方玄昌：从三个角度看环保NGO
该系列视频版权归属于基因农业网。
2013年10月19日，来自全国19个省（直辖市）的300位左右网友组织参与了在武汉华中农业大学举行的“全国首届黄金大米品尝会”暨“湖北第二届转基因大米品尝会”。 此段视频为方玄昌演讲《从三个角度看绿色和平组织》。
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。
卢大儒：NGS的科学问题与行政管理
卢大儒，遗传学博士，复旦大学特聘教授，生命科学院副院长，遗传工程国家重点实验室副主任，主要从事包括肿瘤分子遗传学；基因检测与基因操作研究。在血友病B基因治疗、东亚人群起源和肿瘤的遗传易感基因与药物遗传学发方面作出突出贡献。先后在Nature、Science、Nature Genetics等杂志上发表SCI论文近200篇，承担各类国家和地方科研项目30余项，获得国家和省部级奖励10余项，其中国家自然科学二等奖1项，国家技术发明二等奖1项，省部级科技奖一等奖5项，获得全国优秀教师、全国师德先进个人、中国青年科技奖、国家百千万人才工程国家级人选、全国优秀博士论文、霍英东优秀青年教师一等奖、教育部优秀青年教师奖、上海市优秀学科带头人、上海市高等学校教学名师和国务院政府特殊津贴等荣誉。
邓杏飞：高通量新一代基因测序技术（NGS）在临床医学研究和诊断中的应用
新一代基因测序（NGS）技术正迅猛发展，检测技术日趋成熟，检测费用也不断降低。NGS在医学研究和临床诊断应用方面正在不断扩大。这些都提示NGS正被广泛应用的黄金时光比人们原先预测的来得快。 除了简要分享NGS的技术发展现状，市场应用前景和NGS在临床医学和基因疾病诊断中的重要应用外， 我将特别探讨无创伤产前基因筛查（包括母血游离DNA和完整胎儿细胞单细胞基因检测）和NGS的应用， Ion Torrent基因定型和肿瘤方面的一些最新研究进展和实验资料。
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.
杨巍维：丙酮酸激酶M2亚型在EGFR促进的癌症发生中的作用及机制
肿瘤细胞，即使在氧气充足的情况下，仍倾向于利用糖酵解的方式代谢葡萄糖，在摄取大量葡萄糖的同时排出大量的乳酸，这个现象被称为“WarburG效应”。可以肯定的是，糖酵解赋予了肿瘤细胞独特的生长优势，但这种优势形成的内在机制仍不清楚。
有研究认为，肿瘤细胞利用大部分葡萄糖代谢中间产物合成生物大分子（氨基酸，核酸以及磷脂），从而支持肿瘤细胞的快速生长。我们的研究则发现糖酵解以另外一种全新机制赋予肿瘤细胞生长优势。
本报告将以丙酮酸激酶M2（PKM2）为切入点，围绕细胞核内PKM2的功能，着重探讨了PKM2的“非代谢”功能在癌症发生、发展中的作用及机制。
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).
抽血测EGFR突变--陈巍学基因（18）
现在针对因为EGFR突变引起的肺癌，有好几种靶向药物，例如：易瑞沙等。在这些药物的用药过程中，监控用药的效果，并及时发现耐药突变，是十分必要的。
药明康德公司开发的，基于数字PCR方法检测EGFR突变的方法，灵敏、准确、经济、无创，是一种很有前途的检测方案。
本视频介绍了这种检测方法，和它的优点。