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The symmetries and topological properties of the topological counterparts in 1D non‐Hermitian systems are investigated. It is found that, after applying the non‐unitary similarity transformation, the non‐unitary topological counterpart in real space exhibits completely different global symmetries except for the sublattice symmetry and reveals many brand new local symmetries. Due to the abundant symmetries of non‐unitary topological counterparts, it is also found that the unique overlapping projections about the unit sphere vector representing the eigenstates appear in the nontrivial regions, and the triviality of the point‐gap topology of non‐unitary topological counterpart completely eliminate the intrinsic skin effect in non‐Hermitian systems. It is also shown that the unitary topological counterpart never arises any changes for the original symmetries and topological structures even in real space. Unitary topological counterparts are further summarized about the two‐band Bloch Hamiltonian, which can expand the definition of non‐Bloch winding number. Furthermore, it is demonstrated theoretically that the Bloch Hamiltonian would still hold time‐reversal symmetry, abnormal particle‐hole symmetry, and sublattice symmetry even suffering from the non‐unitary transformation. This work provides a new way to understand the roles of symmetry and topology in non‐Hermitian systems from the perspective of topological counterparts. [ABSTRACT FROM AUTHOR]

Background: Hypoxia, a typical hallmark of solid tumors, exhibits an essential role in the progression of colorectal cancer (CRC), in which the dysregulation of long non-coding RNAs (lncRNAs) is frequently observed. However, the underlying mechanisms are not clearly defined. Methods: The TCGA database was analyzed to identify differential lncRNA expression involved in hypoxia-induced CRC progression. qRT-PCR was conducted to validate the upregulation of lncRNA STEAP3-AS1 in CRC cell lines and tumor-bearing mouse and zebrafish models under hypoxia. ChIP-qRT-PCR was used to detect the transcriptional activation of STEAP3-AS1 mediated by HIF-1α. RNA-seq, fluorescent in situ hybridization, RNA pulldown, RNA immunoprecipitation, co-immunoprecipitation, immunofluorescence and immunoblot experiments were used to ascertain the involved mechanisms. Functional assays were performed in both in vitro and in vivo models to investigate the regulatory role of STEAP3-AS1/STEAP3/Wnt/β-catenin axis in CRC proliferation and metastasis. Results: Here, we identified a hypoxia-induced antisense lncRNA STEAP3-AS1 that was highly expressed in clinical CRC tissues and positively correlated with poor prognosis of CRC patients. Upregulation of lncRNA STEAP3-AS1, which was induced by HIF-1α-mediated transcriptional activation, facilitated the proliferation and metastasis of CRC cells both in vitro and in vivo. Mechanistically, STEAP3-AS1 interacted competitively with the YTH domain-containing family protein 2 (YTHDF2), a N6-methyladenosine (m6A) reader, leading to the disassociation of YTHDF2 with STEAP3 mRNA. This effect protected STEAP3 mRNA from m6A-mediated degradation, enabling the high expression of STEAP3 protein and subsequent production of cellular ferrous iron (Fe2+). Increased Fe2+ levels elevated Ser 9 phosphorylation of glycogen synthase kinase 3 beta (GSK3β) and inhibited its kinase activity, thus releasing β-catenin for nuclear translocation and subsequent activation of Wnt signaling to support CRC progression. Conclusions: Taken together, our study highlights the mechanisms of lncRNA STEAP3-AS1 in facilitating CRC progression involving the STEAP3-AS1/STEAP3/Wnt/β-catenin axis, which may provide novel diagnostic biomarkers or therapeutic targets to benefit CRC treatment. Hypoxia-induced HIF-1α transcriptionally upregulates the expression of lncRNA STEAP3-AS1, which interacts competitively with YTHDF2, thus upregulating mRNA stability of STEAP3 and consequent STEAP3 protein expression. The enhanced STEAP3 expression results in production of cellular ferrous iron (Fe2+), which induces the Ser 9 phosphorylation and inactivation of GSK3β, releasing β-catenin for nuclear translocation and contributing to subsequent activation of Wnt signaling to promote CRC progression. [ABSTRACT FROM AUTHOR]

In this article, we review the worldwide developments of battery-electric buses (a) from medium-sized vehicles (e.g., 6.7 m) to heavy-duty vehicles (e.g., 11 m), and (b) from the slow-charging mode (e.g., 6 hours) to the fast-charging mode (e.g., 10 minutes). We also review the worldwide operations of battery-electric buses (a) from 1907 in London, England, the early 1980s in Denver, Colorado, and the early 1990s in Santa Barbara, California, and Chattanooga, Tennessee, to various international cities now, and (b) from less than 20 vehicles in a transit agency to more than 1,000 vehicles. We summarize the experiences and lessons learned from real-world operations. We examine key technical specifications that are critical to the operations of electric bus systems, in particular the operational distance and charging time. Due to a limited operational range of battery-electric buses, three range remedy methods have been proposed: (a) regular (slow) battery charging with backup vehicles equipped with fully charged batteries; (2) battery swapping; and (3) fast opportunity charging during the layover period. We conduct a qualitative analysis on the strengths and weaknesses of each range remedy method. We also analyze the vehicle cost, energy cost, and emissions of transit buses powered by different sources, and examine potential impacts of fast-charging electric buses on the electric grid. [ABSTRACT FROM PUBLISHER]

A three-dimensional (3D) networking FeTiO3/TiO2@C flexible fiber membrane was successfully fabricated by an electrospinning process and a controlled hot-press sintering method. This FeTiO3/TiO2@C fiber membrane displays a long-range continuous conductive networks, which can be directly used as self-standing anodes. The electrode sintered at 750 °C for 3 h possesses a reversible capacity of 205.4 mAh/g after 100 cycles at a current density of 300 mA/g. The superior cycle and rate performance can be attributed to the synergistic effect of little volume variation of TiO2 matrix, high capacity of FeTiO3 and good electrical conductivity of 3D networking. [ABSTRACT FROM AUTHOR]

In pig-to-human xenotransplantation, the transmission risk of porcine endogenous retroviruses (PERVs) is of great concern. However, the distribution of PERVs in pig genomes, their genetic variation among Eurasian pigs, and their evolutionary history remain unclear. We scanned PERVs in the current pig reference genome (assembly Build 11.1), and identified 36 long complete or near-complete PERVs (lcPERVs) and 23 short incomplete PERVs (siPERVs). Besides three known PERVs (PERV-A, -B, and -C), four novel types (PERV-JX1, -JX2, -JX3, and -JX4) were detected in this study. According to evolutionary analyses, the newly discovered PERVs were more ancient, and PERV-Bs probably experienced a bottleneck ~0.5 million years ago (Ma). By analyzing 63 high-quality porcine whole-genome resequencing data, we found that the PERV copy numbers in Chinese pigs were lower (32.0±4.0) than in Western pigs (49.1±6.5). Additionally, the PERV sequence diversity was lower in Chinese pigs than in Western pigs. Regarding the lcPERV copy numbers, PERV-A and -JX2 in Western pigs were higher than in Chinese pigs. Notably, Bama Xiang (BMX) pigs had the lowest PERV copy number (27.8±5.1), and a BMX individual had no PERV-C and the lowest PERV copy number (23), suggesting that BMX pigs were more suitable for screening and/or modification as xenograft donors. Furthermore, we identified 451 PERV transposon insertion polymorphisms (TIPs), of which 86 were shared by all 10 Chinese and Western pig breeds. Our findings provide systematic insights into the genomic distribution, variation, evolution, and possible biological function of PERVs.

Objective: This paper aims to provide some experimental basis for unveiling the role of PDRG1 (P53 And DNA Damage-Regulated Gene 1) gene silencing in the growth and development of gastric cancer., Methods: PDRG1 levels in gastric cancer tissues and cell lines were measured by Western blotting. Then, gastric cancer BGC-823 cells, divided into Control, PDRG1 siRNA, NC siRNA and PDRG1 siRNA + KU55933 (ATM inhibitor) groups, were used to conduct a series of in vitro experiments including MTT, Flow cytometry, Wound-healing and Transwell assays. Expression of PDRG1 and ATM/p53 pathway-related proteins were determined by Western blot. Eventually, experiment in vivo was carried out to verify the control of PDRG1 on gastric cancer cells after establishing the tumor xenograft model in nude mice., Results: PDRG1 was significantly elevated in gastric cancer tissues and was associated with lower cell differentiation degree, more severe lymph node metastasis and higher tumor stage of gastric cancer patients. The growth of BGC-823 cells were significantly retarded and the cell apoptosis was increased in the PDRG1 siRNA group; besides, cell cycle was arrested in G2/M phase, and the expressions of p-ATM, p53, p21, p-cdc2 and cleaved caspase-3 were up-regulated with the reduced PDRG1. However, KU55933 could reverse the anti-tumor effect of PDRG1 siRNA on BGC-823 cells. The in-vivo experiment confirmed PDRG1 siRNA can inhibit tumor xenograft growth in nude mice., Conclusion: Specific PDRG1 gene silencing may inhibit the growth and metastasis of gastric cancer cells through the activation of ATM/p53 pathway., (Copyright © 2019 Elsevier GmbH. All rights reserved.)