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.
Telomeres and AGing
端粒是染色体末端的特殊结构，它由简单重复的DNA 序列和与之结合的蛋白质构成，保护染色体末端不被降解或融合，并使染色体能够完全复制。端粒长度的维持以及端粒结构的稳定在细胞衰老、癌症发生以及干细胞全能性自我更新能力维持等生命过程中都起重要作用。
Sigma® Life Science——Where bio beGins
生命是一个不断扩大、不断进化的宇宙，充满着发现问题和探索未知的机会。每天，突破性的想法重新调整我们的认识，不断打破我们对生物学的认知边界。Sigma® Life Science正在改变世人关于生物学的思维方式，让研究者以独特的视角去探索科学，鼓舞他们去不懈挑战，这里是生物学开始的地方。
Karen Dell: iBiology:Meet the world's best bioloGists through the Internet
Karen Dell来自美国细胞生物学学会，她将简述通过iBiology来获取生物学学习和交流的资源。
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).
AGilent生物芯片原理--陈巍学基因（29）
欢迎来到【陈巍学基因】，我们这个节目，主要是为大家介绍基因组学，和最新的临床分子诊断的技术进展。
今天，会和大家谈一下AGilent公司（安捷伦公司）的生物芯片，视频主要分为以下几个部分：
1.AGilent生物芯片的扫描仪、合成工艺、大体规格和分析软件等。
2.AGilent芯片的应用主要在“比较基因组杂交”领域；
CGH芯片主要是检测：杂合性缺失（LOH）、单亲二染色体（UPD）、和拷贝数变异（CNV）；
CGH芯片区分SNP位点的方法，是通过“酶切+杂交”。
3.AGilent表达谱芯片的IVT检测原理和三个特点。
Pre-Clinical In Vivo ImaGing Solutions from PerkinElmer
PerkinElmer offers a comprehensive portfolio of pre-clinical in vivo imaGing systems and reagents. Find out more at http://bit.ly/1mnyvwF. Our pre-clinical imaGing instruments include our highly published (over 4000 citations) IVIS Optical imaGing systems, Quantum FX microCT which delivers high quality images at an x-ray dose low enough for lonGitudinal studies, and x-ray systems. We also offer a large portfolio of in vivo imaGing reagents for most areas of research including cancer, infectious disease, stem cell, inflammation, toxicology/drug safety and more.
Synthetic Biology & Metabolic EnGineering Teaching an Old Bacterium New Tricks
在第一部分，普莱瑟博士解释说，合成生物学涉及工程原理应用到生物的系统建立生物机器。在建筑这些机器的关键材料是合成DNA。合成DNA可以添加在不同的组合，以生物宿主，如细菌，把它们变成化学工厂，能生产小分子的选择。
Synthetic Biology & Metabolic EnGineering Teaching an Old Bacterium New Tricks
在2部分，普拉瑟介绍了她的实验室使用的设计原则设计E. coli从葡萄糖生产葡萄糖二酸。葡糖酸不在细菌中自然产生的所以，普拉瑟和她的同事们“bioprospected”从其他生物酶并在大肠杆菌中表达，构建所需的酶途径。普拉瑟走我们通过优化时序的许多步骤，酶表达的定位和水平，以产生最大的产量。