基于Android系统的远程人体生理参数检测系统
其远程生理参数检测仪在2012年12月获得SFDA注册，是一款带有RFID身份识别功能，用于对人体血压、血糖、血氧、脉搏检测，并可录入体温、身高与体重（自动计算BMI指数）等生理参数，并通过GPRS网络与健康信息分析系统进行数据通信，并可配套手机APP进行用户数据绑定及查询的产品。
目前已上市一年多，已销售2500余台，该产品销售额超过500万。
Andres Lozano帕金森氏综合症、抑郁症和关闭它们的开关
大脑深部电击术变得相当精准。借由这项科技，外科医生几乎能将电极置入大脑的任何区域,像电台或恒温器的调节旋钮一项,增强或减弱回路信号。一位罹患帕金森氏综合症的妇女，在电击后立即停止肢体抖动，以及老年痴呆症患者脑部功能恢复，我们看到这项科技带来的巨大改变。
Jonathan drori:存蓄数十亿种子的原因
在TED U 2009的这个简短的演讲中，Jonathan drori鼓励我们保护生物多样性 -- 从一颗颗种子做起。他提醒我们要保护人类赖以生存的植物，同时他也给大家描述了千年种子库这样一个美好的远景，在这里面，将会有逾30亿颗的种子被人类珍藏，这其中甚至还包括那些正日益减少但却必不可少的植物物种。
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).
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.
从外周血中提取drabek基因组DNA
drabek genomic DNA extractions from peripheral blood. Employing a novel DNA extraction procedure adapted from drabek [Biomed. Papers 146(2), 37–39 (2002)] and Nasiri [Journal of Clinical Laboratory Analysis 19:229–232 (2005)]for human peripheral blood samples.
使用Nanodrop ND-1000的分光光度仪测定DNA
Spectrophotometric evaluation of DNA using a Nanodrop ND-1000. Spectrophotometric evaluation of genomic DNA quality and quantity using a microvolumetric Nanodrop ND-1000 optical fibre UV-Vis spectrophotometer.
克氏锥虫和Chagas病 - Norma Andrews P1
本视频由科普中国和生物医学大讲堂出品
Norma Andrews (U. Maryland) Part 1: Trypanosoma cruzi and Chagas’ Disease
Lecture overview:
Trypanosoma cruzi and Leishmania are closely related intracellular protozoan parasites that cause serious diseases throughout the world. In the first part of this lecture, I will present background material on the biology of Trypanosoma cruzi and the history of its discovery as an important agent of human disease in Latin America. I will also discuss the main characteristics of the disease, and the current efforts to stop human transmission.
In the second part of this lecture, I will present background material on Leishmania, the intracellular protozoan parasites responsible for severe human pathology in several parts of the world. I will discuss the main disease forms, the history of identification of the causative agent and form of transmission, and recent discoveries that established important concepts in our understanding of this increasingly serious infectious disease.
In the third part of this lecture, I will discuss current work from our laboratory on mechanisms used by the intracellular parasites Trypanosoma cruzi and Leishmania to interact with mammalian cells. In addition to clarifying specific molecular strategies used by these parasites to infect and survive within host cells, these studies also led, in some instances, to unexpected insights on novel pathways regulating mammalian cell function.
Speaker bio:
Norma Andrews is currently a Professor and Chair of the Department of Cell Biology and Molecular Genetics at the University of Maryland. She received a B.S. degree in biology (1977) and a Ph.D. degree in biochemistry (1983) from the University of São Paulo, Brazil.
In 1990, after completing postdoctoral studies in the laboratory of Victor Nussenzweig at New York University, she was appointed Assistant Professor at Yale University where she remained until 2010.
Andrews was a Burroughs Wellcome New Investigator, a Burroughs Wellcome Molecular Parasitology Scholar and recipient of a NIH MERIT Award. Her laboratory has made numerous contributions to the cell biology of host-pathogen interactions, and discoveries in this area have led to the identification and functional characterization of a novel pathway of Ca2+-regulated lysosomal exocytosis in mammalian cells.
利什曼原虫和利什曼病 - Norma Andrews P2
本视频由科普中国和生物医学大讲堂出品
Norma Andrews (U. Maryland) Part 2: Leishmania spp and Leishmaniasis
In the second part of this lecture, I will present background material on Leishmania, the intracellular protozoan parasites responsible for severe human pathology in several parts of the world. I will discuss the main disease forms, the history of identification of the causative agent and form of transmission, and recent discoveries that established important concepts in our understanding of this increasingly serious infectious disease.
Norma Andrews moved from Yale University to the University of Maryland in 2010.
入侵细胞和在细胞内生存的策略 - Norma Andrews P3
本视频由科普中国和生物医学大讲堂出品
Norma Andrews (U. Maryland) Part 3: Strategies for Cell Invasion and Intracellular Survival
In the third part of this lecture, I will discuss current work from our laboratory on mechanisms used by the intracellular parasites Trypanosoma cruzi and Leishmania to interact with mammalian cells. In addition to clarifying specific molecular strategies used by these parasites to infect and survive within host cells, these studies also led, in some instances, to unexpected insights on novel pathways regulating mammalian cell function.
Norma Andrews moved from Yale University to the University of Maryland in 2010.