COLD SPRING HARBOR, N.Y. — When breast cancer spreads, it moves in gangs of ready-to-rumble tumor cells, a small genetic study suggests. Most of the mutations that drive recurrent tumors when they pop up elsewhere in the body were present in the original tumor, geneticist Elaine Mardis reported May 9 at the Biology of Genomes meeting.
For many types of cancer, it is the spread, or metastasis, of tumor cells that kills people. Because cancer that comes back and spreads after initial treatment is often deadlier than the original tumors, researchers thought most of the mutations in recurrent tumors happened after they spread. But the new findings contradict this assumption and may indicate ways to stop metastasis. Mardis, of Nationwide Children’s Hospital in Columbus, Ohio, and colleagues collected recurrent breast tumors from 16 women who died after their cancer had spread to other parts of the body. Comparing the metastasized tumors with the original breast tumors, the researchers were surprised to learn that multiple, slightly genetically different cells from the original site had broken away together and established the new tumors.
Researchers used to think cancer spread when single cells slipped away and set up shop elsewhere. But recent research in mice suggested cancer cells migrate in groups (SN: 1/10/15, p. 9). The new study doesn’t provide direct evidence of this group migration in human cancer. But genetic similarities between metastasized and original tumors suggest that multiple cells move together to remote sites.
Only two women in the study had cancer-driving mutations — both in an estrogen receptor gene called ESR1 — in their recurrent tumors not seen in the original. All of the tumors that metastasized contained mutations in the TP53 gene. Such mutations could be a warning sign that a breast cancer is prone to spread, Mardis said.
When astronomers in February announced the discovery of seven planets orbiting a supercool star, details about the outermost planet were sketchy. No more. The seventh planet is chilly and definitely no place for life, the international team reports May 22 in Nature Astronomy.
The seven-planet system, TRAPPIST-1, is 39 light-years from Earth in the constellation Aquarius. Follow-up observations of the system reveal that TRAPPIST-1h is about three-quarters the size of Earth and orbits its star in just under 19 days. The planet sits about 9.6 million kilometers from its star, which has only 8 percent of the mass of the sun. As a result, TRAPPIST-1h gets about as much starlight as the icy dwarf planet Ceres, in the asteroid belt, gets from the sun.
Such limited light makes the planet too cold (‒100° Celsius) to harbor liquid water and therefore life as we know it, the researchers report.
Tornadoes in the southeast, Earth’s magnetic field and obesity might not seem to have much in common. Well, now they do.
Under President Donald Trump’s 2018 budget proposal, federal research spending into all three areas — and many others — would decline abruptly. The president delivered his budget request to Congress on May 23, presenting the sharpest picture yet of his administration’s priorities for federal science spending. Some science and technology programs within agencies would see their funds increase, but the administration recommends extensive cuts to basic research overall. The request greatly expands on the “skinny budget” the administration released in March (SN: 4/15/17, p. 15).
Total federal research spending would be slashed by about 17 percent, Rush Holt, CEO of the American Association for the Advancement of Science, said in a conference call with reporters. “If the White House budget plan were to become law, it would devastate America’s science and technology enterprise.”
For many science agencies and programs, the outlook appears stark. Some examples:
The National Science Foundation, which funds research in all fields of science and engineering, would face an 11 percent cut. The U.S. Geological Survey’s budget would be cut by 15 percent. The National Institute of Standards and Technology, where research includes cybersecurity and nanotechnology, would face a 23 percent cut. The National Oceanic and Atmospheric Administration’s primary research arm, which investigates weather, climate and ocean resources, would be cut 32 percent. The Environmental Protection Agency’s Office of Science & Technology would be cut by 37 percent. The budget proposes a 16 percent cut for the Department of Energy’s Office of Science, the largest supporter of basic research in the physical sciences. The U.S. Centers for Disease Control and Prevention would take a 17 percent cut. Food and Drug Administration funding (not including revenue from user fees) would be cut by 30 percent. The U.S. Department of Agriculture’s Agricultural Research Service would fall 22 percent. And, as expected, the National Institutes of Health’s budget would be slashed 22 percent. Those numbers don’t mean much just yet — they are just a starting point for a long and winding route through the political process. But the details do provide more information about what programs and areas of research could be in trouble. NSF’s grant programs, for example, would lose $776 million, dropping the overall budget from $7.5 billion to $6.65 billion. As a result, the agency estimates that in fiscal year 2018, the proposed funds would support about 8,000 new research grant awards, about 800 fewer than in 2016. Among the NSF-funded programs facing potentially severe reductions are clean energy research and development and the Ocean Observatories Initiative, an array of marine and seismic sensors scattered across the Atlantic and Pacific oceans that is expected to provide some of the most detailed ocean measurements to date (SN: 10/19/13, p. 22). The project would see its NSF funding slashed by 44 percent.
A bright spot: The request leaves funding flat for LIGO, which discovered gravitational waves in 2016 (SN: 3/5/16, p. 6). Planned, continued upgrades to the project’s laser interferometer systems are still on, NSF director France Córdova said May 23 at a budget presentation at NSF headquarters in Arlington, Va. NSF has invested about $1.1 billion in the project. “It was the biggest investment NSF has made to date, and it was a big risk,” Córdova said.
Many in the scientific community say the proposed cuts would significantly undermine the nation’s global leadership role in advancing science. And they doubt the administration’s argument that the private sector would make the necessary investments in basic science research.
“Candidly, shareholders are not interested in funding research, which tends to be costly, very long-term and very risky,” said retired aerospace executive Norman Augustine during the AAAS conference call. “Research is a public good.… The rewards tend to go to the public as a whole, and therefore research really warrants government support.”
Funding for DOE’s energy programs, including research into efficiency and renewable energy, would fall about 60 percent. One of those programs, the Advanced Research Projects Agency-Energy, would be eliminated. The administration defends phasing out the roughly $300 million ARPA-E, which funds research on risky but promising energy technologies, by saying the private sector is “better positioned” to finance such research.
Within the DOE Office of Science, the biological and environmental research program, which studies climate modeling among other things, faces the steepest cut — 43 percent, a drop from $612 million to $349 million. High-energy physics research would see an 18 percent reduction, but the program for advanced scientific computing would get an 11 percent bump.
Environmental research would suffer at NOAA, with the Office of Oceanic and Atmospheric Research facing sweeping cuts. Funding for climate research would drop 19 percent, weather and air chemistry research 25 percent and ocean, coastal and Great Lakes research by 49 percent. Programs potentially shuttered include:
Air Resources Laboratory, which researches air chemistry, mercury deposition and the movement of harmful materials through the atmosphere. VORTEX-Southeast, a tornado detection and warning program for the southeastern United States. The Marine Mammal Commission, an independent agency formed in 1972 to help protect marine animals and their habitats. At USGS, the roughly $1.9 million geomagnetism program would be zeroed out. It monitors changes in Earth’s magnetic field, providing data that help NOAA and the U.S. Air Force track magnetic storms due to solar activity. Such storms can disrupt radio communication, GPS systems and, if severe enough, the electric power grid. The agency’s Climate and Land Use Change program, renamed the Land Resources program, would see a 24 percent cut. Most of the funding for a carbon sequestration research program, about $8 million, would be eliminated, with the rest, about $1.5 million, being redirected to the energy and minerals program. That division would see about a 2 percent increase overall.
Health programs and biomedical research would face big challenges under Trump’s budget. At CDC, $1.2 billion would be slashed from the agency’s overall budget. The request proposes cutting $163 million from the agency’s chronic disease prevention programs, which aim to reduce incidence of heart disease, stroke, diabetes and obesity. Prevention programs for domestic HIV/AIDS, sexually transmitted diseases and tuberculosis face a $183 million decrease in funding.
NIH’s overall budget would fall from the enacted 2017 level of $34.6 billion to $26.9 billion. Some of the most striking cuts:
National Cancer Institute — $1.2 billion National Heart, Lung and Blood Institute — $672 million. National Institute of Allergy and Infectious Diseases — $1.1 billion. National Institute of Diabetes and Digestive and Kidney Diseases — $421 million. Congress, however, recently boosted NIH funding — at least for fiscal year 2017 — providing an additional $2 billion over the next five months.
That’s an important reminder that many of the programs facing extensive reductions or elimination have allies on Capitol Hill, a potentially comforting thought for those alarmed by the president’s request. “We’re counting on Congress to, once again, say no to these recommendations,” Mary Woolley, president of the health and medical research advocacy group Research!America, said in the AAAS conference call.
Not all science agencies or programs are threatened. For instance, NASA’s planetary science division would see a funding bump. The final 2017 spending agreement, which Congress recently passed, had already increased the division’s budget from $1.63 billion to $1.85 billion. In Trump’s proposal, that number is nudged even higher, to $1.93 billion. As expected, the administration supports a flyby mission to Europa, one of Jupiter’s moons. The president has requested $425 million for the project, a 55 percent increase from the 2017 enacted level of $275 million.
“We’re pleased by our top-line number of $19.1 billion, which reflects the president’s confidence in our direction and the importance of everything we’ve been achieving,” said NASA acting administrator Robert Lightfoot.
But the agency would lose about 9 percent of its earth science budget, slightly more than expected. Grants for earth science research would be cut, and NASA’s Carbon Monitoring System, which Congress directed the space agency to form in 2010, would be axed. Five space-based earth science projects would also be eliminated. Those projects are meant, in part, to provide data to help understand various aspects of Earth’s climate and how it is changing.
Trump’s budget proposal will not get passed by Congress unchanged. Still, the administration’s lack of support for basic federal research overall has alarmed many scientists and their supporters.
“Science research has been the source of improvements in public health, in our energy, in our quality of life, in our agriculture and ability to feed ourselves and the world,” said Holt. “What we see is not just a reduction in government programs. What we see is a failure to invest in America.”
Zuul is back. But don’t bother calling the Ghostbusters. Zuul crurivastator is a dino, not a demon. A 75-million-year-old skeleton unearthed in Montana in 2014 reveals a tanklike dinosaur with a spiked club tail and a face that probably looked a lot like its cinematic namesake.
The find is the most complete fossil of an ankylosaur, a type of armored dinosaur, found in North America, researchers report May 10 in Royal Society Open Science. It includes a complete skull and tail club, plus some preserved soft tissue, says study co-author Victoria Arbour, a paleobiologist at the Royal Ontario Museum in Toronto. “It really gives us a good idea of what these animals looked like.” The bones reveal that Z. crurivastator had spikes running all the way down its tail, not just on the club itself. That arrangement means the weaponry was more than just a “massive sledgehammer,” Arbour says. The club was a formidable weapon. The term crurivastator comes from the Latin for “shin destroyer.” Arbour previously created mathematical models to calculate the force with which similar ankylosaurs might have swung their tails. These appendages provided a winning combination: good at absorbing impacts and able to smack an opponent hard enough to hurt, she says. Despite their armor and fearsome tail, ankylosaurs were plant eaters. So they probably used their tails to smack predators or compete with other ankylosaurs.
Arbour and museum colleague David Evans plan to investigate the thin sheet of fingernail-like material covering the bony plates on the tail, along with other details of the fossil that are typically lost in such old specimens. The rare, preserved soft tissue might even let scientists extract ancient proteins, Arbour says, providing insight into how these building blocks of life have changed since the days of dinos.
Having all this material in hand, she says, “kind of pushes the envelope about what we can identify in the fossil record.”
People with weakened immune systems might help scientists get a jump on the flu virus.
Some flu virus mutations popped up again and again in cancer patients with long-term infections, researchers report June 27 in eLife. And some of those mutations were the same as ones found in flu viruses circulating around the world a few years later, evolutionary virologist Jesse Bloom of the Fred Hutchinson Cancer Research Center in Seattle and colleagues discovered. The findings may eventually help vaccine developers predict flu strain evolution. “You can’t predict what’s going to happen next year,” — at least not yet, Bloom says. But monitoring infections in many people may indicate which parts of the virus are most likely to change in the future.
Most people who catch the flu get over it in about a week. Previous studies have suggested that the virus doesn’t change much within one person. It must pass through tens to hundreds of people to build up enough mutations to give it an advantage over other flu viruses, Bloom says. That makes predicting flu evolution tricky.
A coffee shop conversation alerted Bloom to a potential treasure: multiple nasal wash samples from four cancer patients who had had the flu for months in 2006 and 2007. Part of their cancer treatments had weakened all four people’s immune systems, making it hard for them to fight off the infections.
Evolutionary biologist Katherine Xue in Bloom’s lab and colleagues examined genetic material from the nasal washes, identifying mutations present in at least 5 percent of flu viruses in each person. The team tracked competition between virus variants within each person over time and compared virus evolution patterns among the patients.
Nine flu mutations popped up in at least two separate patients. Of those, five were in the virus’s hemagglutinin gene. That gene encodes a sugar-studded protein on the virus’s outer surface that helps the virus stick to and invade human cells. The immune system commonly makes antibodies against hemagglutinin that foil the strain’s ability to infect the host again. As a result, the virus has to mutate so that the protein will be different enough to evade the immune system. Four amino acids of the hemagglutinin protein were frequently changed by mutations in the cancer patients’ viruses and popped up years later in flu strains worldwide, too. Those amino acids are the 138th, 193rd, 223rd and 225th links in the chain of amino acids that make up the hemagglutinin protein.
In some cases, the mutations produced the same amino acid change in both the cancer patients’ and the global virus strains circulating after 2010. For instance, the amino acid valine was altered to isoleucine at position 223. That happened in two cancer patients in 2006 and 2007. After about 2012, nearly all viruses circulating worldwide had the same change.
In another case, those same two cancer patients’ viruses had tyrosine at position 193, but globally circulating viruses had either phenylalanine or serine at that position, the researchers found. Those results indicate that at some spots in the protein, particular changes are important, but other positions are more malleable.
Within patients, viruses carrying different amino acids seemed to directly compete against each other; as one became more frequent, the other was reduced in abundance. That’s the same sort of pattern researchers observe at the global level. Knowing which mutations commonly win competitions in immune-compromised patients may give a preview of winners in the global flu fight.
Not all of the flu mutations that arose in the cancer patients were later found in the general population, says infectious disease biologist Katia Koelle of Duke University. For instance, a mutation called L427F (changing leucine at position 427 to phenylalanine) was found in more than 75 percent of flu viruses in three of the cancer patients, but it was never seen in flu viruses circulating globally. That mutation might give flu viruses some advantage within a person, but might not be efficient at spreading from person-to-person, Koelle says. Studies that compare flu alterations in multiple people won’t immediately tell researchers how to design vaccines, she says, but could point to parts of the virus for further investigation.
Xue and Bloom say they would like to repeat the study, perhaps this time in very young children and elderly people — two groups that also have weaker immune systems than most adults.
A majority of football players whose brains were donated for research suffered a degenerative brain disease during their lives, according to the largest sample of players ever studied. The finding provides more evidence that the repetitive injuries to the brain sustained while playing American football are associated with the disease, researchers say.
Of 202 deceased former football players, 177 were diagnosed with chronic traumatic encephalopathy, which can cause a host of mood and behavioral issues as well as thinking and reasoning problems. Among 111 men who had played in the National Football League, 110 — a whopping 99 percent — had developed the disease, researchers report July 25 in JAMA. Three of 14 high school players also showed signs of the brain disease, as well as 48 of 53 college players. Researchers relied on brain autopsies of the players to make the diagnoses and interviewed family members and friends about the symptoms players had experienced. This doesn’t necessarily mean all football players experience chronic traumatic encephalopathy. Many of the families who donated the brains for research could have been motivated to do so because their loved ones had noticeable symptoms, so the sample is not necessarily representative of the general football population. The results are still worrisome, though, researchers say. “The fact that chronic traumatic encephalopathy was so common adds to our concern about the safety of playing football and the risk of developing neurologic symptoms later in life,” says neurologist Gil Rabinovici of the University of California, San Francisco, who wrote an editorial accompanying the article. This “hovers like a dark cloud over the game at all levels, even if the study cannot address how frequent the disease is, or who is at risk.”
Chronic traumatic encephalopathy, or CTE, shows up in athletes and others who’ve had repetitive injuries to the head, such as concussions. The only way to diagnose the disease is with an autopsy. In brains with the condition, a protein called tau goes “bad” and forms clumps in nerve cells and other brain cells. Although tau buildup is found in other brain diseases, like Alzheimer’s, in CTE, the protein congregates in brain cells around small blood vessels. In 2008, a research team set up a brain bank to study the impact of head blows resulting from contact sports or military service. Behavioral neurologist Jesse Mez of Boston University School of Medicine and his colleagues classified players as having mild or severe CTE, depending on how widespread the tau clumps were in the players’ brains. The severity of disease seemed to track with the number of years spent playing football, says Mez. Among NFL players, 95 of the 110 diagnosed cases were severe. All three of the high school players’ cases were mild, while just over half of the college players’ cases were severe.
Yet the players’ reported symptoms while alive were similar, regardless of the severity seen in the brain. Behavioral and mood problems, such as impulsivity, anxiety and depression, were commonly reported in both severe and mild cases of the disease. Cognitive symptoms, including memory loss, were also typical for both groups. One major difference, Mez notes, was that dementia was more common in severe cases of CTE than in mild cases.
As for why players reportedly experienced similar symptoms no matter the severity, “the question is, is there something else going on,” such as inflammation, Mez says. “Or are there regions of the brain that we’re not looking carefully enough at?”
There still isn’t a way to diagnose CTE during life, and that’s “the 800-pound gorilla in the room,” says neurologist David Brody of Washington University School of Medicine in St. Louis.
Detecting the disease in patients will be crucial for understanding how common CTE is in the NFL, “let alone in the millions of people who participated in college, high school and youth football,” says Rabinovici. “In the meantime, we need to focus on prevention of concussions and other head impacts at all levels of contact sports.”
A genetic risk factor for Alzheimer’s disease is a double, make that triple, whammy.
In addition to speeding up the development of brain plaques associated with Alzheimer’s, a gene variant known as APOE4 also makes tau tangles — another signature of the disease — worse, researchers report online September 20 in Nature. APOE4 protein also ramps up brain inflammation that kills brain cells, neuroscientist David Holtzman of Washington University School of Medicine in St. Louis and colleagues have discovered. “This paper is a tour de force,” says Robert Vassar, a neuroscientist at Northwestern University Feinberg School of Medicine in Chicago. “It’s a seminal study that’s going to be a landmark in the field” of Alzheimer’s research, Vassar predicts.
For more than 20 years, researchers have known that people who carry the E4 version of the APOE gene are at increased risk of developing Alzheimer’s. A version of the gene called APOE3 has no effect on Alzheimer’s risk, whereas the APOE2 version protects against the disease. Molecular details for how APOE protein, which helps clear cholesterol from the body, affects brain cells are not understood.
But Holtzman and other researchers previously demonstrated that plaques of amyloid-beta protein build up faster in the brains of APOE4 carriers (SN: 7/30/11, p. 9). Having A-beta plaques isn’t enough to cause the disease, Holtzman says. Tangles of another protein called tau are also required. Once tau tangles accumulate, brain cells begin to die and people develop dementia. In a series of new experiments, Holtzman and colleagues now show, for the first time, that there’s also a link between APOE4 and tau tangles. In one experiment, mice that had no A-beta in their brains developed more tau tangles if they carried the human version of APOE4 than if they had the human APOE3 gene, Holtzman and colleagues found. That finding indicates APOE4 affects tau independently of A-beta. Brains of people who died from various diseases caused by tangled tau had more dead and damaged cells if the people carried APOE4. The researchers also tracked 592 people who had low levels of A-beta in their cerebral spinal fluid — a clue that plaques have formed in the brain — and who showed symptoms of Alzheimer’s. Over a five- to 10-year period, the disease progressed 14 percent faster in people with one copy of APOE4 and 23 percent faster in people with two copies than in people who didn’t have that version of the gene, the researchers found. Those worsening symptoms are presumed to be caused by more rapid buildup of tau tangles in the APOE4 carriers.
APOE4 also seems to make Alzheimer’s worse by causing inflammation, the researchers found. Two kinds of mouse glial brain cells, microglia and astrocytes, making different versions of the APOE protein were grown with brain nerve cells, or neurons, that make disease-causing forms of tau. Mouse neurons grown with glia making no APOE grew well, even though they were making abnormal tau. But neurons grown with glia making APOE4 often died. APOE4 provoked inflammation responses in the normally friendly astrocytes and microglia, leading those cells to kill neurons, the researchers found. Such inflammation can make brain degeneration worse.
The data linking the APOE4 gene to tau tangles and brain inflammation is “super tight,” says molecular neurobiologist Sangram Sisodia of the University of Chicago. But the molecular details behind how APOE4 protein causes those effects are still vexingly absent, he says. Much more work is needed to uncover which molecules APOE4 interacts with, so that researchers can devise ways to counteract its negative effects in the brain.
Any therapies that decrease or eliminate APOE4 will need to be limited to the brain, because the protein is needed in the rest of the body to maintain healthy cholesterol levels, Vassar says. “You don’t want to give a person heart disease to cure Alzheimer’s disease.”
The reappearance of a long-lost meteor shower has finally explained what happened to a missing comet named 289P/Blanpain.
That comet was spotted only once in 1819 and never again, unusual for a body orbiting the sun. But in 2003, astronomers found a small asteroid moving along the Blanpain orbit, suggesting the space rock might be the comet (or a piece of it) after it ejected much of its cometary dust.
Some of that dust may have been what Japanese researchers saw in 1956 when they observed a meteor shower from the constellation Phoenix. Meteor showers occur when dust left behind by a comet burns up as it hits Earth’s atmosphere. Those “Phoenicid” meteors hadn’t been seen before — or since. Astronomer Jun-ichi Watanabe of the National Astronomical Observatory of Japan in Tokyo and colleagues traced the meteors to where the comet’s dust trail should have been. In 2010, the group predicted that the remaining dust would create another shower in 2014.
Team members traveled to North Carolina and Spain’s Canary Islands to test their prediction, and on the first two days of December, 2014, they saw Phoenicids streak across the sky. But there were about 90 percent fewer meteors than expected; Blanpain may have lost its dust more quickly than previously thought, the team reports in the Sept. 1 Planetary and Space Science. The astronomers will get a second chance to check — another shower is expected in 2019.
Self-driving vehicles passed a major milestone in November when Waymo’s minivans hit the streets of Phoenix without backup human drivers — reportedly making them the first fleet of fully autonomous cars on public roadways. Over the next few months, people will get a chance to take these streetwise vehicles for a free spin as the company tries to drum up excitement — and a customer base — for its launch of a driverless taxi service.
But even as these cars are ditching human supervisors, many people doubt the safety of machine motorists. A whopping 85 percent of baby boomers and even 73 percent of millennials confess to being afraid to ride in self-driving cars, according to a recent AAA survey. And while Waymo claims its vehicles are designed to be the world’s most experienced drivers — based on road tests as well as clocking millions of virtual miles — there’s still no consensus among experts about how safe is “safe enough” when it comes to street-smart cars. It’s especially difficult to tell whether self-driving cars have earned their licenses when scientists are still writing the driver’s test.
Besides the sheer convenience of being able to take your hands off the wheel, the major appeal of self-driving cars is safer roadways. After all, mechanical chauffeurs can’t get drunk or distracted — factors involved in 29 and 10 percent of fatal accidents, respectively. But the only surefire way to evaluate autonomous cars’ reliability is test-driving them in real traffic, explains Nidhi Kalra, an information scientist at the RAND Corporation in San Francisco. “I think a lot of people were thinking, ‘Oh, we’ll just wait until the companies do enough test-driving,’” she says. “You could wait until the next millennium until that happens.”
In a 2016 study, Kalra and a colleague showed that self-driving cars would have to trek hundreds of millions or perhaps billions of miles to demonstrate with comfortable certainty that they caused fewer fatalities than the average person (about 1.1 per 100 million miles driven). Based on the current number of self-driving cars, that task could take decades or centuries to complete.
Tech developers hardly have that kind of time, so companies like Waymo assess their vehicles’ safety by pairing real driving time with practice on a private track and millions of miles a day in computer simulations. Still, simulations can’t replace the value of actual road experience, says Philip Koopman, an electrical and computer engineer at Carnegie Mellon University in Pittsburgh. “What about the scenarios they didn’t know [to simulate]?” he says. “Weird, weird, weird stuff happens out on the roadways.”
Since current self-driving safety assurances aren’t exactly airtight, Koopman argues that self-driving cars should be held to a way higher standard than human drivers — say, 10 times safer than the average human — before they’re given the green light. That would provide enough wiggle room in the margin of error to assume that the driverless car actually is safer, Koopman reasons.
But getting to that point could take a long time, and miss the opportunity to save many lives, Kalra says. She’s confident because her team forecast a future — actually lots of different futures — where self-driving cars hit the road when they were 10, 75 or 90 percent safer than the average human driver. At 10 percent, fatalities drop to one death per 100 million miles. Maybe that doesn’t seem like a lot, but with those cars much closer to being ready to roll, some 500,000 lives could be saved between 2020 and 2050, the team forecasts, compared with the imagined futures where people hold out for way higher safety standards.
But just aiming for 10 percent safer doesn’t provide much margin for error, Koopman argues. “You’re cutting it pretty close.”
And a lower safety standard could mean more accidents at first — and a public backlash, says Azim Shariff, a psychologist at the University of California, Irvine. People may be less inclined to accept mistakes made by machines than humans, and research has shown that people are more risk-averse when it comes to risks that they can’t control.
“What happens when a 4-year-old in the back of a car that’s operated by her mother gets killed by an autonomous car?” Shariff asks.
Success depends on buy-in. “So public opinion is really going to matter,” Shariff says.
Right now, most Americans may not be lining up to hop aboard fully autonomous cars. But “once people start knowing people who have been in them and lived to tell the tale, so to speak, I think it will change quickly,” says David Groves, a policy analyst at the RAND Corporation in Santa Monica, Calif.
Kalra also suspects that people will fear autonomous cars less when the National Highway Traffic Safety Administration establishes a self-driving car safety rating, like its crash test ratings for traditional cars. That kind of rating system “will probably come after the technology is on the road, just as it did for regular cars,” she says. “We didn’t have a safety rating system when the Model T came out. It sounds like it’s the cart before the horse to have cars before safety ratings, but that’s often how it happens.”
Death: A Graveside Companion makes for an unusual coffee-table book, with its coppery etched Grim Reaper on the cover. Yet you may be surprised by how much fun it is to pore through the book’s lavish artwork of skulls, cadavers and fanciful imaginings of the afterlife.
There is, after all, a reason for the term “morbid curiosity.” It’s only natural for people to try to understand and come to terms with their inevitable demise, and as the book reveals, it is only in modern Western society that the topic of death has become so taboo. Even as recently as Victorian times, the book notes, the dead were laid out in the family parlor, their hair cut off and twisted to make decorative mementos to hang on the wall. As a founder of New York City’s now-closed Morbid Anatomy Museum, Joanna Ebenstein has set out to help change modern attitudes, by giving us permission to let our morbid curiosity loose. “It is my hope that this book might act as a gesture towards redeeming death, to invite it back into our world in some small way,” she writes. “It is precisely by keeping death close at hand and coming to terms with its inevitability that we are able to lead full rich lives.” She brings together 1,000 images of historical artwork, illustrations and artifacts showcasing humankind’s ongoing quest to imagine and find meaning in death, along with 19 essays by a diverse set of writers, art experts and scientific thinkers. The writings cover spiritual and symbolic aspects of death, such as the origins of Mexico’s Day of the Dead, and the surprising variety of death-themed amusements over the years. An early Coney Island attraction, for instance, re-created the experience of being buried alive. Some essays delve into scientific history, such as miniature crime scenes used in forensic science and the history of cadavers in the study of anatomy. While the essays are illuminating, the illustrations and photographs, along with informative captions, provide most of the book’s substantial heft, as well as its heart. Only by browsing through still life paintings called vanitas, popular in the 16th and 17th centuries, for instance, will you truly grasp what these symbolic masterpieces are meant to convey: the transience of beauty and earthly pursuits. If I have any quibble with this compendium, it’s that the essays (but thankfully not captions) are printed in sepia tones that make them hard to read without good lighting. But given the subject, this book may be best read while sitting next to a sunny window anyway.
