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【bio-news】莱斯大学：突变死病毒？

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Forced Evolution: Can We Mutate Viruses To Death?

http://www.sciencedaily.com/releases/2008/11/081110154034.htm

ScienceDaily (Nov. 11, 2008) — It sounds like a science fiction movie: A killer contagion threatens the Earth, but scientists save the day with a designer drug that forces the virus to mutate itself out of existence. The killer disease? Still a fiction. The drug? It could become a reality thanks to a new study by Rice University bioengineers.

The study, which is available online and slated for publication in the journal Physical Review E, offers the most comprehensive mathematical analysis to date of the mechanisms that drive evolution in viruses and bacteria. Rather than focusing solely on random genetic mutations, as past analyses have, the study predicts exactly how evolution is affected by the exchange of entire genes and sets of genes.

"We wanted to focus more attention on the roles that recombination and horizontal gene transfer play in the evolution of viruses and bacteria," said bioengineer Michael Deem, the study's lead researcher. "So, we incorporated both into the leading models that are used to describe bacterial and viral evolution, and we derived exact solutions to the models."

The upshot is a newer, composite formula that more accurately captures what happens in real world evolution. Deem's co-authors on the study include Rice graduate student Enrique Muñoz and longtime collaborator Jeong-Man Park, a physicist at the Catholic University of Korea in Bucheon.

In describing the new model, Deem drew an analogy to thermodynamics and discussed how a geneticist or drug designer could use the new formula in much the same way that an engineer might use thermodynamics formulas.

"Some of the properties that describe water are density, pressure and temperature," said Deem. "If you know any two of them, then you can predict any other one using thermodynamics.

"That's what we're doing here," he said. "If you know the recombination rate, mutation rate and fitness function, our formula can analytically predict the properties of the system. So, if you have recombination at a certain frequency, I can say exactly how much that helps or hurts the fitness of the population."

Deem, Rice's John W. Cox Professor in Biochemical and Genetic Engineering and professor of physics and astronomy, said the new model helps to better describe the evolutionary processes that occur in the real world, and it could be useful for doctors, drug designers and others who study how diseases evolve and how our immune systems react to that evolution.

One idea that was proposed about five years ago is "lethal mutagenesis." In a nutshell, the idea is to design drugs that speed up the mutation rates of viruses and push them beyond a threshold called a "phase transition." The thermodynamic analogy for this transition is the freezing or melting of water -- which amounts to a physical transition between water's liquid and solid phases.

"Water goes from a liquid to a solid at zero degrees Celsius under standard pressure, and you can represent that mathematically using thermodynamics," Deem said. "In our model, there's also a phase transition. If the mutation, recombination or horizontal gene transfer rates are too high, the system delocalizes and gets spread all over sequence space."

Deem said the new results predict which parameter values will lead to this delocalization.

A competing theory is that a mutagenesis drug may eradicate a virus or bacterial population by reducing the fitness to negative values. The new mathematical results allow calculation of this mechanism when the fitness function and the mutation, recombination and horizontal gene transfer rates are known.

Without theoretical tools like the new model, drug designers looking to create pills to induce lethal mutagenesis couldn't say for certain under what parameter ranges the drugs really worked. Deem said the new formula should provide experimental drug testers with a clear picture of whether the drugs -- or something else -- causes mutagenesis.

The research is supported by the Defense Advanced Research Projects Agency and the Korea Research Foundation.

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2008-11-12 10:42 浏览 : 1313 回复 : 5

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本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领。
申请延时，呵呵！

2008-11-12 20:30

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梦在远方编辑于 2008-11-14 22:46

• 似有胸膜凹陷，强化却不明显，面对如此结节，请你发表高见！（有手术及病理结果）

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Forced Evolution: Can We Mutate Viruses To Death?
强迫演化：我们能够通过变异致死病毒吗？
http://www.sciencedaily.com/releases/2008/11/081110154034.htm
ScienceDaily (Nov. 11, 2008) — It sounds like a science fiction movie: A killer contagion threatens the Earth, but scientists save the day with a designer drug that forces the virus to mutate itself out of existence. The killer disease? Still a fiction. The drug? It could become a reality thanks to a new study by Rice University bioengineers.
科学日报（2008年11月11日）——这听起来像是一个科幻电影：一种致命的传染性病毒威胁着全球生存，但是科学家通过使用一种可以迫使病毒自身变异致死的策划药而转败为胜。这种致命性疾病？仍然是一个虚构。而这种药？由于莱斯大学生物工程师的一项新研究，它可能会变成现实。
The study, which is available online and slated for publication in the journal Physical Review E, offers the most comprehensive mathematical analysis to date of the mechanisms that drive evolution in viruses and bacteria. Rather than focusing solely on random genetic mutations, as past analyses have, the study predicts exactly how evolution is affected by the exchange of entire genes and sets of genes.
这项研究（的相关信息）可以从网上获得并预计发表在《Physical Review E》杂志上。它为驱使病毒和细菌演化的最新机制提供最全面的数学分析。该研究准确的预测了演化是怎样受到整个基因组和基因互换的影响，而不是像以前的分析那样仅仅侧重于随机的基因突变。
"We wanted to focus more attention on the roles that recombination and horizontal gene transfer play in the evolution of viruses and bacteria," said bioengineer Michael Deem, the study's lead researcher. "So, we incorporated both into the leading models that are used to describe bacterial and viral evolution, and we derived exact solutions to the models."
“我们希望将更多的注意力放在重组和水平基因转移在病毒和细菌演化中所扮演的角色，因此，我们将两者都纳入到用来描述细菌和病毒的演化的领导模式，同时我们也得出了该模式确切的解决方案。”该研究的首席科学家Michael Deem生物工程师说道。
The upshot is a newer, composite formula that more accurately captures what happens in real world evolution. Deem's co-authors on the study include Rice graduate student Enrique Muñoz and longtime collaborator Jeong-Man Park, a physicist（physician） at the Catholic University of Korea in Bucheon.
其结果是一个更新的复合公式，它更准确地捕捉现实世界演化中发生的事物，Deem的共著者（关于该研究）包括莱斯大学研究生Enrique Muñoz和长期合作者Jeong-Man Park（来自韩国富川天主教大学的物理学家）。
In describing the new model, Deem drew an analogy to thermodynamics and discussed how a geneticist or drug designer could use the new formula in much the same way that an engineer might use thermodynamics formulas.
在介绍该新模型时，Deem以热力学作为类比，讨论了遗传学家或药物设计者如何以跟工程师使用热力学公式大致相同的方式应用这一新的法则。
"Some of the properties that describe water are density, pressure and temperature," said Deem. "If you know any two of them, then you can predict any other one using thermodynamics.
“密度、压力和温度是水的一些属性，如果你知道它们中的任意两者，那么你就可以通过使用热力学公式而预测出第三者” Deem说道。
"That's what we're doing here," he said. "If you know the recombination rate, mutation rate and fitness function, our formula can analytically predict the properties of the system. So, if you have recombination at a certain frequency, I can say exactly how much that helps or hurts the fitness of the population."
他说“这就是我们正在做的事情，如果你知道重组率、突变率以及适应度函数，我们的公式将可以分析预测该系统的属性。因此，如果你获得一定水平的重组率，我可以准确得出它在多大程度上促进或损害人口的适应性。”
Deem, Rice's John W. Cox Professor in Biochemical and Genetic Engineering and professor of physics and astronomy, said the new model helps to better describe the evolutionary processes that occur in the real world, and it could be useful for doctors, drug designers and others who study how diseases evolve and how our immune systems react to that evolution.
Deem、莱斯大学生物化学和遗传工程John W. Cox教授以及物理学和天文学教授宣称该新模型有助于更好地描述现实世界中发生的演化过程，对于医生、药物设计者和其他研究疾病是如何演化及我们的免疫系统是如何对该演化做出反应的科学家来说，它将可能是有用的。
One idea that was proposed about five years ago is "lethal mutagenesis." In a nutshell, the idea is to design drugs that speed up the mutation rates of viruses and push them beyond a threshold called a "phase transition." The thermodynamic analogy for this transition is the freezing or melting of water -- which amounts to a physical transition between water's liquid and solid phases.
“致命性诱变”是大约五年前提出的一个想法。简而言之，该想法就是设计可以加速病毒突变率并使之超出所谓的“相变”阈值的药物。热力学上与这一转变相类似是水的凝固和熔化——即这相当于水的液相和固相之间的物理转变。
"Water goes from a liquid to a solid at zero degrees Celsius under standard pressure, and you can represent that mathematically using thermodynamics," Deem said. "In our model, there's also a phase transition. If the mutation, recombination or horizontal gene transfer rates are too high, the system delocalizes and gets spread all over sequence space."
“在标准大气压下的零摄氏度，水将由液相变为固相。而且你可以利用热力学公式从算术上阐明此现象。” Deem说道，“在我们的模型中也有一个相变。如果突变、重组或水平基因转移率太高，该系统就会偏离原位并蔓延至整个序列空间。”
Deem said the new results predict which parameter values will lead to this delocalization.
Deem说这项新结果预测出哪一参数值将导致该离域。
A competing theory is that a mutagenesis drug may eradicate a virus or bacterial population by reducing the fitness to negative values. The new mathematical results allow calculation of this mechanism when the fitness function and the mutation, recombination and horizontal gene transfer rates are known.
一个竞争性的理论是诱变药物通过降低对负面价值的适应性而根除病毒或细菌群体。当适应度函数和突变、重组及水平基因转移率已知时，该项新的数学上的结果可以使这一机制运算化。
Without theoretical tools like the new model, drug designers looking to create pills to induce lethal mutagenesis couldn't say for certain under what parameter ranges the drugs really worked. Deem said the new formula should provide experimental drug testers with a clear picture of whether the drugs -- or something else -- causes mutagenesis.
如果没有类似该新模式的理论工具，企图创造出诱发致命性突变药物的设计者就不能确定该药物真正的在哪些参数范围内发挥作用。Deem说该新公式可以为实验性药物测试提供清晰的信息，到底是药物，还是其他什么东西造成突变。
The research is supported by the Defense Advanced Research Projects Agency and the Korea Research Foundation
这项研究受到国防高级研究项目署和韩国研究基金会的资助。

2008-11-16 15:01

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梦在远方编辑于 2008-11-16 15:05

• 广西一患者遵医嘱服用十倍药物后进 ICU

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强迫演化：我们能够通过变异致死病毒吗？
科学日报（2008年11月11日）——这听起来像是一个科幻电影：一种致命的传染性病毒威胁着全球生存，但是科学家通过使用一种可以迫使病毒自身变异致死的策划药而转败为胜。这种致命性疾病？仍然是一个虚构。而这种药？由于莱斯大学生物工程师的一项新研究，它可能会变成现实。
这项研究（的相关信息）可以从网上获得并预计发表在《Physical Review E》杂志上。它为驱使病毒和细菌演化的最新机制提供最全面的数学分析。该研究准确的预测了演化是怎样受到整个基因组和基因互换的影响，而不是像以前的分析那样仅仅侧重于随机的基因突变。
“我们希望将更多的注意力放在重组和水平基因转移在病毒和细菌演化中所扮演的角色，因此，我们将两者都纳入到用来描述细菌和病毒的演化的领导模式，同时我们也得出了该模式确切的解决方案。”该研究的首席科学家Michael Deem生物工程师说道。
其结果是一个更新的复合公式，它更准确地捕捉现实世界演化中发生的事物，Deem的共著者（关于该研究）包括莱斯大学研究生Enrique Muñoz和长期合作者Jeong-Man Park（来自韩国富川天主教大学的物理学家）。
在介绍该新模型时，Deem以热力学作为类比，讨论了遗传学家或药物设计者如何以跟工程师使用热力学公式大致相同的方式应用这一新的法则。
“密度、压力和温度是水的一些属性，如果你知道它们中的任意两者，那么你就可以通过使用热力学公式而预测出第三者” Deem说道。
他说“这就是我们正在做的事情，如果你知道重组率、突变率以及适应度函数，我们的公式将可以分析预测该系统的属性。因此，如果你获得一定水平的重组率，我可以准确得出它在多大程度上促进或损害人口的适应性。”
Deem、莱斯大学生物化学和遗传工程John W. Cox教授以及物理学和天文学教授宣称该新模型有助于更好地描述现实世界中发生的演化过程，对于医生、药物设计者和其他研究疾病是如何演化及我们的免疫系统是如何对该演化做出反应的科学家来说，它将可能是有用的。
“致命性诱变”是大约五年前提出的一个想法。简而言之，该想法就是设计可以加速病毒突变率并使之超出所谓的“相变”阈值的药物。热力学上与这一转变相类似是水的凝固和熔化——即这相当于水的液相和固相之间的物理转变。
“在标准大气压下的零摄氏度，水将由液相变为固相。而且你可以利用热力学公式从算术上阐明此现象。” Deem说道，“在我们的模型中也有一个相变。如果突变、重组或水平基因转移率太高，该系统就会偏离原位并蔓延至整个序列空间。”
Deem说这项新结果预测出哪一参数值将导致该离域。
一个竞争性的理论是诱变药物通过降低对负面价值的适应性而根除病毒或细菌群体。当适应度函数和突变、重组及水平基因转移率已知时，该项新的数学上的结果可以使这一机制运算化。
如果没有类似该新模式的理论工具，企图创造出诱发致命性突变药物的设计者就不能确定该药物真正的在哪些参数范围内发挥作用。Deem说该新公式可以为实验性药物测试提供清晰的信息，到底是药物，还是其他什么东西造成突变。
这项研究受到国防高级研究项目署和韩国研究基金会的资助。

2008-11-16 15:08

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