考研 医学英语 翻译

One man’s genes show DNA is still mysteryThe first detailed map of a man’s genes shows the genetic code is even more complex than anyone thought. For instance, science still cannot pinpoint what makes a person’s eyes blue.Initial study of genome en trepreneur Craig Venter’s own DAN map shows 4.1 million places where his genetic code is different from the basic “reference” human genome. This is many more than had been expected, including big differences that extend far beyond the single-letter changes that account for much of the variation seen so far.The researchers at the J. Craig Venter Institute in Maryland, along with teams at The Hospital for Sick Children in Toronto and the University of California San Diego, analyzed Venter’s genetic code t o compare it with the rival human genome maps published in 2001 by Venter’s private company and the publicly funded Human Genome project.Both the 2001 genomes used DNA from several volunteers, pooled and then sequenced. Writing in the public Library of Science journal PLOS Biology, the researchers said it would also be useful as a rare exercise to thoroughly examine a single person’s genome and compare it to these averages.James Watson, who helped discover the double-helix structure of DNA in 1953, has also had his personal genome sequenced and is offering it to other scientists for study. Both Venter and Watson have said they wanted to serve as examples to a public often afraid of genetic sequencing, in part for fear of being denied jobs or insurance coverage and in part because of privacy concerns.One thing the researchers wanted to find was if an individual’s risk for disease is one—if a person carries the mutated Huntington’s gene, he or she will develop the deadly and incurable disease. But most other diseases are the result of a more complex interaction between genes and environment.Venter, 61, said his father died at the age of 59 of sudden cardiac arrest. Venter has versions of three genes believed to lower the risk of heart disease and carries two copies of a gene mutation that raise the risk of a heart attack, the study found, Venter said he started taking a cholesterol-lowering statin drug years ago, even though his cholesterol levels were below those recommended for taking such medications.“I don’t have to have a 100 percent chance of heart disease to think of talking preventative measures,” Venter said. His mother is 84 and still active, he noted. “Knowing something dosen’t change what’s in our genetic code. But knowing things maybe gives us a chance to change what could be part of our genetic destiny,” Venter said.An article about HIVI think some of the excitement about this revolves around that very point. About10 years ago, we became much more knowledgeable about how HIV gets inside of a cell. Previous to that time, we thought it was a pretty simple process whereby the virus simply attached to an outside molecule on the human T cell and then basically got pulled in. We now know that the process is a little more complex than that and includes at least three different steps.One of those steps, the middle step, is one in which the virus has to use a specific kind of receptor on the outside of the cell. The scientific name for it is a chemokine coreceptor. Using a lock-and-key mechanism, the virus has to use a specific type of coreceptor to gain entrance into the cell. The CCR5 inhibitors block that key-and-lock mechanism such that the virus cannot put its key, so to speak, into the lock on the outside of the cell and then interact with the cell in a key-and-lock mechanism sort of way to gain entrance inside the cell.These new mechanisms of action have been very exciting because our previous classes of anti-HIV medications have worked only after the virus has gotten inside the cell and has already been doing some of its infection processes. This new class of medication works at a much earlier point in the HIV infection cycle so that it blocks the virus's ability to get inside the cell to begin with.So it's an entry inhibitor.Exactly. It is classified as a type of entry inhibitor as well as a CCR5 inhibitor.我认为涉及这个热点的一些问题很重要。

大约10年前我们对于HIV是如何感染细胞已的过程已经了解的很多了。

在那之前，大家认为病毒是靠简单的粘附于T 细胞分子表面然后侵入这样简单的过程感染细胞的。

现在表明其实这个过程要比以前想的复杂一些，至少要包括3个步骤。

中间的一步是这样的，病毒要利用细胞表面的一种特殊的受体。

这种受体的学名叫趋化因子复合受体。

病毒通过一种“开关”机制，利用一种特别类型的复合受体侵染进入细胞。

CCR5抑制剂能够抑制此种“开关机制”，也就是说，病毒就不能用它的钥匙打开细胞外的锁，来用这种开关机制感染到细胞内部并作用与细胞。