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This study explored the effect of Ustilago esculenta infection on differentially expressed genes (DEGs) in male Manchurian wild rice (Zizania latifolia). We injected male Jiaobai plants at the five-leaf stage with U. esculenta suspension, and leaves at different timepoints after inoculation were collected for transcriptome sequencing. Transcriptome sequencing identified 1,226 DEGs mainly enriched in resistance-related processes. Weighted gene coexpression network analysis (WGCNA) showed that ‘plant–pathogen interaction’ and ‘MAPK signalling pathway-plant’ were the two most important upregulated pathways, and 16 candidate genes related to response to U. esculenta infection were screened. The results provide a basis for determining the molecular mechanisms of the response of male Z. latifolia to U. esculenta infection.

Fe-based superelastic alloys, which show both superelasticity and high damping capacity, can be divided into four alloy systems based on the characteristics of the martensite transformation that is responsible for these effects, viz., Fe-Pt, Fe-Pd, Fe-Mn-Si, and Fe-Ni-Co. Since 2010, Fe-Ni-Co-Al-based alloys that exhibit a large superelastic effect have attracted widespread attention. In this paper, the characteristics of the phase transformation from austenite ( γ ) to martensite ( α ') and the effects of the martensite variants in Fe-Ni-Co-Al-based superelastic alloys are summarized. The effects of alloying elements, precipitates and texture on the thermoelastic martensite transformation and the superelastic properties are reviewed. The factors affecting the superelastic effect and recoverable strain along with the related mechanisms are discussed. In addition, research progress on the damping performance, microwire structures, and modeling of Fe-Ni-Co-Al-based superelastic alloys are outlined. Finally, the challenges and future developments of the superelastic effect in Fe-Ni-Co-Al-based alloy are explored. [ABSTRACT FROM AUTHOR]

China has become the largest country for e-bikes in the past decade, leading to a surge in road-related accidents. Chinese provinces and cities have successfully formulated local regulations, which set fines for not wearing helmets levying on e-bike riders. Without considering psychological resistance which is universal under the premise of compulsory legislation, the legislation and enforcement activities cannot continuously promote electric bikers' helmet use. This study aims to investigate the predictors that influence e-bike riders' intention to wear helmets by designing a research methodology that incorporates the theory of planned behavior (TPB), the protection motivation theory (PMT), and the psychological reactance theory (PRT). A multi-method analytical approach, including structural equation modeling (SEM), fuzzy-set qualitative comparative analysis (fsQCA), and a Bayesian Network (BN) with a sample dataset of 846 respondents. SEM and fsQCA explored the intentions to wear helmets from linear and nonlinear perspectives. BN verifies the degree of influence between different configurations resulting from fsQCA, to predict which mental configurations could get the most significant impact on helmet use. A total of 11 configurations lead to high helmet-wearing intention, and 4 lead to low helmet-wearing intention. Policymakers could design safety policies on our research, such as driving licenses and special lectures for e-bike riders. [ABSTRACT FROM AUTHOR]

2-Deoxy-D-glucose (2-DG) is a glucose analog used as a promising anticancer agent. It exerts its effects by inhibiting the glycolytic energy metabolism to deplete cells of energy. The larval stage of Echinococcus relies on glycolysis for energy production. Therefore, in this study, we investigated the in vitro and in vivo efficacy of 2-DG against the larval stage of Echinococcus granulosus and E. multilocularis. 2-DG exhibited significant time- and dose-dependent effects against in vitro cultured E. granulosus protoscoleces and E. multilocularis metacestodes. A daily oral administration of 500 mg/kg 2-DG in E. multilocularis-infected mice effectively reduced the weight of metacestodes. Notably, the combination treatment, either 2-DG (500 mg/kg/day) + albendazole (ABZ) (200 mg/kg/day) or 2-DG (500 mg/kg/day) + half-dose of ABZ (100 mg/kg/day), exhibited a potent therapeutic effect against E. multilocularis, significantly promoting the reduction of metacestodes weight compared with the administration of 2-DG or ABZ alone. Furthermore, the combination significantly promoted apoptosis of the cells of metacestodes and inhibited glycolysis in metacestodes, compared with the administration of 2-DG or ABZ alone. In conclusion, 2-DG exerts an effective activity against the larval stage of Echinococcus. Thus, it may be a promising anti-Echinococcus drug, and its combination with ABZ may provide a new strategy for the treatment of echinococcosis in humans. Author summary: Echinococcosis is a serious but neglected helminthic zoonosis caused by the larval stage of Echinococcus granulosus and E. multilocularis. At present, clinical pharmacotherapy of echinococcosis, such as albendazole (ABZ) and mebendazole, has limited effectiveness. Thus, the development of novel therapeutic drugs for human echinococcosis is urgently needed. 2-Deoxy-D-glucose (2-DG) is a glucose analog used as a promising anticancer agent, and it exerts its effects by inhibiting the glycolytic energy metabolism to deplete cells of energy. Echinococcus in the host depends on glycolysis for energy production and glycolysis intermediates for other metabolic processes. Therefore, in this study, we investigated the efficacy of 2-DG against Echinococcus. 2-DG exerted an effective in vitro and in vivo activity against E. granulosus protoscoleces and E. multilocularis metacestodes, and the combination of this drug with ABZ further improved the therapeutic effect. Therefore, 2-DG can be developed as a promising anti-Echinococcus drug, and its combination with ABZ may provide a new strategy for the treatment of human echinococcosis in the future. [ABSTRACT FROM AUTHOR]

Molecular genetic changes in acute myeloid leukemia (AML) play crucial roles in leukemogenesis, including recurrent chromosome translocations, epigenetic/spliceosome mutations and transcription factor aberrations. Six1, a transcription factor of the Sine oculis homeobox (Six) family, has been shown to transform normal hematopoietic progenitors into leukemia in cooperation with Eya. However, the specific role and the underlying mechanism of Six1 in leukemia maintenance remain unexplored. Here, we showed increased expression of SIX1 in AML patients and murine leukemia stem cells (c‐Kit+ cells, LSCs). Importantly, we also observed that a higher level of Six1 in human patients predicts a worse prognosis. Notably, knockdown of Six1 significantly prolonged the survival of MLL‐AF9‐induced AML mice with reduced peripheral infiltration and tumor burden. AML cells from Six1‐knockdown (KD) mice displayed a significantly decreased number and function of LSC, as assessed by the immunophenotype, colony‐forming ability and limiting dilution assay. Further analysis revealed the augmented apoptosis of LSC and decreased expression of glycolytic genes in Six1 KD mice. Overall, our data showed that Six1 is essential for the progression of MLL‐AF9‐induced AML via maintaining the pool of LSC. [ABSTRACT FROM AUTHOR]

Abstract: Arrays of oriented poly(3,4-ethylenedioxythiophene) (PEDOT) micro/nanorods are synthesized by electrochemical galvanostatic method at the current density of 1mAcm−2 in the cetyltrimethylammonium bromide (CTAB) aqueous solution whose pH value is 1. The CTAB is used both as the surfactant and the supporting salt in the electrolyte solution. The electrochemical properties of PEDOT films are characterized by cyclic voltammetry and galvanostatic charge/discharge techniques, which indicate that the arrays of oriented PEDOT micro/nanorods can be applied as the electrode materials of supercapacitors. In addition, the cycling performance of PEDOT micro/nanorods is much better than that of traditional PEDOT particles. The effects of the concentration of CTAB, the current density, and pH value of electrolyte solutions on the morphologies and electrochemical properties of PEDOT films are investigated. The mechanism of different morphologies formation is discussed in this study as well. [Copyright &y& Elsevier]

Acute myeloid leukemia (AML) is a devastating blood cancer with high heterogeneity and ill-fated outcome. Despite numerous advances in AML treatment, the prognosis remains poor for a significant proportion of patients. Consequently, it is necessary to accurately and comprehensively identify biomarkers as soon as possible to enhance the efficacy of diagnosis, prognosis and treatment of AML. In this study, we aimed to identify prognostic markers of AML by analyzing the cohorts from TCGA-LAML database and GEO microarray datasets. Interestingly, the transcriptional level of microtubule-associated protein TBCB in AML patients was noticeably increased when compared with normal individuals, and this was verified in two independent cohorts (GSE9476 and GSE13159) and with our AML patients. Furthermore, univariate and multivariate regression analysis revealed that high TBCB expression was an independent poor prognostic factor for AML. GO and GSEA enrichment analysis hinted that immune-related signaling pathways were enriched in up-regulated DEGs between two populations separated by the median expression level of TBCB . By constructing a protein-protein interaction network, we obtained six hub genes, all of which are immune-related molecules, and their expression levels were positively linked to that of TBCB . In addition, the high expression of three hub genes was significantly associated with a poor prognosis in AML. Moreover, we found that the tumor microenvironment in AML with high TBCB expression tended to be infiltrated by NK cells, especially CD56 bright NK cells. The transcriptional levels of NK cell inhibitory receptors and their ligands were positively related to that of TBCB , and their high expression levels also predicted poor prognosis in AML. Notably, we found that the down-regulation of TBCB suppressed cell proliferation in AML cell lines by enhancing the apoptosis and cell cycle arrest. Finally, drug sensitivity prediction illustrated that cells with high TBCB expression were more responsive to ATRA and midostaurin but resistant to cytarabine, dasatinib, and imatinib. In conclusion, our findings shed light on the feasibility of TBCB as a potential predictor of poor outcome and to be an alternative target of treatment in AML., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

Nowadays, adolescents would like to share their daily lives via social media platforms, which presents an excellent opportunity for us to leverage these data to develop techniques to measure their mental health status, such as depression. Previous researches focus on the more accurate detection of depression through statistical learning and ignore psychological understanding of depression. However, psychologists have given lots of theoretical evidence for depression. Such as according to cognitive psychology research, cognitive distortions will result in depression. Thus, in this study, we propose a new task, explainable depression detection, to not only automatically detect depression but also try to give clues to depression based on cognitive distortion theory. For this purpose, we construct a multi-task learning model based on a pre-trained model to detect depression and identify cognitive distortion. And we use many analytical means including word clouds for data analysis to draw our conclusion. Previous social media users' depression corpus and our cognitive distortion corpus are utilized for analysis and experiment. Our experimental results outperform the baseline results and interesting conclusions about adolescent depression are drawn., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Wang, Zhao, Lu and Qin.)

Long non-coding RNA (lncRNA) has become an important regulator of many cellular processes, including cell proliferation. Although studies have shown that a variety of lncRNAs play an important role in the occurrence and development of hematopoietic malignancies, a more comprehensive and unbiased method to study the function of lncRNAs in leukemia cell lines is lacking. Here, we used short hairpin RNA (shRNA) library combined with high-throughput sequencing to screen lncRNAs that may affect the proliferation of leukemia cell lines, and identified lncRNA C20orf204-203 among 74 candidate lncRNAs in this study. Further experiments showed that C20orf204-203 was localized in the cytoplasm in both K562 and THP-1 cell lines. C20orf204-203 knockdown decreased the proliferation of K562 and THP-1 cell lines accompanied with the increased proportion of early apoptotic cells. We observed the increased mRNA level of BAD gene while decreased protein level of TP53 and BCL2. The expression of Caspase 3 decreased and Caspase 3-cleaved protein increased in THP-1 cell line. However, their changes were inconsistent in the two cell lines. Our experimental results showed that knockdown of lncRNA C20orf204-203 in leukemia cell lines affected cell proliferation although the mechanism of action in different cell lines may differ. Importantly, our research demonstrated the feasibility of using shRNA library combined with high-throughput sequencing to study the role of lncRNA in leukemia cell lines on a large scale.

Colony-stimulating factor 3 receptor (CSF3R) mutations have been identified in a variety of myeloid disorders. Although CSF3R point mutations (eg, T618I) are emerging as key players in chronic neutrophilic leukemia/atypical chronic myelogenous leukemia , the significance of rarer CSF3R mutations is unknown. Here, we report a 32-year-old female who was diagnosed as Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph + ALL) with the CSF3R M696T mutation and was undergone unrelated donor hematopoietic stem cell transplantation. The patient achieved complete remission with chemotherapy in combination with tyrosine kinase inhibitor (TKI) and long-term survival by unrelated donor transplantation. Meanwhile, we performed a series of experiments using murine interleukin 3 (IL-3)-dependent Ba/F3 cell line to evaluate the transforming capacity of the CSF3R M696T mutation. We confirmed the presence of a CSF3R M696T germline mutation in this patient which was inherited from her mother. The in vitro experiment results showed that the CSF3R M696T mutation contributes marginally to the tumor transformation of Ba/F3 cells, indicating that CSF3R M696T mutation was neutral in tumor transformation ability. We concluded that TKI is effective in patients with the CSF3R M696T mutation in Ph + ALL and donors with CSF3R M696T mutation might still be selected as the candidate for transplantation., (Copyright © 2021 The Authors. Published by Wolters Kluwer Health Inc., on behalf of the Chinese Association for Blood Sciences.)

Epigenetic regulations play crucial roles in leukemogenesis and leukemia progression. SUV39H1 is the dominant H3K9 methyltransferase in the hematopoietic system, and its expression declines with aging. However, the role of SUV39H1 via its-mediated repressive modification H3K9me3 in leukemogenesis/leukemia progression remains to be explored. We found that SUV39H1 was down-regulated in a variety of leukemias, including MLL-r AML, as compared with normal individuals. Decreased levels of Suv39h1 expression and genomic H3K9me3 occupancy were observed in LSCs from MLL-r-induced AML mouse models in comparison with that of hematopoietic stem/progenitor cells. Suv39h1 overexpression increased leukemia latency and decreased the frequency of LSCs in MLL-r AML mouse models, while Suv39h1 knockdown accelerated disease progression with increased number of LSCs. Increased Suv39h1 expression led to the inactivation of Hoxb13 and Six1, as well as reversion of Hoxa9/Meis1 downstream target genes, which in turn decelerated leukemia progression. Interestingly, Hoxb13 expression is up-regulated in MLL-AF9-induced AML cells, while knockdown of Hoxb13 in MLL-AF9 leukemic cells significantly prolonged the survival of leukemic mice with reduced LSC frequencies. Our data revealed that SUV39H1 functions as a tumor suppressor in MLL-AF9-induced AML progression. These findings provide the direct link of SUV39H1 to AML development and progression.