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.<Br> <Br> 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. <Br> <Br> 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. <Br> <Br> 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. <Br> <Br> 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 <Br><Br> 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. <Br><Br>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. <Br><Br>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. <Br><Br> 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]. <Br><Br> 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]. <Br><Br>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’). <Br><Br> 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. <Br><Br> 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：<Br> 1.RiBoZero与Poly（T）方法对比的技术优势<Br> 2.RiBoZero的技术原理<Br> 3.建定向的RNA库的方法：<Br> 1）掺入U碱基的方法来标识cDNA的第二条链<Br> 2）ScriptSeq方法
BRCA基因检测--陈巍学基因（16）
BRCA基因是什么？自从美国著名女影星安吉丽娜.朱莉宣布,在体检中她发现自己有BRCA1基因突变,所以她选择做乳腺切除手术,然后又做了卵巢切除手术,自此,BRCA1和BRCA2这两个基因就一夜之间名声大噪。<Br><Br> 本节课程将为您介绍BRCA1和BRCA2基因的检测。
Keith Barry的大脑魔术表演
这是第一次, Keith Barry告诉我们的大脑如何愚弄我们的身体.Keith Barry邀请了观众参与令人瞠目结舌(甚至有点危险)的大脑魔术表演.
孙毅：RNA深度测序相关(TBD)
孙毅，博士，同济大学教授。美国加州大学洛杉矶分校终身教授，***“***” 国家***。长期致力与神经系统发育和疾病的表观遗传学及分子机制研究。在神经发育方面主要贡献在于阐明了神经干细胞或祖细胞在往神经元或胶质细胞分化过程中命运决定的分子机制，包括首次发现LIF 激动的JAK-STAT pathway 是星形胶质细胞命运决定的主要通路(co 1st author Science, 1997)，首次阐明决定神经元命运的pro-neural BHLH 因子和JAK-STAT pathway 之间的相互抑制作用(1st author Cell, 2001)。<Br><Br> 2001年孙毅教授在美国加州大学(UCLA) 建立实验室后潜心研究DNA 甲基化，组蛋白修饰，及非编码RNA 在神经系统发育，包括细胞命运决定，神经元功能成熟，及其可塑性变化过程中的作用。在神经疾病研究方面，她的实验室是最早开始用人类ES 细胞iPS 细胞做神经系统疾病模型的实验室之一，并取得了突破性成果。<Br><Br> 2009年回国后，开始进行大量转化医学研究主要在干细胞治疗脊髓损伤方面开始了一系列原创性的研究。另外在用干细胞建立孤独症模型方面已取得突破性成果。她带领的团队在同济大学原创性地研发了体细胞单细胞全基因组转录本的RNA 深度测序方法并用于研究成体神经干细胞的分子生物学性状，探讨成体干细胞及肿瘤干细胞静息活化过程中的机制，该技术对未来寻找各类疾病包括衰老的分子标记会有划时代的推动。
金颖：Fox3 suppresses NFAT-mediated differentiation to maintain self-renewal of emBryonic stem cells
金颖教授为分子发育生物学研究室主任，健康科学中心研究员。金教授介绍了Fox3通过抑制NFAT介导的分化维持了胚胎干细胞的自我更新的机制等前沿发现。<Br><Br>Pluripotency-associated transcription factor Foxd3 is required for maintaining pluripotent cells. However, molecular mechanisms underlying its function are largely unknown. <Br><Br>Here, we report that Foxd3 suppresses differentiation induced By Calcineurin-NFAT signaling to maintain the ESC identity. Mechanistically, Foxd3 interacts with NFAT proteins and recruits co-repressor Tle4, a memBer of the Tle suppressor family highly expressed in undifferentiated ESCs, to repress NFATc3’s transcriptional activities. <Br><Br>Furthermore, gloBal transcriptome analysis shows that Foxd3 and NFATc3 co-regulate a set of differentiation-associated genes in ESCs. Collectively, our study estaBlishes a molecular and functional link Between a pluripotency-associated factor and an important ESC differentiation-inducing pathway.
Fluidigm BioMark-陈巍学基因（22）
Fluidigm公司出品的BioMark系统，是一个基于微流控的，高通量的实时定量PCR系统。它可以高效、快速地对多个样本的、多个基因的表达量进行检测，也可以对多个样本的、多个SNP位点进行分型。同时它还可以大量地节约试剂、人工、实验时间。<Br><Br>本视频介绍了BioMark系统的工作原理，和其优势、特点。
GCBI 生物云平台--陈巍学基因（24）
其明公司开发的 GCBI 生物云平台，可以让生物学家方便地、自助式地进行生物信息学分析，无需特别的软件、编程专业知识。<Br><Br>本视频介绍了这个平台，并演示了在这个平台上，以搭积木地方式，方便地、自助式地进行分析的过程。