New approach to BSE successful in lab
A new method of treatment can appreciably slow down the progress of the fatal brain disease scrapie in mice. This has been established by researchers from the Universities of Munich and Bonn together with their colleagues at the Max Planck Institute in Martinsried. To do this they used an effect discovered by the US researchers Craig Mello and Andrew Fire, for which they were awarded this year’s Nobel Prize for Medicine. Scrapie is a variant of the cattle disease BSE and the human equivalent Creutzfeld-Jakob disease. However, it will take years for the method to be introduced to medicine, the researchers warn. Their findings are published in the next issue of the Journal of Clinical Investigation (Vol. 116, No. 12, December 2006).
Scrapie, Creutzfeld-Jakob and BSE are among the most unusual diseases known to medical research. Unusual because the pathogens are apparently neither viruses nor bacteria, being simply protein molecules known as protein prions. What is even more peculiar: exactly the same prion proteins occur in healthy animals. The only difference is that they have a different shape. When there is contact with their ‘diseased twins’ they change their shape, also becoming ‘diseased.’ The result is an irresistible chain reaction. The malformed prion proteins can be deposited in the brain, thereby destroying brain tissue. Prion diseases are always fatal, often, however, not until months after the outbreak of the disease. As yet there is no cure.
In mice suffering from scrapie the pathogenic prion protein is known as PrP-Scr, whereas the normal variant is PrP-C. PrP-C seems to have a protective effect in diseases like a stroke. Interestingly, mice which cannot produce any PrP-C appear to be completely healthy. This has become the starting point for a new therapeutic approach which for some years now has been current in research circles: can we not simply switch off the production of ‘healthy’ PrP-C in infected animals, thereby depriving the ‘diseased’ PrP-Scr of its ability to spread" In this way the chain reaction would be interrupted.
New therapeutic approach
Scientists from Munich’s Ludwig Maximilian University and the University of Bonn, in conjunction with colleagues from the Max Planck Institute in Martinsried, have been testing whether this approach works. In doing so they cut back the production of PrP-C in mice by means of an ingenious procedure. The researchers used a special RNA molecule for this purpose. RNA is related to the genetic molecule DNA. There are types of RNA known as siRNAs which can attach themselves to specific genes, thereby preventing these from being ‘read’. The production of the appropriate protein is thus shut down. This effect is known as RNA interference; its discovery was rewarded with this year’s Nobel Prize for Medicine. “We modified the brain cells of mice in such a way that they were able to produce siRNAs in place of the ‘healthy’ PrP-C protein,” explains Professor Alexander Pfeifer, director of the Institute of Pharmacology of the University of Bonn. “In cell cultures the production of PrP-C was thereby cut back by up to 97 per cent.”
The researchers then tested what effect these siRNAs had on mice which had scrapie. ‘If brain cells are to produce siRNAs, you have to smuggle in the corresponding gene,’ says Professor Kretschmar, director of the Prion Centre of Munich’s Ludwig Maximilian University. ‘But presumably we’ll never manage to equip all the cells in the brain with this gene.’ This is why the researchers also wanted to find out how many cells they have to ‘revamp’ genetically to treat scrapie or similar diseases successfully. For this purpose they bred mice that only had some brain cells which could produce siRNAs. ‘Whereas the untreated mice died on average after 165 days, the mice which had been treated lived appreciably longer,’ is how Professor Kretschmar summarises the results.
BSE-resistant cattle"
It varied how much longer they lived: if only a few cells could produce siRNAs, the mice died at almost the same time as the control mice, i.e. on average after 170 days. However, if the majority of the brain cells were protected by siRNA, the mice survived the prion disease for up to 230 days, in other words about a third longer.
‘Basically siRNAs seem to be a promising therapeutic option for scrapie, CJD or BSE,’ Professor Pfeifer emphasises. ‘However, it will take years before the method can be used on human beings.’ The method is also relevant for animal breeding: in principle it can be used to breed cattle which cannot produce any PrP-C. They would then be resistant to BSE. Source : University of Bonn
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New approach to BSE successful in lab
实验室治疗疯牛病的新方法
A new method of treatment can appreciably slow down the progress of the fatal brain disease scrapie in mice. This has been established by researchers from the Universities of Munich and Bonn together with their colleagues at the Max Planck Institute in Martinsried. To do this they used an effect discovered by the US researchers Craig Mello and Andrew Fire, for which they were awarded this year’s Nobel Prize for Medicine. Scrapie is a variant of the cattle disease BSE and the human equivalent Creutzfeld-Jakob disease. However, it will take years for the method to be introduced to medicine, the researchers warn. Their findings are published in the next issue of the Journal of Clinical Investigation (Vol. 116, No. 12, December 2006).
一种新的治疗方法能减慢致命性脑病羊痒病的进程，这已经被来自于慕尼黑和波恩大学的研究人员和Martinsried马普研究所的同事所证实。他们利用美国研究员Craig Mello 和Andrew Fire获得今年诺贝尔医学奖的一个结果。羊痒病是疯牛病和人克雅氏病的一个变异。但是这种方法要运用到医学还要花很长时间，研究人员警告说。他们的结果发表在下一期的《Journal of Clinical Investigation》（2006年12期，116卷）
Scrapie, Creutzfeld-Jakob and BSE are among the most unusual diseases known to medical research. Unusual because the pathogens are apparently neither viruses nor bacteria, being simply protein molecules known as protein prions. What is even more peculiar: exactly the same prion proteins occur in healthy animals. The only difference is that they have a different shape. When there is contact with their ‘diseased twins’ they change their shape, also becoming ‘diseased.’ The result is an irresistible chain reaction. The malformed prion proteins can be deposited in the brain, thereby destroying brain tissue. Prion diseases are always fatal, often, however, not until months after the outbreak of the disease. As yet there is no cure.
羊痒病、克雅氏病和疯牛病是医学研究中最罕见的疾病之一。说它罕见是因为引起疾病的病因既不是病毒也不是细菌，而是一种叫做蛋白质传染因子的蛋白质分子。更奇特的是：这种蛋白质在健康动物中也存在。唯一的差别是它们有不同的形状。当它们与异常的个体接触后，它们就会改变自己的形状，成为致病的蛋白。这是一个不可抗拒的链式反应。致病性的朊病毒蛋白质在脑中沉积并损伤脑组织。朊病毒病是致命的，常常在发病后数月死亡，但是目前还没有有效的治疗方法。
In mice suffering from scrapie the pathogenic prion protein is known as PrP-Scr, whereas the normal variant is PrP-C. PrP-C seems to have a protective effect in diseases like a stroke. Interestingly, mice which cannot produce any PrP-C appear to be completely healthy. This has become the starting point for a new therapeutic approach which for some years now has been current in research circles: can we not simply switch off the production of ‘healthy’ PrP-C in infected animals, thereby depriving the ‘diseased’ PrP-Scr of its ability to spread" In this way the chain reaction would be interrupted.
在羊痒病小鼠中致病的朊病毒蛋白是PrP-Scr，而正常变异是PrP-C。PrP-C似乎对中风等疾病有保护作用，有趣的是，那些无法产生PrP-C的小鼠看起来是完全健康的。这个现象成为这些年研究新的治疗方法的立足点：我们可以只是简单的阻断感染动物中健康的PrP-C的产生，这样就可以控制致病性PrP-Scr的扩散，通过这种方式打断链式反应。
New therapeutic approach
新的治疗方法
Scientists from Munich’s Ludwig Maximilian University and the University of Bonn, in conjunction with colleagues from the Max Planck Institute in Martinsried, have been testing whether this approach works. In doing so they cut back the production of PrP-C in mice by means of an ingenious procedure. The researchers used a special RNA molecule for this purpose. RNA is related to the genetic molecule DNA. There are types of RNA known as siRNAs which can attach themselves to specific genes, thereby preventing these from being ‘read’. The production of the appropriate protein is thus shut down. This effect is known as RNA interference; its discovery was rewarded with this year’s Nobel Prize for Medicine. “We modified the brain cells of mice in such a way that they were able to produce siRNAs in place of the ‘healthy’ PrP-C protein,” explains Professor Alexander Pfeifer, director of the Institute of Pharmacology of the University of Bonn. “In cell cultures the production of PrP-C was thereby cut back by up to 97 per cent.”
来自于慕尼黑和波恩大学的研究者和Martinsried马普研究所的合作者已经验证了这种方法是否可行，通过一种精巧的方法他们阻断了PrP-C的产生，他们使用了一种特殊的RNA分子。RNA可以和遗传物质DNA结合，这种RNA称为siRNAs，它们可以和特定的基因结合从而阻止这些基因的表达，因此特定的蛋白质的产生被阻断。这个过程叫做RNA干扰。这项发现获得了今年的诺贝尔医学奖。“我们通过修饰小鼠的脑细胞，使得这些细胞能产生siRNAs而不是健康的PrP-C蛋白，”波恩大学药理学研究所主任Alexander Pfeifer教授解释道：“在细胞培养中，PrP-C的产生减少了97%。”
The researchers then tested what effect these siRNAs had on mice which had scrapie. ‘If brain cells are to produce siRNAs, you have to smuggle in the corresponding gene,’ says Professor Kretschmar, director of the Prion Centre of Munich’s Ludwig Maximilian University. ‘But presumably we’ll never manage to equip all the cells in the brain with this gene.’ This is why the researchers also wanted to find out how many cells they have to ‘revamp’ genetically to treat scrapie or similar diseases successfully. For this purpose they bred mice that only had some brain cells which could produce siRNAs. ‘Whereas the untreated mice died on average after 165 days, the mice which had been treated lived appreciably longer,’ is how Professor Kretschmar summarises the results.
随后，研究人员在羊痒病小鼠上检验了siRNAs的作用，慕尼黑大学朊病毒研究中心主任Kretschmar教授说，如果大脑能产生siRNAs，你将不得不转运进相关的基因，但是，假设我们不能把所有的脑细胞都用这种基因修饰，我们就必须找到需要修饰多少细胞才能有效的治疗羊痒病或相似的疾病，这正是科学家研究的原因。为此，他们饲养了一些仅有少量能产生siRNAs脑细胞的小鼠，结果未处理的小鼠在平均165天后死亡，处理的小鼠似乎存活的时间更长些。
BSE-resistant cattle"
对疯牛病有免疫的牛
It varied how much longer they lived: if only a few cells could produce siRNAs, the mice died at almost the same time as the control mice, i.e. on average after 170 days. However, if the majority of the brain cells were protected by siRNA, the mice survived the prion disease for up to 230 days, in other words about a third longer.
生存期是不同的：如果只有少数的细胞可以产生siRNAs，小鼠几乎与对照组小鼠同时死亡，比如在170天后。但是，如果大多数脑细胞可被siRNAs所保护，患有朊病毒病的小鼠可以存活到230天，换而言之，生存期延长了三分之一。
‘Basically siRNAs seem to be a promising therapeutic option for scrapie, CJD or BSE,’ Professor Pfeifer emphasises. ‘However, it will take years before the method can be used on human beings.’ The method is also relevant for animal breeding: in principle it can be used to breed cattle which cannot produce any PrP-C. They would then be resistant to BSE.
Pfeifer教授强调：“看起来siRNAs是治疗羊痒病、克雅氏病或疯牛病的有前景的方法，但是，在它能用于人之前还要很长时间。”这种方法也可用于动物育种：可用于繁殖不能产生PrP-C的牛，这些牛将能够抵抗疯牛病。
Source : University of Bonn
来源：波恩大学
实验室治疗疯牛病的新方法
慕尼黑和波恩大学的研究人员和Martinsried马普研究所的合作者证实一种新的治疗方法能减慢致命性脑病羊痒病的进程。这项结果发表在下一期的《Journal of Clinical Investigation》（2006年12期，116卷）。但是这种方法要运用到医学还要花很长时间，研究人员警告说。羊痒病是疯牛病和人克雅氏病的一个变异，它们是医学研究中最罕见的疾病之一。说它罕见是因为引起疾病的病因既不是病毒也不是细菌，而是一种叫做朊病毒蛋白质的蛋白质分子。更奇特的是：这种蛋白质在健康动物中也存在，唯一的差别是它们有不同的形状。在羊痒病小鼠中致病的朊病毒蛋白是PrP-Scr，而正常变异是PrP-C。当PrP-C与异常的PrP-Scr接触后，PrP-C就会改变自己的形状，成为致病的蛋白。这是一个不可抗拒的链式反应。致病性的朊病毒蛋白质在脑中沉积并损伤脑组织。朊病毒病是致命的，常常在发病后数月死亡，但是目前还没有有效的治疗方法。PrP-C似乎对中风等疾病有保护作用，有趣的是，那些无法产生PrP-C的小鼠看起来是完全健康的。这个现象成为这些年研究新的治疗方法的立足点：我们可以只是简单的阻断感染动物中健康的PrP-C的产生，这样就可以控制致病性PrP-Scr的扩散，通过这种方式打断链式反应从而达到治疗的目的。慕尼黑和波恩大学的研究者和Martinsried马普研究所的合作者已经验证了这种方法是否可行，他们通过一种特殊的RNA分子阻断了PrP-C的产生。RNA可以和遗传物质DNA结合，这种RNA称为siRNAs，RNA可以和特定的基因结合从而阻止这些基因的表达，因此使得基因表达蛋白质的产生被阻断。这个过程叫做RNA干扰（RNA干扰获得了今年的诺贝尔医学奖）。波恩大学药理学研究所主任Alexander Pfeifer教授解释道：“我们通过修饰小鼠的脑细胞，使得这些细胞取代PrP-C蛋白产生siRNAs，在培养的细胞中，PrP-C的产生减少了97%。” 随后，研究人员在羊痒病小鼠上检验了siRNAs的作用，慕尼黑大学朊病毒研究中心主任Kretschmar教授说，如果大脑能产生siRNAs，将不得不转运进相关的基因，但是，假设我们不能把所有的脑细胞都用这种基因修饰，我们就必须找到需要修饰多少细胞才能有效的治疗羊痒病或相似的疾病，这正是科学家研究的原因。为此，他们饲养了一些仅有少量能产生siRNAs脑细胞的小鼠，结果发现未处理的小鼠在平均165天后死亡，处理的小鼠似乎存活的时间更长些。但是这种方法的生存期是有差异的：如果只有少数的细胞可以产生siRNAs，小鼠几乎与对照组小鼠同时死亡，比如在170天后。但是，如果大多数脑细胞可被siRNAs所保护，患有朊病毒病的小鼠可以存活到230天，换而言之，生存期延长了三分之一。Pfeifer教授强调：“看起来siRNAs是治疗羊痒病、克雅氏病或疯牛病的有前景的方法，但是，在它能用于人之前还要很长时间。”这种方法也可用于动物育种：可繁殖不产生PrP-C的牛，这些牛将对疯牛病有免疫力。
来源：波恩大学
请将内容整理编译。
interesting! thanks
高新技术，虽然原理很简单，但是实际操作应该有不少问题，估计得5年才能研究出来吧。
RNA is related to the genetic molecule DNA. RNA可以和遗传物质DNA结合，
这句话翻译不合适吧？
When there is contact with their ‘diseased twins’ 当它们与异常的个体接触后，
这样翻译很影响理解。
后来看到整理后的理解对了。
谢谢！
很不错
等待好消息
