面对新冠病毒大流行，全球关于建立疾病大流行预警系统的呼声越来越强烈。其实这件事情说起来容易，做起来很难。因为疾病大流行的预警就像地震的预测预警一样，是一个世界难题，甚至有人认为对疾病大流行进行预警是不可能的。 我们认为，传染病预测预警是以监测为基础，根据传染病的发生、发展规律及有关因素早期发现异常的先兆或事件发展的不良趋势，从而提高传染病预防控制工作的主动性和预见性。预测预警是对公众的预防行为进行超前调控的一种手段，其目的是把事后补救转变为事先防范，建立一种积极主动的保障机制，避免传染病事件造成影响的不断扩大。要想建立大流行预警系统， 关键是搞清楚导致疾病大流行的关键因素，只有根据关键因素去有针对性的开展监测 ，才能早期发现疾病大流行的先兆，进而根据先兆指标提前采取行动将损失降到最低。实际上，疾病大流行是可以预测的。 我们在2019年11月25日发表在 Current Science 的论文 SpaceWeatherandPandemicWarnings? 中明确指出，由于太阳黑子活动处于近100年最弱的时期，全球宇宙射线大幅增强，并紧急提醒全球接下来几个月很快会出现新的病毒并引起大流行，公共卫生部门必须提高警惕并采取适当的行动，并提前发布了预警，新型冠状病毒肺炎的大流行验证了该预警的准确性。在这篇预警论文中，我们做到了 精准预警 。精准在哪里？首先，我们明确指出是大流行，用的是Pandemic这个单词，这个单词一般应用于流感大流行，而实际上世界卫生组织于2020年3月12日才被迫向全球发布大流行警告。其次，我们是2019年11月25日发表的论文，明确指出接下来几个月全球很快会出现一种新的病毒并引起大流行，论文发表后一个月，就在中国武汉出现了不明原因肺炎，后经实验室证实是新型冠状病毒。 论文见： Space weather and pandemic warnings.pdf 近日，由本人和世界著名宇宙学家Chandra Wickramasinghe共同撰写的论文： The world should establish an early warning systemfor new viral infectious diseases by space-weather monitoring 即将发表。预则立，不预则废。面对新型冠状病毒大流行引发的巨大灾难， 我们希望全球早日建立以“太空射线监测”为基础的大流行预警系统！ 有研究人员认为，需要建立一个严格且分散的 全球野生动物疾病监测系统 ，以应对潜在的新型人畜共患病暴发。这样一个系统可以在病毒成为全球卫生危机之前，识别出它的源头。他们提到，通过将更多利益攸关方纳入其中，可以促进全球参与。相关论文7月10日刊登于《科学》。我们认为这两个预警系统可以互为补充，提高疾病大流行预警效率。 Rigorous wildlife disease surveillance Mrinalini Watsa 1 , 2 , Wildlife Disease Surveillance Focus Group 3 Science 10 Jul 2020: Vol. 369, Issue 6500, pp. 145-147 DOI: 10.1126/science.abc0017 Evidence suggests that zoonotic (animal origin) coronaviruses have caused three recent emerging infectious disease (EID) outbreaks: severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), and the current coronavirus disease 2019 (COVID-19) pandemic. In the search for an intermediate host for SARS coronavirus 2 (SARS-CoV-2, which causes COVID-19), studies have identified SARS-CoV-2–like strains in bats ( 1 ) and pangolins ( 2 ), but these do not contain the same polybasic cleavage site that is present in SARS-CoV-2 ( 3 ). It is unknown what the intermediate host for this spillover event was because to date there are no international or national conventions on pathogen screening associated with animals, animal products, or their movements, and capacity for EID diagnostics is limited along much of the human-wildlife interface. EID risks associated with the wildlife trade remain the largest unmet challenge of current disease surveillance efforts. Although viruses represent a fraction of ～1400 known human pathogens, they place a disproportionate burden on global health ( 4 ). Around 89% of the 180 recognized RNA viruses with the potential to harm humans are zoonotic. Coronaviruses are only the tip of the spillover iceberg: HIV came from nonhuman primates, Ebola came from bats, and H5N1 and H1N1 influenza strains came from birds and pigs, respectively. Indeed, 60% of EIDs are zoonotic in nature, and more than 70% of these have an origin in wildlife ( 5 ). Unchecked exploitation of wildlife—whether for sustenance or profit, legal or illegal—puts humans in direct contact with myriad unfamiliar species. Increased contact occurs in the global practice of bushmeat and game hunting and in wildlife farms, which often unsustainably and illegally supply wildlife for consumption or trade ( 6 ). Imported, hunted, and farmed wildlife then reach a common endpoint, wildlife markets. There, animals endure debilitating and immunocompromising conditions that promote disease transmission: packed cages, poor biosecurity, and unhygienic shedding of animal excreta ( 7 ). Direct human-wildlife contact, mixing of nonendemic wildlife species, and limited health and safety standards are all criteria for a zoonotic hotspot. Many wildlife markets around the world meet these criteria, yet disease surveillance in them is largely absent. More broadly, although the Convention on the International Trade in Endangered Species (CITES) regulates international wildlife trade on the basis of species' endangered status, only a few countries use strict veterinary import controls, and there are no global regulations on pathogen screening associated with the international trade in wildlife. Pathogen biosurveillance and how humans interact with wildlife are at the crux of EID risk management and response. After bats were identified as likely reservoirs for a range of zoonotic events (such as Hendra, Nipah, SARS, MERS, and Ebola) ( 8 ), surveillance of a single cave in southwest China between 2011 and 2015 revealed 11 novel coronaviruses ( 9 ). From 2015 to 2017, of 1497 people tested in the surrounding Yunnan, Guangxi, and Guangdong districts, nine (0.6%) were positive for prior bat coronavirus antibodies, and 265 (17%) reported SARS- or influenzatype symptoms associated with contact with poultry, carnivores, rodents, shrews, or bats ( 10 ). These findings, formally reported in September 2019, provided a warning about the risk of zoonotic coronaviruses that was neither heard nor heeded. The COVID-19 pandemic is evidence that bridging the gap between research and response is critical to anticipating and mitigating future spillover events. PREDICT, the intermittently federally funded offshoot of the 2009 United States Agency for International Development (USAID) Emerging Pandemic Threats program that partially financed the study of bat coronaviruses ( 10 ), screened 164,000 animals and humans and detected 949 novel viruses in zoonotic hotspots across 30 countries between 2009 and 2019. The Global Virome Project—a collaboration between experts in global health and pandemic prevention—aims to sequence all animal virus strains over a 10-year period, with a projected cost of $1.2 billion. Both projects share stakeholders, and although their missions are likely to adapt to a post–COVID-19 world, one of their stated goals includes strengthening existing laboratory capacities along the human-wildlife interface. But are there sufficient numbers of animal pathogen reference laboratories? According to the World Organisation for Animal Health (OIE) ( 11 ), there are 125 reference laboratories certified to screen for one or more target pathogens (and not for broad pathogen surveillance). Their global distribution does not reflect EID risks. Southeast Asia, Africa, and Central and South America carry the burden of EID risk, yet 78 (62%) of reference laboratories are in Europe and North America; only 33 (26%) are in Asia (14 in China and 8 in Japan), with 12 (34%) spread between 7 countries; 3 (～2%) are in Africa; 4 (～3%) are in Australia, and 8 (～6%) are in South America. Although this does not account for laboratory size or screening methods and capacity, it is evident that many regions with zoonotic hotspots lack testing facilities with the capability of conducting disease surveillance. Markets selling live animals, including wildlife such as this slow loris at the Borito Market in Jakarta, Indonesia, are hotspots for zoonotic spillover and should be monitored to better manage emerging infectious diseases. PHOTO: TOM LE LIEVRE/REDUX What can be done to mitigate future zoonotic EIDs? Centralized biosurveillance efforts produce results but are expensive, maintained by a select few countries, and subject to political whims, as evidenced by the 2019 shift in funding for PREDICT, a recent recall of U.S. National Institutes of Health (NIH) support for the EcoHealth Alliance, and the withdrawal of the United States from the World Health Organization (WHO). As such, they are not immediately scalable, nor do they stimulate widespread capacity. The international wildlife trade is a substantial global industry in need of greater oversight. Because ill-conceived restrictions would affect millions of people and likely drive these activities deeper underground, further impeding regulation ( 12 ), the first step is to establish a more cost-effective, decentralized disease surveillance system. It would empower local wildlife and public health professionals to test for diseases year round, at source, without criminalizing public participation in screening programs. Such screening was not technologically feasible after the emergence of the H1N1 influenza virus in 2009, but now, affordable modern technologies enable quick in situ biosample processing, whole-genome sequencing, metagenomics, and metabarcoding of pathogens. This would enable proactive, broad, routine wildlife pathogen screening in remote areas rather than reactive targeted testing. Decentralized laboratories must be able to extract genomic material and conduct metagenomic sequencing and targeted pathogen testing if necessary. As demand increases, individual technologies have evolved to be smaller, simpler, and more affordable. Multiplex polymerase chain reaction (PCR)–based viral enrichment protocols with portable DNA sequencers (such as MinION) have been deployed for in situ monitoring of Ebola virus, Zika virus, and now SARS-CoV-2 infections ( 13 ). Practical training in applying these laboratory solutions (such as miniature centrifuges, thermocyclers, and electrophoresis setups) is well documented, even in remote locations ( 14 ). However, most pathogen screening efforts that use such equipment have been in response to human disease outbreaks. These technologies could be used to regularly monitor entire pathogen families of increased global concern in animals and areas with increased risk of zoonotic spillover, including wildlife markets or farms and free-ranging high-risk taxa such as primates and bats ( 15 ). Local wildlife scientists and health care workers can be trained on how to safely use facilities with broadly accessible molecular equipment in local facilities with standard biosecurity practices to prevent risk of pathogen spillover into the community. Restricting such training and activities to relatively few specialized centers impedes broad surveillance efforts. Any animal surveillance program should integrate with testing programs for humans to capture early zoonotic pathogen circulation between human and nonhuman populations. Sources of zoonotic pathogens are frequently unclear and often not possible to determine after the early stages of a spillover event. Monitoring could remove much of this uncertainty, allowing molecular epidemiology to inform short- and long-term responses on both a local and global level. To complement decentralized laboratories, a publicly accessible, centralized, curated system for monitoring pathogens must be established for three main reasons: (i) This would provide instant pathogen classifications based on comparative genomics, further cross-linked to reference data on prevalence by species and region. (ii) A centralized curated system could alert to EID indicators, including gains and losses of strains, pathogen-specific changes in host species numbers, rapid increases in mutation rates that may indicate pathogen spillover into a naive host, and pathogen detection in traded animals that do not occur in wild counterparts. (iii) For virus families that are poised to spillover into human populations, genomic sequence data can reveal diversity of key pathogen proteins in circulating strains (for example, the spike protein that mediates human cell entry of coronaviruses, and the RNA-dependent RNA polymerase that is important for viral replication). Such approaches assist in identifying broad-spectrum antivirals and vaccination targets as well as treatment-resistant pathogen variants that pose a risk of generating future EIDs. An example of a disease-focused public database that could be expanded is the GISAID (global initiative on sharing all influenza data) EpiFlu repository, a global initiative developed for sharing influenza virus sequence data and currently also documenting SARS-CoV-2 sequences. It facilitates data access for registered users while securing data ownership by requiring that contributors be acknowledged in derivative research. Additionally, the database could include report-generating features such as those in the Zoological Information Management Software (ZIMS), used by more than 1000 Species360–accredited zoological institutions worldwide to upload biomedical data and compute reference ranges across multiple variables and species. An internationally recognized standard for managing wildlife trade on the basis of known disease risks should be established. Currently, few countries consider disease risk as a factor in regulating wildlife imports and exports, and a disease status equivalent to CITES is lacking. Pathogen screening is also not required nor facilitated before, during, or after translocating wildlife products, leaving pathogen status to be declared by the shipper, who may not have the experience to make such determinations. Because a large number of animals naturally carry pathogens that could spillover to humans if improperly handled, the means to identify the species for which security standards should be enhanced, or for which trade and consumption should potentially be prohibited, is needed. An important caveat is that such classifications can stigmatize animals to their detriment and incite fear-based human behaviors that may threaten species conservation. A decentralized network could improve feedback between those who screen samples and those who curate data to bolster the safety of wildlife and humans, a fundamentally “One Health” approach. This would increase localized knowledge of EID risks, provide earlier warnings and faster global responses to spillovers, and inform wildlife trade policy. This model is more robust to shifting political landscapes and funding and does not ignore the role of advanced regional research laboratories, which also provide vital targeted pathogen screening. Research laboratories can also provide samples for or generate high-quality host de novo reference genome assemblies and expand regional capacity for biobanking, including cell cultures, which will improve understanding of the co-evolutionary processes that underlie pathogen-host range and susceptibility. By giving more parties a stake in the effort, decentralization is more likely to succeed in garnering geographically representative participation that explicitly includes the most at-risk, under-resourced regions. Supplementary Materials science.sciencemag.org/content/369/6500/145/suppl/DC1 http://www.sciencemag.org/about/science-licenses-journal-article-reuse Rigorous__wildlife disease__surveillance.pdf https://v.sciencenet.cn/detail/v_5f07cab0e4b061de7cb5a195/3 https://science.sciencemag.org/content/369/6500/145 传染病预测预警方法的研究进展 http://blog.sciencenet.cn/blog-529903-839249.html
在《甲醛与认知》一书中，老朽提出了一个观点：“部分老年性痴呆病人存在意识损害”。当然，这一观点需要进一步证实。 In the book of Formaldehyde and Cognition, I hypothesized: Some Alzheimer's patients may suffer from consciousness impairent. Of course, this hypothesis needs further investigating. Please See: Rongqiao He. Cognitive ability and impairment related to formaldehyde in Formaldehyde and Congition, 1st Ed, Springer Nature , pp. 143-166 . doi : https://doi.org/10.1007/978-94-024-1177-5_8 URL： https://link.springer.com/chapter/10.1007/978-94-024-1177-5_8#citeas
Gender difference in valproic acid-induced neuroprotective effects on APP/PS1 double transgenic mice modeling Alzheimer's disease Zhimin Long, Qinghua Zeng, Kejian Wang, Akhilesh Sharma and Guiqiong He Chongqing Key Laboratory of Neurobiology, Chongqing Medical University, Chongqing 400016, China Acta Biochim Biophys Sin 2016, 48: 930–938; doi: 10.1093/abbs/gmw085 Alzheimer's disease (AD) is a neurodegenerative disorder that causes progressive memory and cognitive impairment with gender difference in specific cognitive ability domains, pathology, and risk of AD. Since valproic acid (VPA) is a widely used mood stabilizer and an antiepileptic drug, which exhibits multiple neuroprotective activities on AD, this study intended to investigate the gender difference in the effect of VPA on APP/PS1 double transgenic mice modeling AD. Behavioral experiments showed that VPA reduced the autonomous behaviors, improved learning and memory, and exhibited gender differences in AD mice compared with the control mice. The decrease in senile plaque, amyloid β (Aβ) 40, and Aβ42 caused by VPA in the male AD mice was more notable than that in the female AD mice. Meanwhile, VPA protected brain cells from dying notably in the male AD mice but only slightly in the female AD mice, and VPA treatment thickened the postsynaptic density and markedly increased the number and density of presynaptic vesicles in both male and female AD mice. However, the effects of rescuing early synaptic structural and functional deficits by VPA were more obvious in the male mice. Overall, these results supported the hypothesis that gender difference significantly influences AD and indicated that VPA may be a promising remedy for AD if basic biological differences and gender specificity were prudently taken into account. VPA protected gender-dependent neurons from dying 阅读全文: http://www.abbs.org.cn/arts.asp?id=4076 相关论文: 1 Valproic acid inhibits A beta production, neuritic plaque formation, and behavioral deficits in Alzheimer 's disease mouse models 2 Histone Deacetylase Inhibitor Valproic Acid Inhibits Cancer Cell Proliferation via Down-regulation of the Alzheimer Amyloid Precursor Protein 3 Valproic acid induces caspase 3-mediated apoptosis in microglial cells 4 Valproic acid stimulates clusterin expression in human astrocytes: Implications for Alzheimer 's disease 5 Valproic acid as a promising agent to combat Alzheimer 's disease 6 VALPROIC ACID ENHANCES MICROGLIAL PHAGOCYTOSIS OF AMYLOID-beta(1-42) 7 Valproic Acid Attenuates Neuronal Loss in the Brain of APP/PS1 Double Transgenic Alzheimer 's Disease Mice Model 8 Valproic Acid Alleviates Memory Deficits and Attenuates Amyloid-beta Deposition in Transgenic Mouse Model of Alzheimer 's Disease 关注ABBS
Risk predisposition for Crohn disease - Extranet du CHU https://extranet.chu-nice.fr/.../531_BrestAUTOPHAGY.pdf 文件格式: PDF/Adobe Acrobat - 快速查看 作者：P Brest - 2011 - 被引用次数：2 - 相关文章 influenced by common variants at many loci like the exonic synonymous IRGM . SNP (rs10065172, NM_001145805.1, c . 313C T ). We recently showed that ... Variable Genome: Synonymous SNPs are not so synonymous varigenome.blogspot.com/.../ synonymous - s ... - 网页快照 - 翻译此页 2 Feb 2011 – The exonic SNP c . 313C T (rs10065172) is in perfect linkage ... The c . 313C T variant alters codon 105 of the IRGM protein from CTGTTG. Risk predisposition for Crohn disease - 医脉通 paper.medlive.cn/literature/31525 - 网页快照 Susceptibility to Crohn disease (CD), an inflammatory bowel disease, is influenced by common variants at many loci like the exonic synonymous IRGM SNP (rs10065172, NM_001145805.1, c . 313C T ). We recently showed that miR-196 is ...
摘要 ：简述我如何判定南京发生泻湖病，如何进行文献搜索，在此基础上如何将科学知识结合在一起给出可能是正确的判断。进一步交待我讽刺松鼠会有关科普的原因，评论松鼠会新出有关科普因为意气之争而变成劣质科普，科学被意气污染，科学上有错误，而且明显忘了科普基本写作规范——读者始终是对的。谴责与讽刺民众科学素质的科普基本上都是劣质科普（他们都懂了，还希罕你科普么）。 全文 ： 南京发生泻湖病，医生诊断为横纹肌溶解，由于怀疑生产加工环节中的疏漏，导致了当地政府与民众高度紧张，过度反应，成立了以市长为首的工作小组，试图彻查小龙虾产业，要找到致病原因，同时，网络与媒体上也充斥着大量的业余或者专业科学人员的相关讨论，不少人试图按照福尔摩斯的探案技巧，来解决这个世界难题。 我一开始并未关注该事件，但我的编辑来约稿，于是就关注了一下，编辑给我的链结是 松鼠会群雄坐而论道，试图解密小龙虾至横纹肌溶解的相关科普 。松鼠会不少人发言很有见地，但也有人不太靠谱，对比我找到的资料，我发现他们实际上拥有所有文献资料，在这种情况下，无人提到泻湖病，就让我感到有点好笑了，如果你思路走上歧路，解密小龙虾事件就无疑成了大跃进式的笑话，这个世界难题存在几千年了，几个人坐而论道就解决了？ 说来说去，都怪诊断该病的医生只给了横纹肌溶解这么一个诊断，而横纹肌溶解是一个很基础的肌肉损伤机制，其病因归纳起来，数不胜数，这是福尔摩斯的最大挑战。现代医学的福尔摩斯遇到前所未有的难题，一定先查文献，松鼠会群雄的确查了文献，但遗憾的是，他们大多不是医生，其中有医生，但好象又不太懂行。 南京小龙虾事件如果医生查文献，一定会首先怀疑泻湖病，这跟美国当年鉴定小龙虾导致泻湖病不是一回事。首先我们说说如何查文献。 南京事件中即使是媒体非专业人员都能把小龙虾跟患者的横纹肌溶解联系在一起，那么你无疑是要用两个专业术语搜索，一是小龙虾，二是横纹肌溶解（此综合征易于诊断，否则还会怀疑诊断是否准确，查询方法会有变化）。用常用的Medline搜索，事实上你搜不到任何文献，这多半不是没有文献，而是你的搜索方法有问题，需要进一步扩大。 你可以去掉横纹肌溶解的限制或者小龙虾的限制，但此案中，横纹肌溶解相对很确定，故而需要保留，而扩大小龙虾，扩大它的上一级生物学分类概念，事实上你可以采用跳跃式的逼近法，先跳到很大的概念，比如鱼类，看看有多少文献，Medline产生21个结果，Bingo，你的搜索任务完成一半，这些文献中要么会给予你此前是否有过类似病例，要么提供一定线索，可能会从小龙虾升级到它的属、亚科、科、亚目、或者一至向上走，或者什么都没有，你的确有一个新病或者得从其它方面寻求答案。 从文献的数量上，你可以得出初步信息，那就是这是罕见疾病状态，对于罕见病，你可以猜测这些文献大多数是个案报道或者回顾。无论是个案，还是回顾，其中都会回顾已往病例，给你足够的基础信息，让你可以更有效地组织下一步的文献查询工作。 对于罕见疾病，你读文献从最新的开始（好象是废话，读文献总是从最新的读起）。最重要的是，对于罕见病来说，文献搜索是靠不住的，你还得从查到的文献所列举的参考文献进行追索。很快，你就会阅读到Langley与Bobbitt的“Haff Disease After Eating Salmon”一文（Southern Medical Journal 2007；100（11）：1147-50），这就是了，你甚至不需要进一步读就知道你研究的方向在哪里了，因为Langley与Bobbitt清清楚楚地列出了在美国发生的病例并且明确地提到在露易丝安纳州的9个小龙虾中毒病例。 一看Langley与Bobbitt一文，你就知道为什么在文献搜索中你搜不到文献了，露易丝安纳州的病例是州卫生部门的疾病通报中报告的，这样的文献不被现有的文献索引收集。你如果不愿意进一步寻求露州疾病报告，Langley与Bobbitt一文已经给予你足够的信息了，小龙虾能导致Haff Disease，而Haff Disease目前致病毒素不明，但学界似乎认定存在着相应的毒素致病，并对其性质有一定了解。 基于这样的信息，再结合南京发生的病例情况，事实上南京发生泻湖病就呼之欲出，而如果你细读露州疾病报告，几乎可以肯定南京发生了泻湖病。南京发生泻湖病的关键判定依据如下： 1. 小龙虾致泻湖病已有先例 2. 南京连普通人都在怀疑小龙虾 3. 流行趋势高度一致（大体极度散发，具体案例却又集中） 4. 当地卫生部门与医生进行了排查，没有发现其它致病原因，或者提供的致病原因可以明显排除 作用当地卫生行政部门，对相应产业进一步检查当然是公共义务，但面对这么多的科学证据，也应把泻湖病当着最大可能性的诊断，而对发现致病根本原因或者毒素不要抱太大希望，免得浪费资源，也避免挠民过度。 你一看我的整个思路，就明白我为什么忍不住要讽刺科普爱好者了，Langley与Bobbitt把诊断写在标题上，你们东扯一个可能，西扯一个可能，就是不提泻湖病。但不妨碍这些科学爱好者经常性地把民众科学素质低下放在嘴里，好象不接受他们观点的，就是缺乏科学。方舟子综合征也太容易传染了吧？ 我直接点破南京发生泻湖病，估计专家恨我要死，松鼠们也看我大为不爽，这不，松鼠会马上又发大作来“复仇”来了。《 当我们谈论小龙虾时我们在谈论些什么 》作者 游识猷 ，就是松鼠会论坛管理人员之一，特点是讽刺松鼠者他严格执行论坛规则，而松鼠们则不必担心，科学松鼠会是中国人过美国大学兄弟会瘾的地方，成了兄弟会正式成员就有享受侮辱新成员的权利。 游识猷老师高才，寻正讽刺了松鼠一把，他辛苦辛苦地抄来哲人的教导， 我们知道，世界上存在着已知的已知事物，也就是说有些事情我们知道自己知道。而我们也知道世上存在着被人所知不明事物，这就是说有些事情我们知道自己不知道。同时，世上还存在着我们不知道的不明事物，也就是说我们不知道自己不知道。——拉姆斯菲尔德 这位哲人是谁呢？他就是著名的美国前国防部长Donald Rumsfeld，哲人的话其实不难懂，美国以伊拉客有大规模杀伤武器与搞恐怖活动为名侵入伊拉客，结果发现有点证据缺乏，于是能说会道的Rumsfeld玩了一把语言游戏，有作者存在反党反政府倾向，因此说Rumsfeld是诗人，比如游识猷老师就引用了他的名诗： The Unknown As we know, There are known knowns. There are things we know we know. We also know There are known unknowns. That is to say We know there are some things We do not know. But there are also unknown unknowns, The ones we don't know We don't know. 未知 我们知道， 世界上存在着已知的已知事物， 也就是说有些事情我们知道自己知道。 而我们也知道 世上存在着被人所知不明事物， 这就是说 有些事情我们知道 自己不知道。 同时，世上还存在着我们不知道的不明事物， 也就是说我们不知道自己不知道。 游识猷老师的教导，寻正虽然只是少年先锋队（亲友团）的成员，但闻弦歌而知雅意，只能说，辛苦了，松鼠会的面子，在知与不知搅得一塌糊涂的时候，估计挽回来了。不过，看了游识猷老师的科普，我实在是忍不住要发声，我向往松鼠会，那是因为其中专业人员多，专业精神足，科学味儿够，怎么从松鼠会写圣元奶粉开始，频出劣质科普呢？比如DNA的《 导致性早熟的一定是雌激素吗？ 》，箫汲的《 “微小青春期”未必与食物有关 》，或者李清晨的《 外科之花的艰难绽放 》。游识猷老师的大作《 当我们谈论小龙虾时我们在谈论些什么 》也很有些失水准的。 DNA既然要洗白圣元，起码也该交待一下其奶粉可不可能含激素，国际标准又该不该含激素吧？箫汲的文章更是古怪，除了标题谈微小青春期，全文就跟微小青春期无缘，但不妨碍为圣元洗污，李清晨的《艰难绽放》可笑至极，基本事实与人物没搞清楚，连基本的写作规范都不顾及。最后说说游识猷老师的大作，让人忍俊不住，做科学的基本素质是头脑清醒，不让意气之争损害自己的判断能力，可惜老师一激动，就无法保持科学的纯洁，但具有讽刺意味的是，老师还不忘淳淳教导：民众就是喜欢伪科学。 民众不仅仅喜欢伪科学，他们还更喜欢科学，前提是你得有足够的科学。象完全缺乏相关常识而拼命绕着道儿为圣元洗污的“科普”，想让人喜欢，我看民众还不如喜欢伪科学的好，受了骗起码得了心理上的安慰，而你们的“科学”害了人，还要被你们骂得象孙子样的。看看你们这些劣质科普后面的留言，我几乎都要怀疑你们染上了方舟子病了，故意化名相互吹捧。到底是你们缺乏科学，还是你们贬斥的民众不懂科学？我还真的越来越怀疑了，两年前科学松鼠会倡导科普作者要谦卑，但我看到的是一个又一个地肚子挺得圆，对着方舟子这类有影响的人物很谦卑，达到唾面自干的程度了，而面对真正的读者，稍有质疑，恶言相向。如果谦卑就是畏强凌弱，还是不要也罢。 我以专业知识为基础，判断南京发生了泻湖病，其实也不算扫松鼠会的面子，毕竟我还是松鼠会的少先队员不是？不过，松鼠们我得罪多了，包括游识猷老师的选择性执法，也在我的批判之列，故而不把我当自己人，要找回场子，可以理解。但哪里跌了一跤，还要在哪里陷进去，就不能不说愚昧了。 游识猷老师的大作，洋洋洒洒如同研究生的读书报告，民众最关心三个问题，A，我们不知道，B，我们不知道，C，我们不知道。搞了半天，游识猷老师还没能把科普与研究生报告区别开来，呵呵，难怪喜欢超凡入圣的哲学诗： 我们知道， 世界上已知的已知事物， 我们不知道， 世界上不知的未知事物， 但我们就是知道， 民众不知道我们的不知道， 也不知道我们的知道， 只知道我们不知道， 只知道我们想要他们知道。 三个湾带到柯尼斯堡（Konigsberg）的新泻湖（Frisches Haff），柯尼斯堡在二战后被苏联强占，苏联改名加里宁格勒，而新泻湖，也变成了维斯图拉泻湖（Vistula Lagoon），德语仍然称之为新泻湖。 图示维斯图拉泻湖卫星照片与新泻湖与柯尼斯堡地图 新泻湖，也就是现在的维斯图拉泻湖，就是泻湖病的最先发现的地区，因此，该病被称为Haff Disease，中文正确的译法，无疑就是泻湖病，但是，在我译出此病之前，有人将之错误地译为哈夫病，而我不客气地纠正了这一错误。对于名词的译法，人名音译，地名则视情况而定，比如Frishes在德文中指新鲜的意思，可音可意，但Haff本意指泻湖，译成哈夫则不知所云，铁定的错误译法。在我纠正错误译法之后，游识猷老师偏要将错就错，似乎故意跟寻正叫板似的，而两只松鼠也就跳了出来，好象寻正又犯了大错似的： 松鼠会相互极力吹捧，一篇不合格的科普（但适合做研究生进展讨论是无疑的）一会儿是科普典范，一会儿又是要挂一年，好象民众真缺了这之中的“科学”似的。坐井观天是要惹笑话的，尤其是不自量力要坐而论道解决世界性难题之时。我给出了正确的提示，就无形之中是一个提醒，那一番一会知，一会不知的教训，是应当首先内部消化的，不是用来搪塞民众的。但似乎我的提示又成某些人炫耀科学知识的契机，不能不说，人啊，真有些意思。 当然，游识猷老师是极度不服气的，松鼠们也是不服气的，少年先锋队的，只够资格挨贬，还在五七干校劳教着呢，怎么这么不客气造起反来了！游识猷老师说，唉呀，我的科学知识，是没有问题的么，不就一个名词，你依理我依例，说那么多干什么？你找一条我的错误试试？真的莫叫我试，方舟子前车之鉴，李清晨也跌了好几跟斗，如果要练他们一样的厚脸皮，尽可挑战我来试。咱们还是少年先锋队的，纠错点到为止，目的是学习与教育，不必闹得象李清晨跟方舟子一样，动辄要我“身败名裂”，这样的人多了，我受得住，但影响网络环境。 好啦，咱们看一段游识猷老师的描述： 正是在此调查后，美国对哈夫病有了更深入的了解，对此病的临床诊断也有了比较清晰的标准。因此，2001年，美国路易斯安那州方圆三十英里内的地区，在七天内发生九起食用小龙虾后三到十六小时内发生横纹肌溶解症的疫情时，医生便迅速根据此前的研究结果，判断为哈夫病并迅速给予对症治疗。 对于2001年发生的案例，我前面交待了，是报道在州疾病报告中的，我不知道游识猷老师是否读过原始报道，还是根据二手材料推测的，不管怎样，都是错误的。原始文献如下： 露易丝安纳州疾病报告原文 我发文批评中国医生诊断不准让大家虚惊一场，那是因为有了露易丝安纳州的先例，有了泻湖病的流行病学规律才有这一批评的，如果中国案例涉嫌一个新的鱼种，那么我的批评就不适当，医生就得按露易丝安纳州的处理方式进行：排除法。排除其它可能性，然后判定为泻湖病（即使南京病例可以初步诊断为泻湖病，仍然需要常规进行一些其它病因的排除）。当露易丝安纳州的病例判定为泻湖病时，病人都出院好久了，什么“ 医生便迅速根据此前的研究结果，判断为哈夫病 ”，纯粹是臆想。 科学不排斥意气之争，但切不可用意气亵渎科学，其后果么，嗯，还真不严重，不过，会引发我的嘲笑，有的人习惯了，有的人还需要进一步习惯。
阿尔茨海默病（Alzheimers disease，AD）是一种严重影响人类健康的神经退行性疾病。但AD的发病原因目前学术上还众说纷纭，公说公有理，婆说婆有理。但研究表明，-淀粉样蛋白（Amyloid- peptide，A）与AD发生发展密切相关。大脑内A异常沉积与AD呈正相关性。芬兰东方大学Irina Alafuzoff教授及其合作者给出了A与AD相关的有一例证，其成果发表在2010年第20期Journal of Alzheimers Disease上。该研究采用多种A抗体免疫成像检测大脑内A水平，尸检标本包含：10例2-92岁不等脑部未损伤死者，1例患轻度认知损伤(Mild cognitive impairment, MCI)100岁死者，7例57-87岁不等患AD死者，7例50-93岁患含43KD TAR DNA 结合蛋白的额颞叶变性(Frontotemporal Lobar Degeneration with TAR DNA binding protein 43,FTLD-TDP43)神经退行性疾病死者。无一例外地，AD死者尸检表明，其 内嗅皮质 及海马神经元胞外富含大量的A成分，而其余尸检标本除了MCI及特殊3例脑部未损伤死者（52岁，72岁，92岁）检测到含有较多A外，未能检测到明显的A成分。细胞核周围A单抗体检测表明，无论是AD患者还是正常及FTLD-TDP43患者，即使是2岁的正常大脑内也能检测到细胞内A的存在，这提示A可能是神经元正常的代谢产物，但其生理功能目前还是个谜。
英国内科医生詹姆斯帕金森博士最早系统描述了帕金森病。为引起人们对这种疾病的重视，自1997年开始，帕金森博士的生日、每年的4月11日被确定为世界帕金森病日(World Parkinson's Disease Day)。 James Parkinson (11 April 1755 21 December 1824) was an English apothecary surgeon , geologist , paleontologist , and political activist . He is most famous for his 1817 work, An Essay on the Shaking Palsy , in which he was the first to describe paralysis agitans, a condition that would later be named Parkinson's disease after him. http://en.wikipedia.org/wiki/James_Parkinson 下面的链接里介绍了帕金森早期的描述，里面有比较丰富的资料。 James Parkinson life and time http://www.movementdisorders.org/james_parkinson/life.html 另：有许多名人老年得了帕金森病，如邓小平，巴金，拳王阿里，美国总统里根，希特勒...... 二战溃不成军 帕金森病功不可没 http://www.cnkang.com/yxzs/yxzx/yysh/yxs/200801/102993.html 在不久前召开的第13届国际帕金森病学术交流大会上，一位来自美国得克萨斯大学的神经病学专家向与会者报告了他的研究成果：正是由于希特勒患了晚期帕金森病，他的思维变得迟钝，因而难以及时、准确地做出判断，最终导致了德军在诺曼底战役中的失败和第三帝国的灭亡。 战争的胜负最终由其性质决定，非正义的战争必然会失败。但毫无疑问，帕金森病在二战中助了盟军一臂之力。 帕金森病有多厉害 帕金森病是一种慢性神经系统疾病，常见于中、老年人。其病因至今不明，可能与中毒、脑炎、动脉硬化、外伤等有关，部分患者有遗传倾向。该病主要表现是：四肢不由自主地震颤、肌肉僵直、行动迟缓等。这些病状可单独存在，也可同时具有。开始多为单侧，可逐渐发展至对侧。一般不会自行好转，有时可在数年内迅速发展，导致病人完全残废。在本病晚期，患者全身僵硬，卧床不起，生活不能自理，健康状况每况愈下，最后常死于各种并发症。 由此可见，帕金森病对患者的危害非常大。患了晚期帕金森病的希特勒屡出败招，再加其所做所为不得人心，最后落个兵败身死的下场，也便不足为奇了。 聪明反被聪明误 帕金森病是大脑中称为多巴胺的物质含量减少而导致的一种运动功能紊乱病。目前尚无有效的根治方法，所有治疗都是为了改善症状，提高生活质量。 据研究，早在1934年，希特勒就患有帕金森病，他当时的症状是肢体震颤和运动迟缓。但是，自以为是的希特勒通过服药掩盖了这些症状，他还和助手一起对部下及其他人隐瞒了病情。但随着帕金森的不断发展，症状也逐渐加重、增多。到1945年，希特勒已出现了不少晚期症状，包括思维迟钝、反应迟缓、睡眠障碍等，而且，激动时这些症状容易加重。此时，由于药效在不断下降，即便再增加药物的剂量也无济于事。因此，当时希特勒已无力处理一些复杂的问题，也很少公开活动了。 当盟军在诺曼底登陆时，希特勒正在睡大觉，其助手不敢去叫醒他。盟军从诺曼底登陆后，他的如意算盘全被推翻了。由于有思维迟钝、反应迟缓等帕金森病的症状，所以他没能及时组织反攻，从而在一定程度上影响了整个战局。希特勒最后兵败自杀而亡。 帕金森病该怎样治 药物对大部分晚期患者的作用下降，即使增加剂量，也难以达到以前的疗效。多年来，人们一直在探索使用手术的方法来阻断导致帕金森病的神经通络，以达到控制症状的目的。典型的手术是采用立体定向法。近几年，国外又发展了一种利用微电极、计算机的新型精确定向手术，治疗帕金森病取得了极大的成功。由于新的手术方法定位精确，所以疗效确切、持久，可达到立竿见影的效果，并且极少发生严重的手术并发症。大部分患者手术后可再服用少量多巴胺类药物，这样可使症状完全消失或得到基本控制。
http://www.gopubmed.org/web/gopubmed/4?WEB01gbk0re9iby58I2I1I00f01000j10040001rl secondary prevention and ischaemic heart disease and primary care 485 documents semantically analyzed 1 2 Top Years Publications 2009 50 2005 38 2002 36 2008 35 2003 35 2007 34 2001 34 2006 32 2004 29 2000 28 1999 26 1998 25 1997 19 1996 14 1995 6 1990 6 1985 6 2010 4 1994 4 1992 4 1 2 1 2 Top Countries Publications USA 128 United Kingdom 95 Germany 27 Canada 26 Italy 20 Spain 19 France 17 Sweden 16 Netherlands 12 Ireland 9 Australia 9 Japan 7 India 4 Poland 4 New Zealand 4 Switzerland 4 Norway 4 Israel 3 China 3 Brazil 2 1 2 1 2 3 ... 10 Top Cities Publications London 21 Aberdeen 14 Boston 12 Barcelona 9 Paris 8 Glasgow 7 Oxford 7 Toronto 6 Munich 6 Houston 6 Rome 6 Baltimore 6 Edmonton 5 Dublin 5 Utrecht 5 Birmingham 5 Malm 5 Atlanta 5 Galway 4 Florence 4 1 2 3 ... 10 1 2 3 ... 12 Top Journals Publications Bmj 20 Heart 14 Am J Cardiol 12 Circulation 11 Am Heart J 10 Int J Cardiol 9 Aten Primaria 8 Am J Med 7 Can J Cardiol 7 Z Kardiol 7 J Am Coll Cardiol 6 J Gen Intern Med 6 Med Clin-barcelona 6 Drugs 6 Fam Pract 6 Primary Care 6 Eur J Cardiov Prev R 5 Arch Mal Coeur Vaiss 5 Bmc Cardiovasc Disord 4 Pharm World Sci 4 1 2 3 ... 12 1 2 3 ... 97 Top Authors Publications Campbell N 9 Ritchie L 8 Thain J 6 Whincup P 5 Byrne M 4 Bennett K 4 Ray K 4 Gohlke H 4 Morris R 4 Cambou J 4 Ebrahim S 4 Murchie P 4 Deans H 4 Israelsson B 4 Grundy S 4 Jankowski P 3 Smith S 3 Jukema J 3 Simoons M 3 Grobbee D 3 1 2 3 ... 97 1 2 3 ... 78 Top Terms Publications Humans 476 Patients 380 Coronary Disease 320 Heart Diseases 267 Middle Aged 249 Risk Factors 226 Aged 224 Myocardial Infarction 215 Infarction 187 Primary Health Care 169 Cholesterol 159 Mortality 140 Adult 139 Primary Prevention 133 Pharmaceutical Preparations 126 Arteries 120 Hospitalization 119 Hospitals 114 Coronary Artery Disease 110 Evaluation Studies as Topic 103 1 2 3 ... 78 最新研究进展： Buckley BS, Byrne MC, Smith SM. Service organisation for the secondary prevention of ischaemic heart disease in primary care. Cochrane Database Syst Rev. 2010 Mar 17;3:CD006772. (Review) PMID: 20238349 ReadAbstract Clinical Evidence Topics: Secondarypreventionofischemicevents PrimarypreventionofCVD:physicalactivity PrimarypreventionofCVD:dietandweightloss DISCIPLINE RELEVANCE TO PRACTICE IS THIS NEWS? Endocrine General Internal Medicine-Primary Care(US) General Practice(GP)/Family Practice(FP) Internal Medicine Save Article Delete Article Email this article to a colleague Printer Friendly Version Abstract BACKGROUND: Ischaemic heart disease (IHD) is a major cause of mortality and morbidity and its prevalence is set to increase. Secondary prevention aims to prevent subsequent acute events in people with established IHD. While the benefits of individual medical and lifestyle interventions is established, the effectiveness of interventions which seek to improve the way secondary preventive care is delivered in primary care or community settings is less so. OBJECTIVES: To assess the effectiveness of service organisation interventions, identifying which types and elements of service change are associated with most improvement in clinician and patient adherence to secondary prevention recommendations relating to risk factor levels and monitoring (blood pressure, cholesterol and lifestyle factors such as diet, exercise, smoking and obesity) and appropriate prophylactic medication. SEARCH STRATEGY: We searched the Cochrane Central Register of Controlled Trials (CENTRAL, The Cochrane Library 2007, Issue 4), MEDLINE (1966 to Feb 2008), EMBASE (1980 to Feb 2008), and CINAHL (1981 to Feb 2008). Bibliographies were checked. No language restrictions were applied. SELECTION CRITERIA: Randomised or quasi-randomised controlled trials of service organisation interventions in primary care or community settings in populations with established IHD. DATA COLLECTION AND ANALYSIS: Analyses were conducted according to Cochrane recommendations and Odds Ratios (with 95% confidence intervals) reported for dichotomous outcomes, mean differences (with 95% CIs) for continuous outcomes. MAIN RESULTS: Eleven studies involving 12,074 people with IHD were included. Increased proportions of patients with total cholesterol levels within recommended levels at 12 months, OR 1.90 (1.04 to 3.48), were associated with interventions that included regular planned appointments, patient education and structured monitoring of medication and risk factors, but significant heterogeneity was apparent. Results relating to blood pressure within target levels bordered on statistical significance. There were no significant effects of interventions on mean blood pressure or cholesterol levels, prescribing, smoking status or body mass index. Few data were available on the effect on diet. There was some suggestion of a ``ceiling effect`` whereby interventions have a diminishing beneficial effect once certain levels of risk factor management are reached. AUTHORS` CONCLUSIONS: There is weak evidence that regular planned recall of patients for appointments, structured monitoring of risk factors and prescribing, and education for patients can be effective in increasing the proportions of patients within target levels for cholesterol control and blood pressure. Further research in this area would benefit from greater standardisation of the outcomes measured.
知识发现平台： http://arrowsmith.psych.uic.edu/cgi-bin/arrowsmith_uic/show_sentences.cgi 检索策略：parkinson disease and embryonic stem cells 发现的相关研究报道： AB literature B-term BC literature Mitochondrial gene replacement... parkinson disease embryonic stem cells 1: Protection by the NDI1 gene against neurodegeneration in a rotenone rat model of Parkinson's disease .2008 Add to clipboard 2: 2004 Add to clipboard 3: Neuroprotective gene therapy for Parkinson's disease .2002 Add to clipboard 4: Mitochondrial ND1 sequence analysis and association of the T4216C mutation with Parkinson's disease .2000 Add to clipboard 1: The role of Lmx1a in the differentiation of human embryonic stem cells into midbrain dopamine neurons in culture and after transplantation into a Parkinson's disease model.2009 Add to clipboard 2: Cell replacement therapy for Parkinson's disease .2009 Add to clipboard 3: 2009 Add to clipboard 4: Nuclear transfer embryonic stem cells provide an in vitro culture model for Parkinson's disease .2009 Add to clipboard 5: Survival and early functional integration of dopaminergic progenitor cells following transplantation in a rat model of Parkinson's disease .2009 Add to clipboard 6: Granulocyte-macrophage colony-stimulating factor promotes survival of dopaminergic neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced murine Parkinson's disease model.2009 Add to clipboard 7: Multitracer assessment of dopamine function after transplantation of embryonic stem cell-derived neural stem cells in a primate model of Parkinson's disease .2009 Add to clipboard 8: Prospects of stem cell therapy for replacing dopamine neurons in Parkinson's disease .2009 Add to clipboard 9: Effects of GDNF pretreatment on function and survival of transplanted fetal ventral mesencephalic cells in the 6-OHDA rat model of Parkinson's disease .2009 Add to clipboard 10: Treatment of Parkinson's disease model mice with allogeneic embryonic stem cells : necessity of immunosuppressive treatment for sustained improvement.2009 Add to clipboard 11: Autologous neural stem cell transplantation: A new treatment option for Parkinson's disease ?2009 Add to clipboard 12: Bone marrow-derived mesenchymal stem cell therapy as a candidate disease-modifying strategy in Parkinson's disease and multiple system atrophy.2009 Add to clipboard 13: Parkinson's disease .2009 Add to clipboard 14: Future directions: use of interventional MRI for cell-based therapy of Parkinson disease .2009 Add to clipboard 15: Cells therapy for Parkinson's disease -so close and so far away.2009 Add to clipboard 16: The search for a curative cell therapy in Parkinson's disease .2008 Add to clipboard 17: From bench to bed: the potential of stem cells for the treatment of Parkinson's disease .2008 Add to clipboard 18: Comparison of the therapeutic potential of adult and embryonic neural precursor cells in a rat model of Parkinson disease .2008 Add to clipboard 19: Survival, differentiation, and migration of bioreactor-expanded human neural precursor cells in a model of Parkinson disease in rats.2008 Add to clipboard 20: DJ-1-binding compounds prevent oxidative stress-induced cell death and movement defect in Parkinson's disease model rats.2008 Add to clipboard 21: Embryonic stem cell-derived Pitx3-enhanced green fluorescent protein midbrain dopamine neurons survive enrichment by fluorescence-activated cell sorting and function in an animal model of Parkinson's disease .2008 Add to clipboard 22: Embryonic stem cells and Parkinson's disease : cell transplantation to cell therapy.2008 Add to clipboard 23: Therapeutic potentials of human embryonic stem cells in Parkinson's disease .2008 Add to clipboard 24: Human neural stem cells migrate along the nigrostriatal pathway in a primate model of Parkinson's disease .2008 Add to clipboard 25: 2008 Add to clipboard 26: Stem cells and Parkinson's disease : toward a treatment, not a cure.2008 Add to clipboard 27: Functional effect of FGF2- and FGF8-expanded ventral mesencephalic precursor cells in a rat model of Parkinson's disease .2008 Add to clipboard 28: Emerging restorative treatments for Parkinson's disease .2008 Add to clipboard 29: Parthenogenetic dopamine neurons from primate embryonic stem cells restore function in experimental Parkinson's disease .2008 Add to clipboard 30: 2008 Add to clipboard 31: Persistent dopamine functions of neurons derived from embryonic stem cells in a rodent model of Parkinson disease .2007 Add to clipboard 32: Benefits, risks and ethical considerations in translation of stem cell research to clinical applications in Parkinson's disease .2007 Add to clipboard 33: Neural-tube-derived neuroepithelial stem cells: a new transplant resource for Parkinson's disease .2007 Add to clipboard 34: Current advances in the treatment of Parkinson's disease with stem cells.2007 Add to clipboard 35: Stem cell therapy for Parkinson's disease .2007 Add to clipboard 36: 2007 Add to clipboard 37: The future of cell therapies in the treatment of Parkinson's disease .2007 Add to clipboard 38: Restorative cell therapy for Parkinson's disease : a quest for the perfect cell.2007 Add to clipboard 39: Stem cell transplantation: a promising therapy for Parkinson's disease .2007 Add to clipboard 40: Cell transplantation for patients with Parkinson's disease .2006 Add to clipboard 41: Activation of p53 signaling initiates apoptotic death in a cellular model of Parkinson's disease .2006 Add to clipboard 42: Transplantation of human embryonic stem cell-derived cells to a rat model of Parkinson's disease : effect of in vitro differentiation on graft survival and teratoma formation.2006 Add to clipboard 43: Embryonic stem cell-derived neuron models of Parkinson's disease exhibit delayed neuronal death.2006 Add to clipboard 44: Stem cell therapy for Parkinson's disease .2006 Add to clipboard 45: Enriched NCAM-positive cells form functional dopaminergic neurons in the rat model of Parkinson's disease .2006 Add to clipboard 46: Transplanted human neural precursor cells migrate widely but show no lesion-specific tropism in the 6-hydroxydopamine rat model of Parkinson's disease .2006 Add to clipboard 47: Potential application of embryonic stem cells in Parkinson's disease : drug screening and cell therapy.2006 Add to clipboard 48: Neural precursor cells differentiated from mouse embryonic stem cells relieve symptomatic motor behavior in a rat model of Parkinson's disease .2005 Add to clipboard 49: Stem cells may reshape the prospect of Parkinson's disease therapy.2005 Add to clipboard 50: Cripto as a target for improving embryonic stem cell-based therapy in Parkinson's disease .2005 Add to clipboard 51: Cell therapy for Parkinson's disease : problems and prospects.2005 Add to clipboard 52: Regenerative medicine in Parkinson's disease : generation of mesencephalic dopaminergic cells from embryonic stem cells .2005 Add to clipboard 53: Embryonic stem cells as a cell source for treating Parkinson's disease .2005 Add to clipboard 54: Stem cell-based therapy for Parkinson's disease .2005 Add to clipboard 55: Differentiation and migration of long term expanded human neural progenitors in a partial lesion model of Parkinson's disease .2004 Add to clipboard 56: The cellular repair of the brain in Parkinson's disease --past, present and future.2004 Add to clipboard 57: Cell transplantation for Parkinson's disease : present status.2004 Add to clipboard 58: Efficient induction of dopaminergic neurons from embryonic stem cells for application to Parkinson's disease .2004 Add to clipboard 59: Stem cell therapy for Parkinson's disease : where do we stand?2004 Add to clipboard 60: 2004 Add to clipboard 61: Retraction: efficient induction of dopaminergic neurons from embryonic stem cells for application to Parkinson's disease .2004 Add to clipboard 62: 2004 Add to clipboard 63: Embryonic and adult stem cells as a source for cell therapy in Parkinson's disease .2004 Add to clipboard 64: 2003 Add to clipboard 65: Stem cells for cell therapy in Parkinson's disease .2003 Add to clipboard 66: Transplantation of expanded neural precursor cells from the developing pig ventral mesencephalon in a rat model of Parkinson's disease .2003 Add to clipboard 67: Transfer of the von Hippel-Lindau gene to neuronal progenitor cells in treatment for Parkinson's disease .2003 Add to clipboard 68: Genetically modified human embryonic stem cells relieve symptomatic motor behavior in a rat model of Parkinson's disease .2003 Add to clipboard 69: Neurotrophic factor in the treatment of Parkinson disease .2003 Add to clipboard 70: Embryonic ventral mesencephalic grafts to the substantia nigra of MPTP-treated monkeys: feasibility relevant to multiple-target grafting as a therapy for Parkinson's disease .2002 Add to clipboard 71: Will embryonic stem cells be a useful source of dopamine neurons for transplant into patients with Parkinson's disease ?2002 Add to clipboard 72: The potential for circuit reconstruction by expanded neural precursor cells explored through porcine xenografts in a rat model of Parkinson's disease .2002 Add to clipboard 73: Stem cells in the treatment of Parkinson's disease .2002 Add to clipboard 74: Dopamine neurons derived from embryonic stem cells function in an animal model of Parkinson's disease .2002 Add to clipboard 75: Effects of antioxidant pretreatment on the survival of embryonic dopaminergic neurons in vitro and following grafting in an animal model of Parkinson's disease .2002 Add to clipboard 76: Neural stem cells and Parkinson's disease .2002 Add to clipboard 77: Current state of stem cell research for the treatment of Parkinson's disease .2002 Add to clipboard 78: Role of cell therapy in Parkinson disease .2002 Add to clipboard 79: A clonal line of mesencephalic progenitor cells converted to dopamine neurons by hematopoietic cytokines: a source of cells for transplantation in Parkinson's disease .2001 Add to clipboard 80: Promotion of survival and regeneration of nigral dopamine neurons in a rat model of Parkinson's disease after implantation of embryonal carcinoma-derived neurons genetically engineered to produce glial cell line-derived neurotrophic factor.2000 Add to clipboard 信息分析平台： http://www.gopubmed.org/web/gopubmed/WEB10O00d000j100300.y 检索策略：parkinson disease and embryonic stem cells 信息分析结果如下： Top Years Publications 2007 25 2008 23 2004 20 2006 18 2009 17 2002 15 2003 10 2005 9 2001 5 2000 5 1997 2 1996 1 1 2 Top Countries Publications USA 40 Japan 22 United Kingdom 15 Sweden 15 Germany 12 South Korea 7 China 5 Switzerland 4 France 3 Israel 2 Canada 2 Netherlands 2 Spain 2 Belgium 1 Denmark 1 India 1 Australia 1 Italy 1 Mexico 1 Czech Republic 1 1 2 1 2 3 Top Cities Publications Lund 12 Kyoto 10 Cambridge 9 Belmont, MA, USA 7 New York 6 Denver 4 Cologne 4 London 3 Stockholm 3 Philadelphia 3 Bethesda 3 Seoul 3 San Francisco 2 Berne 2 Tochigi 2 Leipzig 2 Beijing 2 Madison 2 Los Angeles 2 Chicago 2 1 2 3 1 2 3 ... 6 Top Journals Publications Stem Cells 12 Brain Res 4 Rinsho Shinkeigaku 3 Neurosurg Focus 3 J Neurosurg 3 Nat Med 3 Cell Transplant 2 Proc Natl Acad Sci U S A 2 Stem Cells Dev 2 Eur J Neurosci 2 Parkinsonism Relat D 2 J Gerontol A-biol 2 Exp Neurol 2 Plos Biol 2 J Clin Invest 2 Cell Tissue Res 2 Expert Opin Biol Ther 2 Neurol Surg Tokyo 2 Regen Med 2 Neurochem Res 2 1 2 3 ... 6 1 2 3 ... 29 Top Authors Publications Barker R 7 Isacson O 7 Brundin P 6 Li J 5 Dunnett S 5 Beal M 4 Svendsen C 3 McKay R 3 Arenas E 3 Lindvall O 3 Morizane A 3 Tyers P 3 Hescheler J 3 Snchez Pernaute R 3 Schwarz J 3 Fukuda H 3 Takahashi J 3 Kim K 3 Chung S 3 Sasai Y 2 1 2 3 ... 29 1 2 3 ... 54 Top Terms Publications Parkinson Disease 150 Neurons 124 stem cell differentiation 123 Animals 122 stem cell development 121 Humans 112 Dopamine 87 Stem Cells 78 Stem Cell Transplantation 77 Cell Differentiation 69 Tissues 65 Tissue Therapy 57 Cell Transplantation 51 Rats 49 Mesencephalon 44 Patients 42 Mice 42 Embryonic Stem Cells 41 Therapeutics 39 Neurodegenerative Diseases 36 1 2 3 ... 54
标签: disease
