Mosquitoes take weird insect flight to new heights.

The buzzing bloodsuckers flap their long wings in narrow strokes really, really fast — more than 800 times per second in males. That’s four times faster than similarly sized insects. “The incredibly high wingbeat frequency of mosquitoes is simply mind-boggling,” says David Lentink, who studies flight at Stanford University.

Mosquitoes mostly hover. Still, it takes a lot of oomph and some unorthodox techniques to fly that slowly. Mosquitoes manage to stay aloft thanks primarily to two novel ways to generate lift when they rotate their wings, Richard Bomphrey and colleagues write March 29 in Nature. The insects essentially recycle the energy from the wake of a preceding wing stroke and then tightly rotate their wings to remain in flight.
Most insects (and some birds and bats) rely on long wing strokes that create tiny low-pressure tornadoes called leading-edge vortices. The sharp front edge of the wing splits airflow in two, creating a bubble of swirling air along the front of the wing. Having low-pressure air above a wing and high-pressure air below generates lift.

But mosquitoes rapidly flap their wings up and down around a roughly 40-degree angle on average. Such short, speedy wingbeats make it impossible to generate enough lift from leading-edge vortices to stay in the air. “We knew something funny had to be going on. We just didn’t know what,” says Bomphrey, a biomechanist at the Royal Veterinary College of the University of London. So his team aimed eight high-speed cameras at hovering house mosquitoes (Culex quinquefasciatus) to model the physics of mosquito flight.
It turns out the insects flap their wings in a tight figure eight formation. Leading-edge vortices generate some lift as the wings briefly cut through the air horizontally. Then, as the wings start to rotate into the curve of the figure eight, they trap the wake of the previous stroke to create another series of low-pressure swirling vortices, this time along the back edge of the wing. “This doesn’t require any power. It’s a particularly economical way of generating lift,” says Bomphrey.
As the wings rotate, they also push air down, redirecting low-pressure air across the top of the wings. The wings rotate around an axis at their front edge, but if they go too far past vertical, they start to lose lift. So, the mosquito subtly shifts its wings’ turning axis from the front to the back of the wing, creating a more horizontal surface that allows the wings to continue to push air down. This also sets up the insect to benefit from the vortices along the trailing edge of the wing coming out of the turn.

Switching the axis mid-rotation “is impressive, especially since mosquito nerve cells fire just once for every few wingbeats,” says Itai Cohen, a Cornell University physicist not affiliated with the work. “Somehow this animal has evolved a complex wing stroke that takes advantage of aerodynamic forces and the mechanical infrastructure of the wing to generate complex motions with very few signals from the brain,” he says.

Bomphrey suspects that using these lift-driving forces may be common in mosquitoes and other insects that hover. But Lentink, who was not affiliated with the work, thinks it’s unlikely that lots of insects fly this way “because it seems so inefficient.”

Another force of nature may have driven mosquitoes to such illogical flight patterns: sex. Mosquito wingbeats make high-pitched tones, and males and females harmonize these tones in their search for a mate (SN: 01/31/09, p. 10). A flight style that entails fast flapping may have evolved as a result of sexual pressure to reach higher frequencies. That’s one theory anyway, and Cohen thinks it’s an interesting idea: “You’re talking about an insect sacrificing its flying capabilities in order to mate.”

It is the dazzling star of the biotech world: a powerful new tool that can deftly and precisely alter the structure of DNA. It promises cures for diseases, sturdier crops, malaria-resistant mosquitoes and more. Frenzy over the technique — known as CRISPR/Cas9 — is in full swing. Every week, new CRISPR findings are unfurled in scientific journals. In the courts, universities fight over patents. The media report on the breakthroughs as well as the ethics of this game changer almost daily.

But there is a less sequins-and-glitter side to CRISPR that’s just as alluring to anyone thirsty to understand the natural world. The biology behind CRISPR technology comes from a battle that has been raging for eons, out of sight and yet all around us (and on us, and in us).

The CRISPR editing tool has its origins in microbes — bacteria and archaea that live in obscene numbers everywhere from undersea vents to the snot in the human nose. For billions of years, these single-celled organisms have been at odds with the viruses — known as phages — that attack them, invaders so plentiful that a single drop of seawater can hold 10 million. And natural CRISPR systems (there are many) play a big part in this tussle. They act as gatekeepers, essentially cataloging viruses that get into cells. If a virus shows up again, the cell — and its offspring — can recognize and destroy it. Studying this system will teach biologists much about ecology, disease and the overall workings of life on Earth.

But moving from the simple, textbook story into real life is messy. In the few years since the defensive function of CRISPR systems was first appreciated, microbiologists have busied themselves collecting samples, conducting experiments and crunching reams of DNA data to try to understand what the systems do. From that has come much elegant physiology, a mass of complexity, surprises aplenty — and more than a little mystery.
Spoiled yogurt
The biology is complicated, and its basic nuts and bolts took some figuring out. There are two parts to CRISPR/Cas systems: the CRISPR bit and the Cas bit. The CRISPR bit — or “clustered regularly interspaced short palindromic repeats” — was stumbled on in the late 1980s and 1990s. Scientists then slowly pieced the story together by studying microbes that thrive in animals’ guts and in salt marshes, that cause the plague and that are used to make delicious yogurt and cheese.

None of the scientists knew what they were dealing with at first. They saw stretches of DNA with a characteristic pattern: short lengths of repeated sequence separated by other DNA sequences now known as spacers. Each spacer was unique. Because the roster of spacers could differ from one cell to the next in a given microbe species, an early realization was that these differences could be useful for forensic “typing” — investigators could tell whether food poisoning cases were linked, or if someone had stolen a company’s yogurt starter culture.
But curious findings piled up. Some of those spacers, it turned out, matched the DNA of phages. In a flurry of reports in 2005, scientists showed, to name one example, that strains of the lactic acid bacterium Streptococcus thermophilus contained spacers that matched genetic material of phages known to infect Streptococcus. And the more spacers a strain had, the more resistant it was to attack by phages.

This began to look a lot like learned or adaptive immunity, akin to our own antibody system: After exposure to a specific threat, your immune system remembers and you are thereafter resistant to that threat. In a classic experiment published in Science in 2007, researchers at the food company Danisco showed it was so. They could see new spacers added when a phage infected a culture of S. thermophilus. Afterward, the bacterium was immune to the phage. They could artificially engineer a phage spacer into the CRISPR DNA and see resistance emerge; when they took the spacer away, immunity was lost.

This was handy intel for an industry that could find whole vats of yogurt-making bacteria wiped out by phage infestations. It was an exciting time scientifically and commercially, says Rodolphe Barrangou of North Carolina State University in Raleigh, who did a lot of the Danisco work. “It was not just discovering a cool system, but also uncovering a powerful phage-resistance technology for the dairy industry,” he says.

The second part of the CRISPR/Cas system is the Cas bit: a set of genes located near the cluster of CRISPR spacers. The DNA sequences of these genes strongly suggested that they carried instructions for proteins that interact with DNA or RNA in some fashion — sticking to it, cutting it, copying it, unraveling it. When researchers inactivated one Cas gene or another, they saw immunity falter. Clearly, the two bits of the system — CRISPR and Cas — were a team.
It took many more experiments to get to today’s basic model of how CRISPR/Cas systems fight phages — and not just phages. Other types of foreign DNA can get into microbes, including circular rings called plasmids that shuttle from cell to cell and DNA pieces called transposable elements, which jump around within genomes. CRISPRs can fend off these intruders, as well as keep a microbe’s genome in tidy order.

The process works like this: A virus injects its genetic material into the cell. Sensing this danger, the cell selects a little strip of that genetic material and adds it to the spacers in the CRISPR cluster. This step, known as immunization or adaptation, creates a list of encounters a cell has had with viruses, plasmids or other foreign bits of DNA over time — neatly lined up in reverse chronological order, newest to oldest.

Older spacers eventually get shed, but a CRISPR cluster can grow to be long — the record holder to date is 587 spacers in Haliangium ochraceum, a salt-loving microbe isolated from a piece of seaweed. “It’s like looking at the last 600 shots you had in your arm,” says Barrangou. “Think about that.”

New spacer in place, the microbe is now immunized. Later comes targeting. If that same phage enters the cell again, it’s recognized. The cell has made RNA copies of the relevant spacer, which bind to the matching spot on the genome of the invading phage. That “guide RNA” leads Cas proteins to target and snip the phage DNA, defanging the intruder.
Researchers now know there are a confetti-storm of different CRISPR systems, and the list continues to grow. Some are simple — such as the CRISPR/Cas9 system that’s been adapted for gene editing in more complex creatures (SN: 4/15/17, p. 16) — and some are elaborate, with many protein workhorses deployed to get the job done.

Those who are sleuthing the evolution of CRISPR systems are deciphering a complex story. The part of the CRISPR toolbox involved in immunity (adding spacers after phages inject their genetic material) seems to have originated from a specific type of transposable element called a casposon. But the part responsible for targeting has multiple origins — in some cases, it’s another type of transposable element. In others, it’s a mystery.

The downsides
Given the power of CRISPR systems to ward off foes, one might think every respectable microbe out there in the soils, vents, lakes, guts and nostrils of this planet would have one. Not so.

Numbers are far from certain, partly because science hasn’t come close to identifying all the world’s microbes, let alone probe them all for CRISPRs. But the scads of microbial genetic data accrued so far throw up interesting trends.

Tallies suggest that CRISPR systems are far more prevalent in known archaea than in known bacteria — such systems exist in roughly 90 percent of archaea and about 35 percent of bacteria, says Eugene Koonin, a computational evolutionary biologist at the National Institutes of Health in Bethesda, Md. Archaea and bacteria, though both small and single-celled, are on opposite sides of the tree of life.

Perhaps more significantly, Koonin says, almost all the known microbes that live in superhot environments have CRISPRs. His group’s math models suggest that CRISPR systems are most useful when microbes encounter a big enough variety of viruses to make adaptive memory worth having. But if there’s too much variety, and viruses are changing very fast, CRISPRs don’t really help — because you’d never see the same virus again. The superhot ecosystems, he says, seem to have a stable amount of phage diversity that’s not too high or low.

And CRISPR systems have downsides. Just as people can develop autoimmune reactions against their own bodies, bacteria and archaea can accidentally make CRISPR spacers from bits of their own DNA — and risk chewing up their own genetic material. Researchers have seen this happen. “No immunity comes without a cost,” says Rotem Sorek, a microbial genomicist at the Weizmann Institute of Science in Rehovot, Israel.

But mistakes are rare, and Sorek and his colleagues recently figured out why in the microbe they study. The researchers reported in Nature in 2015 that CRISPR spacers are created from linear bits of DNA — and phage DNA is linear when it enters cells. The bacterial chromosome is protected because of its circular form. Should it break and become linear for a spell, such as when it’s being replicated, it contains signals that ward off the Cas proteins.

There are other negatives to CRISPR systems. It’s not always a bonus to keep out phages and other invaders, which can sometimes bring in useful things. Escherichia coli O157:H7, of food poisoning fame, can make humans sick because of toxin genes it harbors that were brought in by a phage, to name just one of myriad examples. Even CRISPR systems themselves are spread around the microbial kingdom via phages, plasmids or transposable elements.

For microbes that lack CRISPR systems, there are many other ways to repel foreign DNA — as much as 10 percent of a microbial genome may be devoted to hawkish warfare, and new defense systems are still being uncovered.

Countermeasures
The war between bacteria and phages is two-sided, of course. Just as a microbe wants to keep doors shut to protect its genetic integrity and escape destruction, the phage wants in.

And so the phage fights back against CRISPRs. It genetically morphs into forms that CRISPRs no longer recognize. Or it designs bespoke artillery. Microbiologist Joe Bondy-Denomy, now at the University of California, San Francisco, happened upon such customized weapons as a grad student in the lab of molecular microbiologist Alan Davidson at the University of Toronto. The team knew that the bacterium Pseudomonas aeruginosa, which lives in soil and water and can cause dangerous infections, has a vigorous CRISPR system. Yet some phages didn’t seem fazed by it.

That’s because those phages have small proteins that will bind to and interfere with this or that part of the CRISPR machinery, such as the Cas enzyme that cuts phage DNA. The binding disables the CRISPR system, the researchers reported in 2015 in Nature. Bondy-Denomy and others have since found anti-CRISPR genes in other phages and other kinds of interloping DNA. The genes are so common, Davidson says, that he wonders how many CRISPR systems are truly active.

In an especially bizarre twist, microbiologist Kimberley Seed of the University of California, Berkeley found a phage that carries its own CRISPR system and uses it to fight back against the cholera bacterium it invades, she and colleagues reported in 2013 in Nature. It chops up a segment of bacterial DNA that normally inhibits phage infection.

Of course, in this never-ending scuffle one would expect the microbes to again fight back against the phages. “It’s something I often get asked: ‘Great, the anti-CRISPRs are there, so where are the anti-anti-CRISPRs?’ ” Bondy-Denomy says. Nobody has found such things yet.

Evolution drivers
It’s one thing to study CRISPR systems in well-controlled lab settings, or in just one type of microbe. It’s another to understand what all the various CRISPRs do to shape the ecosystem of a bubbling hot spring, human gut, diseased lung or cholera-tainted river. Estimates of CRISPR abundance could drop as more sampling is done, especially of dark horse microbes that researchers know little about.

In a 2016 report in Nature Communications, for example, geomicrobiologist Jill Banfield of UC Berkeley and colleagues detected 1,724 microbes in Colorado groundwater that had been treated to boost the abundance of types that are difficult to isolate. CRISPR systems were much rarer in this sample than in databases of better-known microbes.

Tallying CRISPRs is just the start, of course. Microbial communities — including those inside our own guts, where there are plenty of CRISPR systems and phages — are dynamic, not frozen. How do CRISPRs shape the evolution of phages and microbes in the wild? Banfield’s and Barrangou’s labs teamed up to watch as S. thermophilus and phages incubated together in a milk medium for hundreds of days. The team saw bacterial numbers fall as phages invaded; then bacteria acquired spacers against the phage and rallied — and phage numbers fell downward in turn. Then new phage populations sprang up, immune to S. thermophilus defenses because of genetic changes. In this way, the researchers reported in 2016 in mBio, CRISPRs are “one of the fundamental drivers of phage evolution.”

CRISPR systems can be picked up, dropped, then picked up again by bacteria and archaea over time, perhaps as conditions and needs change. The bacterium Vibrio cholerae is an example of this dynamism, as Seed and colleagues reported in 2015 in the Journal of Bacteriology. The older, classical strains of this medical blight harbored CRISPRs, but these strains went largely extinct in the wild in the 1960s. Strains that cause cholera today do not have CRISPRs.

Nobody knows why, Seed says. But scientists stress that it is a mischaracterization to paint the relationship between microbes and phages, plasmids and transposable elements as a simplistic war. Phages don’t always wreak havoc; they can slip their genomes quietly into the bacterial chromosome and coexist benignly, getting copied along with the host DNA. Phages, plasmids and transposable elements can confer new, useful traits — sometimes even essential ones. Indeed, such movement of DNA across species and strains is at the heart of how bacteria and archaea evolve.

So it’s about finding balance. “If you incorporate too much foreign DNA, you cannot maintain a species,” says Luciano Marraffini, a molecular microbiologist at the Rockefeller University in New York City whose work first showed that DNA-cutting was key to CRISPR systems. But you do need to let some DNA in, and it’s likely that some CRISPR systems permit this: The system he studies in Staphylococcus epidermidis, for example, only goes after phages that are in their cell-killing, or lytic, state, he and colleagues reported in 2014 in Nature.
Beyond defense
One thing is very clear about CRISPR systems: They are perplexing in many ways. For a start, the spacers in a microbe should reflect its own, individual story of the phages it has encountered. So you’d think there would be local pedigrees, that a bacterium sampled in France would have a different spacer cluster from a bacterium sampled in Argentina. This is not what researchers always see.

Take the nasty P. aeruginosa. Rachel Whitaker, a microbial population biologist at the University of Illinois at Urbana-Champaign, studies Pseudomonas samples collected from people with cystic fibrosis, whose lungs develop chronic infections. She’s found no sign that two patients living close to each other carry more-similar P. aeruginosa CRISPRs than two patients thousands of miles apart. Yet surely one would expect nearby CRISPRs to be closer matches, because the Pseudomonas would have encountered similar phages. “It’s very weird,” Whitaker says.

Others have seen the same thing in heat-loving bacteria sampled from very distant bubbling hot springs. It’s as if scientists don’t truly understand how bacteria spread around the world — there could be a strong effect of far-flung passage by air or wind, says Konstantin Severinov, who studies CRISPR systems at Rutgers University in New Brunswick, N.J.
Another weirdness is the differing vigor of CRISPR systems. Some are very active. Molecular biologist Devaki Bhaya of the Carnegie Institution for Science’s plant biology department at Stanford University sees clear signs that spacers are frequently added and dropped in the cyanobacteria of Yellowstone’s hot springs, for example. But other systems are sluggish, and E. coli, that classic workhorse of genetics research, has a respectable-looking CRISPR system — that is switched off.

It may have been off for a long time. Some 42,000 years ago, a baby woolly mammoth died in what is now northwestern Siberia. The remains, found in 2007, were so well-preserved that the intestines were intact and E. coli DNA could be extracted.

In research published in Molecular Ecology in January, Severinov’s team found surprising similarities between the spacers in the mammoth-derived E. coli CRISPR cluster and those in modern-day E. coli. “There was no turnover in all that time,” Severinov marvels. If the CRISPR system isn’t active, why does E. coli bother to keep it?

That quandary leads neatly to what some researchers refer to as an intellectually “scandalous situation.”

In some cases, the genetic sequence of spacers nicely matches phage DNA. But overall, only a fraction (around 1 to 2 percent) of the spacers scientists know about have been matched to a virus or a plasmid. In E. coli, the spacers don’t match common, classic phages known to infect the bacterium. “Is it the case that there is a huge, unknown amount of viral dark matter in the world?” says Koonin — or are phages evolving superfast? “Or is it something completely different?”

Faced with this conundrum, some researchers strongly suspect — and have evidence — that CRISPR systems may do more than defend; they may have other jobs. Communication, perhaps. Or turning genes on and off.

But some microbes’ CRISPR sequences do make sense, especially if looking at the spacers most recently added, and others may be clues to phages still undiscovered. So even as they scratch their heads about many things CRISPR, scientists are also excited by the stories CRISPR clusters can tell about the viruses and other bits of DNA that bacteria and archaea encounter and that they choose, for whatever reason, to note for the record. What do microbes pay attention to? What do they ignore?

CRISPRs offer a bright new window on such questions and, indeed, already are unearthing novel phages and facts about who infects whom in the microscopic world.

“We can catalog everything that’s out there. But we don’t really know what matters,” says Bondy-Denomy. “CRISPRs can help us understand.”

A severe coral bleaching event spurred by high ocean temperatures has struck the Great Barrier Reef for an unprecedented second time in 12 months, reveal aerial surveys released April 10 by scientists at James Cook University in Townsville, Australia. While last year the northern third of the reef was hardest hit, this time around the reef’s midsection experienced the worst bleaching. The two bleaching events together span around 1,500 kilometers of the 2,300-kilometer-long reef.

“It takes at least a decade for a full recovery of even the fastest growing corals, so mass bleaching events 12 months apart offers zero prospect of recovery for reefs that were damaged in 2016,” James Kerry, one of the researchers behind the finding, said in a statement.

Bleached corals aren’t dead. Trauma, disease or warm water can cause an exodus of the symbiotic algae that provide corals with food and vibrant color schemes. If better conditions, such as cooler waters, return, the algae may return to their homes. If they don’t come back, though, the corals starve.

Warming caused by El Niño exacerbated last year’s bleaching event. With El Niño now long gone, the researchers blame this year’s bleaching largely on global warming. If humans don’t curb emissions of planet-warming greenhouse gases, scientists warn that the entire reef could be in jeopardy.

Sometimes, the improbable happens. The stock market crashes. A big earthquake shakes a city. A nuclear power plant has a meltdown. These seemingly unpredictable, rare incidents — dubbed black swan events — may be unlikely to happen on any specific day, but they do occur. And even though they may be rare, we take precautions. A smart investor balances their portfolio. A California homeowner stores an earthquake preparedness kit in the closet. A power plant designer builds in layers of safeguards.

Conservation managers should be doing the same thing, scientists warn. Black swan events happen among animals, too, and they rarely have positive effects, a new study finds.

How often do black swan events impact animals? To find out, Sean Anderson of the University of Washington in Seattle and colleagues looked at data for 609 populations of birds, mammals and insects. Often, the data were noisy; there could be lots of ups and downs in population sizes, not always with good explanations for what happened. But, Anderson notes, “it turns out that there are plenty of black swan events that are so extreme that we can easily detect them with available data.”

The researchers looked for upswings or declines that were so big they would be observed only once every 10,000 years. For example, the team found a population of gray herons in England that experienced large die-offs in the 1920s, ’40s and ’60s. Those declines were well outside the normal ups and downs found in the population. Harsh winters meant limited food availability for the birds, and the population crashed several times. “The last event actually involved population crashes two years in a row, and it took three times longer for the population to recover than expected,” Anderson notes.

About 4 percent of the populations in the study experienced a black swan event, the team reports in the March 21 Proceedings of the National Academy of Sciences. And this was usually a sharp decline in population size. That’s because there are limits to how fast a population can grow — organisms can only have so many babies per year. But there are no limits to how fast the members of a group can die.

Whether that 4 percent figure holds for the entire animal world is hard to tell. But it does confirm that these events do happen and that they are rarely good. And, given the nature of the events that disrupted populations, it’s possible they may become more common due to climate change.

“We found that most black swan events were caused by things like extreme climate or disease, and often an unexpected combination of factors,” Anderson says. Climate change is expected to increase the frequency and magnitude of events such as heat waves and drought. “We may observe more black swan events in animal populations in the future because of these climate extremes,” he says.
Conservationists can’t predict when such events will happen, but there are ways to minimize their impact when they do, Anderson and colleagues suggest. For animals, this could mean making sure a population doesn’t get so small that something like a disease outbreak — such as the one that happened with saiga antelope in 2015 — or a really bad winter results in extinction.

A handful of measurements of decaying particles has seemed slightly off-kilter for years, intriguing physicists. Now a new decay measurement at the Large Hadron Collider in Geneva has amplified that interest into tentative enthusiasm, with theoretical physicists proposing that weird new particles could explain the results. Scientists with the LHCb experiment reported the new result on April 18 in a seminar at the European particle physics lab CERN, which hosts the LHC.

“It’s incredibly exciting,” says theoretical physicist Benjamin Grinstein of the University of California, San Diego. The new measurement is “a further hint that there’s something new and unexpected happening in very fundamental interactions.”
Other physicists, however, are more cautious, betting that the series of hints will not lead to a new discovery. “One should always remain suspicious of an effect that does not show up in a clear way” in any individual measurement, Carlos Wagner of the University of Chicago wrote in an e-mail.

Taken in isolation, none of the measurements rise beyond the level that can be explained by a statistical fluctuation, meaning that the discrepancies could easily disappear with more data. But, says theoretical physicist David London of the University of Montreal, there are multiple independent hints, “and they all seem to be pointing at something.”

The measurements all involve a class of particle called a B meson, which can be produced when protons are smashed together in the LHC. When a B meson decays, it can produce a type of particle called a kaon that is accompanied either by an electron and a positron (an antimatter version of an electron) or by a muon — the electron’s heavier cousin — and an antimuon.

According to physicists’ accepted theories, muons and electrons should behave essentially identically aside from the effects of their differing masses. That means the two kinds of particles should have an even chance of being produced in such B meson decays. But in the new result, the scientists found only about seven decays with muons for every 10 with electrons.

There are several varieties of B mesons. All are made up of one quark — a type of fundamental particle that also makes up protons and neutrons — and one antiquark. One of the two particles is a type called a “bottom” quark (or antiquark), hence the B meson’s name.
Earlier measurements of another variety of B meson decay also found a muon shortage. What’s more, measurements of the angles at which particles are emitted in some types of B meson decay also appear slightly out of whack, adding to the sense that something funny may be going on in such decays.

“We are excited by how [the measurements] all seem to fit together,” says LHCb spokesperson Guy Wilkinson, an experimental physicist at the University of Oxford in England. If more data confirm that B mesons misbehave, a likely explanation would be a new particle that interacts differently with muons than it does with electrons. One such particle could be a leptoquark — a particle that acts as a bridge between quarks and leptons, the class of particle that includes electrons and muons. Or it could be a heavy, electrically neutral particle called a Z-prime boson.

Physicists spawned a similar hubbub in 2016, when the ATLAS and CMS experiments at the LHC saw hints of a potential new particle that decayed to two photons (SN: 5/28/16, p. 11). Those hints evaporated with more data, and the current anomalies could do likewise. Although the two sets of measurements are very different, says Wolfgang Altmannshofer of the University of Cincinnati, “from the point of the overall excitement, I would say the two things are roughly comparable.”

Luckily, LHCb scientists still have a lot more data to dig into. The researchers used particle collisions only from before 2013, when the LHC was running at lower energy than it is now. “We have to get back to the grindstone and try and analyze more of the data we have,” says Wilkinson. Updated results could be ready in about half a year, he says, and should allow for a more definitive conclusion.

Mapping the relationships between different dog breeds is rough (get it?), but a team of scientists at the National Institutes of Health did just that using the DNA of 1,346 dogs from 161 breeds. Their analysis, which appears April 25 in Cell Reports, offers a lot to chew on.

Here are five key findings from the work:

Dogs were bred for specific jobs, and this shows in their genes.
As human lifestyles shifted from hunting and gathering to herding to agriculture and finally urbanization, humans bred dogs (Canis familiaris) accordingly. Then over the last 200 years, more and more breeds emerged within those categories. Humans crossed breeds to create hybrids based on appearance and temperament, and those hybrids eventually became new breeds.

DNA from hybrid dogs backs up historical records.
Genetic backtracking indicates that, for example, mixing between bulldogs and terriers traces back to Ireland between 1860 and 1870. That timeframe and location coincides with historical records indicating a dog-fighting fad that’s linked with crossing breeds to make better fighters.

Geography also matters.
While herder dog breeds showed a lot of genetic diversity, they fall into two general groups from the rural United Kingdom and the Mediterranean on the breed family tree. When humans switched from hunting to farming, herding breeds may have emerged independently in different areas. Geography could also explain why these two groups use different herding tactics.

New World dogs aren’t all immigrants.
A genetic legacy of America’s early canine inhabitants lives on in some of today’s breeds. Dogs trekked to the Americas from Asia with people more than 10,000 years ago, but when European groups started to colonize the Americas, they brought European dog breeds with them. Past studies suggest that outside breeds largely replaced New World dogs, but the new dataset shows New World dog DNA actually does persist in a few modern New World breeds, such as Chihuahuas.

Big dogs evolved independently to be big.
European mastiffs and Mediterranean sheepdogs don’t share recent changes in their DNA, meaning their size traits arose separately and for different reasons. While both breed groups specialize in guarding things, mastiffs use their size to intimidate humans, while sheepdogs use their size to overpower animal predators. Larger size may have been one of the first traits that human breeders zeroed in on, the researchers suspect.

Leave it to a researcher who studies icy moons in the outer solar system to come up with an out-there scheme to restore vanishing sea ice in the Arctic.

Ice is a good insulator, says Steven Desch, a planetary scientist at Arizona State University in Tempe. That’s why moons such as Jupiter’s Europa and Saturn’s Enceladus, among others, may be able to maintain liquid oceans beneath their thick icy surfaces. On Earth, sea ice is much thinner, but the physics is the same. Ice grows on the bottom surface of floating floes. As the water freezes, it releases heat that must make its way up through the ice before escaping into the air. The thicker the ice, the more heat gets trapped, which slows down ice formation. That’s bad news for the Arctic, where ice helps keep the planet cool but global warming is causing ice to melt faster than it can be replaced.
The answer to making thicker ice more quickly? Suck up near-freezing water from under the ice and pump it directly onto the ice’s surface during the long polar winter. There, the water would freeze more quickly than underneath the ice, where it usually forms.

In theory, Desch says, the pumps used for this top-down approach to ice growth could be driven by technology no more sophisticated than the windmills that have long provided water to farms and ranches on the Great Plains.
Desch and colleagues envision putting such pumps on millions of buoys throughout the Arctic. During winter, each pump would be capable of building an additional layer of sea ice up to 1 meter thick over an area of about 100,000 square meters, or about the size of 15 soccer fields, the researchers estimate in the January issue of Earth’s Future.
It won’t be easy. The Arctic’s harsh environment poses many problems such as frozen pipes. But many of those hitches are being addressed by engineers familiar with developing and maintaining Arctic infrastructure such as small-scale wind turbines and drinking-water systems, Desch says. To build and ship each ice-making buoy to the Arctic would cost about $50,000, he estimates. Over a decade, covering 10 percent of the Arctic Ocean with buoys would cost about $50 billion per year. “It’s a big project, but the point is, it’s not an impossible one,” he argues.

Now is the time to begin detailed designs and build prototypes, Desch says. The Arctic Ocean’s end-of-summer sea ice coverage has decreased, on average, more than 13 percent per decade since 1979. “There’ll be a time, 10 to 15 years from now, when Arctic sea ice will be accelerating to oblivion, and there’ll be political will to do something about climate change,” Desch says. “We need to have this figured out by the time people are ready to do something.”

A wearable robot could prevent future falls among those prone to stumbles.

The new exoskeleton packs motors on a user’s hips and can sense blips in balance. In a small trial, the pelvic robot performed well in sensing and averting wearers’ slips, researchers report May 11 in Scientific Reports.

Exoskeletons have the potential to help stroke victims and people with spinal cord injuries walk again (SN: 11/16/13, p. 22) — and even kick soccer goals (SN Online: 6/12/14). But this new model focuses on a more ordinary aspect of the human condition: falling on your face or your rear. “Exoskeletons could really help in this case,” says study coauthor Silvestro Micera, an engineer at École Polytechnique Fédérale de Lausanne in Switzerland.
Most exoskeletons guide the movement of the wearer, forcing the person to walk in a particular way. But the new pelvic device allows the user to walk normally and reacts only when it needs to. A computer algorithm measures changes in a wearer’s hip joint angles to detect the altered posture that goes along with slipping. The robot then uses its motors to push the hips back into their natural position to, hopefully, prevent a fall.

At a rehab facility in Florence, eight elderly people and two amputees — two groups at risk for balance issues — tried out the device while walking on a treadmill. The robot picked up on slips within 0.35 seconds of a change of gait.

Still, the device has some hurdles ahead. The exoskeleton is bulky, so Micera and his team are working on a sleeker model that would be less imposing for elderly users. The team is also testing the robot’s skills in other types of balance loss like tripping.

Walter A. Feibelman of the University of Pittsburgh … has found evidence indicating a fourth ring [of Saturn].… Every 14.78 years, the rings of Saturn can be seen edge-on from Earth, and the past winter marked one of these opportunities.… The thin ring “extends to more than twice the known ring diameter” (or a total of 340,000 miles), and is so faint it cannot be photographed except with a large telescope. — Science News, June 3, 1967

Update
Scientists no longer observe Saturn’s rings only from Earth. Four spacecraft have visited the planet and revealed a complex ring system, with the four previously known rings accompanied by multiple fainter ones. NASA’s Cassini spacecraft, which arrived at the planet in 2004, is now swooping between Saturn and its rings to get the closest views yet (SN Online: 4/27/17). Rings have also been spied around Jupiter, Uranus and Neptune, and in 2012, scientists spotted an exoplanet with giant rings (SN: 3/7/15, p. 5).

When my girls were newborns, I spent a lot of time damp. Fluids were everywhere, some worse than others. One of the main contributors was milk, which, in various stages of digestion, came back to haunt me in a sloppy trail down my back.

I was sometimes alarmed at the volume of fluid that came flying out of my tiny babies. And I remember asking our pediatrician if it was a problem. We were lucky in that the amount and frequency of the regurgitations didn’t seem to signal trouble.

But some babies spit up a lot more, and seem to be in distress while doing so. That’s led doctors to prescribe antacids to treat reflux disease in these infants. A U.S.-based survey found that from 2000 to 2003, infant use of a type of antacid called proton-pump inhibitors quadrupled.

Those numbers point to worried doctors and parents who want to help babies feel better. The problem, though, is that antacids come with side effects. Mucking with acid levels can affect the body beyond the stomach, and these unintended effects may be even more meddlesome in babies.

“What we found in adults and what we’re starting to see more in children is that [the drugs] are not as benign as we used to think,” says U.S. Air Force Captain Laura Malchodi, a pediatrician at Walter Reed National Military Medical Center in Bethesda, Md.

Infants who took proton-pump inhibitors, a class of drugs that includes Prilosec and Nexium, in their first six months of life broke more bones over the next several years than children who didn’t receive the drugs. That example comes from research Malchodi presented May 7 at the 2017 Pediatric Academic Societies Meeting in San Francisco.

Malchodi and her colleagues examined medical records of nearly 900,000 healthy children. Of those, about 7,000 were prescribed proton-pump inhibitors by the time they were 6 months old. About 67,000 were prescribed histamine H2-blocking drugs, such as Zantac or Pepcid, and about 11,000 babies were prescribed both types of drugs.
Children who had received proton-pump inhibitors, either alone or in combination with a histamine H2-blocker, had more fractures over the next five years than children who weren’t prescribed that type of drug. The researchers tried to rule out other differences between the groups of babies that might explain the higher number of fractures. When those differences were removed from the analysis, proton-pump inhibitor prescriptions were still linked to fractures.

The study can’t say whether proton-pump inhibitors definitely caused weaker bones. But that’s not an unreasonable hypothesis given what’s seen in adults, for whom the link between long-term use of proton-pump inhibitors and broken bones is stronger.

If proton-pump inhibitors do interfere with bones, it’s still a mystery exactly how. One idea was that the drugs hinder calcium absorption, leading to weaker bones. That idea has fallen out of favor, Malchodi says. Another proposal centers on cells called osteoclasts. To do their job, these cells rely on proton pumps to create acidic pockets around bones. But if osteoclasts aren’t working properly, “in the end, what you get is disorganized bone,” Malchodi says.

Reflux disease is not the same thing as reflux, which babies are nearly guaranteed to experience. For one thing, the amount of liquid they’re slurping down relative to their body weight is huge. And that liquid is held down by an esophageal sphincter that’s often underdeveloped in babies. (One technical term for reflux is “poor gastric compliance,” but I bet you’ve got more colorful descriptions.)

Antacids won’t stop babies from spitting up, says Malchodi. “We definitely counsel parents all the time that this is not going to stop the reflux,” she says. Instead, the drugs are thought to change the pH of the liquid coming back up in an attempt to make it less irritating.

Some babies may need that pharmaceutical help. But many may not. If babies are growing well and don’t seem to be in long-lasting distress, then it’s possible that they may need the “tincture of time” to outgrow the reflux. (Malchodi points out that so-called “happy spitters” are probably not smiling while they’re barfing, because obviously, throwing up is not fun. It’s just that these babies don’t seem to be bothered long after the spitting.)

She hopes that her research and other studies like it will prompt more careful discussions between parents and doctors before antacids are prescribed. And if they are deemed necessary, “have a stop point in mind,” she says.