当代研究生英语下册课文原文

UNIT 1 PASSAGES OF HUMAN GROWTH (I)1 A person’s life at any given time incorporates both external and internal aspects. The external system is composed of our memberships in the culture: our job, social class, family and social roles, how we present ourselves to and participate in the world. The interior realm concerns the meanings this participation has for each of us. In what ways are our values, goals, and aspirations being invigorated or violated by our present life system? How many parts of our personality can we live out, and what parts are we suppressing? How do we feel about our way of living in the world at any given time?2 The inner realm is where the crucial shifts in bedrock begin to throw a person off balance, signaling the necessity to change and move on to a new footing in the next stage of development. These crucial shifts occur throughout life, yet people consistently refuse to recognize that they possess an internal life system. Ask anyone who seems down, “Why are you feeling low?” Most will displace the inner message onto a marker event: “I’ve been down since we moved, since I changed jobs, since my wife went back to graduate school and turned into a damn social worker in sackcloth,” and so on. Probably less than ten percent would say: “There is some unknown disturbance within me, and even though it’s painful, I feel I have to stay with it and ride it out.” Even fewer people would be able to explain that the turbulence they feel may have no external cause. And yet it may not resolve itself for several years.3 During each of these passages, how we feel about our way of living will undergo subtle changes in four areas of perception. One is the interior sense of self in relation to others. A second is the proportion of safeness to danger we feel in our lives. A third is our perception of time—do we have plenty of it, or are we beginning to feel that time is running out? Last, there will be some shift at the gut level in our sense of aliveness or stagnation. These are the hazy sensations that compose the background tone of living and shape the decisions on which we take action.4 The work of adult life is not easy. As in childhood, each step presents not only new tasks of development but requires a letting go of the techniques that worked before. With each passage some magic must be given up, some cherished illusion of safety and comfortably familiar sense of self must be cast off, to allow for the greater expansion of our own distinctiveness.Pulling Up Roots5 Before 18, the motto is loud and clear: “I have to get away from my parents.” But the words are seldom connected to action. Generally still safely part of our families, even if away at school, we feel our autonomy to be subject to erosion from moment to moment.6 After 18, we begin Pulling Up Roots in earnest. College, military service, and short-term travels are all customary vehicles our society provides for the first round trips between family and a base of one’s own. In the attempt to separate our view of the world from our family’s view, despite vigorous protestations to the contrary—“I know exactly what I want!”— we cast about for any beliefs we can call our own. And in the process of testing those beliefs we are often drawn tofads, preferably those most mysterious and inaccessible to our parents.7 Whatever tentative memberships we try out in the world, the fear haunts us that we are really kids who cannot take care of ourselves. We cover that fear with acts of defiance and mimicked confidence. For allies to replace our parents, we turn to our contemporaries. They become conspirators. So long as their perspective meshes with our own, they are able to substitute fo r the sanctuary of the family. But that doesn’t last very long. And the instan t they diverge from the shaky ideals of “our group”, they are seen as betrayers. Rebounds to the family are common between the ages of 18 and 22.8 The tasks of this passage are to locate ourselves in a peer group role, a sex role, an anticipated occupation, an ideology or world view. As a result, we gather the impetus to leave home physically and the identity to begin leaving home emotionally.9 Even as one part of us seeks to be an individual, another part longs to restore the safety and comfort of merging with another. Thus one of the most popular myths of this passage is: We can piggyback our development by attaching to a Stronger One. But people who marry during this time often prolong financial and emotional ties to the family and relatives that impede them from becoming self-sufficient.10 A stormy passage through the Pulling Up Roots years will probably facilitate the normal progression of the adult life cycle. If one doesn’t have an identity crisis at this point, it will erupt during a later transition, when the penalties may be harder to bear.The Trying Twenties11 The Trying Twenties confront us with the question of how to take hold in the adult world. Our focus shifts from the interior turmoils of late adolescence—“Who am I?”“What is truth?”—and we become almost totally preoccupied with working out the externals. “How do I put my aspirations into effect?” “What is the best way to start?” “Where do I go?” “Who can help me?” “How did you do it?”12 In this period, which is longer and more stable compared with the passage that leads to it, the tasks are as enormous as they are exhilarating: To shape a Dream, that vision of ourselves which will generate energy, aliveness, and hope. To prepare for a lifework. To find a mentor if possible. And to form the capacity for intimacy, without losing in the process whatever consistency of self we have thus far mustered. The first test structure must be erected around the life we choose to try.13 Doing what we “should” is the most pervasive theme of the twenties. The “shoulds” are largely defined by family models, the press of the culture, or the prejudices of our peers. If the prevailing cultural instructions are that one should get married and settle down behind one’s own door, a nuclear family is born.14 One of the terrifying aspects of the twenties is the inner conviction that the choices we make are irrevocable. It is largely a false fear. Change is quite possible, and some alteration of our original choices is probably inevitable.15 Two impulses, as always, are at work. One is to build a firm, safe structure for the future by making strong commitments, to “be set”. Yet people who slip into a ready-made form without much self-examination are likely to find themselves locked in.16 The other urge is to explore and experiment, keeping any structure tentative and therefore easily reversible. Taken to the extreme, these are people who skip from one trial job and one limited personal encounter to another, spending their twenties in the transient state.17 Although the choices of our twenties are not irrevocable, they do set in motion a Life Pattern. Some of us follow the locked-in pattern, others the transient pattern, the wunderkind pattern, the caregiver pattern, and there are a number of others. Such patterns strongly influence the particular questions raised for each person during each passage through the life.18 Buoyed by powerful illusions and belief in the power of the will, we commonly insist in our twenties that what we have chosen to do is the one true course in life. Our backs go up at the merest hint that we are like our parents, that two decades of parental training might be reflected in our current actions and attitudes.19 “Not me,” is the motto, “I’m different.”UNIT 2 AIDS IN THE THIRD WORLD A GLOBAL DISASTER1 In rich countries AIDS is no longer a death sentence. Expensive drugs keep HIV-positive patients alive and healthy, perhaps indefinitely. Loud public-awareness campaigns keep the number of infected Americans, Japanese and West Europeans to relatively low levels. The sense of crisis is past.2 In developing countries, by contrast, the disease is spreading like nerve gas in a gentle breeze. The poor cannot afford to spend $10,000 a year on wonder pills. Millions of Africans are dying. In the longer term, even greater numbers of Asians are at risk. For many poor countries, there is no greater or more immediate threat to public health and economic growth. Yet few political leaders treat it as a priority.3 Since HIV was first identified in the 1970s, over 47 million people have been infected, of whom 14 million have died. Last year saw the biggest annual death toll yet: 2.5 million. The disease now ranks fourth among the wor ld’s big killers, after respiratory infections, diarrhea disorders and tuberculosis. It now claims many more lives each year than malaria, a growing menace, and is still nowhere near its peak. If India and other Asian countries do not take it seriously, th e number of infections could reach “a new order of magnitude”, says Peter Piot, head of the UN’s AIDS programme.4 The human immunodeficiency virus (HIV), which causes acquired immune deficiency syndrome (AIDS), is thought to have crossed from chimpanzees to humans in the late 1940s or early 1950s in Congo. It took several years for the virus to break out of Congo’s dense and sparsely populated jungles but, once it did, it marched with rebel armies through the continent’s numerous war zones, rode with truckers from one rest-stop brothel to the next, and eventually flew,perhaps with an air steward, to America, where it was discovered in the early 1980s. As American homosexuals and drug infectors started to wake up to the dangers of bath-houses andneedle-sharing, AIDS was already devastating Africa.5 So far, the worst-hit areas are east and southern Africa. In Botswana, Namibia, Swaziland and Zimbabwe, between a fifth and a quarter of people aged 15-49 are afflicted with HIV or AIDS. In Botswana, children born early in the next decade will have a life expectancy of 40; without AIDS it would have been near 70. Of the 25 monitoring sites in Zimbabwe where pregnant women are tested for HIV, only two in 1997 showed prevalence below 10%. At the remaining 23 sites,20-50% of women were infected. About a third of these women will pass the virus on to their babies.6 The region’s giant, South Africa, was largely protected by its isolation from the rest of the world during the apartheid years. Now it is host to one in ten of the world’s new infections—more than any other country. In the country’s most populous province, KwaZulu-Natal, perhaps a third of sexually active adults are HIV-positive.7 Asia is the next disaster-in-waiting. Already, 7 million Asians a re infected. India’s 930 million people look increasingly vulnerable. The Indian countryside, which most people imagined relatively AIDS-free, turns out not to be. A recent study in Tamil Nadu found over 2% of rural people to be HIV-positive: 500,000 peopl e in one of India’s smallest states. Since 10% had other sexually transmitted diseases (STDS), the avenue for further infections is clearly open. A survey of female STD patients in Poona, in Maharashtra, found that over 90% had never had sex with anyone but their husband; and yet 13.6% had HIV.8 No one knows what AIDS will do to poor countries’ economies, for nowhere has the epidemic run its course. An optimistic assessment, by Alan Whiteside of the University of Natal, suggests that the effect of AIDS on measurable GDP will be slight. Even at high prevalence, Mr. Whiteside thinks it will slow growth by no more than 0.6% a year. This is because so many people in poor countries do not contribute much to the formal economy. To put it even more crudely, where there is a huge oversupply of unskilled labour, the dead can easily be replaced.9 Other researchers are more pessimistic. AIDS takes longer to kill than did the plague, so the cost of caring for the sick will be more crippling. Modern governments, unlike medieval ones, tax the healthy to help look after the ailing, so the burden will fall on everyone. And AIDS, because it is sexually transmitted, tends to hit the most energetic and productive members of society. A recent study in Namibia estimated that AIDS cost the country almost 8% of GNP in 1996. Another analysis predicts that Kenya’s GDP will be 14.5% smaller in 2005 than it would have been without AIDS, and that income per person will be 10% lower.The cost of the disease10 In general, the more advanced the economy, the worse it will be affected by a large number of AIDS deaths. South Africa, with its advanced industries, already suffers a shortage of skilled manpower, and cannot afford to lose more. In better-off developing countries, people have more savings tofall back on when they need to pay medical bills. Where people have health and life insurance, those industries will be hit by bigger claims. Insurers protect themselves by charging more or refusing policies to HIV-positive customers. In Zimbabwe, life-insurance premiums quadrupled in two years because of AIDS. Higher premiums force more people to seek treatment in public hospitals: in South Africa, HIV and AIDS could account for between 35% and 84% ofpublic-health expenditure by 2005, according to one projection.11 At a macro level, the impact of AIDS is felt gradually. But at a household level, the blow is sudden and catastrophic. When a breadwinner develops AIDS, his (or her) family is impoverished twice over: his income vanishes, and his relations must devote time and money to nursing him. Daughters are often forced to drop out of school to help. Worse, HIV tends not to strike just one member of a family. Husbands give it to wives, mothers to babies.12 The best hope for halting the epidemic is a cheap vaccine. Efforts are under way, but a vaccine for a virus that mutates as rapidly as HIV will be hugely difficult and expensive to invent. For poor countries, the only practical course is to concentrate on prevention. But this, too, will be hard, for a plethora of reasons.Sex is fun... Many feel that condoms make it less so. Zimbabweans ask: “Would you eat a sweet with its wrapper on?”... and discussion of it is often taboo. In Kenya, Christian and Islamic groups have publicly burned anti-AIDS leaflets and condoms, as a protest against what they see as the encouragement of promiscuity.Poverty. Those who cannot afford television find other ways of passing the evening. People cannot afford antibiotics, so the untreated sores from STDS provide easy openings for HIV.Migrant labour. Since wages are much higher in South Africa than in the surrounding region, outsiders flock in to find work. Migrant miners (including South Africans forced to live far from their homes) spend most of the year in single-sex dormitories surrounded by prostitutes. Living with a one-in-40 chance of being killed by a rockfall, they are inured to risk. When they go home, they often infect their wives.War. Refugees, whether from genocide in Rwanda or state persecution in Myanmar, spread HIV as they flee. Soldiers, with their regular pay and disdain for risk, are more likely than civilians to contract HIV from prostitutes. When they go to war, they infect others. In Africa the problem is dire. In Congo, where no fewer than seven armies are embroiled, the government has accused Ugandan troops (which are helping the Congolese rebels) of deliberately spreading AIDS. Unlikely, but with estimated HIV prevalence in the seven armies ranging from 50% for the Angolans to an incredible 80% for the Zimbabweans, the effect is much the same. Sexism. In most poor countries, it is hard for a woman to ask her partner to use a condom. Wives who insist risk being beaten up. Rape is common, especially where wars rage. Forced sex is a particularly effective means of HIV transmission, because of the extra blood. Drinking. Asia and Africa makemany excellent beers. They are also home to a lot of people for whom alcohol is the quickest escape from the stresses of acute poverty. Drunken lovers are less likely to remember to use condoms.How to fight the virus13 Pessimists look at that situation and despair. But three success stories show that the hurdles to prevention are not impossibly high.14 First, Thailand. One secret of Thailand’s success has been timely, accurateinformation-gathering. HIV was first detected in Thailand in the mid-1980s, among male homosexuals. The health ministry immediately began to monitor other high-risk groups, particularly the country’s many heroin addicts and prostitutes. In the first half of 1988, HIV prevalence among drug injectors tested at one Bangkok hospital leapt from 1% to 30%. Shortly afterwards, infections soared among prostitutes.15 The response was swift. A survey of Thai sexual behaviour was conducted. The results, which showed men indulging in a phenomenal amount of unprotected commercial sex, were publicized. Thais were warned that a major epidemic would strike if their habits did not change. A “100% condom use” campaign persuaded prostitutes to insist on protection 90% of the time with non-regular customers.16 Most striking was the government’s success in persuading people that they were at risk long before they started to see acquaintances die from AIDS. There was no attempt to play down the spread of HIV to avoid scaring off tourists, as happened in Kenya. Thais were repeatedly warned of the dangers, told how to avoid them, and left to make their own choices. Most decided that a long life was preferable to a fast one.17 Second, Uganda. Thailand shows what is possible in a well-educated, fairly prosperous country. Uganda shows that there is hope even for countries that are poor and barely literate. President Yoweri Museveni recognized the threat shortly after becoming president in 1986, and deluged the country with anti-AIDS warnings.18 The key to Uganda’s success is twofold. First, Mr. Museveni made every government department take the problem seriously, and implement its own plan to fight the virus. Accurate surveys of sexual behaviour were done for only $20,000-30,000 each. Second, he recognized that his government could do only a limited amount, so he gave free rein to scores ofnon-governmental organizations (NGOS), usually foreign-financed, to do whatever it took to educate people about risky sex.19 Third, Senegal. If Uganda shows how a poor country can reverse the track of an epidemic, Senegal shows how to stop it from taking off in the first place. This West African country was fortunate to be several thousand mi les from HIV’s origin. In the mid-1980s, when other parts of Africa were already blighted, Senegal was still relatively AIDS-free. In concert withnon-governmental organizations and the press and broadcasters, the government set up a national AIDS-control programme to keep it that way.20 Contrast these three with South Africa. On December 1st, World AIDS Day, President Nelson Mandela told the people of KwaZulu-Natal that HIV would devastate their communities if not checked. The speech was remarkable not for its quality—Mr. Mandela is always able to move audiences—but for its rarity. Unlike Mr. Museveni, South Africa’s leader seldom uses his authority to encourage safer sex. It is a tragic omission. Whereas the potholed streets of Kampala are lined with signs promoting fidelity and condoms, this correspondent has, in eight months in South Africa, seen only two anti-AIDS posters, both in the UN’s AIDS office in Pretoria.UNIT 3 NEW FINDINGS OF HIV1 For almost four years, research into HIV has been dominated by a single theory about how the virus causes the catastrophic collapse of the immune defences that leads to AIDS. But the consensus on this theory is now crumbling, thanks in part to the work of a Dutch team led by immunologist Frank Miedema. If the Dutch team is right, the consequences will be profound. People with HIV may hope for new types of treatment. And some of the most cherished dogmas ofa multibillion-dollar research industry may be overturned.2 The prevailing view about how HIV causes AIDS is that every day the virus makes billions of copies of itself and, in doing so, kills billions of the key defence cells that it infects, a class of T cell known as CD4 cells. These vital cells orchestrate the body’s immune response. Every da y the infected person’s immune system attempts to replace these cells. After years of waging this immunological war, the body eventually fails to keep pace with the virus and the numbers of CD4 cells become dangerously low, leaving the body unable to defend itself against microorganisms and cancerous cells.3 But Miedema and his colleagues at the University of Amsterdam see things differently. They agree that the number of CD4 cells ultimately dwindles, but not because the virus is killing them off. In their view, the virus impairs the body’s ability to produce new CD4 cells, and—critically—it traps existing cells in lymph nodes and other tissues, preventing their movement in and out of the bloodstream. As large numbers of CD4 cells become trapped in this way, and the body fails to produce a sufficient number of new ones, the dwindling population of circulating cells becomes increasingly restricted in its range and ability to respond to different invading microbes.4 Naturally, the champions of the prevailing theory dispute the Dutch ideas. David Ho, chief architect and proponent of the accepted view, at the Aaron Diamond AIDS Research Center in New York, has told colleagues that “the whole field would have to be turned upside down if they were right”. But elsewhere, the controversial Dutch theory is gaining ground. Indeed, it builds on ideas that have been circulating since about 1990, among researchers such as Yvonne Rosenberg at TherImmune, a company in Maryland, and John Sprent, at the University of California, San Diego. Earlier this month, Miedema’s latest findings were aired at a major international meeting in Glasgow on new therapies for HIV—a sign that the ideas are attracting interest from those at the sharp end of AIDS treatment.5 The widely accepted view, that HIV is a mass murderer of cells, first took hold in 1995, when Ho and his colleagues in New York, and another group led by George Shaw of the University of Alabama at Birmingham, published two seminal papers in the journal Nature. These papers reported that there was a large and rapid turnover of CD4 cells in people with HIV infection, and that therapy with a powerful cocktail of antiviral drugs brought about huge and immediate increases in the numbers of these cells. The fact that the cells bounced back so quickly was due, Ho and Shaw reasoned, to the effects of the antiviral drugs. By stopping HIV from building new copies of itself, the drugs stopped the virus from killing (or “lysing”)cells, while new cells continued to be produced at a rapid rate. This compelling idea offered a simple explanation for how HIV could wreak such havoc. Overnight, the theory became dogma.6 Then, in November 1996, Miedema proposed an alternative view. His work at that time centred on telomeres. These are the small sections of DNA at each end of a chromosome that are shortened with each cycle of cell division. Miedema and his colleagues reasoned that if CD4 cells were being constantly destroyed, then the unremitting cell division needed to supply the new cells would wear away their telomeres.7 Yet the length of the telomeres turned out to be stable. “This means that cells are not being turned over in massive numbers,” Miedema said at the time. “Our data cannot be interpreted any other way.” He sugg ested that if the cells are disappearing but not being destroyed, then HIV must be hitting their production instead.8 Ho disagreed. He said that an enzyme called telomerase, which rebuilds telomeres in cells that need to carry on dividing indefinitely, such as reproductive cells, is overactive in people with HIV. The enzyme is active in their immune cells, where normally it is absent. He argued that this overactivity could explain why the telomeres do not shorten. But Miedema’s group has tested T cells from people with HIV and has found no evidence of increased telomerase activity. Ho retorts that their tests are not sufficiently sensitive, and that special assays are needed.9 Ho’s views find support from Tomas Lindahl, a telomere specialist at Britain’s Imperial Cancer Research Fund. “I don’t think the telomere argument... is very strong,” he says. “Telomerase activity is notoriously difficult to measure.”10 Indeed, other researchers now suggest that Miedema may have misinterpreted his original results. They believe that he found the average length of telomeres to be stable because he missed those cells that were disappearing most rapidly—the very cells that would have the shortest telomeres if they were turning over at the rate Ho suggests.11 Whether the telomere research is significant or not, a growing number of researchers now believe that HIV does prevent the production of new T cells. Mike McCune at the University of California, San Francisco, suggests that the site of this inhibition could be the thymus, the organwhere CD4 cells develop. But the Dutch group and others were increasingly convinced that there was another possibility. If T cells were disappearing from the blood, perhaps it was not just because new cells were failing to appear. It could also be that existing cells were being hidden away in other tissues. Miedema and his colleagues were puzzled by the flood of CD4 cells rushing into the blood that Ho and others had observed when infected people start to take antiviral drugs. They knew that the rise was rapid and then reached a plateau, and so they argued that it could not be due to the production of new cells because this would lead to a slow, more sustained increase. Instead, it must be due to the release of existing CD4 cells trapped in lymph nodes and elsewhere.12 Their own experiments supported their hunch. When they analysed T cells in the blood of people with HIV as they started antiviral treatment, they found the same steep rise of CD4 cells, reaching a plateau within three weeks. The findings also appear to explain a phenomenon that has puzzled doctors, namely that the more advanced a person’s HIV infection, the greater the initial rise in their CD4 cell count when they start antiviral therapy. This, says Miedema, is because more and more cells become trapped as infection persists. If Ho and Shaw were right, the increase in CD4 cells should be modest in such people, because the virus would have killed so many of their cells.13 But the nature of the newly appeared cells gave the Dutch team further support. They were virtually all so-called CD4 memory cells——that is, cells that had already come into contact with antigens from specific invading microbes. What is more, so-called naive CD4 cells——those that have not yet met an antigen—did not immediately appear. These findings strengthen the argument that antiviral drugs were not preventing HIV from killing cells, but simply releasing into the blood mature CD4 cells that had been trapped elsewhere.14 An obvious response to the suggestion that CD4 cells are disappearing from blood into lymph tissue might be: “ Why not count them?” Unfortunately, this is easier said than done. Removinglymph tissue is awkward and unpleasant—and may be unhelpful to patients whose immune systems are already disrupted. Equally important, researchers would not know exactly how many CD4 cells a patient had in the first place, and therefore would have no baseline figure with which to compare their estimate. Finally, even in healthy individuals, the number of CD4 cells in the bloodstream is a tiny proportion—between 1 and 2 per cent—of the total. So even if the researchers measured their decline in the bloodstream and estimated their numbers in the lymph nodes over a period of time, the margin of error would probably be too wide for the counts to be meaningful.15 The Dutch group now has the backing of a growing number of immunologists. Brigitte Autran at the Pitié-Salpetrière Hospital in Paris has found that, in people with HIV who take powerful drug cocktails, the immune system appears to be able to take a break from the damaging effects of the virus and boost its numbers of naive CD4 cells. This implies that the unchecked virus does indeed prevent the production of new CD4 cells. And, in the latest move, also reported at the Glasgow meeting, Miedema found that the immature。