过去已有无数证据表明节食即热量限制(calorie restriction)能延长动物寿命,也能改善人的代谢状况,如增强胰岛素敏感性,避免发生糖尿病和心血管病,还能降低患癌风险。至于节食对于免疫系统尤其是免疫细胞功能的影响,目前还所知甚少。 最近,英国伦敦大学学院与西班牙科学家在《自然—免疫学》(Nature Immunology)上发表论文称,营养、代谢和免疫均参与衰老过程,并证明营养与衰老信号共同调节T淋巴细胞功能,从而打消了人们长期以来对它们是否有关联的疑虑。 当人衰老时,免疫功能下降,患传染病和得癌症的机会增大,而且严重程度也增加。同时,接种疫苗的抗病效果会随年龄增长而降低。导致这个现象的根本原因是T细胞的衰老,而采用丝裂原激活蛋白的激酶( MAPK) p38 抑制剂可以逆转 T细胞衰老,提示可以通过药物控制免疫功能因 衰老而下降。 该研究发现,T细胞中的p38可被低水平营养和DNA损伤信号所激活,从而自动发生磷酸化。低营养与基因损伤对p38的活化依赖AMP激酶(AMPK)及骨架蛋白TAB1的共同作用,从而 抑制 端粒酶活性、T细胞增殖和T细胞抗原受体(TCR)表达。 由 英国癌症研究院、 伦敦大学学院、牛津大学 和 意大利科学家在《临床调查杂志 》(JCI)发表的 一篇最新论文也表明,抑制p38的激活可以恢复衰老T细胞的免疫功能,包括促进线粒体增殖和细胞分裂,而这得益于自噬活性增强。 由此可见,p38的活性可以通过药物或食物进行控制。现在已有制药公司研制出p38抑制剂,用于缓解慢性炎症。但是,通过食物调节p38的活性更健康和更简便。由于p38可被低营养(饥饿)激活,故在日常生活中 老年人 应注意加强营养,而不是经常节食或天天素食。 Are you as old as what you eat? Researchers learn how to rejuvenate aging immune cells Date: August 24, 2014 Source: Biotechnology and Biological Sciences Research Council Summary: Researchers have demonstrated how an interplay between nutrition, metabolism and immunity is involved in the process of aging. It has been suspected for a long time that these are linked, and this paper provides a prototype mechanism of how nutrient and senescence signals converge to regulate the function of T lymphocytes. Researchers from UCL (University College London) have demonstrated how an interplay between nutrition, metabolism and immunity is involved in the process of aging. The two new studies, supported by the Biotechnology and Biological Sciences Research Council (BBSRC), could help to enhance our immunity to disease through dietary intervention and help make existing immune system therapies more effective. As we age our immune systems decline. Older people suffer from increased incidence and severity of both infections and cancer. In addition, vaccination becomes less efficient with age. In previous BBSRC funded work, Professor Arne Akbar's group at UCL showed that aging in immune system cells known as 'T lymphocytes' was controlled by a molecule called 'p38 MAPK' that acts as a brake to prevent certain cellular functions. They found that this braking action could be reversed by using a p38 MAPK inhibitor, suggesting the possibility of rejuvenating old T cells using drug treatment. In a new study published in Nature Immunology the group shows that p38 MAPK is activated by low nutrient levels, coupled with signals associated with age, or senescence, within the cell. It has been suspected for a long time that nutrition, metabolism and immunity are linked and this paper provides a prototype mechanism of how nutrient and senescence signals converge to regulate the function of T lymphocytes. The study also suggests that the function of old T lymphocytes could be reconstituted by blocking one of several molecules involved in the process. The research was conducted at UCL alongside colleagues from Complejo Hospitalario de Navarra, Pamplona, Spain. The second paper, published in The Journal of Clinical Investigation, showed that blocking p38 MAPK boosted the fitness of cells that had shown signs of aging; improving the function of mitochondria (the cellular batteries) and enhancing their ability to divide. Extra energy for the cell to divide was generated by the recycling of intracellular molecules, a process known as autophagy. This highlights the existence of a common signaling pathway in old/senescent T lymphocytes that controls their immune function as well as metabolism, further underscoring the intimate association between aging and metabolism of T lymphocytes. This study was conducted by researchers from UCL, Cancer Research UK, University of Oxford and University of Tor Vergata, Rome, Italy. Professor Arne Akbar said: Our life expectancy at birth is now twice as long as it was 150 years ago and our lifespans are on the increase. Healthcare costs associated with aging are immense and there will be an increasing number of older people in our population who will have a lower quality of life due in part to immune decline. It is therefore essential to understand reasons why immunity decreases and whether it is possible to counteract some of these changes. An important question is whether this knowledge can be used to enhance immunity during aging. Many drug companies have already developed p38 inhibitors in attempts to treat inflammatory diseases. One new possibility for their use is that these compounds could be used to enhance immunity in older subjects. Another possibility is that dietary instead of drug intervention could be used to enhance immunity since metabolism and senescence are two sides of the same coin. Story Source: The above story is based on materials provided by Biotechnology and Biological Sciences Research Council . Note: Materials may be edited for content and length. Journal Reference : Alessio Lanna, Sian M Henson, David Escors, Arne N Akbar. The kinase p38 activated by the metabolic regulator AMPK and scaffold TAB1 drives the senescence of human T cells . Nature Immunology , 2014; DOI: 10.1038/ni.2981
夏季温差变化影响老人死亡率 美国哈佛大学公共卫生学院的研究者日前报告说,夏季最高温度与最低温度之差如果显著拉大,有可能提高老年慢性病患者的死亡率。 这份发表在美国《国家科学院院刊》( PNAS )的报告指出,研究人员利用美国“医疗保健”系统在1985年至2006年间收集的数据,追踪研究约370万名65岁以上慢性病患者的长期健康状况。排除其他影响因素后,研究人员发现,在这些老人居住的135个城市中,如遇上夏季温差变化较大的年份,老人的死亡率会随之升高。 总体而言,夏季温差每升高1摄氏度,老年慢性病患者的死亡率平均增加2.8%至4%,其中糖尿病患者死亡率增加4%,心脏病患者的死亡率增加3.8%,这一几率在慢性肺病和心衰患者中则分别增加3.7%和2.8%。 科学界近年来预测,气候变化不仅会提升全球气温,而且会扩大夏季气温变化幅度,特别是在中纬度地区。这项新研究结果说明,这种温差变化可能引起公共卫生问题。 报告作者之一、哈佛大学教授乔尔·施瓦茨说,人们不容易适应异常的气温变化,随着人口老化,糖尿病等慢性病的患病比例逐渐增高,气候变化导致更多异常气温波动,这类公共卫生问题可能变得越发突出。(来源:新华社 任海军) Summer temperature variability and long-term survival among elderly people with chronic disease meijin 添加于 2012-4-13 15:28:50 27次阅读 | 0次推荐 | 0个评论 Time series studies show that hot temperatures are associated with increased death rates in the short term. In light of evidence of adaptation to usual temperature but higher deaths at unusual temperatures, a long-term exposure relevant to mortality might be summertime temperature variability, which is expected to increase with climate change. We investigated whether the standard deviation (SD) of summer (June–August) temperatures was associated with survival in four cohorts of persons over age 65 y with predisposing diseases in 135 US cities. Using Medicare data (1985–2006), we constructed cohorts of persons hospitalized with chronic obstructive pulmonary disease, diabetes, congestive heart failure, and myocardial infarction. City-specific yearly summer temperature variance was linked to the individuals during follow-up in each city and was treated as a time-varying exposure. We applied a Cox proportional hazard model for each cohort within each city, adjusting for individual risk factors, wintertime temperature variance, yearly ozone levels, and long-term trends, to estimate the chronic effects on mortality of long-term exposure to summer temperature SD, and then pooled results across cities. Mortality hazard ratios ranged from 1.028 (95% confidence interval, 1.013– 1.042) per 1 °C increase in summer temperature SD for persons with congestive heart failure to 1.040 (95% confidence interval, 1.022–1.059) per 1 °C increase for those with diabetes. Associations were higher in elderly persons and lower in cities with a higher percentage of land with green surface. Our data suggest that long-term increases in temperature variability may increase the risk of mortality in different subgroups of susceptible older populations. 作 者: Zanobetti, Antonella; O'Neill, Marie S.; Gronlund, Carina J.; Schwartz, Joel D. 期刊名称: Proceedings of the National Academy of Sciences 期卷页: 第卷 第期 ~页 学科领域: 医学科学 老年医学 老年医学 添加人是否为作者: 否 原文链接: http://www.pnas.org/content/early/2012/04/03/1113070109.abstract DOI: 10.1073/pnas.1113070109 ISBN: 0027-8424 关键词: 备 注:
青蒿素的研究充分体现了当时全国一盘棋,大会战的特色。单纯的归功于某一个或者某几个人是不合适的。 老人们经常回忆起当年搞青蒿素的情形,基本上半个中国的力量都动用了。 听中药所的同行说过一些情况,当时屠教授的一些研究不是她完成的——她也没这个能力完成,是所长书记出面协调,请动某些大佬搞的,中药所加实验药厂为了青蒿素搞攻关会战,人人参与。 结果,最后,光荣属于一个人。屠做人上也不是没有缺陷,据说青蒿素被她视为禁脔,不许别人研究。不说国内其他单位,就是本单位对她不满的人也很多。 她评院士,评过两次,每次消息传来,老人们都会说,她得罪的人太多,不可能评上。果然! 评院士不是评水平,而是“”评得罪的人多少”。 你也承认屠教授没评上院士,不是因为她的贡献和水平,而是得罪了你们这帮人。 换句话,如果她把成就拱手相让,那么早就是院士了。什么逻辑! 她曾几次获院士提名 默默无闻多年后得到这么多关注,是“时来运转”吗?非也。 青蒿素类抗疟药是中国唯一被世界承认的原创新药。 当年青蒿素类抗疟药最主要的一群发现者,如今无一人做大官,无一人成富翁,无一人当院士。 屠呦呦教授也曾经几次被提名院士,但始终没有当选。 不过为“五二三”付出的心血,她始终无怨无悔。 http://blog.sina.com.cn/s/blog_65674ed00100i3k1.html Artemisia annua L and Artemisinin Medicines – A Scientific White Paper in Anti-Malaria History 《青蒿及青蒿素类药物》 - 一本抗疟史上的科技白皮书 - Artemisinin (青蒿素)博客 Artemisia annua L and Artemisinin Medicines authored by Professor You You Tu and published by China Chemical Industry Press records the details of how Artemisinin ( 青蒿素 pronounced as Qinghaosu in Chinese) – a potent anti-malaria compound was discovered by professor Tu in 1972 and a series of medicines derived from Artemisinin had beendeveloped by Professor Tu’s team and other scientists in China since its discovery. The book, based on sound scientific evidence, tells the world a true, yet mystery discovery history and highlights the successful outcomes of exploring ancient Traditional Chinese Medicine legacy through wisdom and hard workcontributed bycontemporary Chinese pharmaceutical scientists. The book covers wide range of scientific information, including Botany, Phytochemistry, Synthetic Chemistry, Analytical Chemistry around Artemisia annua L and Artemisinin Medicines as well as detailed data package generated during the course of new drug development. Professor Tu was the first scientist who established that a mixture extractedfrom Artemisia annua L leave byher unique isolation technique provided an effective therapy to animal models contrasted with multi-drug resistant strains of falciparum malaria. She then successfully purified artemisinin, a potent compound from the extracts in 1972. In 1986, based on her findings, she and her team launched Artemisinin as an innovative anti-malaria medicine in China after a thorough and lengthy development process. Late in 1992, she developed and launched another potent medicine Dihydroartemisinin, an Artemisinin derivative in the simplest format but yet the most effective compound among Artemisinin derivatives. Professor Tu’s achievement is well recognized both nationally and internationally. Recently, a Special Issue "Artemisinin (Qinghaosu): Commemorative Issue in Honor of Professor Youyou Tu on the Occasion of her 80th Anniversary" was published by Journal Molecules in which a number of top researchers in the fields offered their papers. It’s worth to comment that without Professor Tu’s breakthrough discovery, Human beings as a whole would have lost our battles against malaria, especially the multi-drug resistant falciparum malaria. Her achievement deserves more and much distinguishedinternational awards. Professor Tu is currently a professor and director of Qinghaosu (Artemisinin) Research Center, Institute of Chinese Materia Medica, China Academy of Chinese Medical sciences. She also serves as a fellow of China Association of Invention. 《青蒿及青蒿素类药物》由屠呦呦教授编著,中国化工出版社出版,详细记录了屠教授于 1972 年发现青蒿素的经过以及她的团队和其他中国科学家在她发现青蒿素以后所做的工作。 本书以大量的科学证据告诉了世界一段真实而神奇的历史 - 一个用中国药物科学家的智慧和努力成功开拓中华医学遗产的范例。本书覆盖了大量的资料,包括围绕植物青蒿及青蒿类药物的植物学、植物化学、合成化学、分析化学资料以及新药开发过程中大量的研究数据。 屠教授是首位发现青蒿(黄花蒿)提取物有强抗疟活性的科学家。又是她于 1972 年首先分离出有效单体 - 青蒿素。 1986 年,根据她的发现和深入开发,她和她的团队首先将青蒿素作为新药在中国上市。 1992 年,她和她的团队又将另一新药 - 双氢青蒿素,一个结构最简单但最有效的青蒿素衍生物在中国上市。 屠教授的贡献被中国及国际社会公认。最近 , 《分子学杂志》为祝贺她的贡献,在她 80 岁生日时出版了《青蒿素专辑》。许多该领域的顶尖专家为专辑供稿。 值得一提的是, 如果没有屠教授突破性发现,全人类将惨败于抗疟战场。她的成就值得更多、更高的国际嘉奖。 屠教授目前是中国中医科学院中药研究所终身研究员,青蒿素研究中心主任及中国发明协会理事 。 青蒿素的故事,考验和教育了中国科学家 http://blog.sciencenet.cn/home.php?mod=spaceuid=280034do=blogid=486631