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A blood cancer uses a secret weapon for tearing bone apart. That same mechanism may allow breast cancer and other types of tumors to spread to bones, a new study suggests.

In patients with the blood cancer multiple myeloma, an enzyme called thymidine phosphorylase sets off a chain reaction that leads to bone destruction, researchers report August 24 in Science Translational Medicine. Drugs that inhibit the enzyme caused mice to lose less bone.

The findings may lead to new therapies for stopping bone loss from multiple myeloma or other cancers that spread to bone. Halting bone destruction may even make bones less hospitable for tumors, stopping their growth, too, says Jing Yang, a cancer researcher at the University of Texas MD Anderson Cancer Center in Houston.
Multiple myeloma is a cancer that grows in bone marrow. Myeloma cells talk directly to bone-remodeling cells. The tumor cells’ messages send bone-building cells on permanent vacation while stimulating bone-demolishing cells. The result is weak bones, holes, fractures and bone pain.

Yang and colleagues had previously discovered that a biological process in myeloma cells that weakens bones also boosts production of thymidine phosphorylase. The enzyme was known to be more abundant in many types of cancers where it stimulates blood vessel growth to tumors and stops tumor cells from dying. No one knew it was involved in poking holes in bones.

Thymidine phosphorylase in myeloma cells kicks off a series of steps that convert a building block of DNA called thymidine into a small molecule called 2-deoxy-D-ribose, or 2DDR. Myeloma cells secrete 2DDR and bone cells pick it up, sending a signal to turn off genes that control bone cell activity. When bone-building cells called osteoblasts get the message, they stop working, Yang and colleagues discovered. But bone-eating cells called osteoclasts work harder. That tips the cycle of bone remodeling toward destruction.

Yang’s team injected myeloma cells into the femurs of mice. After the cancer was established, the researchers treated some of the mice with drugs that inhibit thymidine phosphorylase. Those mice lost less bone than untreated mice with myeloma did.

The drugs have already been approved for treating other types of cancer. If the results of the mouse study hold up in human clinical tests, the drugs may also preserve bone in myeloma patients and people with other cancers that have spread to their bones, Yang says. She hopes that the drugs may even help repair bone damage.
“We’re getting better at getting rid of myeloma cells,” says Rebecca Silbermann, a hematologist at Indiana University School of Medicine in Indianapolis. “But we have no way to heal those bone lesions at this point, even if a person’s myeloma is gone.”

Currently, drugs used to maintain bone strength slow bone-dissolving cells, but don’t put bone-building cells back to work, Silbermann says. Drugs like the thymidine phosphorylation inhibitors used in the study might have better results because they may prod bone-building cells to do their jobs again.

Because thymidine phosphorylase’s message passes through multiple receivers and transmitters, researchers also have multiple options for interrupting the relay, says Yibin Kang. That interference may one day allow doctors to stop or even reverse bone loss from cancer and maybe even from osteoporosis, says Kang, a cancer researcher at Princeton University who studies how breast cancer spreads to bone.

While the study provides important new clues about how myeloma breaks down bone, it’s not clear whether thymidine phosphorylase starts the process early in cancer or just helps perpetuate it later, says Qing Yi, a myeloma researcher at the Cleveland Clinic. It’s also too early to tell whether breast cancer and others use the same process for breaking down bone, he says. “This has a long way to go before it can ever reach the patient.”

Hawaiian honeycreepers are a marvel of evolution. Millions of years ago, some finches arrived on the Hawaiian Islands and began to diversify. As the Pacific Plate moved over the Hawaiian hotspot and new islands formed and others shriveled away, these colorful songbirds evolved into more than 50 species that differed so much in what they ate, where they lived and how they looked that it took scientists quite a while to figure out that they were all related.

More than half of those species are now gone. “Many extinctions took place when the islands were first settled by Polynesian people,” notes Helen James, who, as curator of birds at Smithsonian’s National Museum of Natural History, has studied the birds’ evolutionary history. Then Westerners arrived and bird populations started to disappear more quickly due to a combination of threats, including habitat loss, introduction of invasive species and the arrival of diseases such as avian malaria.

Bird populations on Hawaii’s oldest island, Kauai, have been hit especially hard. Kauai lost at least eight species of honeycreepers — as well as several other “marvelous species” of birds, James notes — before people began keeping good records of the island’s fauna. And now a new study warns that the birds’ situation will get worse — and soon. The honeycreepers that are left on the island are declining fast, and some species could disappear in as little as a decade.

Eben Paxton of the U.S. Geological Survey Pacific Islands Ecosystems Research Center at Hawaii Volcanoes National Park and colleagues looked at population trends for seven species of native forest birds living on Kauai’s Alakai Plateau, the eroded crater of a long-extinct volcano. On other Hawaiian islands, only high-elevation areas have generally been cool enough to keep out the mosquitoes that spread avian diseases. But on lower-lying Kauai, its forests have tended to be cooler than similar-elevation regions on the other islands, so spots such as the Alakai Plateau have been disease-free refuges for native birds.
Or, they were. A 2014 study found that disease prevalence in birds had more than doubled there between 1994-1997 and 2007-2013. Climate change had warmed the plateau enough that disease-laden mosquitoes could spread.
In the new study, Paxton and his colleagues found that six of seven native forest birds surveyed (an eighth proved too wily for scientists to accurately count) are rapidly disappearing and their ranges contracting. All six are honeycreepers, and four are now found only in small, remote parts of the plateau. Fewer than 1,000 Akekee and fewer than 500 Akikiki remain, the team reports September 2 in Science Advances.

“If native species linearly decline at a rate similar to or greater than that of the past decade, then multiple extinctions are likely in the next decade,” the team writes.

James says that she hopes the new findings will be a call to action. “Their data show alarming declines in population and geographic ranges of endemic Hawaiian honeycreepers on the island of Kauai,” she says. The birds’ extinction “would be a tremendous loss.”

Even without avian diseases and climate change, the honeycreepers still face threats from habitat loss, introduced predators and competition with non-native birds (some of whom, such as the Japanese bush-warbler, are thriving on the plateau, the study finds). Reducing those threats could buy the honeycreepers some time to adapt to the growing threat of disease. Scientists can also help by developing genetically modified mosquitoes and figuring out why honeycreepers are so susceptible to avian malaria — and how to protect them from it, James notes.

“The Hawaiian honeycreepers are a classic example of adaptive radiation in animals, second only to Darwin’s finches,” she says. Losing Kauai’s endemic honeycreepers “would definitely cost us in terms of our opportunities to study, understand and appreciate nature.”

Language is a tricky thing to write about. You’re using it while dissecting it. That sort of recursion can trip you up. As a philosopher friend of mine once said, a zoologist studying tigers, while riding on the back of a tiger, should be very careful.

Of all the writers who’ve ever taken on the task of writing about language, nobody of any consequence has ever tripped himself up quite so much as Tom Wolfe. His new book, The Kingdom of Speech, has been widely denigrated (deservedly) by scientists who have encountered it. Wolfe has taken it upon himself to explain various aspects of science — having to do with biological evolution, linguistics, psychology and cognitive neuroscience — to scientists, in the process disparaging titans in their fields such as Charles Darwin and Noam Chomsky. It’s kind of like Brad Pitt or Angelina Jolie trashing George Washington and Abraham Lincoln. Wolfe pontificates about language without realizing that he’s riding on the back of a linguistic tiger.

It’s difficult to criticize him, though, without lapsing into the same sort of abominable adhominemism with which he assaults Darwin and Chomsky. It’s not enough just to assert disagreement with Darwin’s views on how language evolves or Chomsky’s theory that evolution endowed all human babies with a built-in hardwired “universal grammar.” Wolfe attacks their character.

He presents Chomsky as a demon, a bully, a knave. When criticizing another’s research, Chomsky “pulls out a boning knife and goes to work,” Wolfe writes; he refers to Chomsky’s “audacity” and accuses him of “double talk.” He calls him “an angry god raining fire and brimstone.” He lambastes Chomsky for attacking his critics as liars, charlatans and frauds. In short, Wolfe attacks Chomsky for using against others the same linguistic strategy that Wolfe uses against Chomsky. Riding on a tiger.

Wolfe gives the impression of being jealous of Chomsky’s fame, which seems odd for a writer so famous himself. As for Darwin, Wolfe presents the greatest biologist in history as a petty thief who stole credit for the theory of evolution by natural selection from Alfred Russell Wallace, who was (Wolfe alleges) screwed over by the British gentlemen’s club conspirators who rigged the system to give Darwin credit for priority. And then Wolfe ridicules Darwin for reporting observations on the behavior of his dog.

But the poverty of Wolfe’s intellectual rhetoric does not cement the case against him. Just as belittling Darwin and Chomsky personally does not really rebut their science, condemning Wolfe’s rhetorical juvenility does not confront the substance of his thesis — that humans invented speech (and subsequent forms of language derived from it) — and that evolution had nothing to do with it. And that speech, and speech virtually alone, makes humans superior to other animals.

Somehow Wolfe manages to claim that he and he alone has figured out what no one else (at least, “no licensed savant”) ever thought of, that speech is the “cardinal distinction between man and animal.” It did not evolve. “Man, man unaided, created language,” Wolfe says. Language is a system of mnemonics, based on sounds that represent meaning, enabling people to remember, think and plan. And humans invented that system. Yes, invented it!!! (That’s how Wolfe writes: his rhetoric would collapse if denied the use of italics and exclamation points.) In any case, the question is not whether Wolfe dismisses Darwin and Chomsky unfairly, but rather whether he marshals sufficient factual evidence to support his central claim.
But facts are not Wolfe’s strong suit. On page 5, for instance, he announces that Watson and Crick discovered DNA. How unfair to Friedrich Mieschler, who discovered the molecule deoxyribonucleic acid in 1869. Watson and Crick discovered its double helix structure. Given such a weak grasp of such an elementary fact, Wolfe’s subsequent assertions on subtle points of evolutionary theory warrant suspicion.

There’s more. In one of his book’s most tweeted passages, he asserts that evolution fails all the tests of what makes “science”:

“Had anyone observed the phenomenon…? Could other scientists replicate it? Could any of them come up with a set of facts that, if true, would contradict the theory (Karl Popper’s ‘falsifiability’ test)? Could scientists make predictions based on it? Did it illuminate hitherto unknown or baffling areas of science?”
To which questions Wolfe answers “no … no … no … no … and no.” But to which any long-time reader of Science News would have responded “yes, yes, yes, yes and yes” (as would any knowledgeable scientist, as biologist Jerry Coyne, among others, has pointed out).

Wolfe’s citing of Popper is especially lame; although in early writings Popper criticized natural selection, in his later years he assented that natural selection could be posed in testable terms (he even thought that it failed the test under certain circumstances).

Nonetheless it is true that ideas about the evolutionary origin of language are difficult to test. Wolfe, in fact, anchors his argument with two recent papers (2014), each with Chomsky as a coauthor, asserting that “the most fundamental questions about the origins and evolution of our linguistic capacity remain as mysterious as ever.” Evidence on this issue is either “inconclusive or irrelevant,” Chomsky and colleagues wrote in Frontiers in Psychology. Evidence of Neandertal ability to produce speech does not help trace the beginnings of language, he and collaborators wrote in PLOS Biology. Speech ability “is undoubtedly a necessary condition for the expression of vocally externalized language,” but “is not a sufficient one, and … is evidently no silver bullet for determining when human language originated.”

Others would disagree on how well the evidence illuminates language’s origins, just as some experts in linguistics have disagreements with Chomsky on many other points. But even if you acknowledge a lack of “conclusive” evidence, that’s not the same thing as saying there is “no evidence” — as Wolfe repeatedly alleges.

Of course, both papers clearly state that language did, in fact, evolve — it’s just that science can not yet say exactly how. And it’s true that the origin of speech is among the most stubborn of mysteries. So are the origin of the universe, the origin of life and the origin of baseball. Science has not yet fully understood the causes of Alzheimer’s disease, either (and certainly has found no cure); the logical conclusion is not that man just decided to get Alzheimer’s disease. Research continues on the premise that its biological basis might yet be discovered.

Boiled down to its essentials, Wolfe’s case amounts to a fairly sparse syllogism: Science has not been able to establish how human language originated and evolved. Therefore, it did not evolve. And furthermore, I (Wolfe) know how it originated. Humans invented it.

Wolfe apparently doesn’t seem to care that his major premise is based on two papers that assert that language did in fact evolve. Or that his argument against language evolution hinges on a lack of testable evidence, while he declares that he knows how language originated — without any testable evidence. Tigers.

And Wolfe certainly missed the irony of one sentence in the paper in PLOS Biology he cites. “Evolutionary analysis of language is often plagued by popular, naïve, or antiquated conceptions of how evolution proceeds,” Chomsky and collaborators wrote. As in Wolfe’s book.

DNA in cancerous tissues of tobacco smokers shows mutation patterns that differ from those in cancerous tissues of nonsmokers, a new analysis finds. The new study, in the Nov. 4 Science, reveals how smoking contributes to different cancers, enhancing several kinds of DNA damage.

“We are doing a sort of molecular archaeology,” says cancer geneticist Ludmil Alexandrov of Los Alamos National Laboratory in New Mexico, who led the analysis. While smoking’s link to cancer has been known for decades, “it’s always been a bit of a mystery why smoking increases the risk of cancers like bladder or kidney — tissues that aren’t exposed to smoke.”
Mutations in DNA arise naturally in a person’s lifetime, but some genetic changes — such as those spurred by smoking — increase the risk of certain cancers. Scientists have identified several patterns of DNA mutations that consistently show up in tissues of some cancers. These patterns, which may appear over and over again in a stretch of tumor DNA, can serve as a signature of the underlying mechanism that led to the mutations, offering clues to how different cancers strike.

“When someone has a cancer, we only see what is now — we don’t know what happened 20 years ago when that cancer was only one cell,” says cancer biologist Gerd Pfeifer of the Van Andel Research Institute in Grand Rapids, Mich.

“These signatures give us a really good clue of what might have happened,” says Pfeifer, who was not involved with the study.

Alexandrov and an international team of researchers found several differences in the number of altered DNA signatures in tumors of smokers compared with those from nonsmokers with the same type of cancer. The research adds dismal specifics to what’s already known about smoking: It is really bad for you.

“Tobacco smoking leaves permanent mutations — it erodes the genetic material of most cells in your body,” says Alexandrov. “Even if you are a just a social smoker who occasionally has one or two or five cigarettes, there is still a cumulative effect.”
Alexandrov and colleagues compiled data on DNA extracted from more than 5,000 human samples representing 17 cancers for which smoking is a known risk factor. About half of the samples were from smokers. The team then searched the DNA for various patterns of damage, or “mutational signatures.”

One suite of mutations, called signature 4, was consistently found in tissues exposed to tobacco smoke. While this signature also appeared in nonsmokers’ tumors, it occurred far less often. Smokers with lung squamous cancer, lung adenocarcinoma and larynx cancers had an especially high number of signature 4 mutations. Signature 4 signals damage to guanine (the structural component of DNA known as “G”). This signature also appears in the DNA of cells in a lab dish that are exposed to a chemical found in burnt products, including polluted air and the tar in cigarette smoke.

Signature 4 mutations also showed up in cancers of the oral cavity, pharynx and esophagus, but much less often. The researchers aren’t sure why these tissues, which are also directly exposed to smoke, don’t have as heavy a mutational load. Those tissues may metabolize smoke differently, the researchers speculate.

DNA damage in smokers also differed from that in nonsmokers for another suite of mutations, known as signature 5. This signature typically shows up in all cancers and across all tissue types. The cause of signature 5 remains unknown, but scientists do know that the number of signature 5 mutations is “clocklike” — it increases with age. The new analysis revealed that the signature 5 “clock” ticks faster in smokers. Depending how heavily a person smoked, the more signature 5 mutations were found.

In patients with lung adenocarcinoma, far more mutations associated with two other signatures, 2 and 13, had accumulated in smokers than in nonsmokers. There are hints that these mutations result from overactive DNA editing machinery. But because these signatures are found in many kinds of cancer, it isn’t clear why smoking ups the mutations load. Inflammation from smoke might be activating the cellular machinery that underlies the mutations.

When the researchers took into account the quantity smoked, they discovered that the number of mutations for some cancers was linked to the “pack years” smoked (a pack of cigarettes a day for one year). Breaking these data down into cancer types allowed the team to calculate the mutations caused by smoking for a particular tissue type: A pack a day for one year leads to 150 mutations in a lung cell, 97 in a larynx cell, 39 in the pharynx, 23 in the oral cavity, 18 in the bladder and six in a liver cell.

Lurking beneath New Zealand is a long-hidden continent called Zealandia, geologists say. But since nobody is in charge of officially designating a new continent, individual scientists will ultimately have to judge for themselves.

A team of geologists pitches the scientific case for the new continent in the March/April issue of GSA Today, arguing that Zealandia is a continuous expanse of continental crust covering around 4.9 million square kilometers. That’s about the size of the Indian subcontinent. Unlike the other mostly dry continents, around 94 percent of Zealandia hides beneath the ocean. Only New Zealand, New Caledonia and a few small islands peek above the waves.
“If we could pull the plug on the world’s oceans, it would be quite clear that Zealandia stands out about 3,000 meters above the surrounding ocean crust,” says study coauthor Nick Mortimer, a geologist at GNS Science in Dunedin, New Zealand. “If it wasn’t for the ocean level, long ago we’d have recognized Zealandia for what it was — a continent.”

The landmass faces an uphill battle for continent status, though. Unlike planets and slices of geologic time (SN: 10/15/16, p. 14), no international panel exists to officially rubber-stamp a new continent. The current number of continents is already vague — usually given as six or seven, with geologists referring to Europe and Asia collectively as Eurasia. Proponents will just have to start using the term “Zealandia” and hope it catches on, Mortimer says.
This odd path forward stems from the simple fact that nobody expected another addition to the continental ranks, says Keith Klepeis, a structural geologist at the University of Vermont in Burlington who supports Zealandia’s inclusion. The discovery illustrates that “the large and obvious can be overlooked in science,” he says.

Mortimer and others have been building a case for Zealandia for more than a decade and say they’ve now ticked off the boxes required to meet common definitions of a continent. The region is composed of continental rocks such as granite, for instance, unlike the denser volcanic basalt that forms ocean crust. Zealandia is also spatially distinct from nearby Australia thanks to an intervening stretch of ocean crust.

“If Zealandia was physically attached to Australia, then the big news story here wouldn’t be that there’s a new continent on planet Earth; it’d be that the Australian continent is 4.9 million square kilometers larger,” Mortimer says. Other geologic features rising from the seafloor either are not made of continental crust, such as volcano-built submarine plateaus, or are not distinct from nearby continents, such as Greenland.

Size is a sticking point, though. No minimum size requirement exists for continents. Mortimer and colleagues propose a 1-million-square-kilometer cutoff point. If this limit is accepted, Zealandia would be the scrawniest continent by far, little more than three-fifths the size of Australia. (Both submerged and dry areas contribute to a continent’s overall size.)
Scientists dub smaller fragments of continental crust microcontinents, and microcontinents that are attached to larger continents are subcontinents. About six times the size of Madagascar, one of the larger microcontinents, Zealandia fits better as a continent than a microcontinent, Mortimer and colleagues conclude.
“Zealandia’s in this sort of gray zone,” says Richard Ernst, a geologist at Carleton University in Ottawa. He proposes that an intermediate term could help bridge the gap between microcontinent and full-blown continent: mini-continent. The definition would cover Zealandia as well as other not-quite-continents such as India before it plowed into Eurasia tens of millions of years ago. Such a solution would be similar to the route taken for Pluto, which was demoted from planet to the newly coined “dwarf planet” in 2006.

Scientists previously assumed that New Zealand and its neighbors were an assortment of islands, fragments of long-gone continents and other geologic odds and ends. Recognizing Zealandia as a coherent continent would help scientists piece together ancient supercontinents and study how geologic forces reshape landmasses over time, Mortimer says.

Zealandia probably began as part of the southeastern edge of the supercontinent Gondwana, making up about 5 percent of that supersized landmass, before it began peeling off around 100 million years ago. This breakup stretched, thinned and distorted Zealandia, which ultimately lowered the region below sea level.

It won’t be a tsunami. Nor an earthquake. Not even the crushing impact of the space rock. No, if an asteroid kills you, gusting winds and shock waves from falling and exploding space rocks will most likely be to blame. That’s one of the conclusions of a recent computer simulation effort that investigated the fatality risks of more than a million possible asteroid impacts.

In one extreme scenario, a simulated 200-meter-wide space rock whizzing 20 kilometers per second whacked London, killing more than 8.7 million people. Nearly three-quarters of that doomsday scenario’s lethality came from winds and shock waves, planetary scientist Clemens Rumpf and colleagues report online March 27 in Meteoritics & Planetary Science.

In a separate report, the researchers looked at 1.2 million potential impactors up to 400 meters across striking around the globe. Winds and shock waves caused about 60 percent of the total deaths from all the asteroids, the team’s simulations showed. Impact-generated tsunamis, which many previous studies suggested would be the top killer, accounted for only around one-fifth of the deaths, Rumpf and colleagues report online April 19 in Geophysical Research Letters.
“These asteroids aren’t an everyday concern, but the consequences can be severe,” says Rumpf, of the University of Southampton in England. Even asteroids that explode before reaching Earth’s surface can generate high-speed wind gusts, shock waves of pressure in the atmosphere and intense heat. Those rocks big enough to survive the descent pose even more hazards, spawning earthquakes, tsunamis, flying debris and, of course, gaping craters.

While previous studies typically considered each of these mechanisms individually, Rumpf and colleagues assembled the first assessment of the relative deadliness of the various effects of such impacts. The estimated hazard posed by each effect could one day help leaders make one of the hardest calls imaginable: whether to deflect an asteroid or let it hit, says Steve Chesley, a planetary scientist at NASA’s Jet Propulsion Laboratory in Pasadena, Calif., who was not involved with either study.

The 1.2 million simulated impactors each fell into one of 50,000 scenarios, which varied in location, speed and angle of strike. Each scenario was run with 24 different asteroid sizes, ranging from 15 to 400 meters across. Asteroids in nearly 36,000 of the scenarios, or around 72 percent, descended over water.

The deadliness assessment began with a map of human populations and numerical simulations of the energies unleashed by falling asteroids. Those energies were then used alongside existing casualty data from studies of extreme weather and nuclear blasts to calculate the deadliness of the asteroids’ effects at different distances. Rumpf and his team focused on short-term impact effects, rather than long-term consequences such as climate change triggered by dust blown into the atmosphere.

(The kill count of each effect was calculated independently of the other effects, meaning people who could have died of multiple causes were counted multiple times. This double counting allows for a better comparison across effects, Rumpf says, but it does give deaths near the impact site more weight in calculations.)
While the most deadly impact killed around 117 million people, many asteroids posed no threat at all, the simulations revealed. More than half of asteroids smaller than 60 meters across — and all asteroids smaller than 18 meters across — caused zero deaths. Rocks smaller than 56 meters wide didn’t even make it to Earth’s surface before exploding in an airburst. Those explosions could still be deadly, though, generating intense heat that burns skin, high-speed winds that hurl debris and pressure waves that rupture internal organs, the team found.

Tsunamis became the dominant killer for water impacts, accounting for around 70 to 80 percent of the total deaths from each impact. Even with the tsunamis, though, water impacts were only a fraction as deadly on average as land-hitting counterparts. That’s because impact-generated tsunamis are relatively small and quickly lose steam as they traverse the ocean, the researchers found.

Land impacts, on the other hand, cause considerable fatalities through heat, wind and shock waves and are more likely to hit near large population centers. For all asteroids big enough to hit the land or water surface, heat, wind and shock waves continued to cause the most casualties overall. Land-based effects, such as earthquakes and blast debris, resulted in less than 2 percent of total deaths.

Deadly asteroid impacts are rare, though, Rumpf says. Most space rocks bombarding Earth are tiny and harmlessly burn up in the atmosphere. Bigger meteors such as the 20-meter-wide rock that lit up the sky and shattered windows around the Russian city of Chelyabinsk in 2013 only frequent Earth about once a century (SN Online: 2/15/13). Impacts capable of inducing extinctions, like the at least 10-kilometer-wide impactor blamed for the end of the dinosaurs 66 million years ago (SN: 2/4/17, p. 16), are even rarer, striking Earth roughly every 100 million years.
But asteroid impacts are scary enough that today’s astronomers scan the sky with automated telescopes scouting for potential impactors. So far, they’ve cataloged 27 percent of space rocks 140 meters or larger estimated to be whizzing through the solar system. Other scientists are crunching the numbers on ways to divert an earthbound asteroid. Proposals include whacking the asteroid like a billiard ball with a high-speed spacecraft or frying part of the asteroid’s surface with a nearby nuclear blast so that the vaporized material propels the asteroid away like a jet engine.

The recent research could offer guidance on how people should react to an oncoming impactor: whether to evacuate or shelter in place, or to scramble to divert the asteroid. “If the asteroid’s in a size range where the damage will be from shock waves or wind, you can easily shelter in place a large population,” Chesley says. But if the heat generated as the asteroid falls, impacts or explodes “becomes a bigger threat, and you run the risk of fires, then that changes the response of emergency planners,” he says.
Making those tough decisions will require more information about compositions and structures of the asteroids themselves, says Lindley Johnson, who serves as the planetary defense officer for NASA in Washington, D.C. Those properties in part determine an asteroid’s potential devastation, and the team didn’t consider how those characteristics might vary, Johnson says. Several asteroid-bound missions are planned to answer such questions, though the recent White House budget proposal would defund a NASA project to reroute an asteroid into the moon’s orbit and send astronauts to study it (SN Online: 3/16/17).

In the case of a potential impact, making decisions based on the average deaths presented in the new study could be misleading, warns Gareth Collins, a planetary scientist at Imperial College London. A 60-meter-wide impactor, for instance, caused on average about 6,300 deaths in the simulations. Just a handful of high-fatality events inflated that average, though, including one scenario that resulted in more than 12 million casualties. In fact, most impactors of that size struck away from population centers and killed no one. “You have to put it in perspective,” Collins says.

Planting trees is often touted as a strategy to make cities greener, cleaner and healthier. But during heat waves, city trees actually boost air pollution levels. When temperatures rise, as much as 60 percent of ground-level ozone is created with the help of chemicals emitted by urban shrubbery, researchers report May 17 in Environmental Science & Technology.

While the findings seem counterintuitive, “everything has multiple effects,” says Robert Young, an urban planning expert at the University of Texas at Austin, who was not involved with the study. The results, he cautions, do not mean that programs focused on planting trees in cities should stop. Instead, more stringent measures are needed to control other sources of air pollution, such as vehicle emissions.
Benefits of city trees include helping reduce stormwater runoff, providing cooling shade and converting carbon dioxide to oxygen. But research has also shown that trees and other shrubs release chemicals that can interact with their surrounding environment, producing polluted air. One, isoprene, can react with human-made compounds, such as nitrogen oxides, to form ground-level ozone, a colorless gas that can be hazardous to human health. Monoterpenes and sesquiterpenes also react with nitrogen oxides, and when they do, lots of tiny particles, similar to soot, build up in the air. In cities, cars and trucks are major sources of these oxides.

In the new study, Galina Churkina of Humboldt University of Berlin and colleagues compared simulations of chemical concentrations emitted from plants in the Berlin-Brandenburg metropolitan area. The researchers focused on two summers: 2006, when there was a heat wave, and 2014, when temperatures were more typical.

At normal daily maximum summer temperatures, roughly 25° Celsius on average, plants’ chemical emissions contributed to about 6 to 20 percent of ozone formation in the simulations. At peak temperatures during the heat wave, when temperatures soared to over 30°C, plant emissions spiked, boosting their share of ozone formation to up to 60 percent. Churkina says she and colleagues were not surprised to see the seemingly contrary relationship between plants and pollution. “Its magnitude was, however, quite amazing,” she says.

The results, she notes, suggest that campaigns to add trees to urban spaces can’t be done in isolation. Adding trees will improve quality of life only if such campaigns are combined with the radical reduction of pollution from motorized vehicles and the increased use of clean energy sources, she says.

Patience is a virtue in the hunt for dark matter. Experiment after experiment has come up empty in the search — and the newest crop is no exception.

Astronomical observations hint at the presence of an unknown kind of matter sprinkled throughout the cosmos. Several experiments are focused on the search for one likely dark matter candidate: weakly interacting massive particles, or WIMPs. But those particles are yet to be spotted.

New results, posted online at arXiv.org in recent months, continue the trend. The PandaX-II experiment, based in China, found no hint of the particles, scientists reported August 23. The XENON1T experiment in Italy also came up WIMPless according to a May 18 paper. Scientists with the DEAP-3600 experiment in Sudbury, Canada, reported their first results on July 25. Signs of dark matter? Nada. And the SuperCDMS experiment in the Soudan mine in Minnesota likewise found no WIMP hints, scientists reported August 29.

Another experiment, PICO-60, also located in Sudbury, reported its contribution to the smorgasbord of negative results June 23 in Physical Review Letters.

Scientists haven’t given up hope. Researchers are building ever-larger detectors, retooling their experiments and expanding the search beyond WIMPs, in hopes of glimpsing a dark matter particle.

It’s not every day that a spacecraft gets vaporized by the very planet it sought to explore.

After 13 years studying Saturn and its moons, NASA’s Cassini spacecraft will plunge into the ringed gas giant’s atmosphere. The mission will come to a close at about 7:55 a.m. EDT (4:55 a.m. PDT) Friday, when Saturn’s atmosphere pushes Cassini’s antenna away from Earth, terminating the signal. Shortly thereafter, the spacecraft will disintegrate.

If you want to keep tabs on the action, you’ve got a few options. Science News astronomy writer Lisa Grossman is at the Jet Propulsion Laboratory in Pasadena, Calif. — home of mission control for the Cassini probe. She’ll be popping on to the Science News Facebook page throughout the day Thursday with live updates, and she (@astrolisa) and Science News (@ScienceNews) will have details for you on Twitter as well.

Cassini’s death won’t be captured on film. But thanks to the internet, you can watch NASA scientists react to the probe’s impending doom live. In the early hours of Friday morning (7-8:30 a.m. EDT/4-5:30 a.m. PDT), NASA plans to stream a live video feed from the control room, which you can watch here:
And, you can also watch on NASA JPL’s YouTube channel and NASA’s Facebook page.

For more on Cassini’s exploits, check out all of our past coverage of the mission.

A soft heart keeps Enceladus warm from the inside. Friction within its porous core could help Saturn’s icy moon maintain a liquid ocean for billions of years and explain why it sprays plumes from its south pole, astronomers report November 6 in Nature Astronomy.

Observations in 2015 showed that Enceladus’ icy surface is a shell that’s completely detached from its rocky core, meaning the ocean spans the entire globe (SN: 10/17/15, p. 8). Those measurements also showed that the ice is not thick enough to keep the ocean liquid.
Other icy moons, like Jupiter’s Europa, keep subsurface oceans warm through the energy generated by gravitational flexing of the ice itself. But if that were Enceladus’ only heat source, its ocean would have frozen within 30 million years, a fraction of the age of the solar system, which formed roughly 4.6 billion years ago.

Planetary scientist Gaël Choblet of the University of Nantes in France and his colleagues tested whether friction in the sand and gravel thought to make up Enceladus’ core could heat things up.

The team made computer simulations of water circulating through the spongy core using data from the Cassini spacecraft and geoengineering experiments with sand and gravel on Earth. They found that, depending on the core’s makeup, the ocean should get enough heat to stay liquid for tens of millions to billions of years.

The simulations also showed that certain hot spots in the core, including at the poles, correspond to regions where the ice shell is thinner.
“That was quite cool,” Choblet says. “It explains the internal structure and the way things are organized and the dynamics interior to Enceladus.”

And that could explain why the moon spews plumes of water from its south pole: More heat from the core at that spot could melt the ice and let water out. It doesn’t explain why the north pole is plume-free, though.