复旦大学：《学术英语（医学）》补充阅读练习_Plague.pdf_大学文库

Passage 1 Plague Plague is primarily a disease of densely populated zones, households above all else, and its perpetuation and reinforcement involve complex relationship among wild rodents, bacteria, insect vector, and humans. Occasional plague outbreaks can occur almost anywhere, but for the disease to become rooted an environment must exist which can support a high density of rodent hosts living in proximity with human beings. Endemic plague among rodents remote from human habitation poses a danger only to humans who invade those zones The bacterium responsible for bubonic plague is Yersinia(formerly Pasteurella pestis, one of the most pervasive, persistent, and dangerous life forms in the world. It lives in the bloodstream of dozens of varieties of rodents(rats, ground squirrel marmots,etc. ), but it is most commonly found among rats. The simple presence of Y. Pestis in the rodent population has not always meant an immediate threat to humankind. Once the disease becomes epizootic among rodents in proximity to people, however, epidemic outbreaks have followed with consequences equally disastrous to humans and to the rodent hosts Why an epizootic starts is not clear. The bacterium begins to multiply. As it does SO, it poisons its hosts blood, and the rodent dies. This is why a"rat-fall', the sudden appearance of dead or dying rats has come to be regarded as the precursor of a human epidemic. The most common vector for transferring Y. Pestis from one body to another is the rat flea, Xenopsylla cheopis, though other flea types are almost as efficient. Among the some 200 known fleas which transfer plague, one of the least efficient is the human body flea(Pulex irritans), and it therefore seldom happens that flea-borne plague will travel from one person to another Feeding fleas transfer Y. Pestis from rat to rat or from rat to human. The flea lives in the rat s fur and feeds on blood through the skin when the flea is on an infected rat it draws Y. Pestis into its own stomach with the blood it ingests. In turn, the plague bacterium multiplies in the fleas stomach, eventually plugging it with live bacteria The flea, which can no longer swallow fresh blood, regurgitates live bacteria when next it tries to feed, and those bacteria pass through the break in the skins surface The flea defecates as it attempts to feed, and this provides another source for infective material When the host rat dies and its body cools, the blocked or engorged flea moves or to the next living creature available. If that creature is humane the flea will bite in an effort to feed, thereby introducing Y. Pestis into the human bloodstream. A bubonic infection follows. Rats are the essential plague incubators. Even humans dying of plague have too little of the bacterial agent in their bloodstream to continue the nfective chain, and modern physicians believe that plague victims can be nursed in an pen ward without danger. The exceptions are patients with pneumonic plague, where the bacteria have entered the lungs(rather than remaining in the bloodstream) to b expelled in droplets with every breath or cough. Pneumonic plague is highly contagious, and it is almost al ways fatal

Passage 1 Plague Plague is primarily a disease of densely populated zones, households above all else, and its perpetuation and reinforcement involve complex relationship among wild rodents, bacteria, insect vector, and humans. Occasional plague outbreaks can occur almost anywhere, but for the disease to become rooted, an environment must exist which can support a high density of rodent hosts living in proximity with human beings. Endemic plague among rodents remote from human habitation poses a danger only to humans who invade those zones. The bacterium responsible for bubonic plague is Yersinia (formerly Pasteurella) pestis, one of the most pervasive, persistent, and dangerous life forms in the world. It lives in the bloodstream of dozens of varieties of rodents (rats, ground squirrels, marmots, etc.), but it is most commonly found among rats. The simple presence of Y. Pestis in the rodent population has not always meant an immediate threat to humankind. Once the disease becomes epizootic among rodents in proximity to people, however, epidemic outbreaks have followed with consequences equally disastrous to humans and to the rodent hosts. Why an epizootic starts is not clear. The bacterium begins to multiply. As it does so, it poisons its host’s blood, and the rodent dies. This is why a “rat-fall”, the sudden appearance of dead or dying rats has come to be regarded as the precursor of a human epidemic. The most common vector for transferring Y. Pestis from one body to another is the rat flea, Xenopsylla cheopis, though other flea types are almost as efficient. Among the some 200 known fleas which transfer plague, one of the least efficient is the human body flea (Pulex irritans), and it therefore seldom happens that flea-borne plague will travel from one person to another. Feeding fleas transfer Y. Pestis from rat to rat or from rat to human. The flea lives in the rat’s fur and feeds on blood through the skin. When the flea is on an infected rat, it draws Y. Pestis into its own stomach with the blood it ingests. In turn, the plague bacterium multiplies in the flea’s stomach, eventually plugging it with live bacteria. The flea, which can no longer swallow fresh blood, regurgitates live bacteria when next it tries to feed, and those bacteria pass through the break in the skin’s surface. The flea defecates as it attempts to feed, and this provides another source for infective material. When the host rat dies and its body cools, the blocked or engorged flea moves on to the next living creature available. If that creature is humane, the flea will bite in an effort to feed, thereby introducing Y. Pestis into the human bloodstream. A bubonic infection follows. Rats are the essential plague incubators. Even humans dying of plague have too little of the bacterial agent in their bloodstream to continue the infective chain, and modern physicians believe that plague victims can be nursed in an open ward without danger. The exceptions are patients with pneumonic plague, where the bacteria have entered the lungs (rather than remaining in the bloodstream) to be expelled in droplets with every breath or cough. Pneumonic plague is highly contagious, and it is almost always fatal

Passage 2 Knockout blow a breakthrough in understanding how tuberculosis(TB)lies low in the body could lead to a fast and effective cure for the disease TB is a growing threat as drug- resistant forms emerge. At present, a course of antibiotics lasting between 6 and 12 months is needed to cure tB. It takes this long because the existing drugs target rapidly dividing bacteria, rather than the slow-growing ones responsible for persistent infections But when John McKinney, who is now at the rockefeller University in New York, reviewed research done in the 1950s, he was intrigued by a study of bacteria taken from long-infected lung tissue. Unlike Mycobacterium tuberculosis grown in the lab, these bacteria got their energy from fatty acids, not sugars McKinney and his colleagues then targeted the pathway bacteria use to break down fatty acids. They genetically engineered TB bacteria that lacked a key enzyme called isocitrate lyase. When they infected mice with these mutant bacteria, a normal infection developed but the animals immune systems were able to clear the bacteri The results suggest that the m. tuberculosis bacterium alters its metabolism to counter the immune system's attack. McKinney and his collaborators are now studying the structure of the enzyme and are developing drugs to inhibit it. They hope to begin animal trials by the end of the year 2000 If all goes well, TB patients could soon get the drugs that target rapidly growing bacteria along with another one that targets persistent bugs. This one-two punch could eliminate the bacteria in weeks instead of months, McKinney says It would be wonderful to imagine that we could treat tuberculosis like any other bacterial infection, says James Sacchettini, one of McKinney's collaborators at Texas A&M University in College Station. If we could treat tuberculosis in two to three weeks, I think we'd have a really good chance of eradicating the disease Vocabulary tuberculosis n.肺结核 emerge v.出现,形成 screen 1:筛选 persistent a.持续久]的,持久的 ntrigue vt.激起…兴趣 isocitrate lyase异柠檬酸(裂合)酶 metabolism n新陈代谢 inhibit 1:抑制 target 1:瞄准:把.作为目标[对象 eliminate y消除,排除 eradicate 1:.根除

Passage 2 Knockout Blow A breakthrough in understanding how tuberculosis (TB) lies low in the body could lead to a fast and effective cure for the disease. TB is a growing threat as drug-resistant forms emerge. At present, a course of antibiotics lasting between 6 and 12 months is needed to cure TB. It takes this long because the existing drugs target rapidly dividing bacteria, rather than the slow-growing ones responsible for persistent infections. But when John McKinney, who is now at the Rockefeller University in New York, reviewed research done in the 1950s, he was intrigued by a study of bacteria taken from long-infected lung tissue. Unlike Mycobacterium tuberculosis grown in the lab, these bacteria got their energy from fatty acids, not sugars. McKinney and his colleagues then targeted the pathway bacteria use to break down fatty acids. They genetically engineered TB bacteria that lacked a key enzyme called isocitrate lyase. When they infected mice with these mutant bacteria, a normal infection developed but the animals’ immune systems were able to clear the bacteria. The results suggest that the M. tuberculosis bacterium alters its metabolism to counter the immune system’s attack. McKinney and his collaborators are now studying the structure of the enzyme and are developing drugs to inhibit it. They hope to begin animal trials by the end of the year 2000. If all goes well, TB patients could soon get the drugs that target rapidly growing bacteria along with another one that targets persistent bugs. This one-two punch could eliminate the bacteria in weeks instead of months,4 McKinney says. “It would be wonderful to imagine that we could treat tuberculosis like any other bacterial infection,” says James Sacchettini, one of McKinney’s collaborators at Texas A&M University in College Station. “If we could treat tuberculosis in two to three weeks, I think we’d have a really good chance of eradicating the disease.” Vocabulary tuberculosis n. 肺结核 emerge vi. 出现，形成 screen v. 筛选 persistent a. 持续久]的，持久的 intrigue vt. 激起…兴趣 isocitrate lyase 异柠檬酸(裂合)酶 metabolism n. 新陈代谢 inhibit v. 抑制 target v. 瞄准；把...作为目标[对象] eliminate v. 消除，排除 eradicate v. 根除

Passage 3 Directions: There are 10 blanks in the following passage. For each blank there are four choices marked A, B, C, and D. You should choose the ONE that best fits into the passage. There is increasing 1 that remotely monitoring patients with heart failure using information technology can help improve outcomes and quality of care. Integrating such telemonitoring into existing health care 2 is challenging. The technology used varies from simple to complex, although the 3 of the data to the health care team is straightforward. The best method of displaying the data is 4 to be determined, as is the best combination of variables to monitor. Patient acceptability is rarely a problem, but reimbursement of the costs associated with telemonitoring is often a barrier to implementation. Patients with heart failure are often elderly, have decreased 5 and have less social support. This can make clinic 6 difficult. Local review by the family doctor may be more convenient, but the primary care team may lack the specialist knowledge and experience to 7 monitor heart failure. Home visit by a specialist nurse is helpful but expensive, and few health care systems can provide this service for any length of time. Telehealth has the potential to improve 8 to high-quality disease management, and telemonitoring has developed rapidly over the past decade. In the simplest model, a patient receives support from a health care professional 9 the telephone. The patient monitors his or her symptoms and weight and reports these during a 10 structured telephone call. 1. A. evidence B. incidence C. occurrence D. relevance 2. A. exercise B. practice C. training D. career 3. A. transmission B. transfusion C. transcription D. translation 4. A. not B. none C. yet D. still 5. A. mobility B. morbidity C. mortality D. morality 6. A. appearance B. attendance C. activities D. task 7. A. occasionally B. possibly C. easily D. optimally 8. A. acceptance B. entry C. access D. entrance 9. A. in B. over C. by D. with 10. A. lectured B. structured C. constructed D. nurtured