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。
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。
Targets-based thERapy for leukemia: opportunity and challenge
优点主要为：能增强患者的免疫力，防止肿瘤的转移和复发，对病人机体的损伤小。 在我国，现在普遍开展的树突状细胞（DC）和细胞因子诱导的杀伤细胞（CIK）的生物疗法被广泛应用。
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).