated the regulation relationship. VmSP1 was further demonstrated to be a secreted protein and could suppress plant immunity. Deletion of VmSP1 did not affect the vegetative growth but significantly reduced the virulence of V. mali. Further study indicated that VmSP1 could interact with the transcription factor MdbHLH189 of apple. Transiently overexpression of MdbHLH189 enhanced host resistance to V. mali by enhancing the expression of apple defense‐related genes, together with the increased callose deposition. Silencing of MdbHLH189 compromised host resistance to V. mali. Our findings uncovered the novel epigenetic regulation mechanism of a virulence‐associated effector gene mediated by a fungal milRNA at the post‐transcriptional level, and the results enriched the understanding of the function and action mechanism of effectors in tree pathogenic fungi. Significance Statement: Fungal effectors are proposed as major contributors to plant disease development. However, the regulation mechanism of the effector gene is largely unknown. Combining bioinformatics, molecular biology, genetic, and biochemistry methods, we report a new strategy that post‐transcriptional regulation of the virulence‐related effector gene VmSP1 by the milRNA‐mediated sequence‐specific cleavage, and the action mechanism of VmSP1 by targeting an apple resistance‐related transcription factor, which enhances the survival and host adaption of plant pathogenic fungi. [ABSTRACT FROM AUTHOR]

Aim: The aims of the study were to analyse the current situation of health literacy (HL), self‐management and health‐related quality of life (HRQOL) in patients with diabetic peripheral neuropathy (DPN), to explore the correlation between the three and to verify the mediating role of self‐management in HL and HRQOL. Design: A cross‐sectional survey. Methods: The convenience sampling method was used to select 401 DPN patients attending the First Hospital of Jinzhou Medical University in Liaoning Province, China, from December 2020 to December 2021 as the study population. The research instrument included socio‐demographic characteristics questionnaire, Health Literacy Management Scale (HeLMS), Summary of Diabetes Self‐Care Activities (SDSCA) and Short‐Form 12‐item Health Survey (SF‐12). SPSS 25.0 was applied to the data for descriptive analysis, Pearson correlation analysis and stratified multiple regression analysis. Mediating effects were tested using SPSS PROCESS macro 4.0 software. Results: HL and self‐management of DPN patients correlated positively with HRQOL. The mediation role of self‐management was significant in the relationship between HL and physical and mental HRQOL (physical component summary: β = 0.26, P < 0.01; mental component summary: β = 0.18, P < 0.01), with mediating effects accounting for 35.62% and 34.62% of the total effect. Conclusions: There was a positive correlation between HL, self‐management and HRQOL in patients with DPN. Self‐management plays a partially mediating role in the relationship between HL and HRQOL in DPN patients. It means that HRQOL in this population can be improved by increasing HL and thus self‐management in DPN patients. Patient or Public Contribution: None. [ABSTRACT FROM AUTHOR]

High capacitance and good rate performance supercapacitors are needed to power sensors and miniaturized electrical devices. Thick electrodes are promising to increase the mass loading of active materials in supercapacitors, but the 3D geometries and microstructures in thick electrodes still hinder the development with high electron and ion exchange rate and accessible active sites. The scaffold 3D electrodes of reduced graphene oxide:manganese oxide/carbon nanotube (rGO:MnOx/CNT) are manufactured by material extrusion 3D printing (ME3DP), where the mass ratio of rGO to MnOx/CNT composites, thickness, and mass loading per unit area are controllable. The increasing amount of MnOx/CNT composites boosts the areal capacitance. Although the rate capability decays fast with the increasing of MnOx/CNT, it remains stable at different thicknesses (1.2, 1.6, and 2 mm). 2 mm thick rGO:MnOx/CNT (weight ratio 5:3) electrode exhibits an area capacitance of 302.13 mF cm−2 at a current density of 0.5 mA cm−2, due to the highly ordered rGO networks. Compared to the casted electrodes, the microstructures in the 3D printed electrode contribute to lower resistances for the charge and ion transportation. [ABSTRACT FROM AUTHOR]

Food safety and quality are seriously compromised by the growth of spoilage bacteria in food. Various lactic acid bacteria (LAB) may inhibit the growth of spoilage bacteria in food and animal feed. In our study, the antibacterial activity of Lactobacillus acidophilus NX2‐6 was improved by genome shuffling. The starting populations were obtained via 60Coγ‐ray, diethyl sulfate mutagenesis, and UV mutagenesis of protoplasts. The optimal conditions for protoplast formation and regeneration were found to be 30 mg/ml of lysozyme at 37°C for 40 min. The protoplasts were inactivated by UV irradiation for 110 s or by heating at 58°C for 30 min. After two rounds of genome shuffling, the inhibitory activity of strain F50 was improved by 5.6‐fold compared to the original strain. The shuffled strain has broad‐spectrum antibacterial activity and is a promising candidate for bio‐preservative. The antibacterial substances produced by L. acidophilus NX2‐6 can be applied to the preservation of apple juice. The results showed that the growth of Alicyclobacillus acidoterrestris in apple juice was significantly inhibited by the addition of 0.1% culture supernatant with acidocin NX2‐6 at 28°C and 0.2% culture supernatant with acidocin NX2‐6 at 45°C for 30 days. The sugar−acid ratio, pH value, clarity, and fruit flavor of apple juice were well maintained during storage. This study showed that genome shuffling was an effective strategy to improve the bacterial inhibitory activity of LAB and that the shuffled LAB and their metabolites are expected to be used as bio‐based food protectors for food safety. [ABSTRACT FROM AUTHOR]

Summary: Small RNAs (sRNAs) play important roles in various biological processes by silencing their corresponding target genes in most eukaryotes. However, cross‐kingdom regulation mediated by fungal microRNA‐like RNAs (milRNAs) in plant–pathogen interactions is still largely unknown.Using molecular, genetic, histological, and biochemical approaches, we found that the apple tree Valsa canker pathogen Valsa mali milRNA Vm‐milR1 could suppress the host immunity by silencing two host receptor‐like kinase genes, MdRLKT1 and MdRLKT2.Vm‐milR1 was highly induced during V. mali infection. Deletion of Vm‐milR1 precursor abolished the generation of Vm‐milR1 and reduced the virulence of V. mali. Inoculation of Vm‐milR1 deletion mutants induced the host defence responses, including reactive oxygen species (ROS) accumulation, callose deposition, and high expression of defence‐related genes. Furthermore, Vm‐milR1 was confirmed to be able to suppress the expression of MdRLKT1 and MdRLKT2 in a sequence‐specific manner. Moreover, overexpression of either MdRLKT1 or MdRLKT2 enhanced apple resistance to V. mali by activating the host defence responses. Furthermore, knockdown of MdRLKT1 or MdRLKT2 compromised the host resistance to V. mali.Our study revealed that V. mali was equipped with Vm‐milR1 as an sRNA effector to silence host receptor‐like kinase genes, suppress the host defence responses, and facilitate pathogen infection. [ABSTRACT FROM AUTHOR]

MicroRNAs play important roles in various biological processes by regulating their corresponding target genes. However, the function and regulatory mechanism of fungal microRNA‐like RNAs (milRNAs) are still largely unknown. In this study, a milRNA (Vm‐milR37) was isolated and identified from Valsa mali, which causes the most serious disease on the trunk of apple trees in China. Based on the results of deep sequencing and quantitative reverse transcription PCR, Vm‐milR37 was found to be expressed in the mycelium, while it was not expressed during the V. mali infection process. Overexpression of Vm‐milR37 did not affect vegetative growth, but significantly decreased pathogenicity. Based on degradome sequencing, the target of Vm‐milR37 was identified as VmGP, a glutathione peroxidase. The expression of Vm‐milR37 and VmGP showed a divergent trend in V. mali–apple interaction samples and Vm‐milR37 overexpression transformants. The expression of VmGP could be suppressed significantly by Vm‐milR37 when coexpressed in tobacco leaves. Deletion of VmGP showed significantly reduced pathogenicity compared with the wild type. VmGP deletion mutants showed more sensitivity to hydrogen peroxide. Apple leaves inoculated with Vm‐milR37 overexpression transformants and VmGP deletion mutant displayed increased accumulation of reactive oxygen species compared with the wild type. Thus, Vm‐milR37 plays a critical role in pathogenicity by regulating VmGP, which contributes to the oxidative stress response during V. mali infection. These results provide important evidence to define the roles of milRNAs and their corresponding target genes in pathogenicity. [ABSTRACT FROM AUTHOR]

Mammalian sirtuin 6 (SIRT6) is involved in the regulation of many essential processes, especially metabolic homeostasis. SIRT6 knockout mice undergo premature aging and die at age ~4 weeks. Severe glycometabolic disorders have been found in SIRT6 knockout mice, and whether a dietary intervention can rescue SIRT6 knockout mice remains unknown. In our study, we found that at the same calorie intake, a high‐fat diet dramatically increased the lifespan of SIRT6 knockout mice to 26 weeks (males) and 37 weeks (females), reversed multi‐organ atrophy, and reduced body weight, hypoglycemia, and premature aging. Furthermore, the high‐fat diet partially but significantly normalized the global gene expression profile in SIRT6 knockout mice. Regarding the mechanism, excessive glucose uptake and glycolysis induced by the SIRT6 deficiency were attenuated in skeletal muscle through inhibition of insulin and IGF1 signaling by the high‐fat diet. Similarly, fatty acids but not ketone bodies inhibited glucose uptake, glycolysis, and senescence in SIRT6 knockout fibroblasts, whereas PI3K inhibition antagonized the effects of a high‐fatty‐acid medium in vitro. Overall, the high‐fat diet dramatically reverses numerous consequences of SIRT6 deficiency through modulation of insulin and IGF1 signaling, providing a new basis for elucidation of SIRT6 and fatty‐acid functions and supporting novel therapeutic approaches against metabolic disorders and aging‐related diseases. [ABSTRACT FROM AUTHOR]

As a hallmark for glioblastoma (GBM), high heterogeneity causes a variety of phenotypes and therapeutic responses among GBM patients, and it contributes to treatment failure. Moreover, hypoxia is a predominant feature of GBM and contributes greatly to its phenotype. To analyse the landscape of gene expression and hypoxic characteristics of GBM cells and their clinical significance in GBM patients, we performed transcriptome analysis of the GBM cell line U87‐MG and the normal glial cell line HEB under normoxia and hypoxia conditions, with the results of which were analysed using established gene ontology databases as well as The Cancer Genome Atlas and the Cancer Cell Line Encyclopedia. We revealed core signal pathways, including inflammation, angiogenesis and migration, and for the first time mapped the components of the toll‐like receptor 6 pathway in GBM cells. Moreover, by investigating the signal pathways involved in homoeostasis, proliferation and adenosine triphosphate metabolism, the critical response of GBM to hypoxia was clarified. Experiments with cell lines, patient serum and tissue identified IL1B, CSF3 and TIMP1 as potential plasma markers and VIM, STC1, TGFB1 and HMOX1 as potential biopsy markers for GBM. In conclusion, our study provided a comprehensive understanding for signal pathways and hypoxic characteristics of GBM and identified new biomarkers for GBM patients. [ABSTRACT FROM AUTHOR]

Hypoxia stimulates excessive growth of vascular smooth muscle cells ( VSMCs) contributing to vascular remodelling. Recent studies have shown that histone deacetylase inhibitors ( HDIs) suppress VSMC proliferation and activate eNOS expression. However, the effects of HDI on hypoxia-induced VSMC growth and the role of activated eNOS in VSMCs are unclear. Using an EdU incorporation assay and flow cytometry analysis, we found that the HDIs, butyrate (Bur) and suberoylanilide hydroxamic acid ( SAHA) significantly suppressed the proliferation of hypoxic VSMC lines and induced apoptosis. Remarkable induction of cleaved caspase 3, p21 expression and reduction of PCNA expression were also observed. Increased eNOS expression and enhanced NO secretion by hypoxic VSMC lines were detected using Bur or SAHA treatment. Knockdown of eNOS by si RNA transfection or exposure of hypoxic VSMCs to NO scavengers weakened the effects of Bur and SAHA on the growth of hypoxic VSMCs. In animal experiments, administration of Bur to Wistar rats exposed to hypobaric hypoxia for 28 days ameliorated the thickness and collagen deposition in pulmonary artery walls. Although the mean pulmonary arterial pressure ( mPAP) was not obviously decreased with Bur in hypoxic rats, right ventricle hypertrophy index ( RVHI) was decreased and the oxygen partial pressure of arterial blood was elevated. Furthermore, cell viability was decreased and eNOS and cleaved caspase 3 were induced in HDI-treated rat pulmonary arterial SMCs. These findings imply that HDIs prevent hypoxia-induced VSMC growth, in correlation with activated eNOS expression and activity in hypoxic VSMCs. [ABSTRACT FROM AUTHOR]