為大家準備了雅思閱讀模擬題：Why did a promising heart drug fail?雅思模擬試題在雅思備考過程中所起的作用不可小覷，通過模擬練習題，我們可以很直接地了解到自己的備考狀況，從而可以更有針對性地進行之后的復習。希望以下內(nèi)容能夠對大家的雅思備考有所幫助!更多雅思報名的最新消息，最專業(yè)的雅思備考資料，將為大家發(fā)布。
Why did a promising heart drug fail?
Doomed drug highlights complications of meddling with cholesterol.
1. The failure of a high-profile cholesterol drug has thrown a spotlight on
the complicated machinery that regulates cholesterol levels. But many
researchers remain confident that drugs to boost levels of 'good' cholesterol
are still one of the most promising means to combat spiralling heart
disease.
2. Drug company Pfizer announced on 2 December that it was cancelling all
clinical trials of torcetrapib, a drug designed to raise heart-protective
high-density lipoproteins (HDLs). In a trial of 15000 patients, a safety board
found that more people died or suffered cardiovascular problems after taking the
drug plus a cholesterol-lowering statin than those in a control group who took
the statin alone.
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.
Why did a promising heart drug fail?
Doomed drug highlights complications of meddling with cholesterol.
1. The failure of a high-profile cholesterol drug has thrown a spotlight on
the complicated machinery that regulates cholesterol levels. But many
researchers remain confident that drugs to boost levels of 'good' cholesterol
are still one of the most promising means to combat spiralling heart
disease.
2. Drug company Pfizer announced on 2 December that it was cancelling all
clinical trials of torcetrapib, a drug designed to raise heart-protective
high-density lipoproteins (HDLs). In a trial of 15000 patients, a safety board
found that more people died or suffered cardiovascular problems after taking the
drug plus a cholesterol-lowering statin than those in a control group who took
the statin alone.
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.