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        分子神經(jīng)生物學研究團隊

        作者:佚名    來源:實驗中心    發(fā)布時間:2018/1/8 15:16:35    點擊量:    【打印文章】

        團隊人員

        1.   研究組長:陳捷光博士,1995年博士畢業(yè)于美國印第安納大學,隨后在耶魯大學進行博士后的研究工作(1995-1999)。出站后成為美國愛因斯坦醫(yī)學院的研究人員(1999-2003),后續(xù)在耶魯大學以副研究員的身份工作(2003-2008)。2008年回國在溫州醫(yī)科大學組建了自己的實驗室。

        2.   工作人員:李雪、肖劍、涂曉萌、黃寶珊

        研究方向

        體內(nèi)投射神經(jīng)元發(fā)育及病變的分子機理研究: 我們采用基因表達分析和胚胎內(nèi)基因轉染技術,研究中樞神經(jīng)系統(tǒng),包括大腦皮質和神經(jīng)視網(wǎng)膜中,孤獨癥相關的投射神經(jīng)元發(fā)育異常及其分子機制。神經(jīng)元的發(fā)育包括 神經(jīng)前體細胞的增值和分化,新生神經(jīng)元的遷移,以及軸樹突的生長成熟。這一過程中的任何異常將導致神經(jīng)或精神疾病的產(chǎn)生。

        孤獨癥譜系障礙是一類發(fā)病于兒童早期的廣泛性神經(jīng)發(fā)育障礙性疾病。其臨床特征為交往障礙、語言障礙、重復刻板等行為, 并時常表現(xiàn)出視覺功能異常。已知多個轉錄因子,包括皮質神經(jīng)元發(fā)育的關鍵基因Tbr1, Foxp1, 以及Otx1可能和孤獨癥發(fā)生有關。但這些基因是如何影響孤獨癥目前尚不清楚。在自然科學基金的支持下,我們將分析轉錄因子及其突變體對投射神經(jīng)元發(fā)育的影響,以加深對孤獨癥分子和神經(jīng)基礎的認識。更多信息可參閱我們最近發(fā)表的文章 (JBC 10.1074/jbc.RA117.001249, 2017; JBC 291: 7661-7668, 2016; PLoS One 10:1-19, 2015; Neuroscience 285:139-54, 2015) 。

         

        Laboratory of Molecular Neurobiology

         

        Team Members

        1.       Principle Investigator: Jie-Guang Chen, PhD

        Jie-Guang Chen received his PhD degree at Indiana University, USA in 1995. He did his post-doc at Yale Univeristy. Then, he joined at Albert Einstein College of Medicine as Instructor (1999-2003). Later, he became the Associate Research Scientist at Yale University (2003-2008). After that, he returned to china in 2008 and established his own lab at Wenzhou Medical University.

        2.       Team Staff: Xue Li, Jian Xiao, Tu Xiaomeng, Baoshan Huang

        Scope of Research Proposal

        In Vivo Molecular Studies of Development and Disorders of Projection Neurons: By using gene expression analysis and in utero gene electroporation, our current research aims to reveal the molecular mechanisms underlying the autism-related development disorders of projection neurons in the central nervous system,including the cerebral cortex and neural retina. The development of projection neurons involves the proliferation and differentiation of neural progenitors, migration of nascent neurons, and the growth and maturation of axon and dendrites.  Any disruption of these processes will lead to neurological and or psychiatric diseases.

        Autism spectrum disorders are a group of conditions that onset early in childhood. The clinical features of autism include dyslexia, speech impairment, repeated stereotype behaviors, and often show abnormal visual function. Multiple transcription factors, including Tbr1, Foxp1, and Otx1, the key genes regulating the development of cerebral cortex, are involved in the incidence of autism. But how these genes affect autism is as yet unclear. With the support from the Natural Science Foundation, we are currently studying the functions of these transcription factors and their autism-related mutants in the neural development.  Our studies will provide new understandings on the molecular and neurological bases of autism. For more information, please refer to our recent publications (J Biol Chem. doi: 10.1074/jbc.RA117.001249, 2017; J Biol Chem. 291: 7661-7668, 2016; PLoS One 10:1-19, 2015; Neuroscience 285:139-54, 2015).


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