When someone uses the phrase “sleeping like a baby,” it’s obvious that they don’t really know how babies sleep. Many babies, especially newborns, are lousy sleepers, waking up every few hours to rustle around, cry and eat. For creatures who sleep up to 18 hours per 24-hour period, newborns are exhausting.
That means that bone-tired parents are often desperate to get their babies to sleep so they can rest too. A study published in the September Pediatrics captured this nightly struggle in the homes of 162 Pennsylvanian families. And the results revealed something disturbing: Despite knowing that they were being videotaped, many parents didn’t put their babies into a safe sleeping spot.
The risk of sleep-related infant deaths, including those caused by strangulation or sudden infant death syndrome, goes up when babies are put in unsafe sleeping positions or near suffocation hazards. Babies should be on their back on a firm mattress free of any objects. But that wasn’t the case for the majority of babies in the study, says Ian Paul, a pediatrician at Penn State.
As a parent to three, Paul is sympathetic to the difficulties of soothing babies to sleep. “The first few months are really exhausting,” he says. But as a pediatrician, he also sees the risks of ignoring safe sleep guidelines. “Parents need to realize that these risks are real and might happen to them.”
The videos taken for the study revealed that at 1 month of age, nearly all of the babies were put onto a sleep surface that had a loose or ill-advised item. Some of those objects aren’t surprising: Loose blankets, pillows, stuffed animals, crib bumpers and a SIDS monitor turned up in babies’ sleep areas. “The fact that almost every baby had loose bedding in the crib was disturbing,” Paul says. Stranger objects, such as cords, electrical wires and even a pet, were also observed.
Some of these items, such as sleep positioners and the soft bumpers that run around crib rails, are sold at baby stores. “If they’re selling it, parents think it is safe,” Paul says. “That’s just not the case.” Despite public health messages, babies are still suffocating on bumpers or getting trapped between bumpers and their mattress. There are no federal rules against crib bumpers, but several areas have banned them.
The study also spotted lots of bed hopping. Often, babies would start the night in a safe crib, but by the morning, they’d be in a more dangerous place, such as a bed full of pillows with a parent. The nightly shifts usually went from safe to unsafe as tired parents moved their babies around, Paul and colleagues found.
Paul recommends that parents create a safe place right next to their own beds for their babies to sleep, such as a bassinet or playpen. By designing their environment to encourage good habits at night, tired parents may be more likely to put the baby into a safe spot.
For bacteria, practice makes perfect: Adjusting to ever higher levels of antibiotics preps them to morph into super resistant strains, and scientists can now watch it happen. A new device — a huge petri dish coated with different concentrations of antibiotics — makes this normally hidden process visible, microbiologist Michael Baym and colleagues report in the Sept. 9 Science. The setup gives a step-by-step picture of how garden-variety microbes become antibiotic-resistant superbugs.
“As someone who’s studied evolutionary biology for a long time, I think it has a real wow factor,” says Sam Brown, a microbiologist at the Georgia Institute of Technology in Atlanta who wasn’t involved in the study. The bacteria are “climbing this impossible mountain of antibiotics.” Scientists often study microbial evolution in flasks where everything is mixed together. “Inside that flask, in order for a new strain to evolve, the new mutant has to be more fit than everything around it,” says Baym, of Harvard Medical School. “But in nature, we see a second dynamic: You don’t necessarily need to be more fit than everything around you. You just need to make it into a new environment.”
Baym and colleagues modeled those spatial dynamics using a giant dish more than a meter long instead of a standard palm-sized petri dish. That gave the bacteria more room to diversify and also let the researchers create a gradient of antibiotics on the plate. Low concentrations of trimethoprim or ciprofloxacin antibiotics at the edges ramped up to much higher levels in the middle. Then, the team put Escherichia coli bacteria on each end of the plate and watched the microbes multiply over the next week and a half.
In general, as the E. coli mutated in ways that let them handle higher and higher levels of antibiotics, their descendants could press into new territory on the plate. The bacteria that made it to the middle could tolerate doses of antibiotics a thousand times higher than what was necessary to kill the original bacteria.
But antibiotic resistance didn’t always make bacteria competitive colonizers. Highly resistant bacteria sometimes spread more slowly. Trapped in the back by faster-moving bacteria at the forefront, the stragglers’ descendants formed pockets of super-resistance at lower antibiotic concentrations. Baym and his colleagues think the experimental setup could be used to study microbial evolution under other environmental and spatial constraints, like the availability of particular nutrients.
Scientists may soon find out how tiny neutrinos really are. On October 14, scientists switched on the Karlsruhe Tritium Neutrino experiment, or KATRIN, located at the Karlsruhe Institute of Technology in Germany, which aims to measure the mass of the petite particles for the first time.
KATRIN will study neutrinos, which are less than a millionth the mass of an electron, by sifting through the aftermath of radioactive decays of tritium, an isotope of hydrogen with two neutrons. Tritium decays into helium-3, emitting a neutrino and an electron in the process. Because neutrinos are hard to detect, scientists measure the energy of the electrons emitted and use that information to deduce the neutrino mass.
KATRIN has begun taking test data, but the experiment is not yet filled with the radioactive tritium gas necessary to collect data for analysis. “This was a big milestone because it means that all the other systems are up and ready to go, and we’re taking data,” says KATRIN member Joseph Formaggio of MIT. Official data taking should begin in 2017.
Tweaking activity of one protein may help protect against 10 autoimmune diseases, a new study suggests. The protein, tyrosine kinase 2 or TYK2, helps regulate how strongly the immune system responds to threats.
Using genetic data from more than 36,000 people with a variety of autoimmune diseases, researchers found that one genetic variant in the gene that codes for the TYK2 protein protects against a wide range of diseases that cause the immune system to attack the body. The variant changes one amino acid in the protein. As a result, the protein’s activity is greatly reduced, but not completely eliminated, researchers report November 2 in Science Translational Medicine.
The researchers say the variant strikes just the right balance between incapacitating the immune system and protecting against overreactions that lead to multiple sclerosis, Crohn’s disease and other autoimmune disorders. New drugs that reduce TYK2’s activity would need similar Goldilocks-like precision. But if such a drug could be developed, it could prove useful against a broad range of diseases.
Saved by the Bell Physicists used light from stars to perform a cosmic Bell test, which verified that quantum particles were indeed “spooky,” Emily Conover reported in “Quantum effect passes space test” (SN: 1/21/17, p. 12).
Reader George Mitchell took issue with Conover’s description of entangled photons before they are measured as having multiple polarizations at once. “We don’t know the direction of their polarization,” Mitchell wrote. “It is undefined.”
“Multiple polarizations” in this context is meant to indicate that there are multiple possible outcomes of a polarization measurement; the particle does not have a definite polarization that is simply unknown. “Bell tests like the one in the article confirm this interpretation,” Conover says (SN Online: 1/27/16). It’s similar to how Schrödinger’s cat can be in a “superposition” of both alive and dead at the same time (SN: 11/20/10, p. 15). “It’s not that we don’t know whether the cat is alive or dead; it’s both,” she says. “This is hard to wrap one’s head around.” In any case, it is effectively impossible to put a real cat in a superposition, because it is too large to display the strange properties of quantum mechanics. “But for particles,” she says, “this is acceptable behavior.”
Land ho From Nuna to Pangaea, shifting landmasses have repeatedly reshaped Earth’s surface. Researchers are now picturing a future supercontinent dubbed Amasia, due in 250 million years, Alexandra Witze reported in “Supercontinent superpuzzle” (SN: 1/21/17, p. 18).
Reader Pierre Grillet wondered how subduction — the process by which a tectonic plate is pushed beneath another tectonic plate — could pull continents apart. “I would suggest that a different mechanism is also at work here. Rising material must balance crust material being subducted into the mantle,” he wrote. “It would make sense that this rise should occur in the center of the plate, where the mantle is hotter. Rising material would then spread sideways, pushing the sides of the plate over the oceanic crust and pulling the plate apart.”
The process Grillet describes is a theory proposed by some researchers. Other researchers have doubts (SN: 4/4/15, p. 13). “Plumes of hot material rising from the mantle could rip continents apart, but the plumes would have to rise up at weak points along continental boundaries, which seems unlikely,” says Thomas Sumner, Science News’ earth sciences writer. A competing theory covered in the story suggests that subduction tears continental plates apart by pulling at their edges. Power up A variety of next-generation batteries promise to store energy more efficiently, providing power for longer periods, Susan Gaidos reported in “Charging the future” (SN: 1/21/17, p. 22).
Reader Tom Wicker was disappointed that the beginning of the story equated power and energy. “Everybody wants more power from their batteries,” Gaidos wrote, citing smartphone, laptop and electric-car batteries as examples.
“Laptop batteries can supply more than enough power. You need to charge them frequently because of the limited amount of energy they store,” Wicker wrote. “It is of course correct that drawing more power, more energy per unit time, from a battery will drain it faster. But that is true even though the battery may have no problem supplying the required amount of power. It just can’t do that for as long as required due to insufficient energy storage.”
Wicker’s distinction between energy and power is correct, Gaidos says. “When talking about batteries, the term ‘portable power’ is frequently used, when what is really meant is portable energy. The research under way, as described in the story, aims to create batteries with high power that can maintain that power through a large number of recharge cycles,” she says.
Cancer prevention isn’t the first thing that comes to many parents’ minds when they consider vaccinating their preteens against human papillomavirus, or HPV. And the fact that HPV is transmitted sexually gives the vaccine more baggage than a crowded international flight. But what gets lost in the din is the goal of vaccination, to protect adolescents from infection with HPV types that are responsible for numerous cancers.
Newly released estimates show just how prevalent HPV infections are in the United States. In April, the U.S. Centers for Disease Control and Prevention reported for 2013-2014 that among adults ages 18 to 59, 25 percent of men and 20 percent of women had genital infections with HPV types that put them at risk of developing cancer.
That’s just a snapshot in time. For those who are sexually active, more than 90 percent of men and 80 percent of women can expect to become infected with at least one type of HPV during their lives. About half of those infections will be with a high-risk HPV type.
“People who think, ‘I’m not at risk,’ are really not understanding the magnitude of this virus,” says cancer epidemiologist Electra Paskett of Ohio State University in Columbus.
HPV is the most common sexually transmitted infection in the United States. The HPV group of viruses includes low-risk and high-risk types. Low-risk types 6 and 11 are responsible for 90 percent of all genital warts. The high-risk types of HPV can cause cancer, and the two behind most HPV-related cancers are types 16 and 18. Seventy percent of cervical cancers can be traced back to types 16 and 18, while type 16 also causes cancers of the anus, vagina, penis and the oropharynx, the part of the throat at the back of the mouth. HPV spreads by sexual contact, either vaginal, anal or oral. Nationally, from 2011 to 2014, 11 percent of men ages 18 to 69 had an oral infection with any type of HPV, and for nearly 7 percent of men, it was a high-risk type, the CDC’s National Center for Health Statistics estimated in its April report. For women in this age group, it was 3 percent and 1 percent, respectively.
The numbers are far worse when it comes to genital HPV infections. During 2013 to 2014, 45 percent of men and 40 percent of women ages 18 to 59 had genital infections with any type of HPV. One in four men and one in five women in this age group were infected with a high-risk type.
“It’s a wake-up call for both genders, but particularly for males,” says Jessica Keim-Malpass, a nurse scientist at the University of Virginia in Charlottesville.
For an estimated 19,200 women and 11,600 men each year, HPV infections result in a cancer diagnosis.
Vaccination could greatly relieve this cancer burden. Three different HPV vaccines have been available in the United States. The first, introduced in 2006, covered low-risk types 6 and 11 and high-risk types 16 and 18. The most recent HPV vaccine protects against these four types as well as five more high-risk types, and is the only vaccine currently distributed nationally. A federal advisory committee recommended routine vaccination against HPV at 11 or 12 years of age in 2006 for girls and in 2011 for boys.
But the HPV-cancer prevention message doesn’t seem to be getting through in the United States. HPV vaccination rates lag behind the national coverage goal of 80 percent for 13- to 15-year-olds. In 2015, among U.S. adolescents ages 13 to 17, six out of 10 girls and five out of 10 boys had gotten at least one shot in a three-shot series. But only four out of 10 girls and three out of 10 boys had completed the series.
What’s with the lackluster response?
Parents are part of the issue. “They don’t know about the vaccine, or they have fears about safety, or they say ‘My child is not going to be at risk for HPV infections,’” Paskett says.
The safety of all three vaccines was established in large clinical trials before approval by the U.S. Food and Drug Administration. Since 2006, almost 90 million doses of HPV vaccines have been administered nationally, and the most common side effects are soreness or swelling at the site of the shot.
Some parents think that “by giving the vaccine, you are saying it’s OK to have sex,” notes Keim-Malpass. Research doesn’t back this up. A 2012 study in Pediatrics of 11- to 12-year-old girls found that HPV vaccination was not tied to increased sexual activity, as measured by medical records of sexually-transmitted infection or pregnancy. A 2015 study in JAMA Internal Medicine of 12- to 18-year-old girls found no evidence to link HPV vaccination with higher rates of sexually transmitted infections.
The recommended age for vaccination ensures that preteens are protected before they are exposed to HPV, whenever that may be. “The whole reason the vaccine is targeted to 11- and 12-year-olds is to get kids vaccinated before they enter a sexual relationship,” says Keim-Malpass.
Lack of urgency is a problem, too. The delay between an infection and a future cancer can make people complacent about HPV. “You are protecting yourself from an infection, but it has ramifications years, decades later,” Keim-Malpass says. “It’s not about something you get tomorrow, it’s about something you could get 20 to 30 years from now.”
Another difficulty has been the vaccination schedule. The initial recommendation was for three doses, with the second shot one to two months after the first, and the third shot six months after the first. This schedule was challenging for busy adolescents, notes Keim-Malpass.
Now there is a new dosing regimen. For adolescents who begin vaccination before turning 15, only two shots are required, with the second one coming six to 12 months after the first. This should be easier to accommodate in yearly well-child visits.
Even with the suboptimal vaccination rates, there has been an impact on infections. A 2016 Pediatrics study found that, within six years of the first vaccine’s introduction in 2006, infections with the four HPV types covered decreased 64 percent among 14- to 19-year-old girls. There are also fewer cases of genital warts among U.S. teens since 2006.
Any decline in infection rates is a good thing. But “it’s not to the extent we could have, if from the get- go, people realized this was a cancer vaccine,” says Paskett. “If there was a vaccine for breast cancer, moms would be lining up around the corner with their daughters.”
If you could put Uranus’ moon Cressida in a gigantic tub of water, it would float.
Cressida is one of at least 27 moons that circle Uranus. Robert Chancia of the University of Idaho in Moscow and colleagues calculated Cressida’s density and mass using variations in an inner ring of the planet as Uranus passed in front of a distant star. The team found that the density of the moon is 0.86 grams per cubic centimeter and its mass is 2.5×1017 kilograms. The results, reported August 28 on arXiv.org, are the first to reveal details about the moon. Knowing its density and mass helps researchers determine if and when Cressida might collide with another of Uranus’ moons and what will become of both of them.
Voyager 2 discovered Cressida and several other moons when the spacecraft flew by Uranus in 1986. Those moons, and two discovered later, orbit within 20,000 kilometers of Uranus and are the most tightly packed in the solar system.
Such close quarters puts the moons on collision courses. Based on the newly calculated mass and density of Cressida, simulations suggest it will slam into another moon, Desdemona, in a million years.
Cressida’s density suggests it is made of water ice with some contamination by a dark material. If the other moons have similar compositions, the moon collisions may happen in the more distant future than researchers thought. Determining what the moons are made of will also reveal their ultimate fate after a collision: whether they merge, bounce off each other or shatter into millions of pieces.
Artificial sweeteners can have a not-so-sweet side — a bitter aftertaste. The flavor can be such a turnoff that some people avoid the additives entirely. Decades ago, people noticed that for two artificial sweeteners — saccharin and cyclamate, which can taste bitter on their own — the bitterness disappears when they’re combined. But no one really knew why.
It turns out that saccharin doesn’t just activate sweet taste receptors, it also blocks bitter ones — the same bitter taste receptors that cyclamate activates. And the reverse is true, too. The result could make your bitter batter better. And it could help scientists find the next super sweetener.
Saccharin is 300 times as sweet as sugar, and cyclamate is 30 to 40 times as sweet as the real deal. Saccharin has been in use since its discovery in 1879 and is best known as Sweet’N Low in the United States. Cyclamate was initially approved in the United States in 1951, but banned as a food additive in 1969 over concerns that it caused cancer in rats. It remains popular elsewhere, and is the sweetener behind Sweet’N Low in Canada.
In the 1950s, scientists realized that the combination of the two (sold in Europe under brand names such as Assugrin), wasn’t nearly as bitter as either sweetener alone.
But for the more than 60 years since, scientists didn’t know why the combination of cyclamate and saccharin was such a sweet deal. That’s in large part because scientists simply didn’t know a lot about how we taste. The receptors for bitter flavors were only discovered in 2000, explains Maik Behrens, a molecular biologist at the German Institute of Human Nutrition Potsdam-Rehbruecke.
(Now we know that that there are 25 potential bitter taste receptors, and that people express them in varying levels. That’s why some people have strong responses to bitter flavors such as those in coffee, while others might be more bothered by the bitter aftertaste of the sweetener put in it.)
Behrens and his colleagues Kristina Blank and Wolfgang Meyerhof developed a way to screen which of the bitter taste receptors that saccharin and cyclamate were hitting, to figure out why the combination is more palatable than either one alone. The researchers inserted the genes for the 25 subtypes into human kidney cells (an easier feat than working with real taste cells). Each gene included a marker that glowed when the receptors were stimulated. Previous studies of the two sweeteners had shown that saccharin alone activates the subtypes TAS2R31 and TAS2R43, and cyclamate tickles TAS2R1 and TAS2R38. Stimulating any of those four taste receptor subtypes will leave a bitter taste in your mouth.
But cyclamate doesn’t just activate the two bitter receptors, Behrens and his colleagues showed. It blocks TAS2R31 and TAS2R43 — the same receptors that saccharin stimulates. So with cyclamate around, saccharin can’t get at the bitter taste subtypes, Behrens explains. Bye, bye bitter aftertaste.
The reverse was true, too: Saccharin blocked TAS2R1 — one of the bitter receptors that cyclamate activates. In this case, though, the amount of saccharin required to block the receptors that cyclamate activates would have bitter effects on its own. So it’s probably the actions of cyclamate at saccharin’s bitter receptors that help block the bitterness, Behrens and his colleagues report September 14 in Cell Chemical Biology.
The researchers also tested whether cyclamate and saccharin together could be stronger activators of sweet receptors than either chemical alone. But in further tests, Behrens and his colleagues showed that, no, the sweet sides of saccharin and cyclamate stayed the same in combination.
“This addresses a longstanding puzzle why mixing two different sweeteners changes the aftertaste,” says Yuki Oka, a neuroscientist at Caltech in Pasadena. “They are interrupting each other at the receptor level.” It’s not too surprising that a sweetener might block some receptor subtypes and stimulate others, he notes, but that saccharin and cyclamate have such clear compatibilities is a lucky chance. “Mechanism-wise, it’s surprisingly beautiful.”
Oka notes that no actual tongues tasted artificial sweeteners in these experiments. The tests took place on cells in dishes. But, he says, because the researchers used the human bitter taste receptors, it’s likely that the same thing happens when a diet drink hits the human tongue.
Behrens hopes the cell setup they used for this experiment can do more than solve an old mystery. By using cells in lab tests to predict how different additives might interact, he notes, scientists can develop sweeteners with fewer bitter effects. The technique was developed with funding from a multinational group of researchers and companies — many of which will probably be very interested in the sweet results. And on the way to sweeteners of the future, scientists may be able to resolve more taste mysteries of the past.
Earth may not provide the best blueprint for how rocky planets are born.
An analysis of planets outside the solar system suggests that most hot, rocky exoplanets started out more like gassy Neptunes. Such planets are rocky now because their stars blew their thick atmospheres away, leaving nothing but an inhospitable core, researchers report in a paper posted online October 15 at arXiv.org. That could mean these planets are not as representative of Earth as scientists thought, and using them to estimate the frequency of potentially life-hosting worlds is misleading. “One of the big discoveries is that Earth-sized, likely rocky planets are incredibly common, at least on hotter orbits,” says planetary scientist Eric Lopez of NASA’s Goddard Space Flight Center in Greenbelt, Md., who wasn’t involved in the study. “The big question is, are those hot exoplanets telling us anything about the frequency of Earthlike planets? This suggests that they might not be.”
Observations so far suggest that worlds about Earth’s size probably cluster into two categories: rocky super-Earths and gaseous mini-Neptunes (SN Online: 6/19/17). Super-Earths are between one and 1.5 times as wide as Earth; mini-Neptunes are between 2.5 and four times Earth’s size. Earlier work showed that there’s a clear gap between these planet sizes.
Because planets that are close to their stars are easier for telescopes to see, most of the rocky super-Earths discovered so far have close-in orbits — with years lasting between about two to 100 Earth days — making the worlds way too hot to host life as we know it. But because they are rocky like Earth, scientists include these worlds with their cooler brethren when estimating how many habitable planets might be out there.
If hot super-Earths start out rocky, perhaps it is because the worlds form later than their puffy mini-Neptune companions, when there’s less gas left in the growing planetary system to build an atmosphere. Or, conversely, such planets, along with mini-Neptunes, may start with thick atmospheres. These rocky worlds may have had their atmospheres stripped away by stellar winds. Now, exoplanet astronomer Vincent Van Eylen of Leiden University in the Netherlands and his colleagues have shown that the fault is in the stars. “You really have these two populations, and the influence of the star is what creates this separation,” Van Eylen says. That result could warn astronomers not to rely too heavily on these hot, rocky worlds when calculating how many habitable planets are likely to exist.
To measure the planets’ sizes, astronomers need to know the sizes of their stars. Van Eylen and colleagues analyzed 117 planets whose host stars’ sizes had been measured using astroseismology. This technique tracks how often the star’s brightness changes as interior oscillations ripple through it, and uses the frequency to determine its size.
“Think of the stars as musical instruments,” Van Eylen says. A double bass and a violin produce sound the same way, but the pitch is different because of the instrument’s size. “It’s exactly the same thing with stars.”
The researchers then calculated the planets’ sizes — between one and four times the Earth — with about four times greater precision than in previous studies. As expected, the planets clustered in groups of around 1.5 and 2.5 times Earth’s radius, leaving a gap in the middle.
Next the team looked at how the planets’ sizes changed with distance from the host star. Planets that were rocky from the start should be smaller close to the stars, where studies of other young star systems suggest there should have been less material available when these planets were forming. But if proximity to a star’s winds is key, there should be some larger rocky worlds closer in, with smaller gaseous worlds farther out.
Van Eylen’s planets matched the second picture: The largest of the rocky planets nestled close to the stars were bigger than the distant ones. That suggests the rocky planets once had atmospheres, and lost them.
“It’s not fair to take the close-in planets and assume that the more distant planets are just like them,” says exoplanet astronomer Courtney Dressing of the University of California, Berkeley. “You might be fooling yourself.”
Kleptopredation klep-toe-preh-day-shun n. A food-gathering strategy of eating an organism and the meal it just ate.
A wily sea slug has a way to get two meals in one: It gobbles up smaller predators that have recently gulped in their own prey.
“Kleptopredation” is the term Trevor Willis of the University of Portsmouth in England and his colleagues propose for this kind of food theft by well-timed predation.
Researchers knew that the small Mediterranean nudibranch Cratena peregrina, with a colorful mane of streamers rippling off its body, climbs and preys on pipe cleaner‒skinny, branched colonies of Eudendrium racemosum hydroids, which are distant relatives of corals. The nudibranchs devour the individual hydroid polyps and, new tests show, prefer them well fed. In experimental buffets with fed or hungry polyps, the nudibranchs ate faster when polyps were fat with just-caught plankton. In this way, at least half of a nudibranch’s diet is plankton. This quirk explains why some biochemical signatures that distinguish predators from prey don’t work out clearly for nudibranchs and hydroids, the researchers report November 1 in Biology Letters.
A weird echo of this meal-stealing strategy shows up in certain jumping spiders. The arachnids don’t have the biology to drink vertebrate blood themselves. Instead, they catch a lot of female mosquitoes that have just tanked up (SN: 10/15/05, p. 246).
