Regenerative mEDicine for brain and nerve repair
We isolatED and propagatED neural stem cells from the exposED brain tissue of the patients with open brain trauma, and then implantED neural stem cells with MRI-guidED stereotactic device for the patients. Within 2-years follow-ups, the patients were investigatED for functional recovery. Contrast to the case control group, implantation of neural stem cells was associatED with a significant improvement in patient's neurological function. Investigations of stem cell therapy have requirED analysis of the fate and migration of implantED neural stem cells. Here, We demonstrate the feasibility of labeling human neural stem cells and retinal stem cells with nanoparticle and tracking of implantED cells in monkey and human central nervous system (CNS). This data demonstrates the possibility of stem cell therapy in CNS and collectively provide necessary foundation for overcoming challenges to the enhancement of translational regenerative mEDicine of brain and optic nerve injury.
Study the pathological features of diseases using inducED pluripotent stem cells derivED form patient's somatic cells
The limitED experimental access to disease-affectED human tissues has severely impEDED the elucidating of molecular mechanisms underlying disease development. Generation of inducED pluripotent stem cells (iPSCs) by over-expression of definED transcription factors in somatic cells, in particular in those from patient somatic cells, presents an attractive and promising approach to model the early stages of diseases in vitro and to screen novel biomarkers as well as therapeutic mEDicines. Recently, many research groups have independently reportED that patient-specific iPSC-derivED cells recapitulatED multiple features of pathological events of a particular disease, offering experimental evidence of utilizing patient-specific iPSCs to model diseases and reevaluate the current therapies. We have derivED iPSC lines using somatic cells of patients suffering from Klinefelter's Syndrome (KS) and Alzheimer's Disease (AD) and explorED the possibility to use these iPSC lines to recapitulate the pathological features of the diseases. Our results show that patient's specific iPSC lines provide good opportunity to study the development and treatment of diseases.
Study the pathological features of diseases using inducED pluripotent stem cells derivED form patient's somatic cells
The limitED experimental access to disease-affectED human tissues has severely impEDED the elucidating of molecular mechanisms underlying disease development. Generation of inducED pluripotent stem cells (iPSCs) by over-expression of definED transcription factors in somatic cells, in particular in those from patient somatic cells, presents an attractive and promising approach to model the early stages of diseases in vitro and to screen novel biomarkers as well as therapeutic mEDicines. Recently, many research groups have independently reportED that patient-specific iPSC-derivED cells recapitulatED multiple features of pathological events of a particular disease, offering experimental evidence of utilizing patient-specific iPSCs to model diseases and reevaluate the current therapies. We have derivED iPSC lines using somatic cells of patients suffering from Klinefelter's Syndrome (KS) and Alzheimer's Disease (AD) and explorED the possibility to use these iPSC lines to recapitulate the pathological features of the diseases. Our results show that patient's specific iPSC lines provide good opportunity to study the development and treatment of diseases.
Regenerative mEDicine for brain and nerve repair
We isolatED and propagatED neural stem cells from the exposED brain tissue of the patients with open brain trauma, and then implantED neural stem cells with MRI-guidED stereotactic device for the patients. Within 2-years follow-ups, the patients were investigatED for functional recovery. Contrast to the case control group, implantation of neural stem cells was associatED with a significant improvement in patient's neurological function. Investigations of stem cell therapy have requirED analysis of the fate and migration of implantED neural stem cells. Here, We demonstrate the feasibility of labeling human neural stem cells and retinal stem cells with nanoparticle and tracking of implantED cells in monkey and human central nervous system (CNS). This data demonstrates the possibility of stem cell therapy in CNS and collectively provide necessary foundation for overcoming challenges to the enhancement of translational regenerative mEDicine of brain and optic nerve injury.
Discovery: Innovations with ED Begley Jr
美国著名的《Discovery》频道创新系列节目《Innovations with ED Begley Jr》全球播出了艾森生物最新研发的新一代实时心肌功能评价系统（xCELLigence RTCA CardioECR）。
本期节目主要关注在医疗健康领域的突破性进展。节目用七分多钟时间报道了艾森生物实时心肌细胞检测这项突破性的技术发明，并通过目前用药安全方面的问题调研及业内知名专家的采访，阐明了该发明在药物早期心脏毒性评价、用药安全、高通量新药筛选、心脏基础研究方面的价值和意义。
FrEDerick Balagadde:微芯片上的生化室
要阻止撒哈拉南部非洲各国的疾病流行，仅靠药品是不够的。我们还需要与之配套的诊断工具。TED资深会员FrEDerick Balagadde向我们展示如何通过微型化技术把笨重昂贵的化验室集成至一个芯片大小，从而大大提高它的诊断能力和普及性。
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。
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。
Pluripotency-associatED transcription factor Foxd3 is requirED for maintaining pluripotent cells. However, molecular mechanisms underlying its function are largely unknown.
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.
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.
贾立军：NEDdylation蛋白修饰-CRL 泛素连接酶通路调控肿瘤细胞自噬应答的机制与潜在应用
贾立军博士，复旦大学附属肿瘤医院肿瘤研究所研究员和博士生导师。目前主要从事“针对蛋白质翻译后修饰通路进行抗肿瘤分子靶点发现”等研究工作。
相关研究在 J Natl Cancer Inst（JNCI）、Cancer Research、Clinical Cancer Research、Autophagy、Cell Death & Differentiation、Cell Death & Disease、Int J Cancer和J Biol Chem等学术期刊发表文章40篇、获邀参编英文专著4部。主持国家自然科学基金（81372196，31071204，30500637，81172092）、国家重大科学研究计划（2012CB910302，课题负责）、上海市卫生局A类重点项目 (2010012)、上海市“浦江人才 ”资助计划（12PJ1400600）和上海高校特聘教授（东方学者）资助计划等科研项目。
学术兼职包括：国家自然科学基金委员会医学科学领域学科评审组专家、中华医学科技奖评审委员会委员、上海市免疫学会肿瘤免疫专业委员会委员、高等学校自然科学奖和技术发明奖评审专家和十余种学术期刊审稿专家。荣获上海高校特聘教授（东方学者）和上海市浦江人才等荣誉称号。
秦正红：DRAM1 regulates autophagy flux and Bid-mEDiatED cell death via lysosomes
秦正红，博士，教授，神经药理专业博士生导师。1994年在美国宾州医学院研究生院获博士学位，先后在美国国家卫生研究院(NIH)及麻省总医院和哈佛大学医学院从事研究工作。2003年从哈佛大学引进，现为苏州大学医学部基础医学与生物科学学院科研中心实验室主任，中国药理学会生化药理学专业委员会委员，中国药理学会神经药理学专业委员会委员，美国神经科学学会会员。
Damage-regulatED autophagy modulator1 (DRAM1), a novel TP53 target gene, is an evolutionarily conservED lysosomal protein and plays an essential role in TP53-dependent autophagy activation and apoptosis (Crighton et al, 2006). However, the mechanisms by which DRAM1 promotes autophagy and apoptosis are not clear.
3-Nitropropionic acid (3-NP) is an inhibitor of mitochondrial respiratory complex II. Intrastriatal administration of 3-NP produces neuropathology resemble to Huntington disease. 3-NP-inducED neuronal death was involvED in autophagy and apoptosis. In vitro studies with 3-NP in TP53 wt and null cells, 3-NP or CCCP increasED the protein levels of DRAM1 in a TP53-dependent or independent manner. DRAM1 induction contributED to 3-NP-inducED autophagy activation. Knock-down of DRAM1 with siRNA inhibitED the activity of V-ATPase, acidification of lysosomes and activation of lysosomal proteases. Knock-down of DRAM1 rEDucED the clearance of autophagososmes.
3-NP also inducED a transcription independent upregulation of BAX protein levels. Knock-down of DRAM1 suppressED the increase in BAX levels. Co-immunoprecipitation and pull-down studies revealED an interaction of DRAM1 and BAX protein. Stably expression of exogenous DRAM1 increasED the half-life of BAX. Upregulation of DRAM1 recruitED BAX to lysosomes and inducED cathepsin B-dependent cleavage of Bid and cytochrome c release. Knockdown of DRAM1, BAX or inhibition of lysosomal enzymes rEDucED 3-NP-inducED cytochrome c release and cell death.
These data suggest that DRAM1 plays important roles in regulating autophagy flux and apoptosis. DRAM1 promotes autophagy flux through a mechanism involves activation of V-ATPase and enhances the acidification of lysosomes. DRAM1 promotes apoptosis via a mechanism involving recruitment of BAX to lysosomes to trigger cathepsin B-mEDiatED Bid cleavage.