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  • × 2023
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Communications Physics,2023年

Liyuan Hu, Yao Li, Junwei Li, Yushou Song, Yanyun Yang, Zhen Bai, Shuya Jin, Shiwei Xu, Fangfang Duan, Herun Yang, Peng Ma, Junbing Ma, Jiansong Wang, Meirong Huang, Suyalatu Zhang, Dexin Wang, Kang Wei, Qite Li, Ying Chen, Lisheng Yang, Gen Li, Hui Hua, Shiwei Bai, Xiaofei Yang, Jingjing Li, Jinyan Xu, Kai Ma, Yucheng Ge, Yanlin Ye, Weiliang Pu, Zhiwei Tan, Shujing Wang, Jiahao Chen, Zhihuan Li, Jianling Lou, Ziyao Hu, Longchun Tao, Zaihong Yang, Biao Yang, Wei Liu, Dongxi Wang, Siwei Huang, Hanzhou Yu, Yang Liu, Ying Jiang, Jiaxing Han, Ziming Li

LicenseType:CC BY |

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The shape and internal structure of an atomic nucleus can change significantly with increasing excitation energy, angular momentum, or isospin asymmetry. As an example of this structural evolution, linear-chain configurations in carbon or heavier isotopes have been predicted for decades. Recent studies have found non-stability of this structure in 12C while evidenced its appearance in 16C. It is then necessary to investigate the linear-chain molecular structures in 14C to clarify the exact location on the nuclear chart where this structure begins to emerge, and thus to benchmark theoretical models. Here we show a cluster-decay experiment for 14C with all final particles coincidentally detected, allowing a high Q-value resolution, and thus a clear decay-path selection. Unambiguous spin-parity analyses are conducted, strongly evidencing the emergence of the π-bond linear-chain molecular rotational band in 14C. The present results encourage further studies on even longer chain configurations in heavier neutron-rich nuclei.

    Cell Discovery,2023年

    Wasim Shah, Baolu Shi, Yuanwei Zhang, Qinghua Shi, Yuewen Wang, Xiaohua Jiang, Yang Li, Zishuo Xu, Wei Liu, Xuefeng Xie, Xiangjun Zhang, Muhammad Zubair, Hui Ma, Yue Wang, Huan Zhang, Bo Xu, Jianteng Zhou, Suixing Fan, Yuying Jiao, Jingwei Ye, Hanwei Jiang, Zhipeng Xu

    LicenseType:CC BY |

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    During meiosis, at least one crossover must occur per homologous chromosome pair to ensure normal progression of meiotic division and accurate chromosome segregation. However, the mechanism of crossover formation is not fully understood. Here, we report a novel recombination protein, C12ORF40/REDIC1, essential for meiotic crossover formation in mammals. A homozygous frameshift mutation in C12orf40 (c.232_233insTT, p.Met78Ilefs*2) was identified in two infertile men with meiotic arrest. Spread mouse spermatocyte fluorescence immunostaining showed that REDIC1 forms discrete foci between the paired regions of homologous chromosomes depending on strand invasion and colocalizes with MSH4 and later with MLH1 at the crossover sites. Redic1 knock-in (KI) mice homozygous for mutation c.232_233insTT are infertile in both sexes due to insufficient crossovers and consequent meiotic arrest, which is also observed in our patients. The foci of MSH4 and TEX11, markers of recombination intermediates, are significantly reduced numerically in the spermatocytes of Redic1 KI mice. More importantly, our biochemical results show that the N-terminus of REDIC1 binds branched DNAs present in recombination intermediates, while the identified mutation impairs this interaction. Thus, our findings reveal a crucial role for C12ORF40/REDIC1 in meiotic crossover formation by stabilizing the recombination intermediates, providing prospective molecular targets for the clinical diagnosis and therapy of infertility.

      Inflammation and Regeneration,2023年

      Wei Liu, Jie Yu, Ting Wang, Ying Shen, Jinling Ning, Lu Zhao, Yiqiang Wang

      LicenseType:CC BY |

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      BDJ Open,2023年

      Wei Liu, Yi Sun, Xinni Pan, Baiping Fu, Yuedan Xu, Ling Zhang, Zhiwei Shi, Xinyang Jin

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      npj Clean Water,2023年

      Peifang Wang, Xin Gao, Wei Liu, Huinan Che, Yanhui Ao

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      Heterogeneous photocatalytic systems generally lack thermodynamic dependence on the degradation of organic pollutants in aqueous solution. Therefore, it is important to reveal the reasons for the inhibited surface kinetics but still be neglected. Herein, we reveal the mechanism that BiVO4 can’t degrade organics although it is thermodynamically feasible. The surface solvation and formation of double layer (compact layer and diffuse layer) makes low-polarity organics far away from the surface of BiVO4. We found that the introduction of sulfite can solve this problem. Theory calculation illustrates that sulfite can enter into the compact layer because of its higher adsorption energy on BiVO4 and lower adiabatic ionization potential (AIP). Then, photogenerated holes initiate the chain transformation of sulfite and produce strong oxidizing species which can diffuse out to degrade organics. This paper provides an insight into the understand the effects of solid-liquid interface on heterogeneously photocatalytic degradation of organic pollutants.

        BMC Cancer,,232023年

        Ruidong Zhang, Chanjuan Wang, Wei Liu, Xiaoxi Zhao, Shuguang Liu, Zhigang Li, Weijing Li, Lei Cui

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        BackgroundLittle is known about DNMT3A expression and its prognostic significance in childhood B cell acute lymphoblastic leukemia (B-ALL).MethodsWe determined DNMT3A mRNA expression in 102 children with B-ALL. Correlations with relapse-free survival (RFS) and common clinical characteristics were analyzed. DNMT3A was stably knocked out by CRISPR/Cas9 gene editing technology in Reh and 697 B-ALL cell lines. Cell proliferation activity after treated with daunorubicin (DNR) was determined by CCK8 assay in DNMT3A KO Reh and 697 cell lines.ResultsDNMT3A expression in B-ALL patients who were in continuous complete remission (CCR) was higher than in those who got relapse (P = 0.0111). Receiver operating characteristic curve showed prognostic significance of DNMT3A expression (P = 0.003). Low expression of DNMT3A (≤ 0.197) was significantly correlated with poor RFS (P < 0.001) in children with B-ALL. Knock-out of DNMT3A in Reh and 697 cell lines significantly increased IC50 of DNR (P = 0.0201 and 0.0022 respectively), indicating elevated resistance to DNR.ConclusionLow expression of DNMT3A associates with poor prognosis in children with B-ALL. Knock-out of DNMT3A confers resistance to DNR on leukemic cells.