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  • Oxford University Press (OUP)  (9)
  • 1
    In: The Plant Cell, Oxford University Press (OUP), Vol. 34, No. 4 ( 2022-03-29), p. 1226-1249
    Abstract: Low temperature causes poor coloration of strawberry (Fragaria sp.) fruits, thus greatly reducing their commercial value. Strawberry fruits accumulate anthocyanins during ripening, but how low temperature modulates anthocyanin accumulation in plants remains largely unknown. We identified MITOGEN-ACTIVATED PROTEIN KINASE3 (FvMAPK3) as an important negative regulator of anthocyanin accumulation that mediates the poor coloration of strawberry fruits in response to low temperature. FvMAPK3 activity was itself induced by low temperature, leading to the repression of anthocyanin accumulation via two mechanisms. Activated FvMAPK3 acted as the downstream target of MAPK KINASE4 (FvMKK4) and SUCROSE NONFERMENTING1-RELATED KINASE2.6 (FvSnRK2.6) to phosphorylate the transcription factor FvMYB10 and reduce its transcriptional activity. In parallel, FvMAPK3 phosphorylated CHALCONE SYNTHASE1 (FvCHS1) to enhance its proteasome-mediated degradation. These results not only provide an important reference to elucidate the molecular mechanisms underlying low-temperature-mediated repression of anthocyanin accumulation in plants, but also offer valuable candidate genes for generating strawberry varieties with high tolerance to low temperature and good fruit quality.
    Type of Medium: Online Resource
    ISSN: 1040-4651 , 1532-298X
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
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  • 2
    In: Journal of Applied Microbiology, Oxford University Press (OUP), Vol. 132, No. 2 ( 2022-02), p. 1307-1318
    Type of Medium: Online Resource
    ISSN: 1364-5072 , 1365-2672
    URL: Issue
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 2020421-8
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  • 3
    In: Neuro-Oncology, Oxford University Press (OUP), Vol. 24, No. 11 ( 2022-11-02), p. 1871-1883
    Abstract: Targeting glioblastoma (GBM) energy metabolism through multiple metabolic pathways has emerged as an effective therapeutic approach. Dual inhibition of phospholipid and mitochondrial metabolism with cytoplasmic phospholipase A2 (cPLA2) knockdown and metformin treatment could be a potential strategy. However, the strategic prerequisite is to explore a carrier capable of co-delivering the therapeutic combination to cross the blood-brain barrier (BBB) and preferentially accumulate at the GBM site. Methods Blood exosomes (Exos) were selected as the combination delivery carriers. The cellular uptake of Exos and the therapeutic effects of the combination strategy were evaluated in primary GBM cells. In vivo GBM-targeted delivery efficiency and anti-GBM efficacy were tested in a patient-derived xenograft (PDX) model. Results Here, we showed that the Exos-mediated cPLA2 siRNA/metformin combined strategy could regulate GBM energy metabolism for personalized treatment. Genomic analysis and experiments showed that polymerase 1 and transcript release factor (PTRF, a biomarker of GBM) positively regulated the uptake of Exos by GBM cells, confirming the feasibility of the delivery strategy. Further, Exos could co-load cPLA2 siRNA (sicPLA2) and metformin and co-deliver them across the BBB and into GBM tissue. The mitochondrial energy metabolism of GBM was impaired with this combination treatment (Exos-Met/sicPLA2). In the PDX GBM model, systemic administration of Exos-Met/sicPLA2 reduced tumor growth and prolonged survival. Conclusions Our findings demonstrated that Exos-based combined delivery of sicPLA2 and metformin selectively targeted the GBM energy metabolism to achieve antitumor effects, showing its potential as a personalized therapy for GBM patients.
    Type of Medium: Online Resource
    ISSN: 1522-8517 , 1523-5866
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
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  • 4
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2022
    In:  Forensic Sciences Research Vol. 7, No. 3 ( 2022-07-03), p. 503-509
    In: Forensic Sciences Research, Oxford University Press (OUP), Vol. 7, No. 3 ( 2022-07-03), p. 503-509
    Abstract: In forensic practice, the identification of antemortem burns and postmortem burns is of the utmost importance. Reports from previous studies have shown that miRNAs, with lengths stretching over 18–25 nucleotides, are highly stable and resistant to degradation. However, there has been little research into the application of miRNAs in identifying antemortem and postmortem burns. This study compared the expression of miR-711 and miR-183-3p levels in mouse and postmortem human burned skins using RT-qPCR assay. RT-qPCR examination of burned mouse skins showed that increased miR-711 and miR-183-3p expression in comparison to intact skin tissues. The increased expressions of these two miRNAs were observed until 120 h after death in burned mouse skins, whereas no significant changes were found in postmortem burned skins. In human burned skins, the increased levels of these two miRNAs at 48 h following autopsy occurred in 19 of 26 subjects, which appeared to be related to the severity of the burn. These findings suggest that miR-711 and miR-183-3p may act as biomarkers for vital reaction of skin burn. Key PointsThis study investigated miR-711 and miR-183-3p levels in mouse and postmortem human burned skins using RT-qPCR.Increased miR-711 and miR-183-3p levels were observed in burned mouse skins.The increased expressions of these two miRNAs were observed until 120 h after death in burned mouse skin.The increased levels of these two miRNAs were observed until 48 h after autopsy in 19 of 26 forensic cases, which appeared to be related to the severity of the burn.
    Type of Medium: Online Resource
    ISSN: 2096-1790 , 2471-1411
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
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  • 5
    In: Journal of Economic Entomology, Oxford University Press (OUP), Vol. 112, No. 4 ( 2019-08-03), p. 1866-1874
    Abstract: In this study, the sensitivity of 20 field populations of Chilo suppressalis (Walker) from five provinces in China to seven insecticides was evaluated during 2016–2018. The results indicated that 20 field populations of C. suppressalis had evolved moderate to high levels of resistance to triazophos (RR 64.5–461.3) and chlorpyrifos (RR 10.1–125.0). Furthermore, C. suppressalis exhibited low to moderate levels of resistance to abamectin (RR 6.5–76.5) and decreased susceptibility to cyantraniliprole (RR 1.0–34.0). The population collected from Nanchang in Jiangxi Province (JXNC) showed high resistance to chlorantraniliprole (RR 148.3–294.3), and other geographical populations remained susceptible to moderate levels of resistance (RR 1.0–37.5). In contrast, C. suppressalis remained susceptible to low levels of resistance to spinetoram (RR 1.0–6.7) and spinosad (RR 1.0–4.6). Significant correlations were found between the Log LC50 values of chlorantraniliprole and cyantraniliprole, chlorpyrifos and triazophos, as well as cyantraniliprole and chlorpyrifos and triazophos. Similarly, significant correlations were found among abamectin, chlorpyrifos, and triazophos. In addition, a significant correlation was also observed between the activity of the detoxification enzymes and the log LC50 values of chlorantraniliprole, cyantraniliprole, abamectin, chlorpyrifos, and triazophos. The findings provide an important reference for implementing effective resistance management strategies and the development of new insecticides in insect pest control.
    Type of Medium: Online Resource
    ISSN: 0022-0493 , 1938-291X
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
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  • 6
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2014
    In:  Stem Cells Vol. 32, No. 4 ( 2014-04-01), p. 902-912
    In: Stem Cells, Oxford University Press (OUP), Vol. 32, No. 4 ( 2014-04-01), p. 902-912
    Abstract: Osteoblast differentiation and bone formation (osteogenesis) are regulated by transcriptional and post-transcriptional mechanisms. Recently, microRNAs (miRNAs) were identified as novel key regulators of human stromal (skeletal, mesenchymal) stem cells (hMSC) differentiation. Here, we identified miRNA-34a (miR-34a) and its target protein networks as modulator of osteoblastic (OB) differentiation of hMSC. miRNA array profiling and further validation by quantitative RT-PCR revealed that miR-34a was upregulated during OB differentiation of hMSC, and in situ hybridization confirmed its OB expression in vivo. Overexpression of miR-34a inhibited early commitment and late OB differentiation of hMSC in vitro, whereas inhibition of miR-34a by anti-miR-34a enhanced these processes. Target prediction analysis and experimental validation confirmed Jagged1 (JAG1), a ligand for Notch 1, as a bona fide target of miR-34a. siRNA-mediated reduction of JAG1 expression inhibited OB differentiation. Moreover, a number of known cell cycle regulator and cell proliferation proteins, such as cyclin D1, cyclin-dependent kinase 4 and 6 (CDK4 and CDK6), E2F transcription factor three, and cell division cycle 25 homolog A were among miR-34a targets. Furthermore, in a preclinical model of in vivo bone formation, overexpression of miR-34a in hMSC reduced heterotopic bone formation by 60%, and conversely, in vivo bone formation was increased by 200% in miR-34a-deficient hMSC. miRNA-34a exhibited unique dual regulatory effects controlling both hMSC proliferation and OB differentiation. Tissue-specific inhibition of miR-34a might be a potential novel therapeutic strategy for enhancing in vivo bone formation. Stem Cells  2014;32:902–912
    Type of Medium: Online Resource
    ISSN: 1066-5099 , 1549-4918
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2014
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    detail.hit.zdb_id: 1143556-2
    detail.hit.zdb_id: 605570-9
    SSG: 12
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  • 7
    In: Neuro-Oncology, Oxford University Press (OUP), Vol. 23, No. 3 ( 2021-03-25), p. 387-399
    Abstract: Metabolism remodeling is a hallmark of glioblastoma (GBM) that regulates tumor proliferation and the immune microenvironment. Previous studies have reported that increased polymerase 1 and transcript release factor (PTRF) levels are associated with a worse prognosis in glioma patients. However, the biological role and the molecular mechanism of PTRF in GBM metabolism remain unclear. Methods The relationship between PTRF and lipid metabolism in GBM was detected by nontargeted metabolomics profiling and subsequent lipidomics analysis. Western blotting, quantitative real-time PCR, and immunoprecipitation were conducted to explore the molecular mechanism of PTRF in lipid metabolism. A sequence of in vitro and in vivo experiments (both xenograft tumor and intracranial tumor mouse models) were used to detect the tumor-specific impacts of PTRF. Results Here, we show that PTRF triggers a cytoplasmic phospholipase A2 (cPLA2)–mediated phospholipid remodeling pathway that promotes GBM tumor proliferation and suppresses tumor immune responses. Research in primary cell lines from GBM patients revealed that cells overexpressing PTRF show increased cPLA2 activity—resulting from increased protein stability—and exhibit remodeled phospholipid composition. Subsequent experiments revealed that PTRF overexpression alters the endocytosis capacity and energy metabolism of GBM cells. Finally, in GBM xenograft and intracranial tumor mouse models, we showed that inhibiting cPLA2 activity blocks tumor proliferation and prevents PTRF-induced reduction in CD8+ tumor-infiltrating lymphocytes. Conclusions The PTRF-cPLA2 lipid remodeling pathway promotes tumor proliferation and suppresses immune responses in GBM. In addition, our findings highlight multiple new therapeutic targets for GBM.
    Type of Medium: Online Resource
    ISSN: 1522-8517 , 1523-5866
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
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  • 8
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2015
    In:  Toxicology Research Vol. 4, No. 6 ( 2015), p. 1523-1534
    In: Toxicology Research, Oxford University Press (OUP), Vol. 4, No. 6 ( 2015), p. 1523-1534
    Type of Medium: Online Resource
    ISSN: 2045-452X , 2045-4538
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2015
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    SSG: 15,3
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  • 9
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2022
    In:  Clean Energy Vol. 6, No. 3 ( 2022-06-01), p. 496-502
    In: Clean Energy, Oxford University Press (OUP), Vol. 6, No. 3 ( 2022-06-01), p. 496-502
    Abstract: Solar energy has attracted a lot of attention because it is clean and has no pollution. However, due to the partially shaded condition, the photovoltaic array cannot work uniformly at the maximum power point, resulting in a large power loss. To improve this problem, the research of the maximum power point tracking (MPPT) algorithm is discussed by scholars. In this paper, an improved particle swarm optimization (PSO) algorithm is proposed to achieve the goal of MPPT, which uses Newton interpolation-assisted conventional PSO. After tracking to the maximum power point, the Newton interpolation method is used to calculate the maximum power point, reduce the number of iterations of the conventional PSO algorithm and reduce the steady-state oscillation. The simulation is carried out in MATLAB®/Simulink® and compared with conventional PSO. The results show that the improved PSO has better tracking accuracy and speed than the conventional algorithm, and the initial tracking speed is increased by & gt;30%.
    Type of Medium: Online Resource
    ISSN: 2515-4230 , 2515-396X
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 2924554-0
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