High-Efficiency Monolayer Molybdenum Ditelluride Light-Emitting Diode and Photodetector

Developing a high-efficiency and low-cost light source with emission wavelength transparent to silicon is an essential step toward silicon-based nanophotonic devices and micro/nano industry platforms. Here, a near-infrared monolayer MoTe2 light-emitting diode (LED) has been demonstrated and its emission wavelength is transparent to silicon. By taking advantage of the quantum tunneling effect, the device has achieved a very high external quantum efficiency (EQE) of 9.5% at 83 K, which is the highest EQE obtained from LED devices fabricated from monolayer TMDs so far. When the device is operated as a photodetector, the MoTe2 device exhibits a strong photoresponsivity at resonant wavelength 1145 nm. The low dark current of ∼5pA and fast response time 5.06 ms are achieved due to suppression of hBN tunneling layer. Our results open a new route for the investigation of novel near-infrared silicon integrated optoelectronic devicesThe authors acknowledge Financial support from ANU Ph.D. student scholarship, China Scholarship Council, ANU Major Equipment Committee fund (14MEC34), Australian Research Council (ARC) Discovery Early Career Researcher Award (DECRA) (DE140100805) and ARC Discovery Project (DP180103238)

Genomic insights into antimicrobial potential and optimization of fermentation conditions of pig-derived Bacillus subtilis BS21

Bacillus spp. have been widely used as probiotic supplements in animal feed as alternatives to antibiotics. In the present study, we screened a Bacillus subtilis strain named BS21 from pig feces. Antimicrobial activities, whole genome mining and UHPLC-MS/MS analysis were used to explore its antimicrobial mechanism. Strain BS21 showed Significant growth inhibition against a variety of animal pathogens, including Escherichia coli, Salmonella enterica Pullorum, Salmonella enterica Typhimurium, Citrobacter rodentium, Shigella flexneri and Staphylococcus aureus. Seven gene clusters involved in antimicrobial biosynthesis of secondary metabolites were encoded by strain BS21 genome, including four non-ribosomal peptides (bacillibactin, fengycin, surfactin and zwittermicin A), one ribosomal peptide (subtilosin A), one dipeptide (bacilysin) and one polyketide (bacillaene). Among them, production of surfactin, fengycin, bacillibactin, bacilysin and bacillaene was detected in the supernatant of B. subtilis strain BS21. To develop the potential application of BS21 in animal production, medium components and fermentation parameters optimization was carried out using response surface methodology (RSM). Production of antimicrobial secondary metabolites of strain BS21 was increased by 43.4%, and the best medium formula after optimization was corn flour 2%, soybean meal 1.7% and NaCl 0.5% with optimum culture parameters of initial pH 7.0, temperature 30°C, rotating speed at 220 rpm for 26 h. Our results suggested that strain BS21 has the potential for large-scale production and application as a potential source of probiotics and alternative to antibiotics for animal production

On the total length of external branches for beta-coalescents

In this paper we consider the beta(2 − α, α)-coalescents with 1 < α < 2 and study the moments of external branches, in particular, the total external branch length of an initial sample of n individuals. For this class of coalescents, it has been proved that n α-1 T (n) →D T, where T (n) is the length of an external branch chosen at random and T is a known nonnegative random variable. For beta(2 − α, α)-coalescents with 1 < α < 2, we obtain lim n→+∞ n 3α-

Prediction and Validation of Hub Genes Associated with Colorectal Cancer by Integrating PPI Network and Gene Expression Data

Although hundreds of colorectal cancer- (CRC-) related genes have been screened, the significant hub genes still need to be further identified. The aim of this study was to identify the hub genes based on protein-protein interaction network and uncover their clinical value. Firstly, 645 CRC patients’ data from the Tumor Cancer Genome Atlas were downloaded and analyzed to screen the differential expression genes (DEGs). And then, the Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis was performed, and PPI network of the DEGs was constructed by Cytoscape software. Finally, four hub genes (CXCL3, ELF5, TIMP1, and PHLPP2) were obtained from four subnets and further validated in our clinical setting and TCGA dataset. The results showed that mRNA expression of CXCL3, ELF5, and TIMP1 was increased in CRC tissues, whereas PHLPP2 mRNA expression was decreased. More importantly, high expression of CXCL3, ELF5, and TIMP1 was significantly associated with lymphatic invasion, distance metastasis, and advanced tumor stage. In addition, a shorter overall survival was observed in patients with increased CXCL3, TIMP1, and ELF5 expression and decreased PHLPP2 expression. In conclusion, the four hub genes screened by our strategy could serve as novel biomarkers for prognosis prediction of CRC patients

PLK1 maintains DNA methylation and cell viability by regulating phosphorylation-dependent UHRF1 protein stability

Abstract PLK1 is a key serine/threonine kinase as well as a master mitotic regulator, but it has never been reported that PLK1 regulates DNA methylation. In the present study, we for the first time found that PLK1 inhibition disrupted global DNA methylation and elevated the expression level of tumor suppressor genes. Mechanistically, we found that PLK1 interacts UHRF1 protein to induce its phosphorylation at serine 265. Phosphorylation is required for the maintenance of UHRF1 protein stability by recruiting a deubiquitinase USP7. Conversely, PLK1 inhibition decreases UHRF1 protein interaction with USP7 and activates the ubiquitin-proteasome pathway, thereby accelerating UHRF1 protein degradation. UHRF1 degradation decreases the recruitment of DNMT1 to chromatin, and decreases the level of genome-wide DNA methylation, thereby elevating the expression of tumor suppressor genes and decreasing cell viability. We here presented the first report on the novel role of PLK1 in DNA methylation maintenance through UHRF1-DNMT1 pathway, and revealed a novel anticancer mechanism of PLK1 inhibitors

AR antagonists develop drug resistance through TOMM20 autophagic degradation-promoted transformation to neuroendocrine prostate cancer

Abstract Background Prostate cancer(PCa) is the most commonly occurring male cancer in the USA. Abiraterone or Enzalutamide have been approved for the treatment of metastatic castration-resistant prostate cancer (CRPC). However, the treatment-emergent neuroendocrine PCa (t-NEPC) may develop, resulting in drug resistance in about 10–17% CRPC patients. The detailed mechanisms remain unclear.. Methods The expression correlation of TOMM20 and AR in PCa was determined by analyzing publicly available datasets, or by IHC staining in tumor specimens. The protein interaction of TOMM20 and AR was validated by co-immunoprecipitation or GST pull-down assay. The impact of TOMM20 depletion on drug sensitivity were elucidated by assays of cell proliferation, invasion, sphere formation, xenograft growth and intravenous metastasis. The intracellular ROS level was measured by flow cytometry, and the NEPC transdifferentiation and characteristics of cancer stem-like cells were validated by RNA-seq, RT-PCR and western blotting. Results The protein level of TOMM20 is positively correlated with AR in PCa cells and specimens. TOMM20 protein physically interacts with AR. AR antagonists induced the protein degradation of TOMM20 through autophagy-lysosomal pathway, thereby elevating the intracellular ROS level and activating PI3K/AKT signaling pathway. When TOMM20 was depleted, PCa cells underwent EMT, acquired the characteristics of cancer stem-like cells, and developed resistance to AR antagonists. The stable depletion of TOMM20 promoted the transdifferentiation of PCa adenocarcinoma into NEPC and metastasis. Conversely, the rescue of TOMM20 re-sensitized the resistant PCa cells to AR antagonists. Conclusions TOMM20 protein degradation induced by AR antagonists promoted the transdifferentiation of PCa to NEPC, thereby revealing a novel molecular mechanism by which AR antagonists develop drug resistance through mitochondrial outer membrane-mediated signaling pathway. These findings suggested that the decreasing or loss of TOMM20 expression in PCa tissues might become a useful predictor of PCa resistance to AR antagonists