The next flu drug could come from frog mucus. It’s not as crazy as it sounds: For decades, scientists have searched for new antiviral drugs by mining proteins that animals produce to protect themselves from microbes. In lab tests, proteins found in amphibian secretions can defend against HIV, herpes and now the flu.

David Holthausen of Emory University in Atlanta and colleagues sampled slime from the skin of Hydrophylax bahuvistara, a recently discovered frog species from southern India. They tested the influenza-fighting ability of 32 slime peptides. Four showed promise, but three proved toxic to mammals.
The fourth peptide, however, was safe and showed a propensity for fighting off the flu. When exposed to four H3N2 and eight H1N1 strains, this peptide, dubbed urumin, inhibited H3N2 viruses to a degree but was particularly adept at killing H1N1 viruses, which are more common among humans. The frog slime protein even cut viral numbers in a set of seven drug-resistant strains and protected mice during flu infections. Urumin blows up flu virus particles by targeting the stalk region of the hemagglutinin protein in H1 varieties, the team found. With further development, urumin could form the basis of future influenza drugs, the researchers write in the April 18 Immunity.

The footprints of long-gone glaciers and icebergs are now frozen in time in a stunning new collection of images of Earth’s seafloor.

The Atlas of Submarine Glacial Landforms is a comprehensive, high-resolution atlas of underwater landscapes that have been shaped by glaciers, largely in polar and subpolar regions, and provides a comparative look at how glaciers, ice and related climate shifts transform Earth. Kelly Hogan, a marine geophysicist with the British Antarctic Survey and an editor of the atlas, presented it April 26 in Vienna at a meeting of the European Geosciences Union.
Most of the more than 200 images were generated from research vessels using multibeam bathymetry, which renders the seafloor surface in 3-D, exposing a region’s glacial history. For example, the distinctive asymmetry of 20,000-year-old glacial deposits called drumlins in the Gulf of Bothnia, between Finland and Sweden, suggests that ice flowed south, toward a larger glacier in the Baltic Sea.

Other images reveal the tracks of icebergs that once plowed and scribbled the ocean floor, such as those seen in the Barents Sea in the Arctic Ocean. The tracks may look random, but they tell tales of past currents and water depth.

In all, the seafloor depicted in the atlas covers an area about the size of Great Britain. But the real impact of the project goes beyond individual images, Hogan says. She expects that scholars exploring glacial history, researchers predicting future ice behavior and climate scientists are among those who will keep a copy close at hand.

Fascination with faces is nature, not nurture, suggests a new study of third-trimester fetuses.

Scientists have long known that babies like looking at faces more than other objects. But research published online June 8 in Current Biology offers evidence that this preference develops before birth. In the first-ever study of prenatal visual perception, fetuses were more likely to move their heads to track facelike configurations of light projected into the womb than nonfacelike shapes.

Past research has shown that newborns pay special attention to faces, even if a “face” is stripped down to its bare essentials — for instance, a triangle of three dots: two up top for eyes, one below for a mouth or nose. This preoccupation with faces is considered crucial to social development.
“The basic tendency to pick out a face as being different from other things in your environment, and then to actually look at it, is the first step to learning who the important people are in your world,” says Scott Johnson, a developmental psychologist at UCLA who was not involved in the study.

Using a 4-D ultrasound, the researchers watched how 34-week-old fetuses reacted to seeing facelike triangles compared with seeing triangles with one dot above and two below. They projected triangles of red light in both configurations through a mother’s abdomen into the fetus’s peripheral vision. Then, they slid the light across the mom’s belly, away from the fetus’s line of sight, to see if it would turn its head to continue looking at the image.
The researchers showed 39 fetuses each type of triangle five times. Of the 195 times a facelike triangle was projected, fetuses turned their heads 40 times. In contrast, the nonfacelike triangles elicited only 14 head turns, says study coauthor Vincent Reid of Lancaster University in England. The finding suggests that fetuses share newborns’ predisposition for looking at facelike shapes, the researchers conclude.
Psychologist Melanie Spence of the University of Texas at Dallas, who was not involved in the work, says it’s a leap to draw too many similarities between the visual perceptions of fetuses and newborns. Although the triangle images mimic facelike ones used to test newborns, they aren’t the same, she notes. Scientists typically show babies faces in black and white, with head-shaped borders.

Still, Johnson says evidence that a fundamental aspect of facial perception may be hardwired into humans’ visual system is “very, very exciting.” The new study’s method of projecting images into the womb and watching the fetus’s reaction also “opens up all kinds of new doors to understand human development,” Johnson says. A similar light projection and 4-D ultrasound technique might be used to see whether fetuses can distinguish between different quantities in the same way that babies can.

A protein made by the fetus may lead to preeclampsia in moms.

People born to mothers who had the prenatal disorder were more likely to have certain DNA variations near a gene known to influence blood vessels. The results, published online June 19 in Nature Genetics, point to that gene as a possible preeclampsia culprit, and may help scientists develop ways to stop or prevent the pregnancy complication. Preeclampsia, which is marked by a dangerous spike in blood pressure, affects about 5 percent of pregnancies and is estimated to kill over 70,000 women a year globally.
Scientists have known that preeclampsia can run in families, but the genetics of the fetus hadn’t been scrutinized. “Over the years, people have looked at mothers’ genes,” says geneticist Linda Morgan of the University of Nottingham in England. “This is the first large study to look at babies’ genes.”

Morgan and colleagues compared DNA variations in 2,658 babies, children and adults born to mothers who had preeclampsia with those in more than 300,000 people. (This large group probably included some people born to mothers with the condition, but the vast majority were not.)

A genome-wide association study (GWAS), a technique used to comb through DNA looking for genetic variations that may be linked to a disorder, pinpointed a spot on chromosome 13, near a gene called FLT1. That gene is involved with blood vessel formation, an intricate process for the placenta as it grows into the inside wall of the uterus and merges the baby’s blood supply to the mother’s. The same genetic hot spot turned up in tests of a second group of offspring from mothers who had preeclampsia, Morgan and colleagues report. Another DNA variation near the gene also showed a link to the disorder.

Identifying FLT1 “makes a lot of sense,” says Ananth Karumanchi, a vascular biologist at Beth Israel Deaconess Medical Center in Boston, who was not involved in the study. Earlier experiments by Karumanchi and others suggest that the gene plays a role in preeclampsia.

Preeclampsia is kicked off by the placenta, an organ grown mostly from fetal cells that helps provide nutrients to the fetus. And though the details are unclear, some scientists suspect that unhealthy placentas start to pump out too much Flt-1 protein. A version of the protein called sFlt-1 can then slip into a mother’s bloodstream, where it may damage blood vessels in a way that leads to high blood pressure.
The GWAS results can’t explain the bulk of preeclampsia cases. A fetus carrying a single copy of one of the troublesome variants near FLT1 raised a mother’s risk of preeclampsia by about 20 percent, the analysis suggests. Other risk factors are known to be much stronger, Morgan says, including previous high blood pressure, former preeclampsia diagnoses or carrying twins.

Karumanchi says that the genetic results might not be strong enough on their own to make the case that the gene is involved. But other work points to FLT1. “We feel it’s the right target,” he says.

In Europe, a preliminary clinical trial is testing a filtration method that removes excess sFlt-1 protein from the blood of women with signs of preeclampsia. So far, about 20 women have undergone the procedure, says nephrologist Ravi Thadhani of Massachusetts General Hospital in Boston. Early results are “quite encouraging,” he says, and he hopes to expand the study soon.

A vaccine against meningitis has an unexpected side effect: It appears to target gonorrhea, too. If confirmed, the results represent the first instance of a vaccine reducing gonorrhea infections.

After receiving a vaccine aimed at a type of meningitis, people were less likely to contract gonorrhea, scientists report online June 10 in the Lancet. That’s a big deal because worldwide each year, an estimated 78 million people contract gonorrhea, a sexually transmitted disease that can cause pelvic inflammation, infertility and throat infections. Gonorrhea’s bacterial culprit, Neisseria gonorrhoeae, has developed resistance to many antibiotics, making treatment much more difficult. Some strains of gonorrhea can now resist all known antibiotics, the Word Health Organization announced July 7.
“We are in desperate need for new therapies,” says Christine Johnston, an infectious disease specialist at the University of Washington in Seattle. Attempts to make a gonorrhea vaccine have failed so far. The new results are “the first to show that vaccination against gonorrhea could be possible,” Johnston says.

Finding the link between the two diseases was partly “a story of serendipity,” says study coauthor Helen Petousis-Harris, a vaccinologist at the University of Auckland in New Zealand. She and others had noted curious declines in gonorrhea cases in New Zealand, Cuba and, to a lesser extent, Norway after people had been vaccinated against a group B meningococcal bacterium, a pathogen that can cause meningitis and blood infections.

Bacteria that cause meningitis and gonorrhea are actually close kin, sharing 80 to 90 percent of their DNA. “There was certainly biological plausibility, but we needed some proof” that the vaccine really did curb gonorrhea, Petousis-Harris says.

She and colleagues looked at data from the New Zealand national vaccine registry to see who received a meningococcal vaccine that was available from 2004 to 2008, called MeNZB. That vaccination information was combined with data on over 14,000 15- to 30-year-olds who had either gonorrhea, chlamydia or both in New Zealand between 2004 and 2016.

Compared with unvaccinated people, those who had received the vaccine were about a third less likely to contract gonorrhea, the researchers found. The researchers had no information about people’s exposure to gonorrhea, only whether people were treated for the infection at a clinic. No such link was found between the vaccine and chlamydia.
MeNZB is a type of vaccine called an outer membrane vesicle vaccine. By mimicking bacterial bits released as the bugs proliferate, the vaccine trains the immune system to recognize and attack the bacteria. That exact vaccine is no longer in use, but similar vaccines exist, including Bexsero, which was used to treat a meningitis B outbreak at Princeton University in 2013.

The researchers don’t yet know what part of the MeNZB vaccine may be protective against gonorrhea. “We need to understand what was magical about this vaccine,” Petousis-Harris says. That knowledge could help researchers design a more targeted gonorrhea vaccine. Other meningitis vaccines ought to be scrutinized, too, Petousis-Harris says. “It might be that we’ve got a vaccine out there that could make a significant difference.”

Novartis, the health care company that developed Bexsero, provided funds for the study, but had no input on the design or results, Petousis-Harris says. A different company, GlaxoSmithKline, has since bought Novartis’ vaccine division.

Any new treatment for gonorrhea will eventually spur the bacteria to develop resistance, says Teodora Wi, a medical officer at WHO’s Department of Reproductive Health and Research in Geneva. But a vaccine couldn’t be evaded so easily. The current result “provides a very important breakthrough in the development of gonorrhea vaccines,” she says.

[Millions of diabetics] could be indebted to a strain of diabetic mice being bred in Bar Harbor, Maine. In diabetes research, “this mouse is the best working model to date,” one of its discoverers, Dr. Katharine P. Hummel, says.… A satisfactory animal subject had eluded diabetes researchers, until the mouse was found. — Science News, August 12, 1967

Update
Hummel’s diabetic mice are still used in research to mimic type 2 diabetes in humans, which is linked to obesity. In the mid-1990s, researchers found that the diabetic mice carry a mutation in the leptin receptor gene, which prevents the hormone leptin from signaling fullness and triggering other metabolic processes. In people, however, the disease is more complicated. More than 40 genetic variants are associated with susceptibility to type 2 diabetes. Unlike the mouse mutation, none of those variants guarantee a person will develop the disease.

Across Europe, rivers aren’t flooding when they used to.

Long-term changes in temperature and precipitation are making some rivers flood days, weeks or even months earlier than they did 50 years ago, and pushing flooding in other areas much later, researchers report August 11 in Science. Those changes could impact people, wildlife and farms near rivers.

Previous studies have shown that climate change is likely to increase the severity and frequency of coastal floods, but it can be tricky to concretely link river flooding to climate change, says Günter Blöschl, a hydrologist at the Vienna University of Technology who led the study.
Coastal flooding is worsened largely by one overriding variable that can be tracked: sea level rise. But river flooding is affected by a complex set of factors, says Rob Moore, a policy analyst at the Natural Resources Defense Council in Chicago who specializes in water issues. Both the timing and quantity of precipitation matter, as does the type of soil and whether it’s dry or already waterlogged when rain hits. What’s more, changes in land use around a river or engineering projects such as dams that change river flow can also affect flood risk — but aren’t necessarily related to the climate.
So instead of tracking the size or frequency of river floods, the researchers examined the seasonal timing of those floods. That measurement is less impacted by factors that have nothing to do with climate. Blöschl worked with researchers from 38 countries to analyze hydrological data collected at 4,262 sites across Europe from 1960 to 2010.

Flood season shifted as much as 13 days earlier or nine days later per decade, the researchers found. Over the entire study period, that shift added up to floods in some regions occurring, in the most extreme cases, as much as 65 days earlier or 45 days later. The biggest changes were in Western Europe, where a quarter of the monitoring sites recorded flood timing shifts of more than 36 days over the 50-year period. Elsewhere, effects were more moderate, though still measurable: In northeastern Europe and the area around the North Sea, for instance, more than half of the stations showed shifts of more than 8 days.
The effect varies substantially by region because not all parts of Europe experience the same sorts of floods, says Blöschl. In southern Sweden and the Baltics, floods are mostly driven by snowmelt. Warmer local temperatures make the snow melt earlier in the spring, shifting flood season up, too. In southern England, on the other hand, heavy autumn rains saturate the soil, and subsequent winter deluges can cause flooding. Flood season there is driven by when the soil gets too waterlogged to take in more moisture.

The study shows that flood timing has changed, but does not address specific consequences. It’s clear, though, that off-season flooding could have far-reaching effects, especially if these trends continue. Animals that rely on river conditions at a certain time of year in order to breed or find food could be affected by surprise floods. Out-of-season floods or unexpected dry spells could damage crops.

Plus, people are less prepared when big floods happen off-season, says Moore. While a comprehensive study like this one hasn’t been done in the United States, floods are occurring at unusual times here, too, he notes. Moore cites devastating floods that swelled the upper Mississippi River to a record size in December 2015 — not the time of year when the river is expected to overflow its banks. That flooding, combined with tornadoes spurred by the same storm system, killed more than 50 people and caused almost $2 billion in damage.

Just a stab in the dark, but you’ve probably heard: There is a total solar eclipse today, August 21.

For the first time since 1979, the moon’s shadow will zip across the continental United States. The shadow will travel from Oregon to South Carolina in a swift 92 minutes. For those in the path of totality, total darkness will last only a couple of minutes. There and elsewhere in most of the United States, the moon will partially block the sun for around three hours.
If you don’t already have plans to travel to the 115-kilometer-or-so-wide path of totality, well, you’re probably too late. But here are some links to help you experience the eclipse, whether or not you’re able to see it in person.

The eclipse will be visible in all of North America — as well as in Central America and a small part of South America. Wondering what you’ll see where you live? Check out this interactive map from NASA or this cool tool from Vox.

Still need eclipse glasses? While many retailers have been sold out for days, some organizations are handing out free glasses at eclipse-watching events. Check your local TV/newspaper/radio stations’ newsfeeds for the latest. Make sure your glasses are safe.

No eclipse glasses? Never fear! You can still see the moon eclipsing the sun by making a pinhole projector or a box projector. Or just let sunlight shine through something that has holes, like a colander or Ritz Cracker (look at the ground to see the shape of the shadow the holes cast).

Watching with kids? Check out Growth Curve blogger Laura Sanders’ tips for protecting little ones’ eyes during the eclipse.
Which reminds me: Whatever you do, don’t look directly at the sun. Permanent damage to your eyes may result. If you’re in the path of totality, officials say it’s OK to look directly at the sun once the moon completely blocks it. But that’s very brief, so be prepared to quickly look away or shield your eyes once the moon slips out of total alignment.

Want to do more with your eclipse experience? It’s not too late to participate in a citizen science project.

Stuck indoors, or out of totality? Watch the livestream. NASA’s programming begins at noon Eastern on NASA TV, which you can watch at this link or right here:
Want some tunes to go along with it? The NASA interns made an eclipse playlist. There are also several Spotify playlists around, like this one from WXPN, this from the Washington Post and this one from the Boston Globe.

If all this excitement has you fancying a future in eclipse chasing, check out our interactive map of the next 15 total solar eclipses.

And let’s not forget that there will be a ton of science going on during the eclipse. Here are the big questions physicists and astronomers will seek to answer today.

Still want more? Follow us on Facebook and on Twitter for eclipse updates and RT’s of our correspondents in totality. Watch as the Science News team takes over the Society for Science & the Public’s Snapchat (Society4Science). And come back to Science News later today for a report from our astronomy writer, Lisa Grossman, who is spending the day in Casper, Wyo., with a research team that’s studying the sun’s wispy atmosphere, the corona.

Molecules are seriously chilling out. Scientists report the first cooling of molecules below a previously impassable milestone. The result, in which scientists cooled molecules down to tens of millionths of a degree, is a step toward reaching the ultracold temperatures already achievable with atoms, researchers report August 28 in Nature Physics.

Scientists regularly chill atoms to less than a millionth of a degree above absolute zero (‒273.15° Celsius), even reaching temperatures as low as 50 trillionths of a degree (SN: 5/16/15, p. 4). But molecules are more difficult to cool down, as they can spin and vibrate in a variety of ways, and that motion is a form of heat.
Previously, physicists have made ultracold molecules by convincing prechilled atoms to link up (SN: 12/20/08, p. 22), but the technique works for only a few kinds of molecules. Putting the freeze on already assembled molecules has allowed scientists to chill additional types but, until now, down to only a few hundreds of millionths of degrees.

Using lasers and magnetic fields, the scientists corralled and cooled molecules inside a device called a magneto-optical trap. In the trap, molecules of calcium monofluoride are slowed — and therefore cooled — when they absorb photons from a laser. But only so much cooling is possible with this method. To go beyond what’s called the Doppler limit, the researchers adapted a method used for cooling atoms, known as Sisyphus cooling. Two lasers pointed at one another create an electromagnetic field that acts like an endless hill the molecule must climb, thereby sapping its energy and heat. With these two techniques, the molecules reached a frigid 50 millionths of a degree above absolute zero.
As the art of laser cooling advanced in recent decades, ultracold atoms rapidly became a popular research topic. Now, predicts study coauthor Michael Tarbutt, a physicist at Imperial College London, cold molecule research is “going to explode in exactly the same way that it did for cold atoms.”
Cold molecules could be useful for a variety of scientific purposes: studying how chemical reactions occur, looking for hints of new fundamental particles or simulating complex quantum materials in which many particles interact at once.

“It’s a really exciting result,” says physicist David DeMille of Yale University, who was not involved with the research. “It turns out it’s harder in almost every way to apply laser cooling and trapping to molecules, but there are many, many motivations for doing that.”

Immune cells can turn certain invaders on themselves, forcing them to prematurely self-destruct, researchers have discovered.

In mice, when white blood cells in the lungs engulf spores of a common airborne fungus, these immune cells release an enzyme that sends the fungal cells into programmed cell death. That prevents the spores from setting up shop in the lungs and sparking a potentially deadly lung infection, the researchers report in the Sept. 8 Science.

Found naturally in soil and decaying organic matter, the fungus, Aspergillus fumigatus, releases airborne spores that are found in small doses in the air people breathe every day. The finding may help explain why most people can regularly inhale the spores and not get sick. In people with weakened immune systems, though, this natural defense system doesn’t work. This research could eventually lead to better treatments for these patients.
Programmed cell death is a natural part of a cell’s life cycle — a way for organisms to break down old cells and make way for new ones. “Research in the last couple of decades has shown that microbes can exploit [cell death] pathways to cause disease,” says study coauthor Tobias Hohl, an infectious disease researcher at Memorial Sloan Kettering Cancer Center in New York City. But this study shows that the tables can be turned. “Not only can microbes exploit this in hosts, but host cells can exploit these pathways to instruct certain microbes to kill themselves.”

“The idea that the host triggers the mechanism of [programmed cell death] as a way of defending against infection is very cool,” says Borna Mehrad, a pulmonologist at the University of Florida College of Medicine in Gainesville who wasn’t part of the study.

Hohl and colleagues identified a gene in A. fumigatus that puts the brakes on programmed cell death. The gene, AfBIR1, shares an ancestor with the human gene survivin, which also regulates cell death.

When the researchers amped up the activity of AfBIR1 in a strain of the fungus, half the mice infected with the spores died during the eight-day study period. (Mice infected with unmodified spores were fine.) Cues that would normally send fungal cells to their death didn’t register, so the fungus was able to grow in the mice’s lungs.

In another experiment, the scientists gave mice a drug called S12, which took away AfBIR1’s brake effect. As a result, the mice were able to fight off the infection. “Those two findings suggested to us that this fungal [cell death] pathway really is critical,” Hohl says.
Hohl did this research with a special variety of A. fumigatus that changes color when its suicide instructions kick in. That advance allowed the researchers to make observations that weren’t possible before, Mehrad says.

For instance, Hohl and his colleagues noticed that fungal cells being engulfed by neutrophils, a type of white blood cell, appeared to be undergoing programmed cell death. That suggested that neutrophil activity might set off fungal programmed cell death.

Neutrophils release an enzyme called NADPH oxidase, and mice deficient in the enzyme weren’t as good at fending off the fungus, Hohl found. That makes sense with clinical data in humans too. People with a genetic mutation that causes a deficiency in NADPH oxidase are particularly at risk for developing an Aspergillus infection, Hohl says. People who have fewer neutrophils, due to chemotherapy or HIV infection, for instance, also make less of the enzyme and are less able to resist a fungal infection.

Survival rates vary, but the U.S. Centers for Disease Control and Prevention estimates that 41 percent of organ transplant recipients who contract aspergillosis die within a year. Seventy-five percent of stem cell transplant recipients with the infection die in that same time frame. Someday, a version of S12 that’s modified to work in humans might be able to boost these patients’ defenses against A. fumigatus infections, Hohl suggests.

In the future, he wants to see whether the same mechanisms extend to other fungal species too.