2015年医学博士外语真题试卷

A mother who is suffering from cancer can pass on the disease to her unborn child in extremely rare cases,【C1】______a new case report published in PNAS this week.

According to researchers in Japan and at the Institute for Cancer Research in Sutton, UK, a Japanese mother had been diagnosed with leukemia a few weeks after giving birth,【C2】___tumors were discovered in her daughter’s cheek and lung when she was 11 months old. Genetic analysis showed that the baby’s cancer cells had the same mutation as the cancer cells of the mother. But the cancer cells contained no DNA whatsoever from the father,【C3】___would be expected if she had inherited the cancer from conception. That suggests the cancer cells made it into the unborn child’s body across the placental barrier.

The Guardian claimed this to be the first【C4】___case of cells crossing the placental barrier. But this is not the case — microchimerism,【C5】cells are exchanged between a mother and her unborn child, is thought to be quite common, with some cells thought to pass from fetus to mother in about 50 to 75 per cent of cases and to go the other way about half【C6】___.

As the BBC pointed out, the greater【C7】___in cancer transmission from mother to fetus had been how cancer cells that have slipped through the placental barrier could survive in the fetus without being killed by its immune system. The answer, in this case at least, lies in a second mutation of the cancer cells, which led to the【C8】___of the specific features that would have allowed the fetal immune system to detect the cells as foreign. As a result, no attack against the invaders was launched.

【C9】___, according to the researchers there is little reason for concern of “cancer danger”. Only 17 probable cases have been reported worldwide and the combined【C10】___of cancer cells both passing the placental barrier and having the right mutation to evade the baby’s immune system is extremely low.

The American Society of Clinical Oncology wrapped its annual conference this week, going through the usual motions of presenting a lot of drugs that offer some added quality or extension of life to those suffering from a variety of as-yet incurable diseases. But buried deep in an AP story are a couple of promising headlines that seems worthy of more thorough review, including one treatment study where 100 percent of patients saw their cancer diminish by half.

First of all, it seems pharmaceutical companies are moving away from the more cost-effective one-size-fits-all approach to drug development and embracing the long tail of cancer treatments, engineering drugs that only work for a small percentage of patients but work very effectively within that group.

Pfizer announced that one such drug it’s pushing into late-stage testing is target for 4% of lung cancer patients. But more than 90% of that tiny cohort responded to the drug in initial tests, and nine out often is getting pretty close to the ideal ten out of ten. By gearing drugs toward more boutique treatments rather than broad umbrella pharmaceuticals that try to fit for everyone it seems cancer researchers are making some headway. But how can we close the gap on that remaining ten percent?

Ask Takeda Pharmaceutical and Celgene, two drug makers who put aside competitive interests to test a novel combination of their treatments. In a test of 66 patients with the blood disease multiple myeloma, a full 100 percent of the subjects saw their cancer reduced by half. Needless to say, a 100 percent response to a cancer drug (or in this case a drug cocktail) is more or less unheard of. Moreover, this combination never would’ve been tried if two competing companies hadn’t sat down and put their heads together.

Are there more potentially effective drug combos out there separated by walls of competitive interest and proprietary information? Who’s to say, but it seems like with the vast amount of money and research being pumped into cancer drug development, the odds are pretty good. And if researchers can start pushing more of their response numbers toward 100 percent, we can more easily start talking about oncology’s favorite four-letter word: cure.

Liver disease is the 12th -leading cause of death in the U. S. , chiefly because once it’s determined that a patient needs a new liver it’s very difficult to get one. Even in case where a suitable donor match is found, there’s no guarantee a transplant will be successful. But researchers at Massachusetts General Hospital have taken a huge step toward building functioning livers in the lab, successfully transplanting culture-grown livers into rats.

The livers aren’t grown from scratch, but rather within the infrastructure of a donor liver. The liver cells in the donor organ are washed out with a detergent that gently strips away the liver cells, leaving behind a biological scaffold of proteins and extracellular architecture that is very hard to duplicate synthetically.

With all of that complicated infrastructure already in place, the researchers then seeded the scaffold (支架) with liver cells isolated from healthy livers, as well as some special endothelial cells to line the bold vessels. Once repopulated with healthy cells, these livers lived in culture for 10 days.

The team also transplanted some two-day-old recellularized livers back into rats, where they continued to thrive for eight hours while connected into the rats’ vascular systems. However, the current method isn’t perfect and cannot seem to repopulate the blood vessels quite densely enough and the transplanted livers can’t keep functioning for more than about 24 hours (hence the eight-hour maximum for the rat transplant).

But the initial successes are promising, and the team thinks they can overcome the blood vessel problem and get fully functioning livers into rats within two years. It still might be a decade before the tech hits the clinic, but if nothing goes horribly wrong — and especially if stem-cell research establishes a reliable way to create healthy liver cells from the very patients who need transplants — lab-generated livers that are perfect matches for their recipients could become a reality.

Patients whose eyes have suffered heat or chemical burns typically experience severe damage to the cornea—the thin, transparent front of the eye that refracts light and contributes most of the eye’s focusing ability. In a long-term study, Italian researchers use stem cells taken from the limbus, the border between the cornea and the white of the eye, to cultivate a graft of healthy cells in a lab to help restore vision in eyes. During the 10-years study, the researchers implanted the healthy stem cells into the damaged cornea in 113 eyes of 112 patients. The treatment was fully successful in more than 75 percent of the patients, and partially successful in 13 percent. Moreover, the restored vision remained stable over 10 years. Success was defined as an absence of all symptoms and permanent restoration of the cornea.

Treatment outcome was initially assessed at one year, with up to 10 years of follow-up evaluations. The procedure was even successful in several patients whose burn injuries had occurred years earlier and who had already undergone surgery.

Current treatment for burned eyes involves taking stem cells from a patient’s healthy eye, or from the eyes of another person, and transferring them to the burned eye. The new procedure, however, stimulates the limbal stem cells from the patient’s own eye to reproduce in a lab culture. Several types of treatments using stem cells have proven successful in restoring vision, but the long-term effectiveness shown here is significant. The treatment is only for blindness caused by damage to the cornea; it is not effective for repairing damaged retinas or optic nerves.

Chemical eye burns often occur in the workplace, but can also happen due to mishaps involving household cleaning products and automobile batteries.

The results of the study, based at Italy’s University of Modena and Reggio Emilia, were published in the June 23 online issue of the New England Journal of Medicine.

Here is a shaming statistic: divide the US by race, sex and county of residence, and differences in average life expectancy across the various groups can exceed 30 years. The most disadvantaged look like denizens of a poor African country: a boy born on a Native American reservation in Jackson County, South Dakota, for example, will be lucky to reach his 60th birthday. A typical child in Senegal can expect to live longer than that.

America is not alone in this respect. While the picture is extreme in other rich nations, health inequalities based on race, sex and class exist in most societies—and are only partly explained by access to healthcare.

But fresh insights and solutions may soon be at hand. An innovative project in Chicago to unite sociology and biology is blazing the trail (开创), after discovering that social isolation and fear of crime can help to explain the alarmingly high death rate from breast cancer among the city’s black women. Living in these conditions seems to make tumors more aggressive by changing gene activity, so that cancer cells can use nutrients more effectively.

We are already familiar with the lethal effect of stress on people clinging to the bottom rungs of the societal ladder, thanks to pioneering studies of British civil servants conducted by Michael Marmot of University College London. What’s exciting about the Chicago project is that it both probes the mechanisms involved in a specific disease and suggests precise remedies. There are drugs that may stave tumors of nutrients and community coordinators could be employed to help reduce social isolation. Encouraged by the US National Institutes of Health, similar projects are springing up to study other pockets of poor health in populations ranging from urban black men to white poor women in rural Appalachia.

To realize the full potential of such projects, biologists and sociologists will have to start treating one other with a new respect and learn how to collaborate outside their comfort zones. Too many biomedical researchers still take the arrogant view that sociology is a “soft science” with little that’s serious to say about health. And too many sociologists reject any biological angle—fearing that their expertise will be swept aside and that this approach will be used to bolster discredited theories of eugenics, or crude race-based medicine.

It’s time to drop these outdated attitudes and work together for the good of society’s most deprived members. More important, it’s time to use this fusion of biology and sociology to inform public policy. This endeavor has huge implications, not least in cutting the wide health gaps between blacks and whites, rich and poor.

American researchers are working on three antibodies that many mark a new step on the path toward an HIV vaccine, according to a report published online Thursday, July 8, 2010, in the journal Science.

One of the antibodies suppresses 91 percent of HIV strains, more than any AIDS antibody ever discovered, according to a report on the findings published in the Wall Street Journal. The antibodies were discovered in the cells of a 60-year-old African-American gay man whose body produced them naturally. One antibody in particular is substantially different from its precursors, the Science study says.

The antibodies could be tried as a treatment for people already infected with HIV, the WSJ reports. At the very least, they might boost the efficacy of current antiretroviral drugs.

It is welcome news for the 33 million people the United Nations estimated were living with AIDS at the end of 2008.

The WSJ outlines the painstaking method the team used to find the antibody amid the cells of the African-American man, known as Donor 45. First they designed a probe that looks just like a spot on a particular molecule on the cells that HIV infects. They used the probe to attract only the antibodies that efficiently attack that spot. They screened 25 million of Donor 45’s cell to find just 12 cells that produced the antibodies.

Scientists have already discovered plenty of antibodies that either don’t work at all or only work on a couple of HIV strains. Last year marked the first time that researchers found “broadly neutralizing antibodies, ” which knock out many HIV strains. But none of those antibodies neutralized more than about 40 percent of them, the WSJ says. The newest antibody, at 91 percent neutralization, is a marked improvement.

Still, more work needs to be done to ensure the antibodies would activate the immune system to produce natural defenses against AIDS, the study authors say. They suggest three test methods that blend the three new antibodies together in raw form to prevent transmission of the virus, such as from mother to child; in a microbicide gel that women or gay men could use before sex to prevent infection; or as a treatment for HIV/AIDS, combined with antiretroviral drug.

If the scientists can find the right way to stimulate production of the antibodies, they think most people could produce then, the WSJ says.

Whitening the world’s roofs would offset the emissions of the world’s cars for 20 years, according to a new study from Lawrence Berkeley National Laboratory. Overall, installing lighter-colored roofs and pavements can cancel the heat effect of two years of global carbon dioxide emissions, Berkeley Lab says. It’s the first roof-cooling study to use a global model to examine the issue.

Lightening up roofs and pavement can offset 57 billion metric tons of carbon dioxide, about double the amount the world emitted in 2006, the study found. It was published in the journal Environmental Research Letters.

Researchers used a conservative estimate of increased albedo, or solar reflection, suggesting that purely white roofs would be even better. They increased the albedo of all roof by 0. 25 and pavement by 0. 15. That means a black roof, which has an albedo of zero, would only need to be replaced by a roof of a cooler color — which might be more feasible to implement than a snowy white roof. Berkeley Lab says.

The researchers extrapolated a roof’s CO₂offset over its average lifespan. If all roofs were converted to white or cool colors, they would offset about 24 gigatons (24 billion metric tons) of CO₂, but only once. But assuming roofs last about 20 years, the researchers came up with 1. 2 gigatons per year. That equates to offsetting the emissions of roughly 300 million cars, all the in the world, for 20 years.

Pavements and roofs cover 50 to 65 percent of urban areas and cause a heat-island effect because they absorb so much heat. That’s why cities are significantly warmer than surrounding rural areas. This effect makes it harder—and therefore more expensive — to keep buildings cool in the summer. Winds also move the heat into the atmosphere, causing a regional warming effect.

Energy secretary Steven Chu, a Nobel Laureate in physics (and former Berkeley Lab director), has advocated white roofs for years. He put his words into actions by directing all Energy Department offices to install white roofs. All newly installed roofs will be white, and black roofs might be replaced when it is cost-effective over the lifetime of the roof.

“Cool roofs are one of the quickest and lowest-cost ways we can reduce our global carbon emissions and begin the hard work of slowing climate change. ” He said in a statement.