金丝熊眼角出血睁不开，龙腾网熊可以冬眠

金丝熊眼角出血睁不开，龙腾网熊可以冬眠众所周知灰熊有冬眠这一习性，然而它们的肌肉却不会因为长达几个月的缺乏运动而萎缩。在Michael Gotthardt领导的研究团队的《科学报告》中，讲述了它们如何做到这一点的。灰熊的策略也可以帮助预防人类的肌肉萎缩。Grizzly bears spend many months in hibernation but their muscles do not suffer from the lack of movement. In the journal “Scientific Reports” a team led by Michael Gotthardt reports on how they manage to do this. The grizzly bears’ strategy could help prevent muscle atrophy in humans as we

正文翻译

原创翻译：龙腾网 http://www.ltaaa.com 翻译：s555555555 转载请注明出处

Grizzly bears spend many months in hibernation but their muscles do not suffer from the lack of movement. In the journal “Scientific Reports” a team led by Michael Gotthardt reports on how they manage to do this. The grizzly bears’ strategy could help prevent muscle atrophy in humans as well.

众所周知灰熊有冬眠这一习性，然而它们的肌肉却不会因为长达几个月的缺乏运动而萎缩。在Michael Gotthardt领导的研究团队的《科学报告》中，讲述了它们如何做到这一点的。灰熊的策略也可以帮助预防人类的肌肉萎缩。

A grizzly bear only knows three seasons during the year. Its time of activity starts between March and May. Around September the bear begins to eat large quantities of food. And sometime between November and January it falls into hibernation. From a physiological point of view this is the strangest time of all. The bear’s metabolism and heart rate drop rapidly. It excretes neither urine nor feces. The amount of nitrogen in the blood increases drastically and the bear becomes resistant to the hormone insulin.

一只灰熊只知道一年有三个季节。它的活动时间从三月到五月开始。九月左右，熊开始吃大量的食物蓄积能量。在十一月到一月之间的某个时候，它陷入了休眠状态。从生理的角度看，这是最奇怪的时刻。熊的新陈代谢和心率迅速下降。它既不排尿也不排泄粪便。血液中的氮含量急剧增加，而此时熊对胰岛素也不产生反应。

Understanding and copying the tricks of nature

了解和复制自然的窍门

“Muscle atrophy is a real human problem that occurs in many circumstances. We are still not very good at preventing it ” says the lead author of the study Dr. Douaa Mugahid once a member of Gotthardt’s research group and now a postdoctoral researcher in the laboratory of Professor Marc Kirschner of the Department of Systems Biology at Harvard Medical School in Boston.

“肌肉萎缩是在许多情况下都会发生真正的人类问题。而我们仍然不能很好的去应对它，”该研究的主要作者Douaa Mugahid博士说，Douaa Mugahi博士曾经是Gotthardt教授研究小组的成员，现在是波士顿哈佛医学院系统生物学系的Marc Kirschner教授实验室的博士后研究员。

“For me the beauty of our work was to learn how nature has perfected a way to maintain muscle functions under the difficult conditions of hibernation ” says Mugahid. “If we can better understand these strategies we will be able to develop novel and non-intuitive methods to better prevent and treat muscle atrophy in patients.”

Mugahid说：“对我来说，我们的工作之美在于学习自然如何完善了在困难的冬眠条件下维持肌肉功能的方法。” “如果我们能更好地理解这些策略，我们将能够开发出新颖且可靠的方法来更好地预防和治疗患者的肌肉萎缩。”

To understand the bears’ tricks the team led by Mugahid and Gotthardt examined muscle samples from grizzly bears both during and between the times of hibernation which they had received from Washington State University. “By combining cutting-edge sequencing techniques with mass spectrometry we wanted to determine which genes and proteins are upregulated or shut down both during and between the times of hibernation ” explains Gotthardt.

为了了解熊的策略，由Mugahid和Gotthardt领导的团队在数个连续的冬天里检查了灰熊的肌肉样本，这是他们从华盛顿州立大学收到的。 Gotthardt解释道：“通过将先进的测序技术与质谱分析法相结合，我们希望确定在冬眠期间以哪些基因和蛋白质被上调或关闭。”

“This task proved to be tricky – because neither the full genome nor the proteome i.e. the totality of all proteins of the grizzly bear were known ” says the MDC scientist. In a further step he and his team compared the findings with observations of humans mice and nematode worms.

MDC的科学家说：“这项任务非常棘手-因为我们既不了解完整的基因组，也不了解蛋白质组，即不知道灰熊所有的蛋白质。”下一步，他和他的团队将这些发现与人类，小鼠和线虫蠕虫的观察结果进行了比较。

Tissue samples from bedridden patients

In order to find out which signaling pathways need to be activated in the muscle Gotthardt and his team compared the activity of genes in grizzly bears humans and mice. The required data came from elderly or bedridden patients and from mice suffering from muscle atrophy – for example as a result of reduced movement after the application of a plaster cast. “We wanted to find out which genes are regulated differently between animals that hibernate and those that do not ” explains Gotthardt.

为了找出哪些信号通路需要在肌肉中激活，Gotthardt和他的团队比较了灰熊，人类和小鼠中基因的活性。所需数据来自老年患者或卧床不起的患者以及患有肌肉萎缩症的小鼠，例如打了石膏之后活动减少的病患。 Gotthardt解释说：“我们想找出相比于那些不冬眠的动物，冬眠动物的基因有哪些受到了调控。”

However the scientists came across a whole series of such genes. To narrow down the possible candidates that could prove to be a starting point for muscle atrophy therapy the team subsequently carried out experiments with nematode worms. “In worms individual genes can be deactivated relatively easily and one can quickly see what effects this has on muscle growth ” explains Gotthardt.

但是，科学家们遇到了一系列这样的基因。为了缩小可能被证明是肌肉萎缩治疗起点的候选对象范围，研究小组随后进行了线虫蠕虫实验。 Gotthardt解释说：“在蠕虫中，单个基因可以相对轻松地失活，并且可以迅速看到其对肌肉生长的影响。”

A gene for circadian rhythms

With the help of these experiments his team has now found a handful of genes whose influence they hope to further investigate in future experiments with mice. These include the genes Pdk4 and Serpinf1 which are involved in glucose and amino acid metabolism and the gene Rora which contributes to the development of circadian rhythms. “We will now examine the effects of deactivating these genes ” says Gotthardt. “After all they are only suitable as therapeutic targets if there are either limited side effects or none at all.”

在这些实验的帮助下，他的团队现在已经发现了一些基因，他们希望通过这些基因的影响来进一步研究小鼠。其中包括参与葡萄糖和氨基酸代谢的基因Pdk4和Serpinf1，以及有助于昼夜节律发展的基因Rora。 Gotthardt说：“我们现在将研究使这些基因失活的作用。” “毕竟，只有在副作用有限或根本没有副作用的情况下，它们才适合作为靶向治疗。”

评论翻译

原创翻译：龙腾网 http://www.ltaaa.com 翻译：s555555555 转载请注明出处

[–]At_Work_SND_Coffee

I wonder if this might be able to give us a way to defeat muscle atrophy for coma patients and anyone working in space for long duration''s of time.

我想知道这是否能为我们提供一种治疗肌肉萎缩的方法来治愈那些长期昏迷的病人和任何长期在太空工作的人。

[–]BocceBaller42[S]

The article mentions that attempts to take supplements hasn''t helped bedridden patients and that a key difference is the bears make/deliver the amino acids themselves to the spots that need it.

这篇文章有提到，尝试服用补充剂对卧床不起的病人没有帮助，关键的区别是熊自己制造/运送氨基酸到需要它的地方。

[–]At_Work_SND_Coffee

Sounds like something we''ll need to build our medical monitoring equipment around if we can identify these things it will result in easier recovery for coma/paralysis victims and space travelers.

听起来我们需要建立我们的医疗监控设备，如果我们能识别出这些氨基酸到底是什么东西，将会使昏迷/瘫痪的病人和太空旅行者更容易恢复。

[–]Havanatha_banana

Even if we could are we able to deliver it to localised areas? I thought that one of the difficulty of medicinal administration is delivery to certain areas.

即使我们可以，我们能把它送到细胞内部吗?我认为给药的困难之一就是是把药精准地送到某些位置。

[–]Throwitupyourbutt

The amount of progress being made in the medicle field is stunning.

医疗行业日新月异的发展进步真是让人惊叹。

[–]Olibri

Clearly the correct answer is to start sending bears into space.

很明显把灰熊送上太空就能得到正确答案了。

[–]Fez_and_no_Pants

If we can figure out a way to do it for all the cells... Hypersleep and or immortality maybe?

如果我们能搞清楚所有细胞的机制的话。。长时间休眠甚至是永生都是可行的了？

[–]DrCaesars_Palace_MD

Immortality is a stretch. It''ll prevent muscle atrophy but cells replication process is flawed and gets worse over time. It''s theorized that this is a major contributor to why we age I believe. Our bodies can''t keep up

永生是一种延伸。它可以防止肌肉萎缩，但细胞复制过程是有缺陷的，而且随着时间的推移会变得更糟。我相信，从理论上讲，这是我们变老的主要原因。我们的身体跟不上

[–]fAP6rSHdkd

Manufactured replacement parts would work for organs. Bones would be harder and skin would be very difficult to fully replace but making tailormade parts with your own DNA code and enough telomeres to add 100 years to their life expectancy sounds possible in the next 30-50 years. Replacing brains however that''ll take much longer unless we''re supplementing with computer hardware

人造的替换零件可以替换器官。但骨头会变得更硬，皮肤也很难完全替换，但用你自己的DNA代码和足够的端粒来制造定制的部件，让它们的预期寿命增加100岁，在未来30-50年听起来是可能的。然而，除非我们用电子硬件，否则要替换人脑将需要更长的时间

[–]fAP6rSHdkd

Yep it''s likely unsustainable for a population of 7 billion or at least it will be at first but our kids or grandkids might not have to die from the normal aging process ever again and that''s a cool concept to me. What kinda laws and regulations will pop up around it? Will people rush to save up tens of millions of dollars to have these surgeries and retire for half their lifetime with a young body? What sort of philanthropic or passion projects will be possible for people who don''t need to work for a living because it''s viable to save up for a body replacement? Or will they save up to have the surgery and go back to work to save up for the next one? Will we stop at traditional organs or move on to mechanical parts? The great thing is that if we don''t implode as a species the options are neigh endless and it all starts this century. Sorry if this seems too SciFi for thus point in time but we will live to see all of these things come to fruition and that''s exciting to me

[–]EssenceOfSenescence

Telomeres are not the whole story. All forms of cancer in humans involve telomere expansion because it allows cells to evade senescence an anti-tumour mechanism. There are other ways we age as well like accumulation of mutations ROS mitochondrial dysfunction etc. also adding 100 years to our life expectancy within the next 30-50 years sounds quite optimistic. We can’t even make worms live twice as long and they have about 1000 cells and don’t really have organs the way we do... once we figure this stuff out in worms flies and mice MAYBE we can begin to create therapies in humans. But we can’t even solve aging in simple organisms at the moment and we don’t even know what even causes ageing either so there’s a lot to consider when coming up with a timeline.

端粒并不是全部。人类所有形式的癌症都涉及到端粒的扩展，因为它使细胞逃避衰老，这是一种抗肿瘤机制。我们也有其他衰老的方式，比如突变、活性氧、线粒体功能障碍等的积累，也让我们在未来30-50年的预期寿命增加100年听起来相当乐观。然而我们现在甚至不能让小小的蠕虫多活一倍的寿命，它们有大约1000个细胞，而且没有我们这样的器官……一旦我们在蠕虫、苍蝇和老鼠身上发现了这些东西，也许我们可以开始在人类身上创造治疗方法。但我们现在甚至不能解决简单生物的衰老问题，我们甚至不知道是什么导致衰老，所以在人类发展的时间线上我们还要考虑许多问题。