To examine this pathway in more detail, the researchers deleted the DDAH gene in mice.
为了更具体的验证这个途径，研究者把小鼠的DDAH基因敲除。
They also designed specific inhibitors (small molecules) which bind to the active site of human DDAH.
他们也设计了一个特殊的抑制物(小分子)，它可以结合在人类DDAH的活性位点上。
Genes and their pathways are crucial to our understanding of cardiovascular disease and a better understanding of DDAH-1 could lead to important new treatments.
探索这些基因和它们的途径，对我们了解心血管疾病和更好地了解DDAH - 1可导致新疗法的产生很重要。
CONCLUSION: Endothelial dysfunction induced by OFR is associated with the increase in ADMA concentration and reduction of DDAH activity, but not DDAH expression.
结论：OF R培养下，内皮损伤adma的增加与DDAH的活性减弱有关，而与DDAH的表达无关。
This study suggests for the first time that the loss of the activity of the enzyme DDAH-1 leads to reduced NO production and may cause heart and circulatory disease.
这个研究第一次说明ddah - 1酶活性的丧失导致NO产生的减少并且可能导致心脏和循环疾病。
Scientists have hypothesised that if DDAH function is impaired, NO production is reduced, and that this could be an important feature of increased cardiovascular risk.
科学家假设，如果DDAH的功能被损害了，那么NO的产生也会减少，这可能是心血管疾病风险增加的一个重要特征。
It could help us to establish if genetic variation predisposes certain people to these diseases, or whether environmental factors exert some of their effects through modulation of DDAH activity.
这可以帮助我们弄清是否是遗传性变异促使某些人患这些疾病，还是环境因素通过改变DDAH活性来发挥它们的效应。
It could help us to establish if genetic variation predisposes certain people to these diseases, or whether environmental factors exert some of their effects through modulation of DDAH activity.
这可以帮助我们弄清是否是遗传性变异促使某些人患这些疾病，还是环境因素通过改变DDAH活性来发挥它们的效应。
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