经济学人203:衰老 青春永驻?

 　　Science and technology

　　科学技术
　　Ageing
　　衰老
　　Forever young?
　　青春永驻？
　　A way to counteract 1 part of the process of growing old
　　一个减缓衰老进程的途径
　　BIOLOGISTS have made a lot of progress in understanding ageing.
　　在对人类衰老过程的探索中生物学家们取得了长足的进步。
　　They have not, however, been able to do much about slowing it down.
　　可是如何减缓衰老他们还没有太多的办法。
　　Particular versions of certain genes 3 have been shown to prolong life,
　　与延长寿命相关的特定基因已经找到，
　　but that is no help to those who do not have them.
　　但这还帮不了那些此段基因缺失的人。
　　A piece of work reported in this week's Nature by Darren Baker 4 of the Mayo Clinic, in Minnesota, though, describes an extraordinary result that points to a way the process might be ameliorated.
　　本周《自然》杂志发表了明尼苏达州梅奥诊所的Dr.Darren Baker的一项实验报告，描述了其所采取的方法使得衰老进程得到改善，结果非常好。
　　Dr Baker has shown—in mice, at least—that ageing body cells not only suffer themselves,
　　至少在实验小白鼠体内是这样，
　　but also have adverse 5 effects on otherwise healthy cells around them.
　　Dr.Barker称体细胞不仅自己逐渐衰老,还将不利的影响传达到周围健康的细胞。
　　More significantly, he has shown that if such ageing cells are selectively destroyed, these adverse effects go away.
　　更神奇的是，如果这些衰老的细胞被人为破坏掉，它们对健康细胞的负面影响也会随之消失。
　　The story starts with an observation, made a few years ago, that senescent cells often produce a molecule 6 called P16INK4A.
　　故事还得从几年前的一项实验开始讲起，他们观察到衰老的细胞通常会产生一种叫P16INK4A的分子。
　　Most body cells have an upper limit on the number of times they can divide—and thus multiply in number.
　　大部分体细胞分裂次数会有一个上限－数量的翻倍，
　　P16INK4A is part of the control mechanism 7 that brings cell division to a halt when this limit is reached.
　　当这个上限接近时，P16INK4A作为控制机制的一部分会使细胞的分裂停止。
　　The Hayflick limit, as the upper bound is known, is believed to be an anticancer mechanism.
　　海弗利克极限，即我们所知的上限现在认为可作为一种抗癌机制，
　　It provides a backstop that prevents a runaway 8 cell line from reproducing indefinitely, and thus becoming a tumour 9.
　　它可以拦截、阻断细胞链的无限期、失常的增生，正是这种失常的增生形成了肿瘤。
　　The limit varies from species to species—in humans, it is about 60 divisions—and its size is correlated with the lifespan of the animal concerned.
　　这种极限随物种不同而不同，人类大致的分裂次数上限是60次，极限的大小与相应动物的预期生命期限有关。
　　Hayflick-limited cells thus accumulate as an animal ages, and many biologists believe they are one of the things which control maximum lifespan. Dr Baker's experiment suggests this is correct.
　　细胞的海弗利克极限累加就是动物的寿命长度，很多的生物学家推测它们控制着生命期限最长值。Dr.Barker的实验证明了推测是正确的。
　　Age shall not weary them
　　老而未衰的器官
　　Dr Baker genetically 11 engineered a group of mice that were already quite unusual.
　　Dr. Baker 通过基因工程处理的一组小白鼠非常特别，
　　They had a condition called progeria, meaning that they aged 12 much more rapidly than normal mice.
　　它们的症状也称早老症，意味着它们比一般的小白鼠衰老的更快。
　　The extra tweak he added to the DNA 13 of these mice was a way of killing 14 cells that produce P16INK4A. He did this by inserting into the animals' DNA, near the gene 2 for P16INK4A, a second gene that was,
　　他在这些小白鼠的DNA中加入了可杀死能产生P16INK4A分子的细胞的特别基因，具体做法是在实验小白鼠P16INK4A旁边的基因插入另一段动物基因，
　　because of this proximity 15, controlled by the same genetic 10 switch.
　　因为在它旁边，第二段基因也受相同的遗传开关控制。
　　This second gene, activated 16 whenever the gene for P16INK4A was active, produced a protein that was harmless in itself,
　　这第二段基因编码产生的蛋白质对自身无害，但在特殊的药物作用下，它就会变的很致命，只要P16INK4A分子有活性它就能被激活。
　　but which could be made deadly by the presence of a particular drug. Giving a mouse this drug, then, would kill cells which had reached their Hayflick limits while leaving other cells untouched. Dr Baker raised his mice, administered the drug, and watched.
　　给实验小白鼠服用这种药后，就会杀死那些接近海弗利克极限的细胞，其它细胞则完好无损。 Dr Baker 培养这些小白鼠,给它们服用药物后，观察它们。
　　The results were spectacular.
　　结果是出人意料的。
　　Mice given the drug every three days from birth suffered far less age-related body-wasting than those which were not.
　　小白鼠出生后每3天给一次药,服药小白鼠比没服药小白鼠的与衰老相关的机体耗损要少的多。
　　They lost less fatty tissue. Their muscles remained plump.
　　它们耗损的脂肪组织更少，肌肉丰满,
　　And they did not suffer cataracts 17 of the eye.
　　并且都没患上白内障。
　　They did, though, continue to experience age-related problems in tissues that do not produce P16INK4A as they get old.
　　接下来，他们还对那些老化的但并没有出现P16INK4A分子的器官也进行了衰老相关问题的实验，
　　In particular, their hearts and blood vessels 18 aged normally.
　　特别是它们的心脏和血管，老化的进程很正常，
　　For that reason, since heart failure is the main cause of death in such mice, their lifespans were not extended.
　　小白鼠的主要是死因心脏衰竭，所以它们的预期寿命不会再延长了。
　　The drug, Dr Baker found, produced some benefit even if it was administered to a mouse only later in life.
　　Dr Baker发现，这种药物即使是饲喂给生命快到尽头的的小白鼠也会有一定的疗效，
　　Though it could not clear cataracts that had already formed, it partly reversed muscle-wasting and fatty-tissue loss.
　　尽管对已经形成的白内障没法再变回清澈，但能使肌肉及脂肪组织的耗损部分得以缓解，
　　Such mice were thus healthier than their untreated confrères.
　　这些小白鼠因此比没有服药的更健康。
　　Analysis of tissue from mice killed during the course of the experiment showed that the drug was having its intended effect.
　　对那些在实验中死亡小白鼠的组织进行分析发现，药物达到了预期的效果。
　　Cells producing P16INK4A were killed and cleared away as they appeared.
　　细胞一旦产生了P16INK4A分子就立即被杀死了。
　　Dr Baker's results therefore support the previously 19 untested hypothesis that not only do cells which are at the Hayflick limit stop working well themselves,
　　因此这一结果证实了早先未被验证的推测，即，达到海弗利克极限的细胞不仅自身的不再正常运作。
　　they also have malign 20 effects on their otherwise healthy neighbours.
　　还会还会把负面的影响带给周围正常的细胞。
　　Regardless of the biochemical details, the most intriguing 21 thing Dr Baker's result provides:
　　先不管其中生化方面的细节，Dr.Baker的实验结论最引人入胜的是：
　　is a new way of thinking about how to slow the process of ageing—and one that works with the grain of nature, rather than against it.
　　人类有了延缓衰老进程的新方法－与其抗衡，不如顺应自然法则。
　　Existing lines of inquiry 22 into prolonging lifespan are based either on removing the Hayflick limit, which would have all sorts of untoward 23 consequences, or suppressing production of the oxidative chemicals that are believed to cause much of the cellular 24 damage which is bracketed together and labelled as senescence.
　　延长预期寿命现有的办法，一是通过消除细胞的海弗利克极限，这可能会出现各种不利的后果。
　　But these chemicals are a by-product 25 of the metabolic 26 activity that powers the body.
　　二是抑制体内氧化物水平。氧化物被认为是引起细胞损伤的元凶，和细胞衰老划等号的一个词，但这些化学物质本身就是给身体提供能量的代谢活动所产生的副产品。
　　If 4 billion years of natural selection have not dealt with them it suggests that suppressing them may have worse consequences than not suppressing them.
　　如果40亿年前的自然选择都没有摒弃这体内的代谢副产品，那就意味着抑制它们可能比不抑制它们所带来的后果更严重。
　　By contrast, actually eliminating senescent cells may be a logical extension of the process of shutting them down, and thus may not have adverse consequences.
　　相反的，真正的消除掉衰老细胞可能是延长机体细胞正常运作的一个符合逻辑的作法,也不会再有不利结果了。
　　It is not an elixir 27 of life, for eventually the body will run out of cells, as more and more of them reach their Hayflick limits.
　　世上没有生命可以长生不老，随着机体内越来越多的细胞到了自己的海弗利克极限，最终，机体也就到了消亡的那一天。
　　But it could be a way of providing a healthier and more robust 28 old age than people currently enjoy.
　　但是未来的我们可能会比现在更健康、更有活力的老去。
　　Genetically engineering people in the way that Dr Baker engineered his mice is obviously out of the question for the foreseeable future.
　　毫无疑问，在可预见的未来某天，Dr. Baker在小白鼠身上采用的基因技术就能应用在人类身上。
　　But if some other means of clearing cells rich in P16INK4A from the body could be found, it might have the desired effect.
　　但如果还能找到其它方法消除体内富含P16INK4A分子的细胞，那可能才是我们期望的效果。
　　The wasting and weakening of the tissues that accompanies senescence would be a thing of the past, and old age could then truly become ripe.
　　伴随着衰老而产生的机体组织耗损、衰弱都将成为过去，年老只意味着真正意义上的成熟！
　　1.counteract v.抵制；清除；中和；对抗
　　We must counteract extremism in the party.
　　我们应该抵制党内的极端主义。
　　2.extraordinary a.非凡的；特别的；特派的
　　He has an extraordinary memory.
　　他有非凡的记忆力。
　　3.significant a.重要的；有意义的；意味深长的
　　The question under discussion is significant.
　　讨论中的问题是重要的。
　　4.molecule n.分子；微粒
　　A molecule is made up of atoms.
　　分子由原子组成。
　　5.mechanism n.机制；原理
　　The WTO provides a mechanism for resolving trade disputes.
　　世贸组织提供了一种解决贸易争端的机制。