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.
Eric Topol:未来医疗的无线化
EricTopol说，我们很快就可以通过智能手机来监控我们的生命体征并监测一些慢性疾病。在TEDMED上，他着重介绍了应用在未来医疗上的一些重要无线装置，这些装置可以帮助我们远离医院的病床。
Christopher deCharms:即时扫描大脑的技术
神经科学家和发明家Christopher deCharms展示一种新的方式利用功能磁共振成像显示大脑活动-思想，情感，痛苦-当它正在发生时。换句话说，你可以看到你的感受。
Frederick Balagadde:微芯片上的生化室
要阻止撒哈拉南部非洲各国的疾病流行，仅靠药品是不够的。我们还需要与之配套的诊断工具。TED资深会员Frederick Balagadde向我们展示如何通过微型化技术把笨重昂贵的化验室集成至一个芯片大小，从而大大提高它的诊断能力和普及性。
Stephen Friend：猎寻未知的遗传英雄
我们从那些的了遗传性疾病的人那里获知了什么－在大部分遗传病中，只有部分的急停成员发生了疾病，而其他带有同样基因的却能避开它。斯蒂文.弗兰德建议我们应该开始研究那些没有得病的家庭成员。听听这个弹性课题，以巨大的努力来搜集基因资料可以帮助解码遗传性的失调。
Eric Dishman:健康看护体系需要大家参与
艾瑞克·迪旭曼 (Eric Dishman) 念大学时，医生说他只能再活 2 到 3 年－那已是好久以前的事了。艾瑞克后来经历了不同的诊断及器官移植，他结合个人经验及尖端医学技术，提出了大胆的创新思维，改以病人为治疗团队核心，以重塑健康看护系统。
Jonathan Drori:存蓄数十亿种子的原因
在TED U 2009的这个简短的演讲中，Jonathan Drori鼓励我们保护生物多样性 -- 从一颗颗种子做起。他提醒我们要保护人类赖以生存的植物，同时他也给大家描述了千年种子库这样一个美好的远景，在这里面，将会有逾30亿颗的种子被人类珍藏，这其中甚至还包括那些正日益减少但却必不可少的植物物种。
Erich Gnaiger：Life Style and Mitochondrial Competence – Modern Drugs for T2 Diabetes in Aging and Degenerative Diseases.
D. Swarovski Research Laboratory (Mitochondrial Physiology), Dept. General, Visceral and Transplant Surgery, Innsbruck Medical University; and OROBOROS INSTRUMENTS, Innsbruck, Austria. - Email: erich.gnaiger@oroboros.at
The contribution of mitochondrial dysfunction to the etiology of T2 diabetes and a range of preventable metabolic diseases is the subject of intensive current research with world-wide health implications.
Recently these investigations gained depth and scope by technological advances for diagnosis of mitochondrial function by comprehensive OXPHOS analysis using high-resolution respirometry [1,2]. Fundamental questions of a causal relationship, however, between compromised mitochondrial function and development of T2 diabetes remain to be resolved [3,4] to optimize prevention and treatment of insulin resistance.
For preventable diseases such as T2 diabetes, the evolutionary background of mitochondrial competence provides a solid basis for improved and broad application of a well established modern drug, mtLSD.
Post-industrial societies are characterized by a high-energy input lifestyle with diminished physical activity and high incidence of non-transmittable diseases, in comparison to human populations where physical work is essentially important for sustaining life and in which degenerative diseases (T2 diabetes, various cancers, Alzheimer's) are essentially absent [5]. The capacity of oxidative phosphorylation (OXPHOS) is increased or maintained high by a life style involving endurance exercise and strength training [6].
Life style changes from the age of 20-30 years to the elderly, but is subject to change and intervention. Depending on group selection in cross-sectional studies, OXPHOS capacity declines from the age of 20-30 years [7,8], or is independent of age up to 80 years [9,10].
Independent of age, there is a strong decline of OXPHOS capacity in human vastus lateralis from BMI of 20 to 30 [1]. At a BMI >30, a threshold OXPHOS capacity is reached in human v. lateralis that may be characteristic of a low-grade inflammatory state (‘mitochondrial fever’).
Onset of degenerative diseases (T2 diabetes, neuromuscular degeneration, various cancers) and mitochondrial dysfunction interact in an amplification loop progressing slowly with age, such that cause and effect of mitochondrial dysfunction cannot be distinguished. Diminished antioxidant capacity at low mitochondrial density is an important mechanistic candidate in the state of mitochondrial fever.
For implementing a life style supporting mitochondrial competence and preventing degenerative diseases in modern societies, we need (1) extended research programmes focused on the causative link between mitochondrial competence and effective prevention of degenerative diseases, (2) educational programmes on mitochondrial physiology targeted at general practitioners, teachers and the society at large, (3) cooperation of health care and insurance organizations to support preventive life style activities, and (4) do not miss any opportunity in taking the lead in living the mtLife Style Drug (mtLSD).
riboZero和方向RNA库-陈巍学基因（15）
本节课程主要内容：
1.riboZero与Poly（T）方法对比的技术优势
2.riboZero的技术原理
3.建定向的RNA库的方法：
1）掺入U碱基的方法来标识cDNA的第二条链
2）ScriptSeq方法