<International Circulation>:What kind of data do you see coming out of China in the next couple years? What are you excited about?
　　《国际循环》：在您看来，未来几年，在中国可以得到什么类型的数据?您最高兴看到的是什么?
　　Dr. Koch: China has some advantages in different areas of both clinical and basic research. For an example， a colleague here has DNA and blood samples from over 400 centenarians. You cannot get these resources anywhere else in the world and could be quite powerful if you do the right science with it.
　　Koch博士: 中国在临床与基础研究的不同领域都拥有一些优势。例如， 这里的一个同事拥有超过400个百岁老人的DNA和血液样本。在世界其他地方你是不可能得到这些资源的， 如果进行科学合理的利用，其作用将非常巨大。
　　<International Circulation>: This next question has to do with a paper you published with Prof. Brinks. As we know， there are several mechanism of heart failure progression， such as RAAS and sympathetic nervous systems. What are the roles of GRKs in these mechanisms?
　　《国际循环》：下一个问题和您与布林克教授发表一篇论文有关。众所周知， 心力衰竭包括几种机制， 例如肾素-血管紧张素-醛固酮系统和交感神经系统。那么G蛋白偶联受体激酶（GRKs）在这些机制中的主要作用是什么?
　　Dr. Koch: We feel that study is significant as most of our studies over the last several decades with GRK2 has shown that it is maladapted in chronic heart failure (CHF). Overtime， its increased activity leads to remodeling. The Brinks et al paper actually showed that even acute injuries to the heart can cause permanent damage. We have gone on to show that GRK2 is a pro-death kinase. Some of our unpublished data is showing that this pro-death signaling that GRK2 induces is independent of its role as a kinase against receptors. It has other targets. As a scientist， this is exciting to figure out. Even if you inhibit GRK2 acutely with a heart attack， you can save myocytes from death.
　　Koch博士:我们觉得这项研究与过去几十年我们对G蛋白偶联受体激酶2 （GRK2）对慢性心力衰竭(CHF)的消极影响的大多数研究同等重要。GRK2的过度表达活性升高导致心室重构。布林克等的论文明确表明这种急性损伤甚至可以对心脏造成永久性伤害。我们已经表明， GRK2是死亡预警激酶。我们的一些未公布的数据表明， GRK2产生的死亡预警信号作为受体激酶而独立发生作用。它还有其他的靶位。作为一个科学家， 能够发现这一点让人十分高兴。即使你在心脏病发作只能紧急抑制GRK2的水平， 你也可以通过挽救心肌细胞而避免死亡。

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