Posts Tagged ‘science’

By Rob Picheta

The science is looking pretty unanimous on this one: Drivers of expensive cars are the worst.

A new study has found that drivers of flashy vehicles are less likely to stop and allow pedestrians to cross the road — with the likelihood they’ll slow down decreasing by 3% for every extra $1,000 that their vehicle is worth.

Researchers from the University of Nevada, Las Vegas speculated that the expensive car owners “felt a sense of superiority over other road users” and were less able to empathize with lowly sidewalk-dwellers.

They came to this conclusion after asking volunteers to cross a sidewalk hundreds of times, filming and analyzing the responses by car drivers.

Researchers used one white and one black man, and one white and one black woman — also finding that cars were more likely to yield for the white and female participants. Vehicles stopped 31% of the time for both women and white participants, compared with 24% of the time for men and 25% of the time for black volunteers.

But the best predictor of whether a car would stop was its cost, researchers discovered. “Disengagement and a lower ability to interpret thoughts and feelings of others along with feelings of entitlement and narcissism may lead to a lack of empathy for pedestrians” among costly car owners, they theorized in the study.

And the discovery of a car-value-to-jerkish-behavior correlation isn’t new; the research, published in the Journal of Transport and Health, backed up a Finnish study published last month that found that men who own flashy vehicles are more likely to be “argumentative, stubborn, disagreeable and unempathetic.”

According to that survey of 1,892 drivers by the University of Helsinki, those deemed to have more disagreeable character traits were “more drawn to high-status cars.”

But it also found that conscientious people often favor higher-priced vehicles, too. If you’re reading this while stuck in traffic in your brand new BMW: yes, you’re definitely in that category.

“I had noticed that the ones most likely to run a red light, not give way to pedestrians and generally drive recklessly and too fast were often the ones driving fast German cars,” Helsinki University’s Jan-Erik Lönnqvist said in a press release.

He set out to discover what kind of person is more likely to buy an expensive car, creating a personality test of Finnish car owners.

“The answers were unambiguous: self-centred men who are argumentative, stubborn, disagreeable and unempathetic are much more likely to own a high-status car such as an Audi, BMW or Mercedes,” the press release states.

“These personality traits explain the desire to own high-status products, and the same traits also explain why such people break traffic regulations more frequently than others,” Lönnqvist added.

His study cited previous research that indicated drivers behind the wheel of a costly vehicle are more likely to flout traffic regulations or drive recklessly.

But he also found people with “conscientious” characters seek out pricey models, too.

“People with this type of personality are, as a rule, respectable, ambitious, reliable and well-organised,” the statement said. “They take care of themselves and their health and often perform well at work.”

https://www.cnn.com/2020/02/26/world/expensive-car-drivers-study-scli-scn-intl/index.html


The Harvard Medical School researcher’s work on the genetic basis of protein coding and production led him to make groundbreaking discoveries in immunology, molecular biology, and cancer genetics.

by ASHLEY YEAGER

Harvard Medical School molecular geneticist Philip Leder died last week (February 2). He was 85.

Leder was revered for his work in molecular biology, immunology, and cancer genetics. His first scientific breakthrough came in the 1960s when he was working as a postdoc in geneticist Marshall Nirenberg’s lab at the National Institutes of Health (NIH). Together they developed a technique that confirmed that amino acids were encoded by a sequence of three nucleotides and revealed the triplet code of ambiguous amino acids.

From there, Leder went on to determine the first complete sequence of a mammalian gene, develop the first recombinant DNA vector system safe for use in the lab, identify the structure of genes that encode antibody molecules, discover a gene that caused cancer, and develop the first mouse model of cancer.

“Phil Leder was special. Among great scientists, he was special, and among scientists, he was an icon,” David Livingston, a geneticist at Harvard who worked in Leder’s lab at NIH, tells The Scientist. “He was gifted. He was generous. He was a splendid person to listen to talk, to run experiments by, and be criticized by. He was a splendid human being on top of all of it.”

Leder was born on November 19, 1934 in Washington, DC, and grew up there. He attended Western High School, graduated in 1952, and went on to study at Harvard University. He interned at NIH as an undergraduate, working in biochemist Martha Vaughan’s lab in the National Heart Institute, which is now the National Heart, Lung, and Blood Institute. He finished his bachelor’s degree at Harvard in 1956 and stayed there for medical school, graduating in 1960.

After a two-year residency program at the University of Minnesota Hospitals, he returned to NIH to work with Nirenberg. Leder dove headfirst into the race to decipher the way genes encode proteins and helped to design a filtering instrument to rapidly test 45 amino acid samples simultaneously, instead of one at a time. Leder and Nirenberg could quickly tag amino acids with a radioactive label, bind them to triplet RNA sequences, and put them into the filtering instrument, which helped the team decode unknown amino acid codon sequences, well before other scientists could, according to a remembrance on Leder posted by NIH.

It was one of the most exciting times in Leder’s life, he said. “I would go to bed thinking about the next day’s experiments and then jump out of bed in the morning and rush to the laboratory,” he recalled in a 2012 interview with American Society for Biochemistry and Molecular Biology Today. “I stayed late at night. It was a lot of work, but the intellectual excitement was enormous.” The two published their work on the codons in 1964.

Leder’s “work w/Marshall Nirenberg set the stage for the revolution in molecular genetics,” NIH director Francis Collins wrote on Twitter last Friday (February 7).

In 1965, Leder joined the Weizmann Institute in Rehovot, Israel, as a visiting scientist and stayed until 1966. He returned to the NIH, serving as a research medical officer in the National Cancer Institute from 1966 to 1969 and then became head of the Section on Molecular Genetics in the Laboratory of Molecular Genetics in the National Institute of Child Health and Human Development and in 1972 was promoted to the director of the lab.

During this time and through the 1970s, he and his colleagues worked on deciphering the genetic sequence of alpha globin, a component of hemoglobin, a protein in red blood cells that carries oxygen to the body’s cells and tissues. His work also revealed important details about the genetics of encoding antibodies and that the synthesis of antibodies was not only regulated by genetics but also biochemical processes that ensure specificity to target the right antigen presented by viruses, bacteria, or other invaders in the body.

What made Leder such an outstanding scientist, Livingston explains, was his immense rigor. Control experiments, for example, had to be “at least as incisive or demanding and rigorous as the actual experiments . . . to prove that nothing in the discovery experiment was an artifact,” he says. “And he had an immensely adventurous mind. No problem was beyond at least discussion,” which made Leder unique as a mentor. “In fact, his ability to mentor was internationally celebrated,” Livingston explains. “You could listen to his talks, and you knew he was a fantastic teacher because his mind was utterly clear.”

Leder joined Harvard Medical School (HMS) in 1980, founding its genetics department in 1981 and chairing the department for 25 years. His research there led to the discovery of a specific gene, MYC. With Harvard colleague Timothy Stewart, Leder began using a fine glass needle to insert the cancer-causing gene into mouse embryos just after fertilization, thereby creating OncoMouse, a genetic line of mice that were prone to developing the disease. The duo patented the animal in 1988, giving researchers an unprecedented tool to study cancer and how to treat it.

His work at Harvard was not limited to his research. He made fundamental changes to hiring, instituting nationwide searches for new assistant professors in the genetics department, which increased the likelihood of hiring women, notes Jonathan Seidman, a geneticist at Harvard who worked in Leder’s lab at NIH in the 1970s. Leder also made sure the department didn’t get too big, Seidman says, and he insisted that if faculty were on different floors, spiral staircases—rather than drab stairwells—would connect them, making it easy for researchers to communicate and collaborate.

Leder’s “contributions to science and to HMS cannot be overstated, and he will never be forgotten,” George Daley, Harvard’s dean of the faculty of medicine wrote to colleagues on February 4.

For his work, Leder was honored with the Albert Lasker Award for Basic Medical Research, the US National Medal of Science, the Heineken Prize from the Royal Netherlands Academy of Arts of Sciences, and the William Allan Medal from the American Society of Human Genetics. He was a member of the National Academy of Sciences, a Fellow of the American Association for the Advancement of Science, and a Howard Hughes Medical Institute investigator.

Surviving him are his wife, Aya Leder, his children, Micki, Tani, and Ben, his daughters-in-law, Karen Leder and Mary Leder, and his grandchildren, Jacob, David, Sarah, Eli, Alex, Matt, Amanda, and Annie.

Ashley Yeager is an associate editor at The Scientist. Email her at ayeager@the-scientist.com. Follow her on Twitter @AshleyJYeager.

https://www.the-scientist.com/news-opinion/philip-leder–who-deciphered-amino-acid-sequences–dies-67096

by EMILY MAKOWSKI

Plants pollinated by nectar-drinking bats often have flowers that reflect ultrasonic waves, making it easier for the animals to locate flowers through echolocation. But one cactus does the opposite—it absorbs more ultrasound in the area surrounding its flowers, making them stand out against a “quieter” background, according to a preprint published on bioRxiv last month.

Espostoa frutescens is a type of column-shaped cactus found only in the Ecuadorian Andes mountains. It has small flowers on its side that open at night, attracting bats as they fly from flower to flower in search of nectar. One of its main pollinators is Geoffroy’s tailless bat (Anoura geoffroyi).

“Bats are really good pollinators,” Ralph Simon, a postdoc in Wouter Halfwerk’s lab at Vrije Universiteit Amsterdam and the lead author of the preprint, tells The Scientist. “They carry a lot of pollen in their fur, and they have a huge home range so they can transport pollen from plants that grow far apart. For plants with a patchy distribution pattern like this cactus, it’s especially beneficial to rely on bats for pollination,” he says.

For bats to find the flowers at night, they use echolocation, emitting ultrasonic calls too high for humans to hear that bounce off objects and allow the bats to form a mental map of their surroundings. Some plants have evolved techniques that take advantage of this sonar system and allow bats to better detect flowers, such as making their petals more concave, forming a more reflective surface that can bounce more echolocation back to the bat. But E. frutescens takes a different approach.

Each of E. frutescens’s flowers are surrounded by an area of wooly hairs called the cephalium. Simon and colleagues knew from past measurements that the hairs were sound-absorbent, and were interested in seeing whether this part of the cactus could be involved in helping bats find the flowers. They attached a microphone and speaker to a device resembling the shape and size of a bat head in order to mimic a bat, and played prerecorded echolocation calls to the cacti and measured how much sound was reflected back to the bat replica.

The team found that the hairy cephalium absorbed ultrasound, and that the greatest absorption occurred above 90 kHz, in the range of the frequency of Geoffroy’s tailless bat’s echolocation call. The sound that bounced back to the microphone from the cephalium area was about 14 decibels quieter than the sound that bounced off the non-hairy part of the cacti.

It’s a “totally different mechanism” than the reflection method other cacti use, says Simon. “Instead of making the flowers conspicuous, it dampens the background. The background absorbs the ultrasound, and the flowers show up in [the middle of] this absorbent fur.”

This mechanism makes sense from a communication standpoint, writes May Dixon, a graduate student studying bat behavior in Mike Ryan’s lab at the University of Texas at Austin who was not involved with the study, in an email to The Scientist. “If you are trying to send a message, you have to think not only about the message itself but also the context. For example, if you are calling someone, you should be loud enough for them to hear, sure, but you should also call from a quiet place,” she says.

“There is something wonderful about the ways that plants have found to communicate with animals through evolution,” Dixon notes. “A cactus has no sense of what it is to be a bat—it can’t see, smell, or echolocate—but here it is, sending a bat a message in a language that a bat can understand.”

The cephalium appears to have originally evolved to protect flowers from environmental stressors such as UV rays, drying out, getting too cold, or being eaten, but “during evolution, it co-opted another function, and it functions as a sound absorbing structure as well,” says Simon. The evolution of this mechanism benefits both cactus and bat. “From the bat point of view, with this mechanism, they save time. And for them, it’s important to save time, because they have to visit several hundred flowers each night to get enough energy,” he says.

The current study did not look at whether sites on the plants with the highest sound absorption in the bats’ echolocation range “indeed resulted in the highest detection and visitation rates by bats,” says Jan Komdeur, an evolutionary ecologist at University of Groningen in the Netherlands who did not participate in the research, in an email to The Scientist. In the future, researchers could investigate how often real-life bats approach hairy versus experimentally manipulated hairless flowers, he suggests.

Jorge Schondube, an ecologist at the Universidad Nacional Autónoma de México who was not involved with the study, agrees that research on real-life bats is needed. “The pattern’s very clear, but now [researchers] need to show how the mechanism is actually changing the behavior of the bats,” he says.

Still, he’s impressed by the findings so far. “Nature is very creative. And by being creative, it allows the origin of completely new and unimaginable things. It’s really surprising that something like this can happen, and the paper shows it really, really beautifully. . . . What we’re seeing here is something that has not been seen before in terms of sound.”

https://www.the-scientist.com/news-opinion/ecuadorian-cactus-absorbs-ultrasound–enticing-bats-to-flowers-66981?utm_campaign=TS_DAILY%20NEWSLETTER_2020&utm_source=hs_email&utm_medium=email&utm_content=82166272&_hsenc=p2ANqtz-9in3Tqjl731fVW0JE_k3Ht2NOEvCOnql7E5ADhmEp4j43Rrs5Q6gxTipSPvHXAs-8C6MvOvVFdBpktnFeyya1pvZPF2A&_hsmi=82166272


Dr. Moir’s radical and iconoclastic theories defied conventional views of the disease. But some scientists were ultimately won over.

By Gina Kolata

Robert D. Moir, a Harvard scientist whose radical theories of the brain plaques in Alzheimer’s defied conventional views of the disease, but whose research ultimately led to important proposals for how to treat it, died on Friday at a hospice in Milton, Mass. He was 58.

His wife, Julie Alperen, said the cause was glioblastoma, a type of brain cancer.

Dr. Moir, who grew up on a farm in Donnybrook, a small town in Western Australia, had a track record for confounding expectations. He did not learn to read or write until he was nearly 12; Ms. Alperen said he had told her that the teacher at his one-room schoolhouse was “a demented nun.” Yet, she said, he also knew from age 7 that he wanted to be a scientist.

Dr. Moir succeeded in becoming a researcher who was modest and careful, said his Ph.D. adviser, Dr. Colin Masters, a neuropathologist at the University of Melbourne. So Dr. Masters was surprised when Dr. Moir began publishing papers proposing an iconoclastic rethinking of the pathology of Alzheimer’s disease.

Dr. Moir’s hypothesis “was and is a really novel and controversial idea that he alone developed,” Dr. Masters said.

“I never expected this to come from this quiet achiever,” he said.

Dr. Moir’s theory involved the protein beta amyloid, which forms plaques in the brains of Alzheimer’s patients.

Conventional wisdom held that beta amyloid accumulation was a central part of the disease, and that clearing the brain of beta amyloid would be a good thing for patients.

Dr. Moir proposed instead that beta amyloid is there for a reason: It is the way the brain defends itself against infections. Beta amyloid, he said, forms a sticky web that can trap microbes. The problem is that sometimes the brain goes overboard producing it, and when that happens the brain is damaged.

The implication is that treatments designed to clear the brain of amyloid could be detrimental. The goal would be to remove some of the sticky substance, but not all of it.

The idea, which Dr. Moir first proposed 12 years ago, was met with skepticism. But he kept at it, producing a string of papers with findings that supported the hypothesis. Increasingly, some of the doubters have been won over, said Rudolph Tanzi, a close friend and fellow Alzheimer’s researcher at Harvard.

Dr. Moir’s unconventional ideas made it difficult for him to get federal grants. Nearly every time he submitted a grant proposal to the National Institutes of Health, Dr. Tanzi said in a phone interview, two out of three reviewers would be enthusiastic, while a third would simply not believe it. The proposal would not be funded.

But Dr. Moir took those rejections in stride.

“He’d make a joke about it,” Dr. Tanzi said. “He never got angry. I never saw Rob angry in my life. He’d say, ‘What do we have to do next?’ He was always upbeat, always optimistic.”

Dr. Moir was supported by the Cure Alzheimer’s Fund, and he eventually secured some N.I.H. grants.

Dr. Moir first came to the United States in 1994, when Dr. Tanzi was looking for an Alzheimer’s biochemist to work in his lab. Working with the lab as a postdoctoral fellow and later as a faculty member with his own lab, Dr. Moir made a string of major discoveries about Alzheimer’s disease.

For example, Dr. Moir and Dr. Tanzi found that people naturally make antibodies to specific forms of amyloid. These antibodies protect the brain from Alzheimer’s but do not wipe out amyloid completely. The more antibodies a person makes, the greater the protection against Alzheimer’s.

That finding, Dr. Tanzi said, inspired the development of an experimental drug, which its manufacturer, Biogen, says is helping to treat some people with Alzheimer’s disease. Biogen plans to file for approval from the Food and Drug Administration.

Robert David Moir was born on April 2, 1961, in Kojonup, Australia, to Mary and Terrence Moir, who were farmers. He studied the biochemistry of Alzheimer’s disease at the University of Western Australia before joining Dr. Tanzi’s lab.

Once he learned to read, Ms. Alperen said, he never stopped — he read science fiction, the British magazine New Scientist and even PubMed, the federal database of scientific publications.

“Rob had an encyclopedic knowledge of the natural world,” she said.

He shared that love with his family, on frequent hikes and on trips with his young children to look for rocks, insects and fossils. He also played Australian-rules football, which has elements of rugby as well as American football, and helped form the Boston Demons Australian Rules Football Team in 1997, his wife said.

In addition to his wife, with whom he lived in Sharon, Mass., Dr. Moir’s survivors include three children, Alexander, Maxwell and Holly Moir; a brother, Andrew; and a sister, Catherine Moir. His marriage to Elena Vaillancourt ended in divorce.

Even on land, crocodiles are no fish out of water. While these reptiles might look lazy and slow sunning on the bank, they can easily pick up speed when necessary, and a scary number can gallop or bound like a horse or a dog.

Bounding is when an animal’s forelimbs hit the ground at the same time, with the back legs pushing off soon after; meanwhile, a gallop is a four-beat sequence whereby the fore and hindlimbs take turns landing.

Freshwater crocodiles from Australia (Crocodylus johnstoni) were historically thought to be the only species capable of doing both. But that’s not actually true. Not even close.

It turns out even scientists have underestimated these creatures. Past research suggested only a handful of croc species were able to gallop, but a new study now adds five more to the mix, suggesting it’s a whole lot more common than we ever thought.

Setting up video cameras around a zoological park in Florida, veterinary scientists analysed the gaits and speeds of 42 individuals from 15 species of crocodylia, which includes true crocodiles (family Crocodylidae), alligators and caimans.

While alligators and caimans were only able to trot on land, the team noticed eight species of crocodile capable of galloping or bounding.

They claim their study is the first to properly document galloping in the Philippine crocodile (Crocodylus mindorensis), the Cuban crocodile (C. rhombifer), the American crocodile (C. acutus), the West-African slender-snouted crocodile (Mecistops cataphractus) and the dwarf crocodile (Osteolaemus tetraspis).

Judging by how common this skill appears to be, there might even be more species that can do the same. There have already been anecdotal reports of galloping in species such as the marsh crocodile (C. palustris) and the New Guinea crocodile (C. novaeguineae).

“We were really surprised at one major thing – despite the different gaits crocodiles and alligators use, they all can run about as fast,” John Hutchinson, a specialist in evolutionary biomechanics at the Royal Veterinary College (RVC), told PA.

No matter what their size, almost every species studied was able to reach nearly 18 kilometres per hour (11 mph), whether it be through trotting, galloping or bounding.

Only crocodiles, however, could use their legs asymmetrically, providing longer stride frequencies, especially among those with smaller body sizes. Why alligators cannot do this remains uncertain, but the researchers think this skill is probably ancestral and has less to do with speed than we thought.

“We suspect that bounding and galloping give small crocodiles better acceleration and manoeuvrability, especially useful for escaping from danger,” explains Hutchinson

“It seems like alligators and caiman stand their ground rather than run away with an extreme gait.”

Similar to other studies, the researchers think the crocodile’s unusual asymmetrical gait came from a long-lost ancestor that lived on the land and had longer legs.

If this is right, it could mean that the ancestors of the alligators somehow lost this ability or no longer express it.

But there’s also another possibility that is rarely acknowledged: the common ancestor of today’s 20 crocodile species may have actually evolved this asymmetrical gait as opposed to inheriting it.

Looking at related species could clear up some of the confusion – the gharial is an Asian fish-eating crocodile that lies outside the Crocodyloidea  and Alligatoroidea ancestry, so if they can be shown to have asymmetrical gaits, it could shed light on how this skill appeared.

But similar to crocodiles and alligators, the gaits of the gharial’s are not well documented, so there’s clearly a lot more research that needs to be done.

“Together, our new observations of asymmetrical gaits and our broader dataset on locomotor kinematics spanning the clade Crocodylia considerably expand our knowledge of their behaviours and natural history,” the authors conclude.

“Importantly, this combined evidence strongly refutes the popular notion that only a few crocodiles use asymmetrical gaits.”

The study was published in Scientific Reports.

https://www.sciencealert.com/approach-with-caution-more-crocodile-species-than-we-thought-can-reach-a-gallop

White House officials are working on an executive order that would boost public access to federally funded research, prompting publishers to panic about the future of their business models, according to people familiar with the plan.

Ostensibly, the order would follow longtime bipartisan interest in improving public access to research that is paid for by taxpayers.

It is expected to require that publicly funded science be obtainable for free immediately, building on an Obama initiative, multiple sources said.

A memo adopted in 2013 mandated that the results of such research be made available within one year of publication.

Though there is generally broad support for public access, publishing groups like the Association of American Publishers worry that a tougher order would upend their subscription-based business model.

Once it caught wind of the effort, AAP began drafting a sharply worded letter of concern to the White House, multiple sources said. The letter could be sent as early as tomorrow.

About a dozen sources told E&E News that they were aware the White House has been considering an executive order but the details remain murky. A senior administration official declined to comment on “internal deliberative processes that may or may not be happening.”

“President Trump’s Administration continues to be focused on scientific discovery and economic expansion,” the official added via email.

Michael Stebbins, who helped draft the Obama-era memo, generally expressed support for public access and noted that it could spur innovation. “But the devil is definitely in the details,” he said.

Many academic journals are funded by subscription fees collected in the first year of publication. The Trump mandate could force publishers to shift their model so authors pay hefty article processing charges, or APCs.

“Here’s the challenge: A world in which there is immediate open access will result in serious pain to a scientific society or small publisher who relies on subscription revenue,” Stebbins added. “That revenue will have to be made up somehow for them to survive.”

Some scientific experts, who are generally skeptical of the Trump team, are worried that the initiative parallels what they call the administration’s incessant attack on science and, by extension, provides favors to industry.

“What problem are we trying to solve?” asked Andrew Rosenberg, an advocate with the Union of Concerned Scientists.

Others noted that the order would give international competitors like China access to American research, which has been a concern of the Trump administration.

It’s also unusual, sources noted, that a Republican administration would adopt policies that could seriously affect business models.

Impacts to publishers could vary. A spokeswoman for the American Association for the Advancement of Science had no direct comment on the administration’s reported plans but obliquely expressed concerns about the potential financial impact.

The nonprofit association publishes a half-dozen journals. One offers immediate free access to its articles, and the other five allow open access to peer-reviewed articles after a year for registered users, the spokeswoman, Tiffany Lohwater, said in an email this week. Articles in those five journals are also available for free as soon as they are posted in university archives technically known as “institutional repositories.”

“High-quality scientific publishing, as AAAS does, requires considerable resource investment, including to identify the papers that have the potential to significantly impact the pace of science,” she said.

George Allen, chief scientist with Northeast States for Coordinated Air Use Management, a Boston-based consortium of air pollution agencies, did not doubt the Trump order would get huge pushback from publishers.

“If you completely take away their business model, then they have no incentive to exist,” he said. He thought allowing free access after a year would be “a reasonable compromise

https://www.eenews.net/stories/1061836761


This piglet had some cells from a monkey but died within a week of birth
Tang Hai

By Michael Le Page

Pig-primate chimeras have been born live for the first time but died within a week. The two piglets, created by a team in China, looked normal although a small proportion of their cells were derived from cynomolgus monkeys.

“This is the first report of full-term pig-monkey chimeras,” says Tang Hai at the State Key Laboratory of Stem Cell and Reproductive Biology in Beijing.

The ultimate aim of the work is to grow human organs in animals for transplantation. But the results show there is still a long way to go to achieve this, the team says.

Hai and his colleagues genetically modified cynomolgus monkey cells growing in culture so they produced a fluorescent protein called GFP. This enabled the researchers to track the cells and their descendents. They then derived embryonic stem cells from the modified cells and injected them into pig embryos five days after fertilisation.

More than 4000 embryos were implanted in sows. Ten piglets were born as a result, of which two were chimeras. All died within a week. In the chimeric piglets, multiple tissues – including in the heart, liver, spleen, lung and skin – partly consisted of monkey cells, but the proportion was low: between one in 1000 and one in 10,000.

It is unclear why the piglets died, says Hai, but because the non-chimeric pigs died as well, the team suspects it is to do with the IVF process rather than the chimerism. IVF doesn’t work nearly as well in pigs as it does in humans and some other animals.

The team is now trying to create healthy animals with a higher proportion of monkey cells, says Hai. If that is successful, the next step would be to try to create pigs in which one organ is composed almost entirely of primate cells.

Something like this has already been achieved in rodents. In 2010, Hiromitsu Nakauchi, now at Stanford University in California, created mice with rat pancreases by genetically modifying the mice so their own cells couldn’t develop into a pancreas.

Pig-human chimeras

In 2017, Juan Carlos Izpisua Belmonte’s team at the Salk Institute in California created pig-human chimeras, but only around one in 100,000 cells were human and, for ethical reasons, the embryos were only allowed to develop for a month. The concern is that a chimera’s brain could be partly human.

This is why Hai and his team used monkey rather than human cells. But while the proportion of monkey cells in their chimeras is higher than the proportion of human cells in Belmonte’s chimeras, it is still very low.

“Given the extremely low chimeric efficiency and the deaths of all the animals, I actually see this as fairly discouraging,” says stem cell biologist Paul Knoepfler at the University of California, Davis.

He isn’t convinced that it will ever be possible to grow organs suitable for transplantation by creating animal-human chimeras. However, it makes sense to continue researching this approach along with others such as tissue engineering, he says.

According to a July report in the Spanish newspaper El País, Belmonte’s team has now created human-monkey chimeras, in work carried out in China. The results have not yet been published.

While interspecies chimerism doesn’t occur naturally, the bodies of animals including people can consist of a mix of cells. Mothers have cells from their children growing in many of their organs, for instance, a phenomenon called microchimerism.

Journal reference: Protein & Cell, DOI: 10.1007/s13238-019-00676-8

Read more: https://www.newscientist.com/article/2226490-exclusive-two-pigs-engineered-to-have-monkey-cells-born-in-china/#ixzz67RYaU5XS