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新东方网>上海新东方学校>上海雅思>雅思阅读>正文

雅思阅读全真练习系列(十三)

2018-05-17 13:43

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  答案&解析 Suggested Answers and Explanations

  1. vi

  2. ii

  3. vii 本段介绍了torcetrapib和statin的治病原理,但是同时短语“in contrast”与之前第二段后半段的内容呼应,暗示了这两种药

  在理论上能相辅相成,是理想的搭配。第一个选项无法涵盖整段意义,故选择i是错误的。

  4. iii 本段分析了可能导致torcetrapibl临床试验失败的原因,后半段指出如果以上推测正确,那么未来的药物可借鉴这个试验,设法

  避免torcetrapib的缺陷,研制出有效的药物。viii选项无法涵盖后半段的意思。

  5. ix 见首句。

  6. v

  7. A 见第二段。题目中administer一词意为“用药”,subject一词为“实验对象”之意。

  8. B 见第四段“… to raise levels of HDLs, which ferry cholesterol out of artery-clogging plaques to the liver for removal

  from the body.”即HDLs的作用最终是将choleserol清除出人体:“… for removal from the body”。

  9. B 见第四段“But HDLs are complex and not entirely understood.”

  10. C 见第二段“… plus a cholesterol-lowering statin”,即statin是可以降低cholesterol的。

  11. D 见第六段“So inhibiting CETP, … might actually cause an abnormal and irreversible accumulation of cholesterol

  in the body.

  12. A 见第三段。

  13. C 见第四段“Statins, in contrast, mainly work by lowering the 'bad' low-density lipoproteins.”

  3. The news came as a kick in the teeth to many cardiologists because earlier tests in animals and people suggested it would lower rates of cardiovascular disease. "There have been no red flags to my knowledge," says John Chapman, a specialist in lipoproteins and atherosclerosis at the National Institute for Health and Medical Research (INSERM) in Paris who has also studied torcetrapib. "This cancellation came as a complete shock."

  4. Torcetrapib is one of the most advanced of a new breed of drugs designed to raise levels of HDLs, which ferry cholesterol out of artery-clogging plaques to the liver for removal from the body. Specifically, torcetrapib blocks a protein called cholesterol ester transfer protein (CETP), which normally transfers the cholesterol from high-density lipoproteins to low density, plaque-promoting ones. Statins, in contrast, mainly work by lowering the 'bad' low-density lipoproteins.

  Under pressure

  5. Researchers are now trying to work out why and how the drug backfired, something that will not become clear until the clinical details are released by Pfizer. One hint lies in evidence from earlier trials that it slightly raises blood pressure in some patients. It was thought that this mild problem would be offset by the heart benefits of the drug. But it is possible that it actually proved fatal in some patients who already suffered high blood pressure. If blood pressure is the explanation, it would actually be good news for drug developers because it suggests that the problems are specific to this compound. Other prototype drugs that are being developed to block CETP work in a slightly different way and might not suffer the same downfall.

  6. But it is also possible that the whole idea of blocking CETP is flawed, says Moti Kashyap, who directs atherosclerosis research at the VA Medical Center in Long Beach, California. When HDLs excrete cholesterol in the liver, they actually rely on LDLs for part of this process. So inhibiting CETP, which prevents the transfer of cholesterol from HDL to LDL, might actually cause an abnormal and irreversible accumulation of cholesterol in the body. "You're blocking a physiologic mechanism to eliminate cholesterol and effectively constipating the pathway," says Kashyap.

  Going up

  7. Most researchers remain confident that elevating high density lipoproteins levels by one means or another is one of the best routes for helping heart disease patients. But HDLs are complex and not entirely understood. One approved drug, called niacin, is known to both raise HDL and reduce cardiovascular risk but also causes an unpleasant sensation of heat and tingling. Researchers are exploring whether they can bypass this side effect and whether niacin can lower disease risk more than statins alone. Scientists are also working on several other means to bump up high-density lipoproteins by, for example, introducing synthetic HDLs. "The only thing we know is dead in the water is torcetrapib, not the whole idea of raising HDL," says Michael Miller, director of preventive cardiology at the University of Maryland Medical Center, Baltimore.

  (613 words nature)

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