Study the pathological features of diseases using induced pluripotent stem cells derived form patient's somatic cells
The limited experimental access to disease-affected human tissues has severely impeded the elucidating of molecular mechanisms underlying disease development. Generation of induced pluripotent stem cells (iPSCs) by over-expression of defined transcription factors in somatic cells, in particular in those from patient somatic cells, presents an attractive and promising approach to model the early stages of diseases in vitro and to screen novel biomarkers as well as therapeutic medicines. Recently, many research groups have independently reported that patient-specific iPSC-derived cells recapitulated multiple features of pathological events of a particular disease, offering experimental evidence of utilizing patient-specific iPSCs to model diseases and reevaluate the current therapies. We have derived iPSC lines using somatic cells of patients suffering from Klinefelter's Syndrome (KS) and Alzheimer's Disease (AD) and explored the possibility to use these iPSC lines to recapitulate the pathological features of the diseases. Our results show that patient's specific iPSC lines provide good opportunity to study the development and treatment of diseases.
Study the pathological features of diseases using induced pluripotent stem cells derived form patient's somatic cells
The limited experimental access to disease-affected human tissues has severely impeded the elucidating of molecular mechanisms underlying disease development. Generation of induced pluripotent stem cells (iPSCs) by over-expression of defined transcription factors in somatic cells, in particular in those from patient somatic cells, presents an attractive and promising approach to model the early stages of diseases in vitro and to screen novel biomarkers as well as therapeutic medicines. Recently, many research groups have independently reported that patient-specific iPSC-derived cells recapitulated multiple features of pathological events of a particular disease, offering experimental evidence of utilizing patient-specific iPSCs to model diseases and reevaluate the current therapies. We have derived iPSC lines using somatic cells of patients suffering from Klinefelter's Syndrome (KS) and Alzheimer's Disease (AD) and explored the possibility to use these iPSC lines to recapitulate the pathological features of the diseases. Our results show that patient's specific iPSC lines provide good opportunity to study the development and treatment of diseases.
Stefan Larsson:医生们可以互相学习
不同医院的不同手术有着不同的结果。但是病人不知道数据, 所以使得选外科医生成为了一个高风险的猜测游戏。
史帝芬·拉森（Stefan Larsson）研究了当医生开始衡量并分享他们的髋关节手术的结果时（比如说什么是最有效的方法）会发生的情况。
如果医生们可以相互学习并形成一个反馈循环，医疗保健会不会变得更好、更便宜？
E.O. Wilson论生物多样性
作为2007年的TED大奖得主之一，爱德华·威尔逊代表所有的生物，提出我们应当关注生物圈的倡议，并且宣布要建立一个在线的百科全书，记录物种多样性。
王煜非：从新版Iso标准修订看血糖监测技术发展趋势
王煜非：上海交通大学附属第一人民医院研究员，中国医院协会临床检验管理专业委员会POCT分委会委员、中华糖尿病学会血糖监测学组委员、上海市糖尿病学会委员、上海市糖尿病学会血糖监测学组副组长、上海市内分泌学会基础学组副组长。
随着人民生活水平的提高和生活方式的改变，糖尿病患病率（尤其是2型糖尿病）在不断攀升。良好的血糖控制有助于预防糖尿病性并发症的发生和发展。准确的血糖检测值可正确指导糖尿病患者的临床用药，饮食和运动，稳定血糖监控，改善生活质量，减少致死致残，降低社会医疗负担。
血糖仪的准确性，精确性和抗干扰能力是准确血糖监测数据的保障。Iso15197（2003版）是国际上针对血糖监测系统评估和验证的标准，近年来，国际组织对此标准进行了大规模的修订并于2013年5月15日正式颁布了新标准，过渡期为三年。
新标准大大提高了血糖仪准确性和精确性的要求，对评估方法亦进行了进一步调整。修订内容主要包括：验证项目定义更清楚，验证标准更严苛，统计方法标准更明确，受试人群分布限制更严格，加大关注清洁消毒过程及临床验证步骤的正确性。不少第三方检测机构研究表明，有一部分血糖仪现有标准也无法全数通过，更难以达到严苛的新标准就。
未来血糖仪的发展趋势是：血糖仪本身技术的突破，具有更好的精准性和更强的抗干扰能力。其他如采血部位的改变，采血与测定一体化，可重复测试的感应技术，用组织间质或体液作为葡萄糖检测的样本，埋入式针头或感应器，无创伤、无样本、红外测定。另一方面血糖数据的管理，联网及远程数据传输等等。
秦正红：DRAM1 regulates autophagy flux and Bid-mediated cell death via lysosomes
秦正红，博士，教授，神经药理专业博士生导师。1994年在美国宾州医学院研究生院获博士学位，先后在美国国家卫生研究院(NIH)及麻省总医院和哈佛大学医学院从事研究工作。2003年从哈佛大学引进，现为苏州大学医学部基础医学与生物科学学院科研中心实验室主任，中国药理学会生化药理学专业委员会委员，中国药理学会神经药理学专业委员会委员，美国神经科学学会会员。
Damage-regulated autophagy modulator1 (DRAM1), a novel TP53 target gene, is an evolutionarily conserved lysosomal protein and plays an essential role in TP53-dependent autophagy activation and apoptosis (Crighton et al, 2006). However, the mechanisms by which DRAM1 promotes autophagy and apoptosis are not clear.
3-Nitropropionic acid (3-NP) is an inhibitor of mitochondrial respiratory complex II. Intrastriatal administration of 3-NP produces neuropathology resemble to Huntington disease. 3-NP-induced neuronal death was involved in autophagy and apoptosis. In vitro studies with 3-NP in TP53 wt and null cells, 3-NP or CCCP increased the protein levels of DRAM1 in a TP53-dependent or independent manner. DRAM1 induction contributed to 3-NP-induced autophagy activation. Knock-down of DRAM1 with siRNA inhibited the activity of V-ATPase, acidification of lysosomes and activation of lysosomal proteases. Knock-down of DRAM1 reduced the clearance of autophagososmes.
3-NP also induced a transcription independent upregulation of BAX protein levels. Knock-down of DRAM1 suppressed the increase in BAX levels. Co-immunoprecipitation and pull-down studies revealed an interaction of DRAM1 and BAX protein. Stably expression of exogenous DRAM1 increased the half-life of BAX. Upregulation of DRAM1 recruited BAX to lysosomes and induced cathepsin B-dependent cleavage of Bid and cytochrome c release. Knockdown of DRAM1, BAX or inhibition of lysosomal enzymes reduced 3-NP-induced cytochrome c release and cell death.
These data suggest that DRAM1 plays important roles in regulating autophagy flux and apoptosis. DRAM1 promotes autophagy flux through a mechanism involves activation of V-ATPase and enhances the acidification of lysosomes. DRAM1 promotes apoptosis via a mechanism involving recruitment of BAX to lysosomes to trigger cathepsin B-mediated Bid cleavage.
病毒结构的一般原则 - Stephen Harrison P1
本视频由科普中国和生物医学大讲堂出品
Stephen Harrison (Harvard) Part 1: Virus structures: General principles
Harrison begins his talk by asking why most non-enveloped viruses and some enveloped viruses are symmetrical in shape. He proceeds to show us lovely images of the structures obtained by x-ray crystallography of numerous viral coat proteins. Deciphering these structures allowed scientists to understand that viral coat proteins form multimers, such as dimers and pentamers, which in turn interact with a scaffold that ensures that the coat proteins are correctly placed. This arrangement results in symmetrically shaped viruses.
In Part 1, Harrison also explains that enveloped viruses infect cells by inducing the fusion of the viral and host cell membranes. He delves deeper into the molecular mechanism of membrane fusion driven by the hemagglutinin or HA protein of the influenza virus in Part 2 of his talk.
Non-enveloped viruses, on the other hand, must enter cells by a mechanism other than membrane fusion. This is the focus of Part 3. Using rotavirus as a model, Harrison and his colleagues have used a combination of Xray crystallography and electron cryomicroscopy to decipher how the spike protein on the viral surface changes its conformation and perforates the cell membrane allowing the virus to enter the cell.
病毒的膜融合 - Stephen Harrison P2
本视频由科普中国和生物医学大讲堂出品
Stephen Harrison (Harvard) Part 2: Viral membrane fusion
Harrison begins his talk by asking why most non-enveloped viruses and some enveloped viruses are symmetrical in shape. He proceeds to show us lovely images of the structures obtained by x-ray crystallography of numerous viral coat proteins. Deciphering these structures allowed scientists to understand that viral coat proteins form multimers, such as dimers and pentamers, which in turn interact with a scaffold that ensures that the coat proteins are correctly placed. This arrangement results in symmetrically shaped viruses.
In Part 1, Harrison also explains that enveloped viruses infect cells by inducing the fusion of the viral and host cell membranes. He delves deeper into the molecular mechanism of membrane fusion driven by the hemagglutinin or HA protein of the influenza virus in Part 2 of his talk.
Non-enveloped viruses, on the other hand, must enter cells by a mechanism other than membrane fusion. This is the focus of Part 3. Using rotavirus as a model, Harrison and his colleagues have used a combination of Xray crystallography and electron cryomicroscopy to decipher how the spike protein on the viral surface changes its conformation and perforates the cell membrane allowing the virus to enter the cell.
非包膜病毒如何侵入细胞 - Stephen Harrison P3
本视频由科普中国和生物医学大讲堂出品
Stephen Harrison (Harvard) Part 3: Non-enveloped virus entry
Harrison begins his talk by asking why most non-enveloped viruses and some enveloped viruses are symmetrical in shape. He proceeds to show us lovely images of the structures obtained by x-ray crystallography of numerous viral coat proteins. Deciphering these structures allowed scientists to understand that viral coat proteins form multimers, such as dimers and pentamers, which in turn interact with a scaffold that ensures that the coat proteins are correctly placed. This arrangement results in symmetrically shaped viruses.
In Part 1, Harrison also explains that enveloped viruses infect cells by inducing the fusion of the viral and host cell membranes. He delves deeper into the molecular mechanism of membrane fusion driven by the hemagglutinin or HA protein of the influenza virus in Part 2 of his talk.
Non-enveloped viruses, on the other hand, must enter cells by a mechanism other than membrane fusion. This is the focus of Part 3. Using rotavirus as a model, Harrison and his colleagues have used a combination of Xray crystallography and electron cryomicroscopy to decipher how the spike protein on the viral surface changes its conformation and perforates the cell membrane allowing the virus to enter the cell.
Tagrisso的伴随诊断 - 陈巍学基因(31)
欢迎来到【陈巍学基因】。我们这个节目，主要是介绍基因组学，和临床分子诊断的最新技术进展。
今天，会和大家谈一谈阿斯利康在开发Tagrisso这个新药过程中对4种伴随诊断方法的研究结果。
Tagrisso是阿斯利康公司开发的一个针对EGFR基因有耐药突变的晚期非小细胞肺癌者的药物，是酪氨酸激酶抑制剂类的靶向抗癌药物。
Tagrisso可以选择性地抑制突变型的EGFR，对发生耐药的肿瘤有强抑制作用；而对野生型的EGFR的抑制作用较弱，即对身体正常表皮细胞的生长抑制作用较弱。
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