Water plays big role in shaping dwarf planet Ceres

Ice volcanoes, patches of water ice and a slew of hydrated minerals paint a picture of dwarf planet Ceres as a geologically active world — one where water has played a starring role. That’s the theme of six papers in the Sept. 2 Science that describe data collected by the Dawn spacecraft.

A 4-kilometer-high mountain dubbed Ahuna Mons, with its bowl-shaped summit and ridged flanks, has the appearance of a cryovolcano — one that erupts water instead of magma. The relatively young Oxo crater also appears to be home to splotches of frozen water. Given that ice should last only tens to hundreds of years on Ceres’ surface, the patches must be recent additions, possibly exposed by a landslide or impact with a meteorite. The surface is also slathered with a class of minerals known as phyllosilicates — silicon-bearing substances that form in the presence of water — which further support the idea that water has been present throughout Ceres’ history.

Ceres is the largest body between Mars and Jupiter. Dawn has been orbiting Ceres since March 6, 2015 (SN: 4/4/15, p. 9), studying its geology and composition to better understand the formation of rocky worlds.

Preteen tetrapods identified by bone scans

Better bone scanning of fossils offers a glimpse of preteen life some 360 million years ago.

Improved radiation scanning techniques reveal accumulating growth zones in chunks of four fossil upper forelimb bones from salamander-shaped beasts called Acanthostega, scientists report online September 7 in Nature. Vertebrate bones typically show annual growth zones diminishing in size around the time of sexual maturity. But there’s no sign of that slowdown in these four individuals from East Greenland’s mass burial of Acanthostega, says study coauthor Sophie Sanchez of Uppsala University in Sweden. They were still juveniles.
The bones came from tropical Greenland of the Devonian Period. Aquatic vertebrates were developing four limbs, which would serve tetrapods well when vertebrates eventually conquered land. This mass die-off doomed at least 20 individuals, presumably when a dry spell after a flood trapped them all in a big, vanishing puddle.
This find makes the strongest case yet for identifying genuine youngsters among ancient tetrapods, Sanchez says. She suspects other individuals trapped could have been juveniles too.

Not many other species were found in the mass burial. So young tetrapods may have stuck together much as today’s young fish school, Sanchez speculates. The limb shape clearly indicates that the youngsters took a long time to start adding hard bone to the initial soft cartilage, she says. So these early tetrapods were at least 6-year-olds and probably 10 years old or more.
For identifying stages of life, the improved technique “allows greater resolution and rigor, so in that regard it is a plus,” says Neil Shubin of the University of Chicago, who studies a fossil fish with some tetrapod-like features called Tiktaalik. There are Tiktaalik preteens, too, he notes.

What interests Nadia Fröbisch of Museum für Naturkunde in Berlin is that some of Acanthostega individuals were different sizes but had reached the same stage of bone development. She muses that they might even have been developing along different trajectories of growth, a flexibility that would be useful in a changeable environment.

Old-school contraptions still work for weighing astronauts

New method to measure mass in space devised — A scale for measuring weight in space that does not depend upon the attraction of gravity has been devised…. In [William Thornton’s] method, the weight of the mass is determined [by] mechanically oscillating a weight in a tray. The heavier the mass, the slower the oscillation rate. The scale is tied to an electronic unit measuring the time required for five cycles of oscillation. A reference to a chart gives the mass’s weight. — Science News, October 1, 1966

UPDATE
Not much has changed. The International Space Station has two spring-based contraptions for weighing in astronauts. An individual rides the Body Mass Measurement Device like a pogo stick — in four or five bounces, it calculates weight. The Space Linear Acceleration Mass Measurement Device uses springs to pull an astronaut; the acceleration reveals weight. In 2012, researchers in Europe experimented with compact computer imaging technology — developed for video games — using photos to estimate mass based on a person’s shape and size.

Gene linked to autism in people may influence dog sociability

Dogs may look to humans for help in solving impossible tasks thanks to some genes previously linked to social disorders in people.

Beagles with particular variants in a gene associated with autism were more likely to sidle up to and make physical contact with a human stranger, researchers report September 29 in Scientific Reports.

That gene, SEZ6L, is one of five genes in a particular stretch of beagle DNA associated with sociability in the dogs, animal behaviorist Per Jensen and colleagues at Linköping University in Sweden say. Versions of four of those five genes have been linked to human social disorders such as autism, schizophrenia and aggression.
“What we figure has been going on here is that there are genetic variants that tend to make dogs more sociable and these variants have been selected during domestication,” Jensen says.

But other researchers say the results are preliminary and need to be confirmed by looking at other dog breeds. Previous genetic studies of dog domestication have not implicated these genes. But, says evolutionary geneticist Bridgett vonHoldt of Princeton University, genes that influence sociability are “not an unlikely target for domestication — as humans, we would be most interested in a protodog that was interested in spending time with humans.”

Most dog studies take DNA samples from pets or village dogs and wild wolves. Jensen’s team instead studied beagles that had been raised in a lab. None of the dogs had been trained. To test sociability, the researchers gave the dogs an unsolvable problem in a room with a female human observer whom the beagles had never seen before. The puzzle was a device with three treats that the dogs could see and smell under sliding lids. One lid was sealed shut and could not be opened.

After opening two lids, the dogs “get very confident that this is not a difficult task, but then they encounter the third lid and that’s where the problem gets impossible,” Jensen says. Wolves would have kept trying to solve the problem on their own (SN: 10/17/15, p. 10). But after some futile attempts, many of the beagles looked to the human observer for help. Some dogs tried to catch her eye, glancing back and forth between the woman and the stuck lid. Other dogs made physical contact with or just tried to stay to close to the woman.

The researchers then looked for places in the dogs’ DNA where the most and least human-friendly dogs differed. A region on chromosome 26 kept popping up, indicating that genes in that region could be involved in social interactions with people.
The finding is a statistical signal, but doesn’t establish what the genes might be doing to influence the dogs’ behavior, says Adam Freedman, an evolutionary geneticist at Harvard University. And since the researchers only examined the beagles, it’s not clear that the same genes would affect behavior in other dogs, he says.

Be careful what you say around jumping spiders

Accidental chair squeaks in a lab have tipped off researchers to a new world of eavesdroppers.

Spiders don’t have eardrums, though their exquisitely sensitive leg hairs pick up vibrations humming through solids like web silk and leaves. Biologists thought that any airborne sounds more than a few centimeters away would be inaudible. But the first recordings of auditory nerve cells firing inside a spider brain suggest that the tiny Phidippus audax jumping spider can pick up airborne sounds from at least three meters away, says Ronald Hoy of Cornell University.
During early sessions of brain recordings, Hoy’s colleagues saw bursts of nerve cell, or neuron, activity when a chair moved. Systematic experiments then showed that from several meters away, spiders were able to detect relatively quiet tones at levels comparable to human conversation. In a hearing test based on behavior, the spiders also clearly noticed when researchers broadcast a low droning like the wing sound of an approaching predatory wasp. In an instant, the spiders hunkered down motionless, the researchers report online October 13 in Current Biology.

Jumping spiders have brains about the size of a poppy seed, and Hoy credits the success of probing even tinier spots inside these (anesthetized) brains to Cornell coauthor Gil Menda and his rock-steady hands. “I close my eyes,” Menda says. He listens his way along, one slight nudge of the probe at a time toward the auditory regions, as the probe monitor’s faint popping sounds grow louder.
When Menda first realized the spider brain reacted to a chair squeak, he and Paul Shamble, a study coauthor now at Harvard University, started clapping hands, backing away from the spider and clapping again. The claps didn’t seem earthshaking, but the spider’s brain registered clapping even when they had backed out into the hallway, laughing with surprise.
Clapping or other test sounds in theory might confound the experiment by sending vibrations not just through the air but through equipment holding the spider. So the researchers did their Cornell neuron observations on a table protected from vibrations. They even took the setup for the scary wasp trials on a trip to the lab of coauthor Ronald Miles at State University of New York at Binghamton. There, they could conduct vibration testing in a highly controlled, echo-dampened chamber. Soundwise, Hoy says, “it’s really eerie.”

Neuron tests in the hushed chamber and at Cornell revealed a relatively narrow, low-pitched range of sensitivity for these spiders, Hoy says. That lets the spiders pick up rumbly tones pitched around 70 to 200 hertz; in comparison, he says, people hear best between 500 and 1,000 Hz and can detect tones from 50 Hz to 15 kilohertz.
Spiders may hear low rumbles much as they do web vibes: with specialized leg hairs, Hoy and his colleagues propose. They found that making a hair twitch could cause a sound-responsive neuron to fire.
“There seems to be no physical reason why a hair could not listen,” says Jérôme Casas of the University of Tours in France. When monitoring nerve response from hairs on cricket legs, he’s tracked airplanes flying overhead. Hoy’s team calculates that an 80 Hz tone the spiders responded to would cause air velocities of only 0.13 millimeters a second if broadcast at 65 decibels three meters away. That’s hardly a sigh of a breeze. Yet it’s above the threshold for leg hair response, says Friedrich Barth of the University of Vienna, who studies spider senses.

An evolutionary pressure favoring such sensitivity might have been eons of attacks from wasps, such as those that carry off jumping spiders and immobilize them with venom, Hoy says. A mother wasp then tucks an inert, still-alive spider into each cell of her nest where a wasp egg will eventually hatch to feed on fresh spider flesh. Wasps are major predators of many kinds of spiders, says Ximena Nelson of the University of Canterbury in Christchurch, New Zealand. If detecting their wing drone turns out to have been important in the evolution of hearing, other spiders might do long-distance eavesdropping, too.

With climate change, grizzly bears may hibernate less

Rocky Mountain hikers might need to start packing more bear spray: Climate change may reduce the time that grizzly bears spend in hibernation — leaving them more time to scare the crap out of any humans wandering in their territory.

Scientists aren’t really concerned about bear hibernation because of unwary hikers, of course. It’s because hibernation is an important time of year for a grizzly bear. By going into hibernation and suppressing their metabolisms, the bears can reduce the amount of energy they expend by some 85 percent and more easily get through months when food supplies are short and weather is bleak. Plus, this is when pregnant females give birth and start raising their young. Disrupt hibernation time and a bear is set for a bad — and potentially deadly — year.

And then there’s the fact that in some places, grizzly bears aren’t doing so well. That’s true in Alberta, Canada, where the bears, already low in number, have been threatened by habitat loss and human hunters and have low reproductive rates.

Karine Pigeon of Laval University in Quebec City and colleagues wanted to know whether they should add climate change to that list of threats. But first they needed more information about the factors that drive the bears into and out of their dens. The bears don’t go into or leave hibernation on specific dates (apparently they don’t use our calendar system), so how do they know when it’s time to hibernate?

To find out, the team captured 15 male and 58 female grizzly bears from 1999 to 2011 in an area along the Alberta-British Columbia border northwest of Calgary. The bears were weighed and measured and fitted with tracking collars. Because the signals from the collars couldn’t be tracked from inside the bears’ dens, the researchers knew when the animals entered and left hibernation. The scientists also collected information about the local weather and the availability of berries, one of the bears’ preferred foods.

No single factor explained the dates on which the grizzlies entered and left hibernation, but some were more important than others, the team reports in the October Behavioral Ecology and Sociobiology. Pregnant females, for instance, entered their dens on average two weeks earlier than males, and the ones that had given birth and had cubs emerged two weeks later. This matched what scientists know about bear denning habits, which are thought to promote the cubs’ safety and development.

The end of hibernation tended to be linked to weather and elevation. A bear denning at high elevation in a year in which spring arrived late would stay snug and warm in its den for longer than a grizzly lower down and when spring arrived early.
The den entry date, though, wasn’t tied to weather. It was partially linked to the availability of food: When there were plenty of tasty berries available, grizzlies tended to stay out and keep eating.

And this is where there’s a problem regarding climate change, the researchers note. Because if longer autumns promote the plentiful production of berries, and earlier springs are bringing milder conditions that prompt bears to leave their dens, then grizzlies may hibernate less. That could have repercussions for females with cubs, the researchers note, because it may lead to smaller, more vulnerable cubs being led out into the open — where humans or other bears could kill them.

New analysis boosts case for smaller proton

Editor’s Note: After this article was published, Horbatsch and colleagues discovered an error in their analysis, which weakened the conclusions. The new calculation of the proton radius falls in between the two previous estimates, and therefore does not add much additional support for the smaller proton.

A spat over the size of the proton just got a bit more complicated.

Measurements of the proton’s radius disagree, with one group of scientists saying it’s smaller than the accepted estimate. Now, a new analysis of old data bolsters the case for a small proton. But the result may dash hopes that the discrepancy could point the way to new physics.
Scientists at York University in Toronto and the Autonomous University of Barcelona reanalyzed data from a 2010 electron scattering experiment at the Mainz Microtron in Germany, in which physicists bombarded protons with electrons and observed how the electrons ricocheted. That scattering, under the influence of the protons’ spheres of positive charge, allows scientists to tease out the size of a proton. The updated estimate came up small, the scientists report November 1 on arXiv.org.

“I think it’s not going to be easy for the proponents of a relatively large proton radius to just discuss this away,” says physicist Randolf Pohl of the Max Planck Institute of Quantum Optics in Garching, Germany. “But I’m not convinced that people will accept it.”

Until several years ago, scientists’ various techniques for sizing up the proton were in agreement. Electron scattering studies like the Mainz experiment implied the same size proton as a second technique, which involves studying the energy levels of hydrogen atoms. These estimates indicated that the proton’s radius was about 0.88 quadrillionths of a meter. But in 2010, a new technique caused a kerfuffle. Measurements of the proton radius using muonic hydrogen — a hydrogen atom with its electron replaced by a heavier relative called a muon — pegged the proton to a size 4 percent smaller than the other estimates (SN: 7/31/10, p. 7).

The flaw among the three techniques might seem likely to lie with the one outlier, the muon experiment. But “there’s actually quite a bit of certainty about those results,” says physicist Marko Horbatsch of York University, a coauthor of the new paper. So Horbatsch and colleagues decided to revisit electron scattering instead, using a subset of the data from the Mainz experiment. Horbatsch’s team focused on glancing collisions where the electron altered its course only slightly. Those collisions are the most essential for determining the proton radius. Then the researchers used theoretical calculations to account for effects that occur in more extreme collisions. Their analysis revealed a slightly scaled-down proton.

If the result is reinforced by future electron scattering measurements, the hydrogen atom data that resulted in the larger-sized proton would still require explanation. But it would also mean that the discrepancy won’t lead to new insights about the universe. Under the standard model of particle physics, muons and electrons should be identical except for mass. Physicists had hoped that the black sheep status of the muonic hydrogen experiment indicated something was different about muons. Agreement of the electron scattering and muonic hydrogen experiments eliminates that possible explanation.
The new analysis is “undoubtedly sensible,” says physicist Judith McGovern of the University of Manchester. “I’m a bit surprised no one has done it before. In fact, I’m a bit surprised I haven’t done it before.”

But that doesn’t mean scientists are fully convinced. MIT physicist Jan Bernauer, one of the authors of the original electron scattering result, says he doesn’t think the puzzle will be solved by reanalysis of existing data. “I’m positive that new data are needed.”

Cretaceous bird find holds new color clue

A 130-million-year-old bird holds a clue to ancient color that has never before been shown in a fossil.

Eoconfuciusornis’ feathers contain not only microscopic pigment pods called melanosomes, but also evidence of beta-keratin, a protein in the stringy matrix that surrounds melanosomes, Mary Schweitzer and colleagues report November 21 in the Proceedings of the National Academy of Sciences.

Together, these clues could strengthen the case for inferring color from dinosaur fossils, a subject of debate for years (SN: 11/26/16, p. 24). Schweitzer, a paleontologist at North Carolina State University in Raleigh, has long pointed out that the microscopic orbs that some scientists claim are melanosomes may actually be microbes. The two look similar, but they have some key differences. Microbes aren’t enmeshed in keratin, for one.

In Eoconfuciusornis’ feathers, Schweitzer and colleagues found round, 3-D structures visible with the aid of an electron microscope. And a molecular analysis revealed bundles of skinny fibers, like the filaments of beta-keratin in modern feathers. The authors don’t speculate on the bird’s color, but they do offer a new way to support claims for ancient pigments.

“Identifying keratin is key to ruling out a microbial source for microbodies identified in fossils,” they write.

Gut microbe mix may spark Parkinson’s

For clues to Parkinson’s brain symptoms, a gut check is in order.

Intestinal microbes send signals that set off the disease’s characteristic brain inflammation and motor problems in mice, researchers report December 1 in Cell. Doctors might someday be able to treat Parkinson’s by fixing this bacterial imbalance.

“It’s quite an exciting piece of work,” says John Cryan, a neuroscientist at University College Cork in Ireland who wasn’t involved in the study. “The relationship between the brain and gut for Parkinson’s has been bubbling up for many years.” The new research, he says, “brings the microbiome really into the forefront for the first time.”
Parkinson’s affects more than 10 million people worldwide, and roughly 70 percent of those patients also have gastrointestinal issues like constipation. Sometimes the GI symptoms show up years before the muscle weakness and other neurological problems. Several recent studies in humans have suggested a link between gut microbes and Parkinson’s. But it wasn’t clear whether intestinal microbes were actually causing the disease, says study coauthor Sarkis Mazmanian, a microbiologist at Caltech. “What our study adds is a functional, mechanistic role for the microbiome.”

Mazmanian’s team studied mice that produced too much alpha-synuclein, the protein that’s believed to cause Parkinson’s when it clumps in the brain. Mice with extra alpha-synuclein acted like they had Parkinson’s: They traversed a narrow beam more slowly, they couldn’t grip as well to a pole and they struggled to pull stickers off their noses. Their brains showed signs of inflammation, too. But when the researchers raised the same type of mice to be germ-free —that is, to not have any gut microbes — the animals acted less sick.

Those mice were still producing boatloads of alpha-synuclein, but the protein wasn’t clumping in their brains. And without the clumps, the mice didn’t have the unsteady gait and muscle weakness typical of Parkinson’s.

In another experiment, the researchers transferred gut microbes from Parkinson’s patients into germ-free mice making too much alpha-synuclein. Those mice developed motor problems when tested 6 or 7 weeks after the transfer, but mice who got microbes from healthy humans were fine.

“Even though the mice that received the healthy microbiota received hundreds of bacteria, they didn’t get the disease,” says Mazmanian. That suggests it’s not the presence or absence of bacteria that triggers Parkinson’s, but the specific composition of the microbial cocktail.
Alpha-synuclein clumps can move from the gut to the brain, a recent study showed. Now, it seems that gut bacteria themselves are also sending important signals.

Researchers are now trying to figure out which signals — and which microbes —are throwing off the balance.

Fecal samples from the mice implanted with bacteria from Parkinson’s patients had higher than normal levels of certain intestinal bacteria. That could be sparking symptoms, says Caltech microbiologist Tim Sampson, who also worked on the study. “I’m interested in trying to understand if there are potential pathogenic microbes that might be individually driving the disease,” he says. “Once we’ve figured that out we’ll be able to understand whether we can remove that group of organisms or block them.”

Abnormally low levels of other bacteria could also factor in. The analyses aren’t large enough to firmly conclude which microbes are particularly important players. But if scientists can figure out what those missing beneficial bacteria are, Mazmanian says, targeted probiotic therapy might be a treatment option in the future.

Aging-associated diseases like Parkinson’s are tricky to study in mice, cautions Stanford University microbiologist Justin Sonnenburg. “They’re typically the result of decades of accumulations of problems,” whereas the mice in the current study were just a couple months old. So the findings will need to be validated in human studies before influencing treatments. Still, he says, “it’s a really important contribution to the growing list of ways that gut microbes can alter our health.”

Year in review: Zika virus devastates Brazil and spreads fear across Americas

A Brazilian mother cradles her baby girl under a bruised purple sky. The baby’s face is scrunched up, mouth open wide — like any other crying child. But her head is smaller than normal, as if her skull has collapsed above her eyebrows.

A week earlier, not far away, a doctor wrapped a measuring tape around the forehead of a 1-month-old boy, held in the arms of his grandmother. This baby too has a shrunken head, a birth defect whose name — microcephaly — has now become seared into the public consciousness.
These images and many more told a harrowing story that case reports alone couldn’t convey: A little-known mosquito-borne virus called Zika appeared to be taking a terrible toll on women and babies, and their families. The world got a gut-wrenching view of microcephaly in 2016, along with a mountain of evidence convincing scientists that Zika bears much of the blame for the dramatic increase in cases.

“Once you’ve seen those pictures from Brazil, you realize what a huge impact this kind of outbreak can have,” says Sonja Rasmussen, a pediatrician at the U.S. Centers for Disease Control and Prevention in Atlanta. Brazil logged its first cases of Zika in 2015, but infections there peaked this spring with perhaps up to 8,000 new infections per week. The virus crept northward and infiltrated many more countries including Panama, Haiti and Mexico. Now, the threat has come to the United States: Cases have been reported in every state except Alaska. They stem mostly from travelers infected abroad, but the virus has staked out new territory in Puerto Rico, the U.S. Virgin Islands, American Samoa and Florida.

As of December 1, Puerto Rico had reported more than 34,000 people with Zika infections. More than 2,700 are pregnant women. And elsewhere in the United States, the CDC has reported well over 4,000 laboratory-confirmed cases of Zika. In these places and others, the images from Brazil have filled expectant mothers (and anyone considering having kids) with uncertainty and fear. “It’s really scary to be pregnant right now,” Rasmussen says. “We don’t know what to tell women.”
The threat to unborn babies wasn’t clear when Zika first hit Brazil, or in earlier, smaller outbreaks on Yap Island in the western Pacific and in French Polynesia. In fact, before 2016, not much was known about the virus at all. The majority of people infected don’t show any symptoms. But in the last year, scientists have thrown themselves at Zika, publishing more than 1,500 papers on different facets of the virus, from what species of mosquito it hides in to what cells it invades.

“We’re learning something new every day,” says obstetrician/gynecologist Catherine Spong, deputy director of the National Institute of Child Health and Human Development in Bethesda, Md.

The studies have scrubbed away some of Zika’s mystery — in particular, what the virus does in the womb. Scientists have found traces of Zika in the brains of human fetuses and confirmed that the virus can infect and kill brain cells in the lab. “This is the year that people became convinced that this mosquito-borne virus could cause birth defects,” Rasmussen says.

Though there was no smoking gun — no single piece of evidence that clinched Zika as the culprit — little clues began adding up, beginning with the conspicuous timing of Brazil’s microcephaly upsurge (SN: 4/2/16, p. 26). In January the CDC first issued a warning to pregnant women to postpone travel to Zika-affected regions. On April 13, a day that may be forever etched into Rasmussen’s memory, she and colleagues reported “a causal relationship” between Zika and microcephaly, along with other birth defects, in a study published online in the New England Journal of Medicine. Since then, Rasmussen says, “The data have become absolutely overwhelming.”
In May, a mouse study offered the first direct proof in animals that in utero Zika infection can lead to microcephaly (SN Online: 5/11/16). In September, researchers reported that a pregnant pigtailed macaque infected with Zika in the third trimester then gave birth to a baby whose brain had stopped growing. In human babies, the range of disorders linked to Zika has ballooned to include problems with the eyes, ears and joints, as well as seizures and extreme irritability (SN: 10/29/16, p. 14). At a workshop in North Bethesda, Md., this fall, a room crowded with doctors and scientists watched videos of inconsolable infants jerking erratically, arms and legs unnaturally stiff. “Heartbreaking,” Rasmussen says.

In December, researchers reported a surge in babies with microcephaly in Colombia (SN Online: 12/9/16), further evidence for Zika’s role in birth defects.

Zika isn’t the first virus to harm babies in the womb. Cytomegalovirus can also cause microcephaly, for example, and rubella, known as “German measles,” can leave babies with hearing, vision and heart problems. Even among these viruses, though, Zika stands out. “It’s such a precedent-setting thing,” Rasmussen says. “Never before has there been a mosquito-borne virus known to cause birth defects.”

Despite what scientists have learned in 2016, there’s little consolation for families already affected by microcephaly. And huge questions remain for expectant mothers. In particular, says Spong, it’s not clear just how risky Zika infection during pregnancy really is. One study published in the New England Journal of Medicine in July estimated that the risk of bearing a child with microcephaly increases to somewhere between 1 and 13 percent for women infected in their first trimester.

Spong hopes that a new study will clarify things. It’s called the Zika in Infants and Pregnancy Cohort Study, or ZIP, and the plan is to enroll 10,000 women in their first trimester. They’ll come from Puerto Rico, as well as Brazil and other countries, Spong says, and include both infected and uninfected women.

Tracking these women through pregnancy, birth and their baby’s first year of life could fill in some answers, like whether an infected pregnant woman who doesn’t have symptoms is better off than one who does. It’s also possible that some type of cofactor, like environmental toxins or other infections, is working with Zika to cause birth defects.

“You’re supposed to avoid stress when you’re pregnant,” Rasmussen says. “How do you avoid stress when you’re thinking that your baby could have these problems related to Zika?”

In the best-case scenario, a Zika vaccine could still be a few years away. And though infection rates may be winding down in some places, in areas with seasonally high temperatures and rainfall, such as Puerto Rico, Zika could become a local fixture. Still, any scrap of new information might help. Results from ZIP and other studies won’t erase the damage, but they could offer a pinprick of light following a year darkened by disease.