To begin with,"muzak"(音乐广播网 )was intended simplyto createasoothing(安慰)atmosphere.Recently,however,it's ecome big business —thanks in part to recentresearch.Dr.Ronald Milliman,an American marketing expert,hasshown that music can boost sales or increase factory roduction by as much as a third.But,it has to be light music.A fast one has no effect atall on sales.Slow music can increase receipts by 38%.This isprobably because shoppers slow down and have more opportunityto spot items they like to buy.Yet,slow music isn't alway sanswer.Dr.Milliman found,for example,that in restaurants slowmusic meant customers took longer to eat their meals,whichreduced overall sales.So restaurants owners might be welladvised to play up-tempo music to keep the customers moving—unless of course,the resulting indigestion leads tocomplaints!

练习：

1.The reason why background music is so popular isthat ______.

A.it can have a powerful effect on those who hear it

B.it can help to create a soothing atmosphere

C.it can boost sales or increase factory production erywhere

D.it can make customers eat their meals quickly

2.Background music means ________.

A.light music that customers enjoy mostB.fast music that makes people move fast

C.slow music that can make customers enjoy their meals

D.the music you are listening to while you are doingomething

3.Restaurant owners complain about background musicbecause ______.

A.it results in indigestion

B.it increases their sales

C.it keeps customers moving

D.it decreases their sales

4.The word"up-tempo music"probably means_____.

A.slow music

B.fast music

C.light music

D.classical music

1.Thefailureofahigh-profilecholesteroldrughasthrownaspotlightonthecomplicatedmachinerythatregulatescholesterollevels.Butmanyresearchersremainconfidentthatdrugstoboostlevelsof'good'cholesterolarestilloneofthemostpromisingmeanstocombatspirallingheartdisease.

2.DrugcompanyPfizerannouncedon2Decemberthatitwascancellingallclinicaltrialsoftorcetrapib，adrugdesignedtoraiseheart-protectivehigh-densitylipoproteins(HDLs).Inatrialof15000patients，asafetyboardfoundthatmorepeoplediedorsufferedcardiovascularproblemsaftertakingthedrugplusacholesterol-loweringstatinthanthoseinacontrolgroupwhotookthestatinalone.

3.Thenewscameasakickintheteethtomanycardiologistsbecauseearliertestsinanimalsandpeoplesuggesteditwouldlowerratesofcardiovasculardisease."Therehavebeennoredflagstomyknowledge,"saysJohnChapman，aspecialistinlipoproteinsandatherosclerosisattheNationalInstituteforHealthandMedicalResearch(INSERM)inPariswhohasalsostudiedtorcetrapib."Thiscancellationcameasacompleteshock."

4.TorcetrapibisoneofthemostadvancedofanewbreedofdrugsdesignedtoraiselevelsofHDLs，whichferrycholesteroloutofartery-cloggingplaquestotheliverforremovalfromthebody.Specifically，torcetrapibblocksaproteincalledcholesterolestertransferprotein(CETP)，whichnormallytransfersthecholesterolfromhigh-densitylipoproteinstolowdensity，plaque-promotingones.Statins，incontrast，mainlyworkbyloweringthe'bad'low-densitylipoproteins.

Underpressure

5.Researchersarenowtryingtoworkoutwhyandhowthedrugbackfired，somethingthatwillnotbecomeclearuntiltheclinicaldetailsarereleasedbyPfizer.Onehintliesinevidencefromearliertrialsthatitslightlyraisesbloodpressureinsomepatients.Itwasthoughtthatthismildproblemwouldbeoffsetbytheheartbenefitsofthedrug.Butitispossiblethatitactuallyprovedfatalinsomepatientswhoalreadysufferedhighbloodpressure.Ifbloodpressureistheexplanation，itwouldactuallybegoodnewsfordrugdevelopersbecauseitsuggeststhattheproblemsarespecifictothiscompound.OtherprototypedrugsthatarebeingdevelopedtoblockCETPworkinaslightlydifferentwayandmightnotsufferthesamedownfall.

6.ButitisalsopossiblethatthewholeideaofblockingCETPisflawed，saysMotiKashyap，whodirectsatherosclerosisresearchattheVAMedicalCenterinLongBeach，California.WhenHDLsexcretecholesterolintheliver，theyactuallyrelyonLDLsforpartofthisprocess.SoinhibitingCETP，whichpreventsthetransferofcholesterolfromHDLtoLDL，mightactuallycauseanabnormalandirreversibleaccumulationofcholesterolinthebody."You'reblockingaphysiologicmechanismtoeliminatecholesterolandeffectivelyconstipatingthepathway,"saysKashyap.Goingup

7.Mostresearchersremainconfidentthatelevatinghighdensitylipoproteinslevelsbyonemeansoranotherisoneofthebestroutesforhelpingheartdiseasepatients.ButHDLsarecomplexandnotentirelyunderstood.Oneapproveddrug，calledniacin，isknowntobothraiseHDLandreducecardiovascularriskbutalsocausesanunpleasantsensationofheatandtingling.Researchersareexploringwhethertheycanbypassthissideeffectandwhetherniacincanlowerdiseaseriskmorethanstatinsalone.Scientistsarealsoworkingonseveralothermeanstobumpuphigh-densitylipoproteinsby，forexample，introducingsyntheticHDLs."Theonlythingweknowisdeadinthewateristorcetrapib，notthewholeideaofraisingHDL,"saysMichaelMiller，directorofpreventivecardiologyattheUniversityofMarylandMedicalCenter，Baltimore.

Questions7-13

Matchtorcetrapib，HDLs，statinandCETPwiththeirfunctions(Questions8-13)..WritethecorrectletterA，B，CorDinboxes8-13onyouranswersheet.NBYoumayuseanylettermorethanonce.

7.Ithasbeenadministeredtoover10,000subjectsinaclinicaltrial.

8.Itcouldhelpridhumanbodyofcholesterol.

9.Researchersareyettofindmoreaboutit.

10.Itwasusedtoreducethelevelofcholesterol.

11.AccordingtoKashyap，itmightleadtounwantedresultifit'sblocked.

12.Itproducedcontradictoryresultsindifferenttrials.

13.ItcouldinhibitLDLs.Listofchoices

A.TorcetrapicB.HDLSC.StatinD.CETP

-----Whataboutthepenyouboughtyesterday?

-----It____________well.Ilikeitverymuch.

new weapon to fight cancer

1. British scientists are preparing to launch trials of a radical new way to fight cancer, which kills tumours by infecting them with viruses like the common cold.

2. If successful, virus therapy could eventually form a third pillar alongside radiotherapy and chemotherapy in the standard arsenal against cancer, while avoiding some of the debilitating side-effects.

3. Leonard Seymour, a professor of gene therapy at Oxford University, who has been working on the virus therapy with colleagues in London and the US, will lead the trials later this year. Cancer Research UK said yesterday that it was excited by the potential of Prof Seymour’s pioneering techniques.

4. One of the country’s leading geneticists, Prof Seymour has been working with viruses that kill cancer cells directly, while avoiding harm to healthy tissue. "In principle, you’ve got something which could be many times more effective than regular chemotherapy," he said.

5. Cancer-killing viruses exploit the fact that cancer cells suppress the body’s local immune system. "If a cancer doesn’t do that, the immune system wipes it out. If you can get a virus into a tumour, viruses find them a very good place to be because there’s no immune system to stop them replicating. You can regard it as the cancer’s Achilles’ heel."

6. Only a small amount of the virus needs to get to the cancer. "They replicate, you get a million copies in each cell and the cell bursts and they infect the tumour cells adjacent and repeat the process," said Prof Seymour.

7. Preliminary research on mice shows that the viruses work well on tumours resistant to standard cancer drugs. "It’s an interesting possibility that they may have an advantage in killing drug-resistant tumours, which could be quite different to anything we’ve had before."

8. Researchers have known for some time that viruses can kill tumour cells and some aspects of the work have already been published in scientific journals. American scientists have previously injected viruses directly into tumours but this technique will not work if the cancer is inaccessible or has spread throughout the body.

9. Prof Seymour’s innovative solution is to mask the virus from the body’s immune system, effectively allowing the viruses to do what chemotherapy drugs do - spread through the blood and reach tumours wherever they are. The big hurdle has always been to find a way to deliver viruses to tumours via the bloodstream without the body’s immune system destroying them on the way.

10. "What we’ve done is make chemical modifications to the virus to put a polymer coat around it - it’s a stealth virus when you inject it," he said.

11. After the stealth virus infects the tumour, it replicates, but the copies do not have the chemical modifications. If they escape from the tumour, the copies will be quickly recognised and mopped up by the body’s immune system.

12. The therapy would be especially useful for secondary cancers, called metastases, which sometimes spread around the body after the first tumour appears. "There’s an awful statistic of patients in the west ... with malignant cancers; 75% of them go on to die from metastases," said Prof Seymour.

13. Two viruses are likely to be examined in the first clinical trials: adenovirus, which normally causes a cold-like illness, and vaccinia, which causes cowpox and is also used in the vaccine against smallpox. For safety reasons, both will be disabled to make them less pathogenic in the trial, but Prof Seymour said he eventually hopes to use natural viruses.

14. The first trials will use uncoated adenovirus and vaccinia and will be delivered locally to liver tumours, in order to establish whether the treatment is safe in humans and what dose of virus will be needed. Several more years of trials will be needed, eventually also on the polymer-coated viruses, before the therapy can be considered for use in the NHS. Though the approach will be examined at first for cancers that do not respond to conventional treatments, Prof Seymour hopes that one day it might be applied to all cancers.

Questions 1-6

Do the following statements agree with the information given in the reading passage? For questions 1-6 write

TRUE if the statement agrees with the information

FALSE if the statement contradicts the information

NOT GIVEN if there is no information on this in the passage

1.Virus therapy, if successful, has an advantage in eliminating side-effects.

2.Cancer Research UK is quite hopeful about Professor Seymour’s work on the virus therapy.

3.Virus can kill cancer cells and stop them from growing again.

4.Cancer’s Achilles’ heel refers to the fact that virus may stay safely in a tumor and replicate.

5.To infect the cancer cells, a good deal of viruses should be injected into the tumor.

6.Researches on animals indicate that virus could be used as a new way to treat drug-resistant tumors.

Question 7-9

Based on the reading passage, choose the appropriate letter from A-D for each answer.

7.Information about researches on viruses killing tumor cells can be found

(A) on TV

(B) in magazines

(C) on internet

(D) in newspapers

8.To treat tumors spreading out in body, researchers try to

(A) change the body’ immune system

(B) inject chemotherapy drugs into bloodstream.

(C) increase the amount of injection

(D) disguise the viruses on the way to tumors.

9.When the chemical modified virus in tumor replicates, the copies

(A) will soon escape from the tumor and spread out.

(B) will be wiped out by the body’s immune system.

(C) will be immediately recognized by the researchers.

(D) will eventually stop the tumor from spreading out.

Questions 10-13

Complete the sentences below. Choose your answers from the list of words. You can only use each word once.

NB There are more words in the list than spaces so you will not use them all.

In the first clinical trials, scientists will try to ……10…… adenovirus and vaccinia, so both the viruses will be less pathogenic than the ……11…….These uncoated viruses will be applied directly to certain areas to confirm safety on human beings and the right ……12…… needed. The experiments will firstly be ……13……to the treatment of certain cancers

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.

Questions 7-13

Match torcetrapib，HDLs，statin and CETP with their functions (Questions 8-13)..Write the correct letter A，B，C or D in boxes 8-13 on your answer sheet.NB You may use any letter more than once.

7.It has been administered to over 10,000 subjects in a clinical trial.

8.It could help rid human body of cholesterol.

9.Researchers are yet to find more about it.

10.It was used to reduce the level of cholesterol.

11.According to Kashyap，it might lead to unwanted result if it's blocked.

12.It produced contradictory results in different trials.

13.It could inhibit LDLs.List of choices

A.TorcetrapicB.HDLSC.StatinD.CETP