上海國際學校,北京國際學校,國際高中,國際學校,國際學校招生國際學校擇校網-專注國際教育,提供高質量的擇校服務。
    擇校小程序
    國際學校小程序

    快速擇校

    微信公眾號
    國際學校公眾號

    政策解讀

    400-805-3685

    國際學校全國統一招生熱線

    北京稻香湖學校學術榮耀照耀美麗校園!

    來源:m.313590.com 時間:2023-12-22 09:45:36

    北京稻香湖學校學術榮耀照耀美麗校園!

    國家英才計劃(生物)于12月7日結束,北京海淀稻香湖學校學生張閎熙再創佳績,獲得了國家優秀學員,生物組順位第一,同輩評議第一,并獲取了參加中國對外交流遴選營資格的輝煌成績。

    The National Talent Program(Biology)ended on December 7th,and Zhang Hongxi,a student from Beijing Daoxianghu School,achieved remarkable results.He was awarded the title of National Excellent Student,ranked first in the Biology Group,and ranked first in peer evaluation.He also achieved brilliant results in qualifying for China's Foreign Exchange Selection Camp.

    什么是國家英才計劃?

    國家英才計劃直屬于中國科技協會,是我國高中生超前培養的重要平臺。“英才計劃”旨在選拔一批學有余力的中學生走進大學,在自然科學基礎學科領域的著名學者指導下參加科學研究、學術研討和科研實踐,進而發現一批具有學科特長、創新潛質的優秀中學生,提前促進學生與大學教育相銜接,建立高校與中學聯合發現和培養頂尖科技創新人才的有效模式,為青少年科技創新人才不斷涌現和成長營造良好的社會氛圍。

    The National Talent Program is directly affiliated with the China Association of Science and Technology and is an important platform for advanced training of high school students in China.The"Talent Plan"aims to select a group of high school students who have spare energy to enter universities,participate in scientific research,academic seminars,and research practices under the guidance of renowned scholars in the field of natural science basic disciplines,and discover a group of outstanding high school students with disciplinary strengths and innovative potential.It promotes the connection between students and university education in advance,and establishes an effective model for universities and high schools to jointly discover and cultivate top scientific and technological innovation talents,To create a favorable social atmosphere for the continuous emergence and growth of young technological innovation talents.

    英才計劃的審核有多嚴格?

    初選:在全國優秀高中中選拔7000位學生參加英才計劃的資格考試,取1500名學生進入英才計劃(筆試兩輪+一輪面試)

    中期評估:學生進入課題組后由中國科協審核每月的成長記錄和演技筆記,不合格者退出英才計劃。

    終期評估:學生提交課題報告、培養報告(包括讀書報告、文獻綜述、實驗記錄、論文等)、《成長日志》、導師評價等材料。中國科協篩選后選取150人參加最終評估(前10%),最后留下30人(前2%)推送至中國對外交流遴選營。生物組評委組組長擔任者為中國科學院院士,普林斯頓大學生物系終身教授,西湖大學校長施一公先生,評委組共12位生物領域著名學者構成,經過四輪密閉交叉答辯得出最后結果。

    Preliminary selection:7000 students will be selected from the national excellent high schools to participate in the qualification exam of the Talent Program,and 1500 students will be selected to enter the Talent Program(two rounds of written exams and one round of interviews)

    Mid term evaluation:After entering the research group,students will have their monthly growth records and acting notes reviewed by the China Association for Science and Technology.Those who fail will be expelled from the Talent Program.

    Final evaluation:Students submit project reports,training reports(including reading reports,literature reviews,experimental records,papers,etc.),growth logs,mentor evaluations,and other materials.After screening by the China Association for Science and Technology,150 people were selected to participate in the final evaluation(the top 10%),and 30 people(the top 2%)were left to be pushed to the China Foreign Exchange Selection Camp.The leader of the jury group of the biology group is Shi Yigong,an academician of the CAS Member,a tenured professor of the Department of Biology of Princeton University,and the president of West Lake University.The jury group consists of 12 famous scholars in the field of biology.After four rounds of closed cross defense,the final result was obtained.

    獲獎課題:

    鐵轉運蛋白基因X調控髓鞘形成和少突膠質細胞發育的機理

    The mechanism of iron transporter gene X regulating myelin formation and oligodendrocyte development

    摘要:

    溶質載體家族(SLCs)作為最大的轉運蛋白家族,在細胞膜上控制著包括糖類、無機鹽、氨基酸、神經遞質、維生素、ATP等在內的多種細胞生長所必須的物質的轉運。SLCs參與這些細胞的生長發育,其功能異常常常與人類健康和疾病息息相關?;騒是識別鐵載體從而實現鐵的跨膜運輸。雖然已經有研究表明其在中樞神經系統尤其是少突膠質細胞上高表達,但是基因X在少突膠質細胞內的生理功能和參與髓鞘形成過程的潛在機制仍然是未解之謎。本文從髓鞘發育和再生的角度詳細闡述了基因X在少突膠質細胞中的特異性敲除嚴重影響了中樞神經系統中的髓鞘形成,這種髓鞘障礙還同時伴隨著少突膠質細胞的分化受阻。考慮到基因X是一類參與鐵運輸的轉運蛋白,而少突膠質細胞的鐵積累是其分化所必須的,因此我們建立了高鐵小鼠模型來探究基因X在少突膠質細胞中的作用是否與其轉鐵功能相關。食物中補充的大量鐵能夠促進髓鞘形成和少突膠質細胞分化進程,然而當基因X缺失這一促進作用明顯減弱,這一結果提示我們基因X可能是通過調控少突膠質細胞的鐵轉運來影響其分化。少突膠質細胞發育障礙導致了多種脫髓鞘神經系統疾病如多發性硬化癥(MS)等的內源性髓鞘再生失敗,探究基因X介導的鐵轉運機制可能成為治療此類疾病的潛在思路。

    The solute carrier family(SLCs),as the largest transporter protein family,control the cell membrane including sugars.Various substances necessary for cell growth,including inorganic salts,amino acids,neurotransmitters,vitamins,ATP,etc.The transfer of quality.SLCs are involved in the growth and development of these cells,and their abnormal functions are often closely related to human health and diseases.Gene X recognizes iron carriers to achieve transmembrane transport of iron.Although there have been studies indicating its high expression in the central nervous system,especially in oligodendrocytes,the physiological function of gene X in oligodendrocytes and the potential mechanisms involved in myelin formation remain unsolved.This article elaborates on the specific knockout of gene X in oligodendrocytes from the perspective of myelin development and regeneration,which seriously affects myelin formation in the central nervous system.This myelin barrier is also accompanied by impaired differentiation of oligodendrocytes.Considering that gene X is a transporter protein involved in iron transport,and iron accumulation in oligodendrocytes is necessary for their differentiation,we established a high-iron mouse model to investigate whether the role of gene X in oligodendrocytes is related to its iron transfer function.The large amount of iron supplemented in food can promote myelin formation and the differentiation process of oligodendrocytes.However,when gene X is missing,this promotion effect is significantly weakened.This result suggests that gene X may affect the differentiation of oligodendrocytes by regulating iron transport.The developmental disorders of oligodendrocytes have led to the failure of endogenous myelin regeneration in various demyelinating nervous system diseases such as multiple sclerosis(MS).Exploring the iron transport mechanism mediated by gene X may become a potential approach for treating such diseases.

    研究論文(節選)

    圖注:

    (A-B)Ki67和Olig2在P28的f/f和f/f;Olig2小鼠胼胝體的免疫熒光染色(A)及數量統計結

    果(B)。綠色為Ki67,紅色為Olig2,藍色為DAPI,標尺為50μm;f/f,n=4;f/f;Olig2,

    n=3,p=8.642E-05;(C-D)Olig2和CC1在P28的f/f和f/f;Olig2小鼠胼胝體的免疫熒光染色

    (C)及數量統計結果(D)。紅色為CC1,綠色為Olig2,藍色為DAPI,標尺為50μm;f/f,

    n=6;f/f;Olig2,n=7;**p=0.0028;(E)原代細胞模型構建流程(G)圖中所示為單細胞追蹤代表圖,原代OPC分別分離自f/f和f/f;Olig2小鼠;(H-I)總遷移路程(H)和平均運動速度(I)無差異。f/f,n=7;f/f;Olig2,n=3,總遷移路程,p=0.9140;平均速度,p=0.4288;

    講解:

    (A-B)共染了KI67和Olig2的抗體,并用共聚焦顯微鏡進行拍攝,觀察到KO組小鼠胼胝體gene X缺失會引起OPC的大量增殖,細胞增殖數量遠高于對照組。這表明geneX敲除導致的髓鞘缺失可能是因為OPC無法向成熟的少突膠質細胞分化導致的

    (C-D)了更好地研究geneX蛋白在少突膠質細胞的生理功能,我們通過Cre重組酶的靶向序列loxp位點,制備了以Cre/loxp系統為依托的Olig2特異的條件性基因敲除小鼠。小鼠4周時候,我們制備了冰凍切片的樣本進行染色觀察。結果顯示,在胼胝體區域,與WT小鼠相比,CC1標記的成熟少突膠質細胞數量減少,統計結果有統計顯著性,因此證明geneX的缺失會抑制少突膠質細胞的分化。

    (E)體外誘導分化實驗都證明缺失也會阻斷少突膠質細胞分化。先讓原代少突膠質質細胞體外分離,取新生小鼠皮層培養成神經干細胞(10天成球),然后用B104細胞系(大鼠神經母細胞瘤細胞系)的上清誘導神經球到少突球的轉變然后再吧少突球接種到共聚焦皿中分化產生少突膠質細胞。

    (F-H)WT(野生型)和ko(基因敲除小鼠)的原代少突細胞分化不同時間點的成熟少突膠質細胞的數量,發現wt組外分化一天后有成熟的MBP+(成熟細胞)體外分化三天有少量的MBP陽性的成熟細胞,分化第五天全部分化完成。而KO組在體外分化三天后才觀察到有MBP陽性的成熟細胞,分化五天只觀察到少量的成熟細胞。ko組表現出明顯的分化滯后性。

    (A-B)Antibodies against KI67 and Olig2 were co stained and photographed using a confocal microscope.It was observed that the absence of gene X in the corpus callosum of KO group mice caused a significant proliferation of OPC,with a much higher number of cell proliferation than the control group.This suggests that the absence of myelin sheath caused by gene X knockout may be due to the inability of OPC to differentiate into mature oligodendrocytes

    To better investigate the physiological function of geneX protein in oligodendrocytes,we prepared Olg2 specific conditional gene knockout mice based on the Cre/loxp system by targeting the loxp site of the Cre recombinase.At 4 weeks of age,we prepared frozen section samples for staining observation.The results showed that in the corpus callosum region,compared with WT mice,the number of mature oligodendrocytes labeled with CC1 was reduced,and the statistical results were statistically significant,indicating that the absence of geneX would inhibit the differentiation of oligodendrocytes.

    (E)In vitro differentiation induction experiments have shown that deficiency can also block the differentiation of oligodendrocytes.Firstly,primary oligodendrocytes were isolated in vitro and cultured into neural stem cells(10 day old)from the cortex of newborn mice.Then,the supernatant of the B104 cell line(rat neuroblastoma cell line)was used to induce the transformation of neurons into oligodendrocytes,and then oligodendrocytes were inoculated into a confocal dish to differentiate into oligodendrocytes.

    (F-H)WT(wild-type)and ko(gene knockout mice)at different time points was determined.It was found that mature MBP+(mature cells)differentiated from the WT group one day later,and a small number of MBP positive mature cells differentiated from the WT group for three days.All differentiation was completed on the fifth day.The KO group only observed mature cells with MBP positivity after three days of differentiation in vitro,and only a small number of mature cells were observed after five days of differentiation.The ko group showed significant differentiation lag.

    以上就是《北京稻香湖學校學術榮耀照耀美麗校園!》介紹。

    國際學校預約看校/在線報名入口
    相關文章推薦
    在線咨詢
    掃碼關注
    國際學校公眾號

    政策解讀

    電話咨詢
    聯系電話
    400-805-3685
    返回頂部
    成人国产精品动漫欧美一区| 久久久99精品一区二区| 人妻无码久久精品| 国产精品偷伦视频观看免费| 亚洲国产人成精品| 国产这里有精品| 国产在线不卡午夜精品2021| 亚洲精品国产美女久久久| 久久99精品久久久久久9蜜桃| 精品一区二区在线观看| 91人前露出精品国产| 国产精品无码午夜福利| 97久久综合精品久久久综合| 日本aⅴ精品中文字幕| 午夜伦情电午夜伦情电影| 日韩精品亚洲专区在线观看| 国产美女精品视频| 国产精品99精品视频网站| 五月花精品视频在线观看 | 国产精品免费一区二区三区| 欧美日韩国产精品自在自线| 久久久久亚洲精品天堂| 成人精品一区二区三区免费看| 伊人精品视频在线| 日韩福利视频精品专区| 久久99精品久久久久久动态图| 老司机亚洲精品影院无码| 69堂午夜精品视频在线| 亚洲精品NV久久久久久久久久| 99国产欧美久久久精品蜜芽| 精品国产三级a∨在线欧美| 精品欧洲AV无码一区二区男男 | 精品国产免费人成网站| 日韩欧精品无码视频无删节| 亚洲精品成人片在线观看精品字幕| 国内精品在线视频| 最新国产成人精品2024| 久久九九亚洲精品| 中文字幕精品一区二区日本| 先锋影音av资源网| 日韩精品www|