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。
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。
各种细胞表达的protein作为抗原的优劣
抗原的制备涉及表达载体选择、表达菌株的选择，以及蛋白纯化方法的选择，其中表达菌株可以有多种选择。本视频通过对不同的表达系统的优势及其局限性进行了详细的阐述。
Western blot 整体解决方案，Amersham WB与您携手实现完美WB
Western blot蛋白免疫印迹技术是分子生物学研究的经典研究手段之一，约60％的科学期刊出版物包含WB实验结果。但WB实验步骤多，耗时长，要获得一个完美的结果十分不易，WB实验结果的不稳定，重复不出来？定量不准确？凝胶又漏了？ GE公司最新推出的Amersham WB系统，4小时内可完成电泳、转印、杂交、孵育、成像、定量分析，一气呵成，为Western blot提供了整体解决方案。每个样品、每一次实验都能获得一致的定量数据。再也无需担心结果难以重复再现，无需反复摸索实验条件！
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。
李于：SIRT1 Regulation of Energy Metabolism: Attenuation of Hepatic Steatosis and Obesity
Fibroblast growth factor 21 (FGF21) is the hepatocyte-derived hormone that regulates fatty acid metabolism and has potential to treat obesity and diabetes. We recently indicate that hepatic overexpression of SIRT1 in diabetic mice attenuates hepatic steatosis and insulin resistance. However, the in vivo long-term consequence of hepatic SIRT1 ablation in liver physiology remains unknown.
We showed that hepatocyte-specific SIRT1 knockout (SIRT1 LKO) mice with the albumin Cre-loxP system exhibited a striking phenotype with greater propensity for obesity on a chow diet, characterized by increased whole body mass and fat mass, reduced energy expenditure, and unaltered food intake and physical activity. The obese phenotypes of SIRT1 LKO mice were associated with reduced hepatic and circulating levels of fasting FGF21.
Hepatic impairment of FGF21 repressed expression of key enzymes involving fatty acid oxidation such as CPT1α and MCAD, and inhibited expression of ketogenic enzymes including ACAT1, HMGCS2, HMGCL, and BDH1, thereby reducing plasma β–hydroxybutyrate levels in SIRT1 LKO mice. Moreover, transcriptional activity of a FGF21 promoter-driven luciferase reporter was stimulated by SIRT1 activators, resveratrol and SRT1720, in SIRT1+/+ MEFs, but not in SIRT1-/- MEFs.
The ability of resveratrol and SRT1720 to stimulate FGF21 protein was abolished by SIRT1 H335A inactive mutant or by nicotinamide and splitomicin in HepG2 cells. Induction of FGF21 by SIRT1 activators enhanced expression of key enzymes for fatty acid oxidation and ketogenesis.
These in vivo and in vitro findings characterize 1) hepatic SIRT1 as a master regulator of FGF21; 2) SIRT1-dependent activation of FGF21 in liver as a component for adaptive fasting response; and 3) defective hepatic SIRT1 and FGF21 signaling as a key pathological determinant of energy metabolic abnormality and obesity susceptibility.
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).
二、初试Endnote X7--软件的安装和界面
在这一部分当中，不是要详细介绍每一部分细节，而是从多数人实际使用场景来介绍基本的使用流程，帮大家快速上手，因为每一个人在学习软件的时候，不可能一下子把所有东西都了解清楚，但我们只要学会了主要的这些功能，我们就可以把软件用起来，如果你之前没有接触过这个软件的话，不妨跟着一起练习一下，本节课程首先介绍的是软件的安装和界面。
本视频由中国科学技术大学图书馆授权播出。
二、初试Endnote X7--创建文献数据库
对于一个文献管理软件来说，最基本的就是要有文献可以管理，所以我们在学习文件管理软件的第一步，就是要知道如何向软件中添加文献，如果这步无法解决的话，我们就无法真正去使用软件，在软件中添加文献的方法有很多种，我们在这部分当中介绍主要的两种方法：1）在线检索2）通过导入PDF的方法。我们一起来练习一下。
本视频由中国科学技术大学图书馆授权播出。