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立德树人,启智润心——2024年广东省初中学业水平考试英语试题笔试部分评价

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英语教师 2025年第4期25卷 82-84页

作者：江碧霞郑钰芳广东省佛山市教育局教学研究室广东佛山528000 广东省佛山市顺德区杏联初级中学广东佛山528000

深入分析2024年广东省初中学业水平考试英语试题的命题特点与育人价值,指出试题在“双减”政策背景下紧紧围绕《课程标准》命制,坚持立德树人,注重考查学生的语言能力、文化意识、思维品质和学习能力。试题通过丰富多样的语言素材和真... 详细信息

深入分析2024年广东省初中学业水平考试英语试题的命题特点与育人价值,指出试题在“双减”政策背景下紧紧围绕《课程标准》命制,坚持立德树人,注重考查学生的语言能力、文化意识、思维品质和学习能力。试题通过丰富多样的语言素材和真实情境的构建,旨在激发学生的科学探索精神,厚植爱国主义情怀,加强品德修养,增长知识,培养奋斗精神和综合素质。试题设计强调高阶思维能力的发展,减少低阶思维题目的比重,依托真实情境强调解决问题,以考促教,推动初中英语教学提质增效。

关键词：立德树人初中学业水平考试英语试题笔试部分试题评价

ANALYSIS OF THE CHAOTIC MOTION FOR A ROTOR SYSTEM WITH A TRANSVERSE CRACK

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Acta Mechanica Solida Sinica 2003年第1期16卷 74-80页

作者： Fu Yiming zheng yufang Zhu Shijian Department of Engineering Mechanics Hunan UniversityChangsha 410082China Institute of Noise and Vibration University of Naval EngineeringWuhan 430033China

The chaotic motion of an elastic shaft-disk rotor system including thegeometric nonlinearity of the shaft with a transverse crack is investigated. The critical conditionfor the system to enter chaotic state is given by the Melnikov method. Meanwhile, whether the chaosoccurs is determined by the Poincare map, phase portrait and time-displacement history diagram.

关键词： geometric nonlinearity cracked rotor chaos

Robust H-infinity control for discrete-time T-S fuzzy systems with input delay

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控制理论与应用（英文版） 2011年第2期9卷 189-194页

作者： Liu, Jianchen Zhang, Jing zheng, yufang He, Min College of Electrical and Information Engineering Hunan University Changsha Hunan 410082 China Institute of Information and Electrical Engineering Hunan University of Science and Technology Xiangtan Hunan 411201 China Department of Electronic and Electrical Engineering Taizhou Vocational and Technical College Taizhou Zhejiang 318000 China

Delay-dependent robust H-infinity control for discrete-time Takagi-Sugeno (T-S) fuzzy systems with interval time-varying input delay is *** constructing a new Lyapunov-Krasovskii functional and using convex combination method,a delay-dependent condition is established,under which the resulted closed-loop systems via a fuzzy state feedback are robust asymptotically stable with given H-infinity norm ***,an iterative algorithm based on the modified SLPMM algorithm is proposed to solve the fuzzy H-infinity ***,a numerical example is used to illustrate the effectiveness and feasibility of the approaches proposed.

关键词： T-S fuzzy system Input delay Discrete-time system H-infinity control

A Disintegrin and Metalloprotease 10 in neuronal maturation and gliogenesis during cortex development

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Neural Regeneration Research 2013年第1期8卷 24-30页

作者： Zhixing Ma Qingyu Li zhengyu Zhang yufang zheng School of Life Sciences Fudan University

The multiple-layer structure of the cerebral cortex is important for its functions. Such a structure is generated based on the proliferation and differentiation of neural stem/progenitor cells. Notch functions as a molecular switch for neural stem/progenitor cell fate during cortex development but the mechanism remains unclear. Biochemical and cellular studies showed that Notch receptor activation induces several proteases to release the Notch intracellular domain （NICD）. A Disintegrin and Metalloprotease 10 （ADAM10） might be a physiological rate-limiting $2 enzyme for Notch activation. Nestin-driven conditional ADAM10 knockout in mouse cortex showed that ADAM10 is cdtical for maintenance of the neural stem cell population during early embryonic cortex development. However, the expression pattern and function of ADAM10 during later cerebral cortex development remains poorly understood. We performed in situ hybridization for ADAMIO mRNA and immunofluorescent analysis to determine the expression of ADAM10 and NICD in mouse cortex from embryonic day 9 （E14.5） to postnatal day 1 （P1）. ADAM10 and NICD were highly co-localized in the cortex of E16.5 to P1 mice. Comparisons of expression patterns of ADAM10 with Nestin （neural stem cell marker）, Tujl （mature neuron marker）, and S100β （gila marker） showed that ADAM10 expression highly matched that of S10013 and partially matched that of Tujl at later embryonic to early postnatal cortex developmental stages. Such expression patterns indicated that ADAM10-Notch signaling might have a critical function in neuronal maturation and gliogenesis during cortex development.

关键词： neural regeneration neurogenesis ADAM10 A Disintegrin and Metalloprotease Notch Notchintracellular domain TujlS100 Nestin cerebral cortex development neuronal maturation glialcell grants-supported paper photographs-containing paper neuroregeneration

Electrophysiological research of synapse formation from beginning to maturity

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Chinese Science Bulletin 1998年第1期43卷 55-59页

作者： XIE Zuoping and zheng yufang State Key Laboratory of Biomembrane and Membrane Biotechnique Department of Biological Sciences and Biotechnology, Tsinghua University, Beijing 100084, China State Key Laboratory of Biomembrane and Membrane Biotechnique Tsinghua University Beijing China Department of Biological Sciences and Biotechnology Tsinghua University Beijing China

The development of synapses is an important question in neurobiology. We employ patchclamp technique to record MEPCs and EPCs of myoballs in Xenopus cell culture. The rate of EPC/MEPC is related with synapses maturation. Accordingly, we define the mature synapses as those whose rate of presynaptic membrane’s EPC to MEPC is more than 8. The process of maturation needs about 2-5 h after neurites contact with myoballs. We divide the development of synapses into three stages: young, developing and mature. The neurotransmitters stack gradually and increase by hundreds of times along with young synapses growing into maturity. So the process of synapses maturation should include presynaptic membrane specialization, postsynaptic membrane specialization and neurotransmitters stack.

关键词： definition of mature synapse α latrotoxin (α LTX) neurotransmitter stack.

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具损伤压电层合板的非线性动力稳定性分析

力学学报 2006年第4期38卷 570-576页

作者：郑玉芳傅衣铭王锋福州大学土木工程学院福州350002 湖南大学工程力学系长沙410082

基于各向异性损伤理论和压电理论,采用能量法和Lagrange方程,建立了具损伤压电智能层合中厚板在参数激励下的非线性运动控制方程,应用增量谐波平衡法,求解了具损伤压电智能层合中厚板的非线性动力稳定性问题．算例中,分析了损伤参数和... 详细信息

基于各向异性损伤理论和压电理论,采用能量法和Lagrange方程,建立了具损伤压电智能层合中厚板在参数激励下的非线性运动控制方程,应用增量谐波平衡法,求解了具损伤压电智能层合中厚板的非线性动力稳定性问题．算例中,分析了损伤参数和压电效应对压电智能层合板非线性动力稳定性的影响,揭示了力电耦合效应的内在特征,并与有关文献的结果进行了比较．

关键词：层合板各向异性损伤压电效应动力稳定性增量谐波平衡法

The function of Dennd1a in the development of mouse neural tube.

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The function of Dennd1a in the development of mouse neural t...

MiR-197 rescues the neurogenesis defects caused by autistic MECP2 mutation

中华医学会第十五次全国医学遗传学学术会议暨中国医师协会医学遗传医师分会第一届全国学术会议暨2016年浙江省医学遗传学年会

作者： Chen Shuxia Yang Xueyan zheng yufang Wang Hongyan The State Key Laboratory of Genetic Engineering and Ministry of Education (MOE)Key Laboratory of Contemporary Anthropology & The Collaborative Innovation Centre of Genetics and Development School of Life Sciences Fudan University Jiangwan Campus

Objective To study the molecular mechanism and function of Dennd1 a in the neural tube defects mouse model. Method A previous large forward screening by using piggy Bac(PB) insertion mouse models for n eural tube defects have revealed that Dennd1 a deficiency could cause mice NTDs. We used this mouse model to further investigate the molecular mechanisms of Dennd1 a in NTDs. The embryo s at E9.5-12.5 were collected and the phenotypes were recorded. Total m RNA was extracted fro m embryo tissues for both genotype confirmation and quantitative polymerase chain reaction(q-P CR) technology. Another set of embryos were used for whole-mount in situ hybridization(ISH) and RNA-seq. Result 1) By using primers spanning the PB insertion point(exon 3 to 5), the m RNA level of Den nd1 a followed the genotype pattern as wild type(WT)>heterozygote(HET)>homozygote(HOMO). The level of a downstream adjacent gene, Lhx2, also shows the downward trend as WT>HET>H OMO. However, q RT-PCR with primers on exon5-7 detected a short form at 3‘ region with the hig hest level of m RNA in HOMO embryos. 2)ISH: The WT embryos have strong signals in the forebr ain, midbrain and hindbrain. The Het and the Homo embryos showed stronger singles than WT a s our probes detect the increased short m RNA of Dennd1 a as the second pair of primers in q-PC R. The Het and Homo embryos also showed signals in the limb bud and spinal cord at tail region.3)RNA-seq: The expression level of total Dennd1 a is up-regulated in Group HOMO, while the Lhx2 is down-regulated. Conclusion 1) PB insertion on Dennd1 a gene caused the brain abnormity, neural tube defects e mbryos and lethality in mice embryos around E10.5. 2)PB insertion destroy the full-length Dennd1 a in mouse, which also had similar effect on Lhx2. 3) PB insertion may cause an alternative splici ng in Dennd1 a gene to induce a short form at 3‘ region.

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MiR-197 rescues the neurogenesis defects caused by autistic ...

The association study of mutations in GLI family and Congenital Heart Diseases

中华医学会第十五次全国医学遗传学学术会议暨中国医师协会医学遗传医师分会第一届全国学术会议暨2016年浙江省医学遗传学年会

作者： Hongyan Wang Yumeng Wang yufang zheng Yasong Du Institute of Reproduction & Development Obstetrics & Gynecology Hospital Fudan University The State Key Laboratory of Genetic Engineering at School of Life Sciences Fudan University Shanghai Mental Health Center Shanghai Jiaotong University

Objective MECP2(Methyl-Cp G-binding protein 2) is a key protein for neurodevelopment with fun ctions in not only transcription regulation but also micro RNA processing. Mutations in MECP2 are associated with neurodevelopment disorders, including MECP2 duplication syndrome(MDS), aut ism spectrum disorders(ASD) and Rett syndrome. Our study is to investigate the functional chan ges of MECP2 mutations from Chinese ASD patients during neural stem cells/progenitor cells(N SC/NPC) differentiation. Method Target sequencing of MECP2 gene in in a Chinese ASD cohort with 288 patients and 369 controls. Five rare missense mutations in MECP2 that were identified. The molecular function of those mutant MECP2 were investigated in both mouse NPC and human glioblastoma cells. In ut ero electroporation was used to study the in vivo function of MECP2 mutants in mouse developin g brain. Result 1. Five rare missense mutations in MECP2 that were identified in six Chinese ASD patient s only but not in control samples. 2. Overexpressing those mutated Me CP2 caused reduced neurogenesis both in vitro and in vivo. 3. Mi R-197 was identified as downstream key molecule of those MECP2 to regulate NOTCH sign aling pathway. Compared to WT MECP2, MECP2 mutants can not up-regulate mi R-197.3. Overexpression of mi R-197 could clearly rescue the differentiation defects caused by Me CP2 mutants both in vitro and in vivo. Conclusion Here we identified a brain-enriched mi R-197 that is critical for Me CP2 promoted neur al stem cells/progenitor cells(NSC/NPC) differentiation through inhibition on Notch signaling. Tho se five new autisitc mutations in MECP2 we identified resulted in a failure of mi R-197 up-regulatio n. Importantly, overexpression of mi R-197 could clearly rescue the defects caused by Me CP2 mu tants both in vitro and in vivo. Our results highlight a potential therapeutic effect of mi R-197 for n eurodevelopment disorders including MDS and ASD.

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The association study of mutations in GLI family and Congeni...