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A green and feasible synthetic protocol for α-polyfluoroarylalcohols was developed with polyfluoroarenes and alcohols via Lewis acid-assisted synergistic photoredox and hydrogen-atom transfer catalysis under batch or flow conditions.

As a core component of the power electronic transformer (PET) in DC network, the multi-level high-frequency power transformer has received great attention due to the insulation material fatigue problems resulting from the hot-spot temperature rises. To solve this problem, a three-winding high-frequency transformer for 10 kVA PET application is designed and made in the laboratory, and the loss and temperature rise distribution is calculated by means of the finite element (FE) electromagnetic-thermal coupling simulation. The influence of temperature on the hysteresis and loss properties of core material has been carefully considered and measured. The influence of skin effect and end effect on the winding loss is taken into account through the establishing three-dimensional FE model. Besides, the convective heat transfer coefficient is solved based on the principle of heat transfer instead of the empirical coefficient method. By compared with the experimental results, the calculated results are validated to be effective in predicting the loss and hot-spot temperature rises of the transformer.

Gliomas are the most common and fatal brain tumors worldwide. Abnormal DNA promoter methylation is an important mechanism for gene loss of tumor suppressors. A long non-coding RNA colorectal adenocarcinoma hypermethylated (CAHM) has been reported to be nearly deleted in glioblastomas (GBMs). Nevertheless, the roles of CAHM in gliomas remain unknown up to now. In the present study, 969 glioma samples downloaded from the CGGA and Gravendeel databases were included. We found that CAHM expression was correlated with glioma grades, molecular subtype, IDH mutation status, and 1q/19p codel status. In glioma cells, CAHM is hypermethylated by DNA methyltransferase1 (DNMT1) and the loss of CAHM expression could be reversed by 5-Aza-2'-deoxycytidine (5-Aza), a specific inhibitor of DNA methyltransferases. Besides, the expression of CAHM was negatively associated with overall survival in both primary and recurrent gliomas. Moreover, the result of Gene Ontology (GO) analysis suggested that CAHM participated in negatively regulating cell development, nervous system development, neurogenesis, and integrin-mediated signaling pathway. Overexpression of CAHM inhibited glioma cell proliferation, clone formation, and invasion. Further exploring results showed that CAHM overexpression suppressed glioma migration and invasion through SPAK/MAPK pathway. Collectively, this study disclosed that CAHM might be a suppressor in gliomas.

Yang Z, Bian E, Xu Y, et al. Onco Targets Ther. 2020;13:989–1000. The Editor and Publisher of OncoTargets and Therapy wish to retract the published article. Concerns were raised regarding the alleged duplication of cell invasion and migration images in Figures 1 and 6. Specifically, Figure 1E, invasion, U251 vector, appears to have been duplicated with Figure 6D, invasion, U251 Control. Figure 6C, migration, U87 Control, appears to have been duplicated with Figure 6D, invasion, U251 Lys05. The authors responded to our queries but were unable to provide a satisfactory explanation regarding the duplicated images, nor were they able to provide original data that could adequately verify the findings. The decision was made to retract the article and the authors have agreed with this. Our decision-making was informed by our policy on publishing ethics and integrity and the COPE guidelines on retraction. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as “Retracted”. This retraction relates to this paper

Cancer-related deaths did not apparently decrease in the past decades despite aggressive treatments. It's reported that cancer will become the leading cause of death worldwide in the twenty-first century. Increasing evidence has revealed that lncRNAs will emerge as promising cancer biomarkers or therapeutic targets in cancer treatment. LncRNA-ATB, a long noncoding RNA activated by TGF-β, was found to be abnormally expressed in certain cancers and participate in the development and progression of tumors. In addition, aberrant lncRNA-ATB expression was also associated with clinical characteristics of tumors. The purpose of this review is to summarize functions and underlying mechanisms of lncRNA-ATB in tumors, and discuss whether lncRNA-ATB can be a biomarker and therapeutic target in cancers.

Background Glioma is one of the most common malignant tumors. Glioblastoma (grade IV) is considered the most malignant form of human brain tumors. Maternal expression gene 3 (Meg3) encodes a non-coding RNA (ncRNA) that plays an important role in the development and progression of cancer. However, the role of Meg3 in glioma cells remains largely unclear. Methods Reverse transcription-quantitative (RT-q) PCR was conducted to evaluate the mRNA expression related to cell autophagy and EMT while protein expression was detected by Western blotting. Staining of acidic vacuoles and immunofluorescence staining were used to detect autophagy. The ability of cells to migrate and invade was detected by Transwell migration and invasion assays. Results In the present study, it was found that the overexpression of Meg3 induced EMT, migration and invasion of glioma cells, whereas Meg3 overexpression induced autophagy of glioma cells. More importantly, the inhibition of autophagy impaired the EMT of glioma cells. In addition, Meg3-induced EMT, migration and invasion could be partially reversed by autophagy inhibitors, chloroquine (CQ) and Lys05, in glioma cells. Conclusion All data suggest that Meg3 induces EMT and invasion of glioma cells via autophagy. Overall, the findings of the present study demonstrate the importance of Meg3 in the molecular etiology of glioma, which also indicate its potential applications in the treatment of glioma.

As a common malicious attack occurring in the network among components in CPS, jamming attacks can result in packet dropouts, which leads to instability of system. Tree-based MPC (TBMPC), as an effective method to deal with probabilistic packet dropouts from jamming attacks, has been proposed in literature [15]. However, the scope of application is limited due to the heavy burden on computation of the existing TBMPC. This paper aims to propose a simplified tree-based model predictive control (STBMPC) method based on attack detection for the packet dropout problem caused by jamming attacks. This method can deal with probabilistic packet dropouts by representing all scenarios along the prediction horizon in the form of binary tree efficiently. Firstly, by combining all possible attacks in the prediction horizon, a combined system considering all scenarios can be obtained. Then, an attack detection method is introduced into the design of controller, which greatly reduces the number of scenarios predicted at each time step. Finally, the simulation results show that, by adopting the attack detection method, STBMPC can greatly shorten the running time without weakening the control performance. The research results of this paper can improve the control efficiency of TBMPC aiming at attacked CPSs

Background The epithelial-to-mesenchymal transition (EMT) has been linked to the regulation of glioma progression. However, the underlying signaling mechanisms that regulate EMT are poorly understood. Methods Quantitative real-time PCR (RT-qPCR) and western blot were performed to detect the expression of MeCP2 in glioma tissues and cell lines. MeCP2 functions were tested with cell immunofluorescence staining and western blot. For in vivo experiments, mouse xenograft model was used to investigate the effects of MeCP2 on glioma. ChIP and Co-IP were used to detect the relationships among MeCP2, miR-200c and Suv39H1. Results In this study, we found that MeCP2 was frequently up-regulated in human glioma tissues and cell lines. MeCP2 knockdown remarkably induced cell epithelial phenotype and inhibited mesenchymal marker ZEB1 and ZEB2 in vitro and in vivo. In addition, MeCP2 in glioma tissues was negatively correlated with miR-200c expression, and miR-200c overexpression partially abrogated mesenchymal phenotype induced by MeCP2. More importantly, we showed that MeCP2 recruited H3K9 to the promoter of miR-200c by interacting with SUV39H1, resulting in EMT of glioma cells. Conclusions This study for the first time reveals MeCP2 as a novel regulator of EMT in glioma and suggest that MeCP2 inhibition may represent a promising therapeutic option for suppressing EMT in glioma. Electronic supplementary material The online version of this article (10.1186/s13046-019-1341-6) contains supplementary material, which is available to authorized users.

Glioma constitutes the most aggressive primary intracranial malignancy in adults. We previously showed that long noncoding RNA activated by TGF-β (lncRNA-ATB) promoted the glioma cells invasion. However, whether lncRNA-ATB is involved in TGF-β-mediated invasion of glioma cells remains unknown. In this study, quantitative real-time polymerase chain reaction and western blot analysis were used for detecting the mRNA and protein expression of related genes, respectively. Transwell assay was performed to assess the impact of lncRNA-ATB on TGF-β-induced glioma cells migration and invasion. Immunofluorescence staining was utilized to characterize related protein distribution. Results showed that TGF-β upregulated lncRNA-ATB expression in glioma LN-18 and U251 cells. Overexpression of lncRNA-ATB activated nuclear factor-κB (NF-κB) pathway and promoted P65 translocation into the nucleus, thus facilitated glioma cells invasion stimulated by TGF-β. Similarly, lncRNA-ATB markedly enhanced TGF-β-mediated invasion of glioma cells through activation P38 mitogen-activated protein kinase (P38/MAPK) pathway. Moreover, both the NF-κB selected inhibitor pyrrolidinedithiocarbamate ammonium and P38/MAPK specific inhibitor SB203580 partly reversed lncRNA-ATB induced glioma cells invasion mediated by TGF-β. Collectively, this study revealed that lncRNA-ATB promotes TGF-β-induced glioma cell invasion through NF-κB and P38/MAPK pathway and established a detailed framework for understanding the way how lncRNA-ATB performs its function in TGF-β-mediated glioma invasion.

NH3 synthesis almost relies on the energy-intensive Haber–Bosch process with abandoned CO2 emission. Electrochemical N2 reduction offers an environmentally friendly process for sustainable artifici...

Neuroinflammatory diseases such as multiple sclerosis are characterized by infiltration of lymphocytes into the central nervous system followed by demyelination and axonal degeneration. While evidence suggests that activated T-lymphocytes induce neurotoxicity and impair function of neural stem cells, the effect of T-cells on oligodendrocyte progenitor cells (OPCs) is still uncertain, partly due to the difficulty in obtaining human OPCs. Here we studied the effect of activated T cells on OPCs using OPCs derived from human hematopoietic stem cells or from human fetal brain. OPCs were exposed to supernatants (sups) from activated T-cells. Cell proliferation was determined by EdU incorporation and CellQuanti-Blue assays. Surprisingly, we found that sups from activated T cells induced OPC proliferation by regulating cell cycle progression. Vascular endothelial growth factor A (VEGF-A) transcripts and protein were increased in T cells after activation. Immunodepletion of VEGF-A from activated T cell sups significantly attenuated its effect on OPC proliferation. Furthermore, VEGF receptor 2 (VEGF-R2) was expressed on OPCs and its inhibition also attenuated activated T cell-induced OPC proliferation. Thus activated T cells have a trophic role by promoting OPC proliferation via the VEGF-R2 pathway.

Stem cells are capable of unlimited proliferation but can be induced to form brain cells. Factors that specifically regulate human development are poorly understood. We found that human stem cells expressed high levels of the envelope protein of an endogenized human-specific retrovirus (HERV-K, HML-2) from loci in chromosomes 12 and 19. The envelope protein was expressed on the cell membrane of the stem cells and was critical in maintaining the stemness via interactions with CD98HC, leading to triggering of human-specific signaling pathways involving mammalian target of rapamycin (mTOR) and lysophosphatidylcholine acyltransferase (LPCAT1)-mediated epigenetic changes. Down-regulation or epigenetic silencing of HML-2 env resulted in dissociation of the stem cell colonies and enhanced differentiation along neuronal pathways. Thus HML-2 regulation is critical for human embryonic and neurodevelopment, while it's dysregulation may play a role in tumorigenesis and neurodegeneration.

Glioma is the most common primary malignant tumor in the human brain. Although there are a variety of treatments, such as surgery, radiation and chemotherapy, glioma is still an incurable disease. Super-enhancers (SEs) are implicated in the control of tumor cell identity, and they promote oncogenic transcription, which supports tumor cells. Inhibition of the SE complex, which is required for the assembly and maintenance of SEs, may repress oncogenic transcription and impede tumor growth. In this review, we discuss the unique characteristics of SEs compared to typical enhancers, and we summarize the recent advances in the understanding of their properties and biological role in gene regulation. Additionally, we highlight that SE-driven lncRNAs, miRNAs and genes are involved in the malignant phenotype of glioma. Most importantly, the application of SE inhibitors in different cancer subtypes has introduced new directions in glioma treatment.

Recent decades, there is significant progress in understanding the mechanisms of tumor progression and immune evasion. The newly discovered protein NLRC5 is demonstrated to participate in regulating cancer immune escape through enhancing MHC class I genes expression in certain tumors. Nevertheless, increasing evidence has revealed that NLRC5 is up-regulated in some other tumors and promote tumor development and progression. The purpose of this review is to describe the role of NLRC5 in tumors and discuss whether NLRC5 can be a potential target in cancer treatment.

Table S1. The clinicopathological features of glioma patients. (DOC 32 kb)

Figure S3. (A) The methylation of miR-200c promoter was observed after transfection with MeCP2 plasmid. (B) The levels of SUV39H1 mRNA expression were examined after transfection with si-SUV39H1. **p

Figure S2. (A) The levels of miR-200c in glioma cells transfected with MeCP2 shRNA. **p

The removal of Pb 2+ from aqueous solution by 732 cation-exchange resin in sodium type (732-CR) has been studied in batch experiments at varying pH (2.0–8.0), Pb 2+ concentration (50–200 mg/L), contact time (5–300 min), temperature (288–308 K) and resin dose (0.125–0.75 g/L). The experimental data show that the ion-exchange process was dependent on pH and temperature, the optimal exchange capacity was found at pH 4.0, and higher temperature was beneficial to lead sorption. Kinetic data indicate that the ion-exchange process followed a pseudo-first order model. The equilibrium exchange capacity could be reached at approximately 4 h, and the maximum sorption capacity of Pb 2+ at pH 4.0 was 396.8 mg/g resin. The equilibrium data were evaluated with Langmuir and Freundlich model, and were best fitted with Langmuir model. The thermodynamic parameters for removal of Pb 2+ indicate that the reaction was spontaneous and endothermic. Additionally, column tests were conducted by using both synthetic solution and effluents from lead battery industry. The regeneration of resin was performed for two sorption-regeneration cycles by 1 M NaOH, and the results show that effective regeneration was achieved by this method.