-----Dad，lookatthebuilding.Itisonfire.

-----Call119____________mobilephonerightnow

Dadwenttobuysome__________as__________formycousin.

Rogue theory of smell gets a boost

1.A controversial theory of how we smell, which claims that our fine sense of odour depends on quantum mechanics, has been given the thumbs up by a team of physicists.

2.Calculations by researchers at University College London (UCL) show that the idea that we smell odour molecules by sensing their molecular vibrations makes sense in terms of the physics involved.

3.That's still some way from proving that the theory, proposed in the mid-1990s by biophysicist Luca Turin, is correct.But it should make other scientists take the idea more seriously.

4."This is a big step forward," says Turin, who has now set up his own perfume company Flexitral in Virginia.He says that since he published his theory, "it has been ignored rather than criticized."

5.Most scientists have assumed that our sense of smell depends on receptors in the nose detecting the shape of incoming molecules, which triggers a signal to the brain.This molecular 'lock and key' process is thought to lie behind a wide range of the body's detection systems: it is how some parts of the immune system recognise invaders, for example, and how the tongue recognizes some tastes.

6.But Turin argued that smell doesn't seem to fit this picture very well.Molecules that look almost identical can smell very different — such as alcohols, which smell like spirits, and thiols, which smell like rotten eggs.And molecules with very different structures can smell similar.Most strikingly, some molecules can smell different — to animals, if not necessarily to humans — simply because they contain different isotopes (atoms that are chemically identical but have a different mass).

7.Turin's explanation for these smelly facts invokes the idea that the smell signal in olfactory receptor proteins is triggered not by an odour molecule's shape, but by its vibrations, which can enourage an electron to jump between two parts of the receptor in a quantum-mechanical process called tunnelling.This electron movement could initiate the smell signal being sent to the brain.

8.This would explain why isotopes can smell different: their vibration frequencies are changed if the atoms are heavier.Turin's mechanism, says Marshall Stoneham of the UCL team, is more like swipe-card identification than a key fitting a lock.

9.Vibration-assisted electron tunnelling can undoubtedly occur — it is used in an experimental technique for measuring molecular vibrations."The question is whether this is possible in the nose," says Stoneham's colleague, Andrew Horsfield.

10.Stoneham says that when he first heard about Turin's idea, while Turin was himself based at UCL, "I didn't believe it".But, he adds, "because it was an interesting idea, I thought I should prove it couldn't work.I did some simple calculations, and only then began to feel Luca could be right." Now Stoneham and his co-workers have done the job more thoroughly, in a paper soon to be published in Physical Review Letters.

11.The UCL team calculated the rates of electron hopping in a nose receptor that has an odorant molecule bound to it.This rate depends on various properties of the biomolecular system that are not known, but the researchers could estimate these parameters based on typical values for molecules of this sort.

12.The key issue is whether the hopping rate with the odorant in place is significantly greater than that without it.The calculations show that it is — which means that odour identification in this way seems theoretically possible.

13.But Horsfield stresses that that's different from a proof of Turin's idea."So far things look plausible, but we need proper experimental verification.We're beginning to think about what experiments could be performed."

14.Meanwhile, Turin is pressing ahead with his hypothesis."At Flexitral we have been designing odorants exclusively on the basis of their computed vibrations," he says."Our success rate at odorant discovery is two orders of magnitude better than the competition." At the very least, he is putting his money where his nose is.

Questions 5-9

Complete the sentences below with words from the passage.Use NO MORE THAN THREE WORDS for each answer.

5.The hypothesis that we smell by sensing the molecular vibration was made by ______.

6.Turin's company is based in ______.

7.Most scientists believed that our nose works in the same way as our ______.

8.Different isotopes can smell different when ______ weigh differently.

9.According to Audrew Horsfield, it is still to be proved that ______ could really occur in human nose.

newweapontofightcancer

1.Britishscientistsarepreparingtolaunchtrialsofaradicalnewwaytofightcancer,whichkillstumoursbyinfectingthemwithviruseslikethecommoncold.

2.Ifsuccessful,virustherapycouldeventuallyformathirdpillaralongsideradiotherapyandchemotherapyinthestandardarsenalagainstcancer,whileavoidingsomeofthedebilitatingside-effects.

3.LeonardSeymour,aprofessorofgenetherapyatOxfordUniversity,whohasbeenworkingonthevirustherapywithcolleaguesinLondonandtheUS,willleadthetrialslaterthisyear.CancerResearchUKsaidyesterdaythatitwasexcitedbythepotentialofProfSeymour’spioneeringtechniques.

4.Oneofthecountry’sleadinggeneticists,ProfSeymourhasbeenworkingwithvirusesthatkillcancercellsdirectly,whileavoidingharmtohealthytissue."Inprinciple,you’vegotsomethingwhichcouldbemanytimesmoreeffectivethanregularchemotherapy,"hesaid.

5.Cancer-killingvirusesexploitthefactthatcancercellssuppressthebody’slocalimmunesystem."Ifacancerdoesn’tdothat,theimmunesystemwipesitout.Ifyoucangetavirusintoatumour,virusesfindthemaverygoodplacetobebecausethere’snoimmunesystemtostopthemreplicating.Youcanregarditasthecancer’sAchilles’heel."

6.Onlyasmallamountofthevirusneedstogettothecancer."Theyreplicate,yougetamillioncopiesineachcellandthecellburstsandtheyinfectthetumourcellsadjacentandrepeattheprocess,"saidProfSeymour.

7.Preliminaryresearchonmiceshowsthatthevirusesworkwellontumoursresistanttostandardcancerdrugs."It’saninterestingpossibilitythattheymayhaveanadvantageinkillingdrug-resistanttumours,whichcouldbequitedifferenttoanythingwe’vehadbefore."

8.Researchershaveknownforsometimethatvirusescankilltumourcellsandsomeaspectsoftheworkhavealreadybeenpublishedinscientificjournals.Americanscientistshavepreviouslyinjectedvirusesdirectlyintotumoursbutthistechniquewillnotworkifthecancerisinaccessibleorhasspreadthroughoutthebody.

9.ProfSeymour’sinnovativesolutionistomaskthevirusfromthebody’simmunesystem,effectivelyallowingthevirusestodowhatchemotherapydrugsdo-spreadthroughthebloodandreachtumourswherevertheyare.Thebighurdlehasalwaysbeentofindawaytodelivervirusestotumoursviathebloodstreamwithoutthebody’simmunesystemdestroyingthemontheway.

10."Whatwe’vedoneismakechemicalmodificationstothevirustoputapolymercoataroundit-it’sastealthviruswhenyouinjectit,"hesaid.

11.Afterthestealthvirusinfectsthetumour,itreplicates,butthecopiesdonothavethechemicalmodifications.Iftheyescapefromthetumour,thecopieswillbequicklyrecognisedandmoppedupbythebody’simmunesystem.

12.Thetherapywouldbeespeciallyusefulforsecondarycancers,calledmetastases,whichsometimesspreadaroundthebodyafterthefirsttumourappears."There’sanawfulstatisticofpatientsinthewest...withmalignantcancers;75%ofthemgoontodiefrommetastases,"saidProfSeymour.

13.Twovirusesarelikelytobeexaminedinthefirstclinicaltrials:adenovirus,whichnormallycausesacold-likeillness,andvaccinia,whichcausescowpoxandisalsousedinthevaccineagainstsmallpox.Forsafetyreasons,bothwillbedisabledtomakethemlesspathogenicinthetrial,butProfSeymoursaidheeventuallyhopestousenaturalviruses.

14.Thefirsttrialswilluseuncoatedadenovirusandvacciniaandwillbedeliveredlocallytolivertumours,inordertoestablishwhetherthetreatmentissafeinhumansandwhatdoseofviruswillbeneeded.Severalmoreyearsoftrialswillbeneeded,eventuallyalsoonthepolymer-coatedviruses,beforethetherapycanbeconsideredforuseintheNHS.Thoughtheapproachwillbeexaminedatfirstforcancersthatdonotrespondtoconventionaltreatments,ProfSeymourhopesthatonedayitmightbeappliedtoallcancers.

Questions1-6

Dothefollowingstatementsagreewiththeinformationgiveninthereadingpassage?Forquestions1-6write

TRUEifthestatementagreeswiththeinformation

FALSEifthestatementcontradictstheinformation

NOTGIVENifthereisnoinformationonthisinthepassage

1.Virustherapy,ifsuccessful,hasanadvantageineliminatingside-effects.

2.CancerResearchUKisquitehopefulaboutProfessorSeymour’sworkonthevirustherapy.

3.Viruscankillcancercellsandstopthemfromgrowingagain.

4.Cancer’sAchilles’heelreferstothefactthatvirusmaystaysafelyinatumorandreplicate.

5.Toinfectthecancercells,agooddealofvirusesshouldbeinjectedintothetumor.

6.Researchesonanimalsindicatethatviruscouldbeusedasanewwaytotreatdrug-resistanttumors.

Question7-9

Basedonthereadingpassage,choosetheappropriateletterfromA-Dforeachanswer.

7.Informationaboutresearchesonviruseskillingtumorcellscanbefound

(A)onTV

(B)inmagazines

(C)oninternet

(D)innewspapers

8.Totreattumorsspreadingoutinbody,researcherstryto

(A)changethebody’immunesystem

(B)injectchemotherapydrugsintobloodstream.

(C)increasetheamountofinjection

(D)disguisethevirusesonthewaytotumors.

9.Whenthechemicalmodifiedvirusintumorreplicates,thecopies

(A)willsoonescapefromthetumorandspreadout.

(B)willbewipedoutbythebody’simmunesystem.

(C)willbeimmediatelyrecognizedbytheresearchers.

(D)willeventuallystopthetumorfromspreadingout.

Questions10-13

Completethesentencesbelow.Chooseyouranswersfromthelistofwords.Youcanonlyuseeachwordonce.

NBTherearemorewordsinthelistthanspacessoyouwillnotusethemall.

Inthefirstclinicaltrials,scientistswilltryto……10……adenovirusandvaccinia,soboththeviruseswillbelesspathogenicthanthe……11…….Theseuncoatedviruseswillbeapplieddirectlytocertainareastoconfirmsafetyonhumanbeingsandtheright……12……needed.Theexperimentswillfirstlybe……13……tothetreatmentofcertaincancers

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