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Science and technology
科学技术

Surviving strokes
挺过中风

Living on
继续活着

Why some cells survive strokes while others don't
为什么有些细胞能幸免于中风，而另一些则不能

WHEN dealing with a stroke—a loss of blood supply to the brain—time is of the essence.
在应对由于大脑失去血液供应造成的中风时，时间是至关重要的。

If the cause is a blocked artery, blood flow can often be restored using clot-busting drugs.
如果原因是动脉阻塞，在使用溶栓药物后，血液流动通常会恢复正常。

If those drugs are swallowed too late, however, they can do more harm than good.
然而，如果这些药物吃得过晚，那么弊大于利。

In one of nature's crueller ironies, the metabolic changes that take place in cells after about three hours without oxygen or glucose mean that restoring blood flow becomes damaging in itself.
自然的残酷讽刺是，细胞在约三个小时没有氧气或葡萄糖时所产生的代谢变化意味着恢复血流本身是具破坏性的。

This is called a reperfusion injury.
这就是所谓的再灌注损伤。

Doctors have long searched for ways to extend the period during which clot-busting pills might help.
医生一直在寻找延长溶栓药片作用时间的方法。

They have tried drugs and even artificially induced hypothermia to help the brain protect itself from the consequences of oxygen and sugar deprivation.
他们曾尝试过麻醉剂，甚至人为地诱导低体温以帮助大脑保护自身由于缺失氧气和糖所造成的后果。

Now, in a paper in Nature Medicine, a group of researchers led by Alastair Buchan, a neurologist at the University of Oxford, describe a new idea.
目前，一篇由牛津大学神经学家阿拉斯泰尔?巴肯所领导的一个研究小组在自然医学杂志中发表的文章中，描述了一个新的想法。

Dr Buchan's team began with an old medical mystery.
但巴肯博士的团队是从一个古老的医学之谜开始的。

It has been known since the 1920s that some nerve cells, or neurons, are more susceptible to stroke damage than others.
自20世纪20年代以来，就有人知道一些神经细胞或神经元比其他的更易遭中风损伤。

In particular, a group of neurons called CA3 cells that live in the hippocampus—a seahorse-shaped chunk of brain tissue involved in forming memories—are much hardier than another sort called CA1 cells, even though the two types are neighbours.
特别是，一组存在于海马状突起中称为CA3的细胞比另一种叫CA1细胞更具有耐受性，尽管这两种细胞是彼此相邻的。

Medical science is often concerned with working out why cells die, says Dr Buchan.We thought we'd look at why some seem to survive.
巴肯博士说：医学经常关注于解决细胞死亡的原因，我们想看看有些细胞幸存下来的原因。

The researchers compared versions of both types of cells taken from rats, looking for differences in their chemistry after they had been subjected to an artificial stroke.
研究人员比较了取自大鼠的这两种类型细胞的变体，以找出它们在遭受人为中风后化学成分的差异。

One conspicuous difference involved a protein called hamartin, which was present in larger amounts in the hardy CA3 cells than in the fragile CA1 cells.
一个显著的区别在于一种名为错构瘤的蛋白质，耐受性强的CA3细胞的错构瘤蛋白数量要比脆弱的CA1细胞中的多。

To check whether hamartin was indeed responsible for the CA3 cells' robustness, the researchers created in a test tube a strain of rat neurons which were unable to produce the protein, and then deprived them of oxygen and sugar for three hours.
为了检验是否错构瘤真的使CA3细胞变得更具耐受性，研究人员在试管中放入一株无法产生错构瘤的大鼠神经元，然后使它们丧失三个小时的氧气和糖。

Sure enough, cell deaths were about a third higher in the modified group than in the controls.
果然，改动组细胞的死亡率比对照组高出约三分之一。

Flipping the experiment around, neurons modified to produce more of the protein than usual had a stroke survival rate 31% higher than their unmodified counterparts.
再将该实验反过来进行，经改良比平常产生更多蛋白质的神经元的中风存活率比未经改良的高出31％。

Experiments in rats themselves showed similar results.
在大鼠身上进行的实验也显示出类似结果。

Hamartin, which is also known as a tumour suppressant, encourages a cellular recycling mechanism called autophagy.
错构瘤，也被称为肿瘤抑制剂，能促进被称为细胞自噬的细胞再生机理。

This breaks down existing bits of cellular machinery so that their chemical components can be reused elsewhere.
它能够分解现有的少量细胞组织以使这些细胞的化学成分可以在其他地方重新使用。

Autophagy presumably arose long ago as a way of helping cells survive lean times.
自噬大概很早以前就出现，作为一种帮助细胞在缺氧缺糖时存活下来的方式。

The theory is that such austerity measures also help neurons survive the hardscrabble environment of a blood-deprived brain.
该理论认为，这种紧缩措施还有助于神经元在大脑缺乏血液的贫瘠环境中存活下来。

So far, of course, the studies have been on rats rather than people.
当然，到目前为止，这些研究仅在大鼠而不是人类身上进行。

But the hippocampus is fairly similar across all of mammaldom.
但所有哺乳动物的海马状突起都完全类似。

Autophagy is a virtually universal property of cells in higher organisms, so it may well be worth investigating this process in other medical conditions in which organs are starved of blood, such as heart attacks.
细胞自噬实际上是高等生物的普遍特征，因此很值得研究它对缺乏血液的身体器官在其他身体状况下的作用，比如心脏病发作时。

And because hamartin is already known to oncologists, some preliminary pharmaceutical groundwork has already been done.
因为错构瘤已为肿瘤学家所了解，一些初步的制药基础原理已经完成。

Dr Buchan and his team are a long way from human trials, let alone a usable drug.
巴肯博士和他的团队离人体试验还有很长的路要走，更不必说可用的药物。

But they have turned up a promising lead.
但是，他们已经找到了一个有希望的线索。