Cell and chemical biology of mitosis
Cell and chemical biology of mitosis
Genomics in the “Century of Biology”
完整基因组测序已为包括肺癌在内的若干种癌症类型的突变谱提供了线索。最新测序技术意味着，现在有可能从全基因组范围内来观察突变差异，而且现在研究人员对肺癌已经做到了这一点
Cell and chemical biology of mitosis
纳米生物效应与安全性实验室在2004年首次发现内含Gd原子的金属富勒烯三明治纳米结构颗粒可以直接作为肿瘤的高效低毒化疗药物以来，已经从分子免疫、神经调控、干细胞分化、血管生成等诸多方面对纳米颗粒直接作为高效低毒化疗药物的药效和机制，进行了长达6年多的研究，在国际学术刊物上连续发表了一系列的研究成果，逐渐形成较大的国际影响力。
Foldit：游戏玩家的生物
猜猜蛋白是如何基于它们的ＤＮＡ序列来折叠的？这非常困难，即便有最高级的计算程序。现在科学家建立了Foldit，这是一个在线游戏，让玩家来做这个工作。
Joe Landolina:可以立即止血的凝胶
忘了伤口缝合吧——有更好的方法让伤口闭合。本 TED 演讲中，TED 伙伴 (TED Fellow) 演讲者 Joe Landolina 讲述他的发明——一种医用凝胶可以即刻停止创伤出血而不需要施加压力。(内含医学影像。)
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。
Moleculo长测序-陈巍学基因（14）
本课程主要介绍Moleculo测序方法
1.Moleculo测序方法的由来
2.Moleculo测序方法的优点
3.Moleculo测序方法的具体介绍
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.