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。
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。
Marcel dicke我们为什么不食用昆虫呢
Marcel dicke马赛·狄基希望把昆虫添加到人们的饮食中，他讲了增进人们食欲昆虫的案例。他还传递给挑剔的厨师与美食家的信息是：像蝗虫和毛虫的美味，在味道，营养，甚至在生态友好上可与肉类媲美。
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。
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).
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.