Tag: disease

Wanted: Collaborative life-scientists for drug discovery

  • Venue: Science Magazine
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The golden age of drug discovery is over—at least for now. Over the past 10 years or so, a number of highly profitable drug patents have expired, and the blockbuster drugs of the 1990s have proved hard to replace. The pharmaceutical industry, which once made billions while transforming lives, has been forced to change how it operates. From megamergers and offshoring to the dramatic restructuring of R&D departments, pharma has become a very different employer.

In such a rapidly shifting industry, it’s hard for anyone to keep tabs on employment opportunities; weary and overwhelmed by experiments, graduate students and postdocs can find themselves completely overmatched.

It is easy to feel despondent when, in the United States alone, the pharmaceutical industry has shed more than 300,000 jobs since 2003, according to Challenger, Gray & Christmas. Yet, even as redundancies continue to make headlines, there are openings for aspiring biotech and pharmaceutical scientists. Those opportunities, though, may not be where they used to be, nor are the risks, incentives, and demands early-career scientists face the same as those of a decade ago.

Who will emerge as the major drug discoverers in the next decade? How can you join their ranks? Science Careers asked scientists from industry and academia to offer tips for those looking to enter the job market in the coming years.

The new world of pharma

One of the most important drivers of change in the pharmaceutical industry was a wave of patent expirations that really picked up steam in 2010. Employees felt the impact of this a decade before, as companies anticipated the drop in profits. By the end of 2012, three dozen of the world’s top brand-name drugs had lost patent protection, paving the way for cheaper generic versions. The ensuing competition among drug companies is estimated to have eroded 90% of top drug companies’ annual U.S. sales.

To make up for these losses, the larger pharmaceutical companies sought savings by cutting R&D departments, which traditionally have eaten up a big chunk of the industry’s spending. To compensate, companies, in effect, outsourced early-stage research to smaller specialty pharmaceutical and biotech companies.

The result: Startups are the big recruiters now, says Richard Bozzato, a senior adviser for MaRS Discovery District in Toronto, Canada, a nonprofit that aims to foster relationships between scientists, venture capitalists, and industry. Oncology and neuroscience are the fields most actively hiring, he adds.

David Lowe, CEO of Aeglea BioTherapeutics, a 1-year-old company based in Austin, Texas, agrees that startups are where the jobs are. Lowe, who took his first job with Genentech in San Francisco, California, almost 30 years ago, when it was still a relatively small company, says that companies today have a different set of needs than when he began. Much of today’s drug discovery focuses on biologically sourced drugs as opposed to chemically synthesized ones.

Because many of the new drugs are ‘biologics,’ developed from the cells of microorganisms, plants, and animals, today’s industry is recruiting more life scientists. “No one studies entomology anymore,” but entomology could be hugely valuable to drug discovery, Lowe says.

Be collaborative and interdisciplinary

Another trend: Small companies are looking for collaborative scientists. Collaboration is “anathema to a lot of scientists, particularly young ones,” Lowe says. In graduate school, “you are supposed to be chief cook and bottle washer on all your own stuff.” Most graduate students are still trained to work independently, to value ownership of their work that leads to primary authorship on articles published in prestigious journals—a major key to success in academia. Scientists employed at large pharmaceutical companies traditionally worked in silos, too, but collaboration is essential for those who wish to thrive in the startup environment.

George Georgiou, a chemical engineer at the University of Texas, Austin, says that industry values people who are not just collaborative but who can work in an interdisciplinary way. Georgiou has mentored 48 students since setting up his lab in 1986; 12 of them have ended up in the industry. He attributes this success, in part, to running a diverse group including chemists, biochemists, molecular biologists, and chemical engineers—and encouraging his team to have a healthy respect for all those disciplines. The result, he hopes, is students who aren’t intimidated by other fields and who understand the jargon used in those fields.

Another advantage of working with such a mixed group is that students have a better understanding of the whole drug-development pipeline. “What I think distinguishes my students from those of other labs is that my students understand not just whether a molecule does what it is meant to do, but … how one might manufacture it,” Georgiou says.

Risks and incentives

Working in Georgiou’s lab was good preparation for industry, says Tom Van Blarcom, a research scientist with Rinat Laboratories in San Francisco, California. Van Blarcom earned a Ph.D. in chemical engineering in 2008 and took a position at Rinat, which develops protein-based therapeutics; Rinat was acquired by Pfizer in 2006 but was allowed to keep operating as an independent biotechnology unit. Van Blarcom was attracted to industry because of the speed with which he could get things done there. “I don’t have to prepare my own media [or] pour my own plates,” he says, nor does teaching cut into his research time. Another advantage of industry, Van Blarcom says, is that young scientists there have access to a larger number of mentors.

Industry also means more diverse employment opportunities for scientists, including for two-scientist couples, as long as they’re willing to settle near a pharma-biotech hub. “I didn’t want to end up somewhere where there [was] only one fulfilling career option in town,” Van Blarcom says—so he and his partner, Diana Van Blarcom, settled in the San Francisco Bay area, a hotbed of pharma and biotech companies, including many startups.

That’s important because layoffs are part and parcel of the new pharmaceuticals industry. “It’s rare for someone to stay at the same company for their entire career,” Van Blarcom says, and there is security in knowing that there is probably another opportunity close by.

Got the skills, get the job

Van Blarcom believes that his interviewing technique helped him get the job. “When I showed up to my interview I was very prepared,” he says. He had read a handful of papers from each of the people he hoped to meet with, so he could converse about their work in more depth. Coming from Georgiou’s lab also helped him, he thinks, because Georgiou’s work is known for having a strong therapeutic bent: With 29 issued patents, more than half licensed to pharmaceutical and biotechnology companies, Georgiou has close ties with industry. “Having that track record from my [graduate adviser] definitely got my foot in the door,” Van Blarcom says.

At Rinat, Van Blarcom focuses on designing, building, and using sequence libraries to discover more effective antibodies. These libraries consist of sequences based on antibodies found in hundreds of people; Van Blarcom uses his bioinformatics knowledge to curate this data. “People could really have a leg-up on the competition if they are proficient in R or Perl,” he says. New sequencing technologies are generating so much data, he says, that automation is becoming essential, so suitable coding skills are becoming indispensable.

An implementation impulse

Van Blarcom says the decision to join Rinat instead of pursuing a university position was philosophical. He sees industry as a place to “produce tangible results,” while academia is more a breeding ground for big ideas. “I never thought I was the type of person that would come up with ground-breaking ideas; I was more of an implementer, so [industry] seemed to be … a natural fit for me.” In industry, he says, success is unlikely to come in the form of a Nature or Science paper but as a chance to develop a drug that ends up helping patients’ lives. “[That’s] ultimately a lot more powerful than another publication,” he says.

Viruses may explain why small animals are more prone to cancer

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Cancer is a numbers game. Larger, longer-lived animals with more cells should get more tumors than do small, short-lived animals. And yet mice are more susceptible to cancer than we are. Now, a new study offers a tantalizing explanation. The genomes of smaller mammals contain more viruses, which the authors suggest may account for their higher rates of cancer.

Aris Katzourakis, an evolutionary biologist at the University of Oxford in the United Kingdom, didn’t set out to explain rates of cancer in animals. He was interested in why over the last 10 million years the genomes of mice have accumulated 10 times more small RNA viruses, called endogenous retroviruses (ERVs), than has the human genome. He teamed up with researchers from Plymouth University and the University of Glasgow in the United Kingdom to mine for retroviruses in the genomes of a range of mammals—including shrews, humans, dogs, and dolphins. The researchers then tested whether differences in how long mammals live and in how quickly they mature affects how many ERVs they harbor.

By the time the team had identified more than 27,000 unique viral sequences across 38 different mammals, it saw a clear pattern emerging: Small mammals have more ERVs than do larger ones. Mice have more than 3000, whereas dolphins have just 55, and humans are somewhere in the middle with 348, the researchers report online today in PLOS Pathogens.

Larger animals have many more cells, and should therefore have more of these endogenous retroviruses. That they have fewer means they must have found efficient ways to remove them, Katzourakis says. That suggests ERVs can be harmful to their hosts, and this harm is more costly, in an evolutionary sense, to large animals.

How do ERVs harm their hosts? Katzourakis suspects that some ERVs cause cancer. The viruses embed in an organism’s genome and make copies of themselves, and these duplicates then split and reinsert randomly at different locations in the genome. More often than not, these viruses do no harm, but occasionally their reinsertion transforms a healthy cell into a cancerous one. One such event led to the untimely death of the world’s first cloned sheep, Dolly, who succumbed to lung cancer caused by the Jaagsiekte sheep retrovirus. Katzourakis proposes that the higher number of ERVs in small-bodied animals may account for their higher rates of cancer.

“It’s nice to see real experimental results that can help explain the vast differences in cancer susceptibility per gram of tissue between small, short-lived animals and large, long-lived animals,” says epidemiologist Richard Peto of the University of Oxford, who was unconnected to the new study. He first recognized the unexpected differences in cancer susceptibilities between animals of different body sizes in the 1970s, an observation that became known as “Peto’s Paradox.”

From an evolutionary perspective, Peto explains, it makes sense that larger animals are better at protecting their genomes from potentially cancer-causing viruses. Large animals tend to live longer and reproduce later, so it is more important for them to postpone the onset of cancer.

Although the findings pinpoint one mechanism underlying the vast difference in cancer rates, they don’t explain all cancers, says George Kassiotis, a virologist at the National Institute for Medical Research in London who studies ERVs in humans and mice. Despite having few ERVs, he explains, humans still get cancers. ERVs are therefore likely to be one of many factors contributing to cancer rates. “One important aspect of this new study is that it provides a framework to quantify the contribution of ERVs to cancer,” he says, “which in turn will inform the contribution of other causes of cancer.”

Working in the Community to Reduce Health Disparities

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Epidemiologist Kristi Allgood of the Sinai Urban Health Institute (SUHI) in Chicago, Illinois, is on a mission to get women to return to the hospital to follow up on suspicious mammograms. For 9 years, she has been involved in a community-based initiative that supports women whose health (and health care) is likely to be overlooked. Allgood and her SUHI colleagues are part of a growing movement across the United States that aims to reduce the nation’s health disparities by increasing the uptake of proven clinical treatments. Allgood, who is now 39, didn’t set out to focus on breast cancer research. After completing a master’s degree in public health from the University of Illinois, Chicago (UIC), she was recruited to SUHI to evaluate HIV education in Chicago’s Mount Sinai Hospital. But Steve Whitman, SUHI’s director, drafted her into a new initiative attempting to mitigate the racial gap in breast cancer survival in the city where she grew up. Funded since 2007, the Helping Her Live: Gaining Control of Breast Cancer project supports a team of community health care workers who help women in Chicago’s African-American and Hispanic communities navigate breast cancer screening, diagnosis, and treatment. Women in these communities, as in the rest of the country, are chronically under or uninsured—and it’s common for women without insurance to fail to return for a follow-up biopsy. The reasons are complex, but mostly have to do with “fear, time, and money,” Allgood says. The upshot: Breast cancer in this population of women tends to be diagnosed at an advanced stage, making it difficult to treat and offering grimmer odds of survival. This breast cancer survival gap hasn’t always existed, explains Bijou Hunt, also an epidemiologist and Allgood’s colleague at SUHI. Twenty years ago, a woman’s race had little bearing on her chance of dying from the disease. Then, starting in the 1990s, white women began to benefit from numerous advances in treatment for breast cancer. African-American women didn’t share the gains. A study published in 2014—Hunt was the lead author—found that in Chicago between 2005 and 2009, African-American women with breast cancer were, on average, 48% more likely than their white counterparts to die from the disease. That makes Chicago the nation’s seventh deadliest city for black women with breast cancer, but the same pattern is seen in many other major U.S. cities. Each year, nationwide, the disparity equates to 1700 extra breast cancer deaths among African-American women, or about five per day. Figures like these motivated SUHI’s director to seek funding to help close the gap. In 2005, he secured half a million dollars to start a project that employed two hospital-based health care workers who would assist patients during procedures, provide guidance in the referral process, help physicians communicate medical concepts clearly, and sometimes “literally walk patients from place to place” at the hospital, Allgood says. When the Avon Foundation for Women provided an additional $1.95 million in 2007, the hospital-based program expanded into the community and took the name “Helping Her Live.” Allgood took a road trip to New York City’s Harlem neighborhood, where a project with similar aims had been running since the early 1990s. She returned to Chicago full of fresh ideas, ready to recruit and train additional health care workers who, in contrast to their hospital-based peers, would work out in the community. This story ties in with Science’s special issue on breast cancer.
Today, these community-based health care workers help women access routine breast screenings, and work to ease delays in test results and follow-ups. They attend community events, present workshops, and canvass women one-on-one to educate them about the reasons behind health disparities, how mammograms work, and how cancer is treated. Allgood describes them as compassionate, effective advocates and well-respected community members who understand the social issues facing the patients they serve. They are, Allgood says, the key to the project’s success. Having got the ball rolling, Allgood was charged, along with Hunt, with evaluating the hospital and community-based projects. The two epidemiologists assemble mammogram results, pathology reports, and clinicians’ suggested treatments, and they combine them with data collected in the community. They then go to work analyzing it. Last year, the project’s hospital-based workers saw more than 3000 patients and assisted them on 12,000 occasions in 50 distinct, documented ways. Over 3 years, the community-based health care workers responded to 5000 requests for help. It is too early to report whether the project is reducing mortality rates, Allgood says. Their analysis shows, however, that their programs are radically improving some interim metrics. Today, 95% of African-American women in the project’s target communities return for a checkup after a suspicious mammogram, up from 66% before the project began.

Wanted: teamwork, statistics, and a passion for social justice

Cancer geneticist Rick Kittles, whose work at UIC identifies genetic and environmental factors that lead to cancer health disparities, says that statistical savvy is important in the work that Allgood is doing—but that social savvy is important, too. Whitman echoes that sentiment: “Too many young people coming into the field of epidemiology … do not know enough about the world and how it works,” he says. The work is highly interdisciplinary and depends on effective communication among scientists, staff, doctors, and patients—as well as with funders and policymakers.

Fundraising, in fact, is one of the job’s biggest challenges. “We work tirelessly to either keep the funding or find new avenues to fund [our] programs,” Allgood says. Allgood, Hunt, and the other epidemiologists write reports for and make presentations to stakeholders who can influence the health policies adopted by the city government.

To get involved in health disparities work, one must, of course, have the basic credential: at least a master’s degree in public health, Whitman says. One needs hands-on experience in gathering, curating, and analysing data; statistics is becoming ever more important as the field becomes more data-driven.

Alongside such training, those pursuing this career should have a passion for social justice and be ready to think critically about how society-level decisions impact individual health, says Jennifer Orsi, a data analyst at Walgreens in Deerfield, Illinois, who previously worked as an epidemiologist at SUHI. An affinity for teamwork is also essential.

The SUHI team is growing. Right now, SUHI is recruiting a community health educator. Since Allgood joined SUHI, the number of epidemiologists has doubled. Each is waging war against a different disease: asthma, diabetes, and HIV, along with more complex conditions such as chronic obstructive pulmonary disease and obesity. Many approaches are shared among projects. “We all work together to help each other,” Allgood says. “It is really nice to have that backup.”

Measleslike Virus Likely Culprit in U.S. Dolphin Die-Off

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A measleslike virus appears to be the chief cause of the droves of dead dolphins that have washed ashore along the Eastern Seaboard of the United States this summer, researchers announced yesterday. Since 1 July, 333 bottlenose dolphins have been recovered from beaches between New York and North Carolina—10 times the number usually recovered at this time of year.

In early August, the large number of strandings prompted the National Oceanic and Atmospheric Administration (NOAA) to declare an Unusual Mortality Event. The declaration freed up federal funding to assist NOAA’s Marine Mammal Health and Stranding Response Program to retrieve and assess the mammals’ remains. The results of their investigation point to a type of morbillivirus as the cause of the die-off—a group that includes viruses that cause measles in humans and distemper in dogs.

The team’s detective work combined traditional techniques that examined tissues from dead animals’ lungs, brains, and lymph systems with molecular techniques to probe for the presence of the virus. So far, researchers have examined 33 dolphins; 32 have tested positive for morbillivirus. Genetic sequencing has confirmed that 11 carry the type of morbillivirus that infects only dolphins, porpoises, and whales.

“Along the Atlantic seaboard this [outbreak] is extraordinary; this is the largest outbreak that we have had since the 1987 die-off,” said Teri Rowles, head of NOAA’s Marine Mammal Health and Stranding Response Program, in a teleconference with reporters. Morbillivirus was also responsible for a devastating 1987 die-off which killed more than 700 dolphins.

Many wild dolphins exposed during that epidemic probably developed immunity to the virus, Rowles says. But a population’s immunity is slowly eroded over time; animals born since 1987 are probably susceptible, Rowles says.

The virus may have taken hold when the dolphin population reached a tipping point, with enough susceptible individuals to sustain its spread, says veterinary epidemiologist Stephanie Venn-Watson of the National Marine Mammal Foundation in San Diego, California. The epidemic will continue until the number of susceptible animals dwindles, researchers predict. There is no feasible way to vaccinate or treat the animals, they add.

It is difficult to predict how many bottlenose dolphins will ultimately succumb to the disease, and the documented strandings probably represent just a fraction of the infected animals. It is also not clear whether the virus will spread to other dolphin species. Typically, morbillivirus strains don’t spread beyond closely related species, researchers say.

As for any threat to people, “there is no indication that this virus could jump into humans,” says virologist Jerry Saliki of the University of Georgia in Athens. However, morbilliviruses suppress the immune system, so many of the washed-up animals are sick with secondary bacterial infections that are communicable to other mammals. Under some circumstances, rotting carcasses could pose a threat to beachgoers and other mammals.

NOAA plans to continue to monitor the spread of the infection and investigate whether marine pollution could be worsening the impact of the outbreak. Rowles explains that high levels of polychlorinated biphenyls, or PCBs, known to suppress mammals’ immune systems, have been reported in some areas along the eastern coastline. “We will be monitoring those areas very closely,” she adds.

Neighbouring cells help cancers dodge drugs

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Cancers can resist destruction by drugs with the help of proteins recruited from surrounding tissues, find two studies published by Naturetoday. The presence of these cancer-assisting proteins in the stromal tissue that surrounds solid tumours could help to explain why targeted drug therapies rapidly lose their potency.

Targeted cancer therapies are a class of drugs tailored to a cancer’s genetic make-up. They work by identifying mutations that accelerate the growth of cancer cells and selectively blocking copies of the mutated proteins. Although such treatments avoid the side effects associated with conventional chemotherapy, their effectiveness tends to be short-lived. For example, patients treated with the recently approved drug vemurafenib initially show dramatic recovery from advanced melanoma, but in most cases the cancer returns within a few months.

Many forms of cancer are rising in prevalence: for example, in the United States, the incidence of invasive cutaneous melanoma — the deadliest form of skin cancer — increased by 50% in Caucasian women under 39 between 1980 and 2004. So there is a pressing need to work out how to extend the effects of targeted drug therapies. But, until now, researchers have focused on finding the mechanism of drug resistance within the cancerous cells themselves.

Two teams, led by Jeff Settleman of Genentech in South San Francisco, California, and Todd Golub at the Broad Institute in Cambridge, Massachusetts, expanded this search into tumours’ surrounding cellular environment.

Settleman’s team tested 41 human cancer cell lines, ranging from breast to lung to skin cancers. The researchers found that 37 of these became desensitized to a handful of targeted drugs when in the presence of proteins that are usually found in the cancer’s stroma, the supportive tissue that surrounds tumours. In the absence of these proteins, the drugs worked well1. By growing cancer cells along with cells typically found in a tumour’s immediate vicinity, Golub and his colleagues showed that these neighbouring cells are the likely source of the tumour-aiding proteins2.

Protein culprit

One of the most startling results of the teams’ experiments was the discovery that a protein called hepatocyte growth factor (HGF) boosts melanoma’s resistance to treatment with vemurafenib. Intrigued by this result, both teams looked at blood samples from people who had undergone treatment with vemurafenib, and found the higher a patient’s HGF levels, the less likely they were to remain in remission.

Martin McMahon, a cancer biologist at the University of California, San Francisco, who was not affiliated with either study, explains that the results have immediate implications for the design of clinical trials, which he says could combine targeted drug therapy with drugs capable of knocking down the production of proteins such as HGF.

“These papers show that the influence of the cell’s microenvironment is important not only for melanoma, but also for pancreatic, lung and breast cancer,” McMahon says, adding that they are “very exciting, because they expand the focus of where we should be looking for the mechanisms of drug resistance”.

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Resistant bed-bugs ‘from tropics’

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New results suggest that insecticide use in the tropics is to blame for the re-emergence of bed-bug infestations.

Exposure to treated bed nets and linens meant that populations of bed-bugs had become resistant to the chemicals used to kill them, researchers said.

The findings could help convince pest controllers to find alternative remedies to deal with the problem.

The results were presented at the American Society of Tropical Medicine and Hygiene’s 60th annual meeting.

Since almost vanishing from homes in industrialised countries in the 1950s, populations of the common bed-bug have become re-established in these regions over the past decade or so.

These mostly nocturnal feeders are difficult to control, not only because they are adept at avoiding detection by crawling into creases of soft furnishing but also because they have developed a resistance to many of the chemicals that have been used to kill them.

Findings presented at the gathering in Philadelphia showed that 90% of 66 populations sampled from 21 US states were resistant to a group of insecticides, known as pyrethroids, commonly used to kill unwanted bugs and flies.

Bed-bugs in furniture (Image: Richard Naylor/University of Sheffield)
Female bed-bugs, hidden in furniture creases, can each lay up to 300 eggs

 

One of the co-authors – evolutionary biologist Warren Booth, from North Caroline State University in Raleigh – explained that the genetic evidence he and his colleagues had collected showed that the bed-bugs infecting households in the US and Canada in the last decade were not domestic bed bugs, but imports.

“If bed-bugs emerged from local refugia, such as poultry farms, you would expect the bed-bugs to be genetically very similar to each other,” explained entomologist and co-author Coby Schal, also from North Carolina State University. “This isn’t what we found.”

In samples collected from across the eastern US, the team discovered populations of bed-bugs that were genetically very diverse.

This suggested that the bugs originated from elsewhere, and relatively recently because the different populations had not had time to interbreed, Dr Schal explained.

He suggested that the source for the new outbreaks was warmer climes, where the creatures would have probably developed a resistance to chemicals.

“The obvious answer is the tropics, where they have used treated bed nets [and] high levels of insecticides on clothing and bedding to protect the military,” Dr Booth told BBC News.

He explained that although bed-bugs were essentially eradicated from industrialised countries in the 1950s, they continued to thrive in Africa and Asia.

“Its very likely that it is from one of these areas where insecticide resistance evolved,” he said.

‘Home-grown’

However, UK-based pest management specialist Clive Boase questioned that hypothesis.

He said bed nets, to protect against mosquito-transmitted malaria and dengue, were only used in parts of Africa that were hot, where the tropical bed-bug (Cimex hemipterus) was found.

But, he added, it was not the tropical bed-bug that was the problem in the US and UK; instead it was their temperate cousin, Cimex lectularius.

Dr Boase explained that comprehensive records showed that infestations of bed-bugs in Europe were less pervasive in the 1970s and 80s, but they were still present.

By continually exposing these populations to insecticides, which came on the market in the late 1970s, these creatures likely developed resistance, he said.

“We don’t have to invoke stories of disease control programmes in Africa; all the evidence here in the UK is that our problem is home-grown.”

Dr Boase wondered that if the US had similar long-term records whether the researchers would have reached a different conclusion.

Evolutionary biologist Richard Naylor from the University of Sheffield agreed: “I am kind of surprised by [their interpretation].

“It doesn’t seem that difficult to develop resistance or lose it; in lab cultures, if you stop exposing [bed-bugs] to pyrethroids it drops out of lab populations very quickly,” he said.

Mr Naylor asked that if the US bed bugs had been exposed to the chemicals elsewhere in the past, “why would they still be resistant?”

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Vaccine developed against Ebola

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Scientists have developed a vaccine that protects mice against a deadly form of the Ebola virus.

First identified in 1976, Ebola fever kills a majority of the people it infects.

The researchers say that this is the first Ebola vaccine to remain viable long-term and can therefore be successfully stockpiled.

The results are reported in the journal Proceedings of National Academy of Sciences.

Ebola is transmitted via bodily fluids, and can become airborne. Sufferers experience nausea, vomiting, internal bleeding and organ failure before they die.

Although few people contract Ebola each year, its effects are so swift and devastating that it is often feared that it could be used against humans in an act of terroism.

All previously developed vaccines have relied on injecting intact, but crippled, viral particles into the body.

Long-term storage tends to damage the virus, paralysing the vaccine’s effectiveness.

The new vaccine contains a synthetic viral protein, which prompts the immune system to better recognise the Ebola virus, and is much more stable when stored long-term.

The vaccine protects 80% of the mice injected with the deadly strain, and survives being “dried down and frozen,” said biotechnologist Charles Arntzen from Arizona State University who was involved in its development.

He said the next step is to try the vaccine on a strain of Ebola that is closer to the one that infects humans.

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Pioneers boast high fertility, say scientists

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Scientists have shown that women who were first to settle in a new land had more children and grandchildren than those who followed.

Researchers analysed the family trees of French settlers who colonised Canada in the 17th and 18th centuries.

Their results could help to explain why some rare genetics diseases are common in communities established by migrations.

The findings have been published in the journal Science.

The team of researchers from Canada and Europe relied on data collected by the parish councils of Charlevoix and Saguenay Lac Saint-Jean, a region 170km north of Quebec, Canada.

The towns not only boast dairy farms, charming villages and sandy beaches but some of the best ever-kept marriage records – comprising more than a million people.

By building a picture of marriages and how many children the pairings produced, the researchers showed that woman who arrived as part of the first wave of immigration had 15% more children than those who arrived a generation later.

The pioneering woman married younger and benefited from scooping up the best local resources, they added.

But the study also found that the pioneering women’s children also had more children.

Lead author Laurent Excoffier, from the University of Bern in Switzerland, explained that the children of women at the front of the wave inherited their mother’s higher rate of fertility.

Yet, the researchers added, there was no such correlation between generations that arrived 30 years later behind the first wave.

Dr Excoffier drew parallels with cane toads. Scientists have observed that the toads at the edge of their range have bigger front legs and stronger back legs; all the better to invade new areas.

And when toads at the frontiers breed, their offspring inherit these longer, stronger limbs.

Such an effect is not unexpected, but until now no one has seen this phenomenon in humans.

“This was a rare chance to study a relatively recent human migration,” said co-author Damian Labuda, a geneticist from the University of Montreal, Canada.

Population geneticist Montgomery Slatkin from University of California, who was not involved in the work, called the study one of the “most interesting, detailed studies” he had seen.

“I think what happened [here] could easily have happened in other populations,” he added.

The findings suggest that families at the front of the wave of migration contributed more to the contemporary gene pool than those that were slower to arrive, explained Dr Labuda.

This could help explain why some rare genetic diseases are more common than expected in the Charlevoix and Saguenay Lac Saint-Jean regions.

That is because any disease causing mutations carried by people by the frontiers would be pass onto their descendents, who make up a large proportion of subsequent generations in the population.

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Rare white kiwi survives surgery

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The world’s only known white kiwi has survived surgery to remove stones from her gizzard, reports a New Zealand Wildlife Centre.

Over a week ago, rangers noted that Manukura, the six-month-old chick, was off her food.

X-rays revealed that two large stones were obstructing the chick’s guts.

In two separate operations, vets at Wellington Hospital in New Zealand used lasers to successfully break apart the rocks.

Pukaha Mount Bruce, New Zealand’s North Island wildlife centre, where Manukura lives, reported that the bird’s heart slowed suddenly during the surgery giving the operating team “a bit of a scare”.

But the little white bird pulled through and is recovering in isolation from other animals.

Kiwis, like other birds, swallow stones to help them digest their food. But Manukura, it seems, swallowed more than she could stomach.

Manukura, a North Island Brown Kiwi, is the 13th kiwi hatched in captivity at the centre this year.

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