Over a six-month period, scientists captured a bounty of 39 sets of gravitational waves. The waves, which stretch and squeeze the fabric of spacetime, were caused by violent events such as the melding of two black holes into one.
The bevy of data, which includes sightings from April to October 2019, suggests that scientists’ gravitational wave–spotting skills have leveled up. Before this round of searching, only 11 events had been detected in the years since the effort began in 2015. Improvements to the detectors — two that make up the Advanced Laser Interferometer Gravitational-Wave Observatory, or LIGO, in the United States, and another, Virgo, in Italy — have dramatically boosted the rate of gravitational wave sightings.
While colliding black holes produced most of the ripples, a few collisions seem to have involved neutron stars, ultradense nuggets of matter left behind when stars explode.
Some of the events added to the gravitational wave register had been previously reported individually, including the biggest black hole collision spotted so far (SN: 9/2/20) and a collision between a black hole and an object that couldn’t be identified as either a neutron star or black hole (SN: 6/23/20).
Gravitational waves are produced when two massive objects, such as black holes, spiral around one another and merge. These visualizations, which are based on computer simulations, show these merging objects for 38 of the 50 known gravitational wave events.
What’s more, some of the coalescing black holes seem to be very large and spinning rapidly, says astrophysicist Richard O’Shaughnessy of the Rochester Institute of Technology in New York, a member of the LIGO collaboration. That’s something “really compelling in the data now that we hadn’t seen before,” he says. Such information might help reveal the processes by which black holes get partnered up before they collide (SN: 6/19/16).
Scientists also used the smorgasbord of smashups to further check Albert Einstein’s theory of gravity, general relativity, which predicts the existence of gravitational waves. When tested with the new data — surprise, surprise — Einstein came up a winner.
It was one of those “big, if true” stories. In September, scientists reported that Venus’ atmosphere seems to be laced with phosphine, a possible sign of life.
Now there’s increasing emphasis on the “if.” As scientists take fresh looks at the data behind the Venus announcement, and add other datasets to the mix, the original claim of inexplicable amounts of phosphine is being called into doubt. And that’s a good thing, many scientists say.
“It’s exactly how science should work,” says planetary scientist Paul Byrne of North Carolina State University in Raleigh, who studies Venus but was not involved in any of the phosphine papers. “It’s too early to say one way or the other what this detection means for Venus.”
Here’s a closer look at efforts to get from “if” to “true:”
The big claim
On September 14, astronomer Jane Greaves of Cardiff University in Wales and colleagues reported that they had seen signs of phosphine in Venus’ clouds using two different telescopes (SN: 9/14/20). The phosphine seemed to be too abundant to exist without some kind of source replenishing it. That source could be strange microbes living in the clouds, or some weird unknown Venusian chemistry, the team said.
Greaves and colleagues first spotted phosphine with the James Clerk Maxwell Telescope in Hawaii and followed up with the powerful ALMA telescope array in Chile. But those ALMA data, and particularly the way they were handled, are now being called into question.
Reading the data: Real molecules or random wiggles?
The key Venus observations were spectra, or plots of the light coming from the planet in a range of wavelengths. Different molecules block or absorb light at specific wavelengths, so searching for dips in a spectrum can reveal the chemicals in a planet’s atmosphere.
Phosphine showed up as a dip in Venus’ spectrum at about 1.12 millimeters, a wavelength of light that the molecule was thought to be absorbing. If Venus’ spectrum could be drawn as a straight line across all wavelengths of light, phosphine would make a deep valley at that wavelength.
But real data are never that easy to read. In real life, other sources — from Earth’s atmosphere to the inner workings of the telescope itself — introduce wiggles, or “noise,” into that nice straight line. The bigger the wiggles, the less scientists believe that the dips represent interesting molecules. Any particular dip might instead be just a random, extra-large wiggle.
That problem gets even worse when looking at a bright object such as Venus with a powerful telescope like ALMA, says Martin Cordiner, an astrochemist at NASA’s Goddard Space Flight Center in Greenbelt, Md. Cordiner uses ALMA to observe other objects in the solar system, like Saturn’s moon Titan, but was not involved in the Venus work.
“The reason those bumps and wiggles are here at all is because of the intrinsic brightness of Venus, which makes it difficult to get a reliable measurement,” Cordiner says. “You could think of it as being dazzled by a bright light: If there’s a bright light in your vision, then your ability to pick out fainter details becomes diminished.”
So astronomers do a few different things to smooth out the data and let real signals shine through. One strategy is to write an equation that describes the wiggles caused by the noise. Scientists can then subtract that equation from the data to highlight the signal they’re interested in, like fuzzing out the background of a photo to let a portrait subject pop. That’s a standard practice, says Cordiner.
But it’s possible to write an equation that fits the noise too well. The simplest equation one could use is just a straight line, also known as a first-order polynomial, described by the equation y=mx+b. A second-order polynomial adds a term with x squared, third-order with x cubed, and so on.
Greaves and colleagues used a twelfth-order polynomial, or an equation with twelve terms (plus a constant, the +b in the equation), to describe the noise in their ALMA data.
“That was a red flag that this needed to be looked at in more detail, and that the results of that polynomial fitting could be untrustworthy,” says Cordiner. Going all the way out to the power of 12 could mean a researcher subtracts more noise than is truly random, allowing them to find things in the data that aren’t really there.
To see if the researchers were a little overzealous in their polynomial fitting, astrophysicist Ignas Snellen, of Leiden University in the Netherlands, and colleagues reapplied the same noise reduction recipe to the ALMA data on Venus and found no statistically significant sign of phosphine, they report in a paper posted at arXiv.org on October 19.
Then the researchers tried the same noise filtering on other parts of Venus’ spectrum, where no interesting molecules should be found. They found five different signals of molecules that aren’t really there.
“Our analysis … shows that at least a handful of spurious features can be obtained with their method, and therefore [we] conclude that the presented analysis does not provide a solid basis to infer the presence of [phosphine] in the Venus atmosphere,” the team wrote.
Looking for other data — and getting no help yet
Meanwhile, scientists at ALMA discovered a separate, unspecified issue in the data that were used to detect the phosphine and took those data off the observatory’s public archive to scrutinize and reprocess, according to a statement from the European Southern Observatory, of which ALMA is a part.
“This does not happen very often,” says Martin Zwaan of the ESO ALMA Regional Center in Garching, Germany, but this isn’t a first. When issues are discovered, it is standard practice to reprocess the data. “In many cases, it does not affect the science outcome significantly,” Zwaan says. “In the case of the phosphine on Venus, this [outcome] has not been established yet.”
What can scientists do while they wait? One of the best ways to confirm the phosphine is to see an equivalent signal at a different wavelength in Venus’ spectrum. Unfortunately, the news isn’t great there either. In a paper to appear in Astronomy & Astrophysics, astronomer Thérèse Encrenaz of the Paris Observatory and colleagues (including Greaves and some other authors of the original paper) looked at archived data from an infrared spectrograph called TEXES that operates in Hawaii. Those observations could have spotted phosphine in Venus’ cloud tops, a lower part of the sky than what ALMA could see.
Greaves and colleagues had approached Encrenaz to look for phosphine in infrared wavelengths before the original paper came out, but those observations were cancelled by the COVID-19 pandemic. So Encrenaz looked through data she had collected between 2012 and 2015 — and found nothing.
“At the level of the cloud tops, there is no [phosphine] at all,” Encrenaz says. That doesn’t necessarily mean there’s no phosphine higher up in the sky — there’s just no clear explanation for how it would get there. “The reasoning in the paper by Jane Greaves was that phosphine was coming from the clouds,” Encrenaz says. “So there is a big problem.”
‘This is just what science looks like.’
There are still ways for Venus’ phosphine to pull through. If it varies with time, for instance, it might be there some of the times that astronomers look and not at others. It’s too early to invoke that scenario, though, Cordiner says. “There’s no point of talking about the time variability of a signal if it isn’t there.”
But this is not a crisis, says Clara Sousa-Silva, an astrochemist at the Harvard-Smithsonian Center for Astrophysics in Cambridge, Mass., and a coauthor of the original paper. Other groups challenging the finding “is completely normal and what I expected (nay, hoped) would happen,” she wrote in an e-mail. “This is usually a phase of a project that I enjoy, and I am hoping people will realize this is just what science looks like.”
The silver lining in all of this is that it’s gotten people excited about Venus, says Byrne, who is a member of NASA’s Venus Exploration Analysis Group.
“These papers provide much value and a needed assessment of these extraordinary claims,” he says. “If nothing else, it has shone a light on just how little we understand about Venus. And the only way we get those answers is if we go to Venus.”
There’s nothing Winifred Frick likes better than crawling through guano-filled caves and coming face-to-face with bats. As chief scientist of Bat Conservation International, she is on a mission to promote understanding of bats and protect imperiled species from extinction.
For months, though, Frick has avoided research that would put her within spitting distance of bats. Her only projects to persist through the pandemic have been conducted from afar, like using acoustic monitors to eavesdrop on the animals’ squeaks and swooshes. In an era of COVID-19, that “hands-off” approach and other precautions are crucial to protect both bats and people, Frick, a biologist at the University of California, Santa Cruz, and over two dozen other scientists argue online September 3 in PLOS Pathogens.
Why the call to action? SARS-CoV-2, the virus that causes COVID-19, likely originated in bats in China (SN: 3/26/20). But neither it nor other coronaviruses belonging to the same genus — Betacoronavirus — have been detected in the more than 40 bat species in North America, although the animals do harbor other types of coronaviruses. Scientists are not worried about catching SARS-CoV-2 from these bats. They’re afraid of giving it to the bats — not an impossibility, the authors argue, given that the United States leads the world in infections, with nearly 8 million as of October 16.
“We can’t tell bats to socially distance,” Frick says. “We want to reduce the chance that there’s any pathogen transfer across animals, full stop.” The goal is to prevent viral “spillover.”
Biologist Winifred Frick advocates for distanced research methods and extra protective gear to safeguard North American bats from the coronavirus.Alan Hicks
Human-to-bat transmission isn’t an unheard-of scenario. People are likely to blame for introducing Pseudogymnoascus destructans, the fungus that causes white nose syndrome, to North American bats. The disease has killed millions of bats throughout the United States and Canada since it was first detected in 2006 (SN: 3/31/16).
It’s unknown if bats are susceptible to SARS-CoV-2 infection, or if the virus would make them sick — bats rarely become ill from the viruses they carry(SN: 2/12/20). But infected bats might spread the virus back to humans, the authors say.
Worse, introducing SARS-CoV-2 to other coronaviruses carried by North American bats could provide the ingredients for creating a new virus (SN: 11/30/17). Either scenario could stoke pre-existing fears about bats spreading disease, presenting a major hurdle for bat conservationists trying to bolster support for the animals.
The International Union for the Conservation of Nature’s bat specialist group, which includes Frick, initially advocated for the hands-off approach in April. Because so little was known in the early days of the pandemic about how SARS-CoV-2 spreads, that group recommended that researchers shut down any projects that involved interacting with bats. In August, the group updated its guidelines to also address spelunking and other activities that might bring humans into bat habitat.
The guidelines still recommend replacing fieldwork with distanced alternatives whenever possible. Picking through guano can identify bat species and reveal the viruses they carry, and cameras positioned outside bat caves and roosts can give a sense of abundance. Scientists can even resurrect evidence of pathogens held in the preserved tissues of bat specimens in museums.
But not all bat research can be socially distanced, and that means taking pandemic precautions, like ensuring field crews aren’t sick with COVID-19 and are wearing personal protective gear. White nose syndrome research already requires disposable Tyvek suits and gloves to reduce spreading the fungus. Now, masks will be a regular part of the ensemble.
For Frick, speaking up for bats has always been a part of being a bat biologist. Besides having a passion for the animals, conservation and human health are inseparable, she says. And bats provide ecosystem services that benefit humans, like pest control that saves North American farmers more than an estimated $3.7 billion per year, according to a study published in 2011 in Science. As human populations expand into shrinking bat habitat, bats and humans increasingly cross paths, making viral spillover events and other harmful interactions more likely. The pandemic has intensified those risks, and for Frick, put the need to speak up “on steroids now.”
Japan’s white-spotted pufferfish are renowned for producing complex, ringed patterns in the sand. Now, 5,500 kilometers away in Australia, scientists have discovered what appear to be dozens more of these creations.
While conducting a marine life survey out on Australia’s North West Shelf near subsea gas infrastructure with an autonomous underwater vehicle, marine ecologist Todd Bond spotted a striking pattern on the seafloor, more than 100 meters deep. “Immediately, I knew what it was,” recounts Bond, of the University of Western Australia in Perth. Bond and his colleagues continued the survey, ultimately finding nearly two dozen more.
Until now, these undersea “crop circles” were found only off the coast of Japan. First spotted in the 1990s, it took two decades to solve the mystery of what created them. In 2011, scientists found the sculptors — the diminutive males of what was then a new species of Torquigener pufferfish. The patterns are nests, meticulously plowed over the course of days and decorated with shells to entice females to lay their eggs in the center.
A hovering autonomous underwater vehicle (HAUV) deployed along subsea natural gas infrastructure off Australia’s coast in September 2018 captured footage of something surprising: a rippled ring carved into the sand. Researchers eventually discovered nearly two dozen of these circles, similar to the elaborate nests crafted by white-spotted pufferfish males near Japan, making it the first such find outside Japan. While it’s not known what species created the Australian rings, an unidentified pufferfish was seen fleeing the site of one of them.
While there’s no video confirmation that pufferfish are building the nests in Australia, the structures are nearly identical to those in Japan, even sharing a similar number of ridges, Bond and his colleagues report in the November 2020 Journal of Fish Biology. And when a colleague deployed an underwater video system in the area, the contraption luckily landed almost directly atop a circle and captured footage of a small pufferfish fleeing the formation.
The Australian circles lie in much deeper waters than Japan’s — 130 meters or more deep compared with about 30 meters deep in Japan. Australian pufferfish known in the area typically inhabit more shallow waters, raising questions about the identity of the species responsible.
Bond says the images captured of the likely piscean culprit are too poor to make a definitive identification. The circles could have been made by the same species that builds Japan’s nests, the white-spotted pufferfish (Torquigener albomaculosus), or the culprit could be a different, local species — possibly one totally new to science.
“It is surprising to find the circles … at a depth where there is not much light,” says Elisabet Forsgren, a behavioral ecologist at the Norwegian Institute for Nature Research in Trondheim. If the nests are meant to be a visual signal to attract females, they may be hard to see in such a dim spot.
Bond says that the discovery raises more questions that may ultimately help us understand the evolution of pufferfishes, a group already awash in eccentricities. Not only are they among the most toxic vertebrates on Earth, but they’ve completely lost their ribs and pelvic bones to make room when they “puff” with water (SN: 8/1/19). Among the questions: If the Australian circles are made by a different species from Japan’s, did the two fishes’ artistic skills evolve separately?
“It’s kind of humbling to know that there’s so much out there that we don’t know,” says Bond. “It’s also a little bit scary as well. This is a reflection of, obviously, a key part to the reproduction of maybe a new species, but we just know nothing about it. We didn’t even know these existed.”
Neurobiologist Kenneth Catania’s passion for scrutinizing odd animal adaptations all started with a creature with a 22-point star on its face.
Catania first saw a star-nosed mole (Condylura cristata) in a children’s book. Later as a 10-year-old, he found a dead one near a stream close to his home in Columbia, Md. From then on, he kept his eyes peeled for more. He had to wait until he was in college, when he landed a research position that required him to trap star-nosed moles in Pennsylvania’s wetlands. At the time, no one knew what that unique nose was good for, and he wanted to figure it out.
In Great Adaptations, Catania describes his pursuit of the mystery behind the mole’s wiggly star-shaped appendage (it helps the subterranean animal sense prey without using sight) as well as a slew of other animal tricks. The account of his adventures as a biological sleuth provides a detailed look at curiosities such as how “hangry” water shrews execute the fastest documented predatory attack by a mammal and how cockroaches resist becoming zombies during parasitoid wasp attacks (SN: 10/31/18).
“It’s part of human nature to be intrigued by mysteries, but the mystery only gets us to the door,” he writes. “You never know what you might find on the other side.”
In search of answers, Catania has set up some odd, but amusing, experiments. To film wasps attacking cockroaches, he built a set fit for a horror flick, by filling a tiny kitchen with warning signs and a plastic human skull for the wasp to store its zombified victim in. Keeping with the horror theme, he also stripped the paint off decorative severed zombie arms and offered the plastic limbs to electric eels (Electrophoruselectricus) to show that the animals leap out of the water as an attack strategy (SN: 6/9/16).
Each chapter follows a logical flow as Catania describes his discoveries, from what first piqued his interest in an animal to his ultimate findings. Science, however, is rarely as straightforward as he makes it seem. Catania’s scientific detective work didn’t always go off without a hitch, but, he notes, including all the failures would have meant a much longer book. Even so, the book alludes to some ideas that didn’t pan out. “The animals are always able to do something unexpected and more interesting than I’d imagined,” he writes.
For instance, the notion that a tentacled snake (Erpeton tentaculatum) might use the short appendages close to itsmouth to lure in nearby fish, just like snapping turtles dowith their tongues, turned out to be wrong. Instead, the tentacleshelp a snake sense a fish’s position in the water andknow when to attack. What’s more, the snakes have hackedtheir prey’s natural escape reflexes. In a fatal mistake, fishflee in the wrong direction — straight toward a snake’smouth — when duped by a twitch of the snake’s neck rightbefore the predator strikes.
Catania’s lighthearted yet informative narrative presents science in a way that’s easy for anyone with a basic knowledge of biology to understand. But even the most seasoned expert will likely learn new details, the type that never make it into a scientific paper. For a particularly daring experiment, in which Catania offered his own arm for an electric eel’s shock to measure the shock’s electricity, Catania admits that he certainly couldn’t subject another animal or a student volunteer to the unpleasant jolt (SN: 9/14/17). His own arm was the “obvious solution.”
In page after page, Catania’s enthusiasm and awe for the animals shine through. When he discovered tentacled snakes are born knowing how to strike at prey rather than learning through failure, Catania recalls that he couldn’t “find enough superlatives to sum up these results.” He also describes a fight between a parasitoid wasp and a cockroach as an “insect rodeo.” The wasp attacks a cockroach’s head in an attempt to lay an egg, but in defense the roach “bucks, jumps, and flails with all its might.”
Some of that enthusiasm will likely rub off on readers and spark a sense of wonder. Great Adaptations packs in plenty of astounding details about some remarkable creatures. As Catania puts it: “I’ve stopped assuming I know the limits of animal abilities.”
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Sound has a speed limit. Under normal circumstances, its waves can travel no faster than about 36 kilometers per second, physicists propose October 9 in Science Advances.
Sound zips along at different rates in different materials — moving faster in water than in air for example. But under conditions found naturally on Earth, no material can host sound waves that outpace this ultimate limit, which is about 100 times the typical seed of sound traveling in air.
The team’s reasoning rests on well-known equations of physics and mathematical relationships. “Given the simplicity of the argument, it suggests that [the researchers] are putting their finger on something very deep,” says condensed matter physicist Kamran Behnia of École Supérieure de Physique et de Chimie Industrielles in Paris.
The equation for the speed limit rests on fundamental constants, special numbers that rule the cosmos. One such number, the speed of light, sets the universe’s ultimate speed limit — nothing can go faster. Another, known as the fine-structure constant, determines the strength with which electrically charged particles push and pull one another. When combined in the right arrangement with another constant — the ratio of the masses of the proton and electron — these numbers yield sound’s speed limit.
Sound waves, which consist of the vibrations of atoms or molecules, travel through a material as one particle jostles another. The wave’s speed depends on various factors, including the types of chemical bonds holding the material together and how massive its atoms are.
None of the sound speeds previously measured in a variety of liquids and solids surpass the proposed limit, condensed matter physicist Kostya Trachenko and colleagues found. The fastest speed measured, in diamond, was only about half the theoretical maximum.
The limit applies only to solids and liquids at pressures typically found on Earth. At pressures millions of times that of Earth’s atmosphere, sound waves move faster and could surpass the limit.
One material expected to boast a high sound speed exists only at such high pressures: hydrogen squeezed hard enough to turn into a solid metal (SN: 6/28/19). That metal has never been convincingly created, so the researchers calculated the expected speed instead of using a measurement. Above about 6 million times Earth’s atmospheric pressure, the sound speed limit would be broken, the calculations suggest.
The role of the fundamental constants in sound’s maximum speed results from how the waves move through materials. Sound travels thanks to the electromagnetic interactions of neighboring atoms’ electrons, which is where the fine-structure constant comes into play. And the proton-electron mass ratio is important because, although the electrons are interacting, the nuclei of the atoms move as a result.
The fine-structure constant and the proton-electron mass ratio are dimensionless constants, meaning there are no units attached to them (so their value does not depend on any particular system of units). Such dimensionless constants fascinate physicists, because the values are crucial to the existence of the universe as we know it (SN: 11/2/16). For example, if the fine-structure constant were significantly altered, stars, planets and life couldn’t have formed. But no one can explain why these all-important numbers have the values they do.
“When I have sleepless nights, I sometimes think about this,” says Trachenko, of Queen Mary University of London. So he and colleagues are extending this puzzle from the cosmic realm to more commonplace concepts like the speed of sound. Trachenko and coauthor Vadim Veniaminovich Brazhkin of the Institute for High Pressure Physics, in Troitsk, Russia, also reported a minimum possible viscosity for liquids in the April 24 Science Advances.
That viscosity limit depends on the Planck constant, a number at the heart of quantum mechanics, the math that governs physics on very small scales. If the Planck constant were 100 times larger, Trachenko says, “water would be like honey, and that probably would be the end of life because the processes in cells would not flow as efficiently.”
Turning a bacterial defense mechanism into one of the most powerful tools in genetics has earned Jennifer Doudna and Emmanuelle Charpentier the Nobel Prize in chemistry.
The award for these genetic scissors, called CRISPR/Cas 9, is “a fantastic prize,” Pernilla Wittung-Stafshede, a member of the Nobel Committee for Chemistry, said at an Oct. 7 news conference held in Stockholm by the Royal Swedish Academy of Sciences to announce the prize. “The ability to cut the DNA where you want has revolutionized the life sciences. We can now easily edit genomes as desired — something that before was hard, or even impossible.”
“The genetic scissors were discovered just eight years ago, but have already benefited humankind greatly,” she said. “Only imagination sets the limits for what this chemical tool … can be used for in the future. Perhaps the dream of curing genetic diseases will come true.” She later amended the statement to say that ethics and law are also important to determine what can and should be done with the tool, as some human gene editing is extremely controversial.
Only five other women have ever won the Nobel Prize in chemistry. “I wish that this would provide a positive message specifically to the young … girls who would like to follow the path of science, and I think to show them that women in science can also be awarded prizes, but more importantly that women in science can also have an impact through the research that they are performing,” Charpentier said in response to a question during the news conference.
The two will split prize money of 10 million Swedish kronor, about $1.1 million.
The tool, a programmable molecular scissors known as CRISPR/Cas9, has been used by bacteria and archaea for millions to billions of years to fight viruses (SN: 4/5/17).
CRISPR stands for Clustered Regularly Interspaced Short Palindromic Repeats. In essence, these short, repeating bits of DNA sandwich bacteria’s version of the FBI’s most wanted list — invading viruses. Every time bacteria encounter a virus, they take a DNA mugshot of it and file it in between the repeats. The next time the bacteria encounters that virus, they make RNA copies of the mugshots. Those RNA photocopies then team up with another bit of RNA known as a trans-activating CRISPR RNA, or tracrRNA, to form an all-points bulletin known as a guide RNA. Guide RNAs shepherd the DNA-cutting enzyme Cas9 to the virus, where the enzyme chops and eliminates the threat.
Doudna of the University of California, Berkeley, and Charpentier, now director of the Max Planck Institute for Infection Biology in Berlin, turned CRISPR/Cas9 from a bacterial defense system into a gene editor. Their innovation was to fuse the mug shot RNA to the tracrRNA, creating a single guide RNA. And the researchers realized that the mugshots didn’t have to be molecular pictures of viruses. Instead, by replacing the mugshot with RNA that matches a gene, the scientists could direct Cas9 to snip that gene — or any gene, really.
These researchers and other scientists have taken these genetic scissors to the next step, using CRISPR/Cas9 to cut and edit genes in human cells. Scientists rave about how cheap, versatile and easy to use CRISPR is. Researchers have used it edit genes in a wide variety of animals, including dogs (SN: 8/30/18), mice (SN: 1/26/17), butterflies (SN: 8/24/16), cows (SN: 2/3/17), pigs (SN: 8/10/17), snails (SN: 5/14/19) and mosquitoes.
With CRISPR’s great power comes great controversy, Doudna warned in her 2017 book A Crack in Creation with coauthor Samuel Sternberg. While the gene editor might be used to stamp out invasive species and prevent mosquitoes from carrying disease, it might also drive entire species extinct or create ecological disasters. Already scientists have wiped out small populations of mosquitoes in the laboratory using a CRISPR-based molecular copy machine known as a gene drive (SN: 9/24/18).
Most controversially, a scientist in China edited genes in human embryos, producing twin baby girls in 2018 (SN: 11/28/18). Backlash against his actions was swift and vocal. But many people fear the door is already open to “designer babies,” health care inequalities and other abuses (SN: 12/17/18).
“This enormous power of this technology means that we need to use it with great care,” Claes Gustafsson, chair of the Nobel Committee for Chemistry, said at the news conference. “But it’s equally clear that this is a technology… that will provide humankind with great opportunities.”
More hopefully, clinical trials testing CRISPR/Cas9’s ability to treat cancer, sickle cell disease, beta-thalassemia and inherited blindness began in 2019 (SN: 8/14/19). If successful, CRISPR/Cas9 may provide therapies, or even cures, for previously untreatable genetic conditions.
CRISPR has also played a role in the coronavirus pandemic, with CRISPR-based diagnostic tests for COVID-19 (SN: 8/31/20) and therapies in development.
Nearly all scientific prizes for CRISPR/Cas9 have honored Doudna and Charpentier. Some prizes have also included Feng Zhang of the Broad Institute of MIT and Harvard, who holds the patent on using the gene editor to make changes in eukaryotic cells, including human and animal cells. Many people thought that the prize would not honor work on CRISPR until the patent dispute was settled. (Zhang is a member of the board of trustees for the Society for Science & the Public, an educational nonprofit in Washington, D.C., that also publishes Science News. He is also an alumnus of the Society’s Regeneron Science Talent Search.)
Two other scientists, Rodolphe Barrangou of North Carolina State University in Raleigh and Philippe Horvath of DuPont Nutrition & Biosciences in Dangé-Saint-Romain, France, have also been honored for discoveries related to CRISPR. The duo discovered CRISPR’s natural role as a bacterial immune system while working with yogurt bacteria at the food ingredient company Danisco.
And two major prizes — the Warren Alpert Foundation prize and the Kavli prize for neuroscience — have honored Virginijus Šikšnys, a biochemist at Vilnius University in Lithuania. Šikšnys authored an independent paper describing the same innovation made by Doudna and Charpentier that was held up in the publishing process, and didn’t hit presses until three months after the UC Berkeley team’s report.
When asked if other scientists had been considered for the prize, Gustaffson said, “this is a question we never answer. We are just extremely happy for this year’s laureates. It’s a big field, and there’s a lot of good science being done.”
Staff writer Maria Temming contributed to this story.
Attacked from behind and at times dismembered, the fallen residents of an ancient Iberian village add to evidence that prehistoric Europe was a violent place.
Finding “partially burnt skeletons and scattered human bones with unhealed injuries caused by sharp weapons demonstrated that this was an extremely violent event,” says archaeologist Javier Ordoño Daubagna of Arkikus, an archaeological research company in Vitoria-Gasteiz, Spain.
Ordoño Daubagna and colleagues examined nine adults, two adolescents, a young child and one infant who died sometime between 365 and 195 B.C., in the ancient village of La Hoya. One of the adults was decapitated in a single blow, the team found. And one of the adolescents, a female, had her arm cut off. The researchers found the arm bones nearly three meters away from the girl’s skeleton, with five copper-alloy bracelets still attached.
Cracks and flaking of the outer layers of some of the bones suggest that the victims were abandoned after they died, rather than buried, the report shows. Other people may have been trapped inside burning buildings — bone shrinkage and discoloration suggest that the remains were in a fire that reached 350° to 650° Celsius. The fact that the bones were only partially burned suggest that they were not scorched during cremation, a common ritual at the time, the researchers say.
“The nature of the injuries, the presence of women and young children as victims and the context of where the human remains were found on the site all indicated that this was not a battle between anything like matched forces,” says coauthor Rick Schulting, an archaeologist at the University of Oxford. “This was not a battle between noble warriors.”
The study supports the idea that Iron Age societies on the Iberian Peninsula were fully capable of resorting to brutal violence as a means of settling disputes, the researchers argue. “We can conclude that the aim of the attackers was the total destruction of La Hoya, perhaps by a rival center for political and economic dominance in the area,” Ordoño Daubagna says.
In-depth accounts of similar attacks during the pre-Roman Iron Age are rare, but this sort of violence may have been more common than scientists have realized. During that time, “power was gained by violence and control over resources,” explains Ludvig Papmehl-Dufay, an archaeologist at Linnaeus University in Kalmar, Sweden, who wasn’t involved in the study. If people think of the past as something peaceful and idealized, he says, “that needs to be revised.”
In the four days since revealing he had COVID-19, President Donald Trump has been treated with three experimental drugs to bring the infection under control: monoclonal antibodies, the antiviral remdesivir and the steroid dexamethasone.
Individually, all three treatments have shown promising results in clinical trials. The U.S. Food and Drug Administration has issued emergency use authorization to give remdesivir to patients ill enough to require hospitalization. Several large studies have shown steroids can reduce the risk of death in critically ill patients. And biotechnology company Regeneron Pharmaceuticals just released preliminary antibody results on September 29 from an early-stage clinical trial with 275 COVID-19 patients suggesting a high-dose cocktail of lab-made immune proteins can help speed recovery.
But it’s unclear how the drugs might work when used together to treat patients, says Rajesh Gandhi, an infectious diseases physician at Massachusetts General Hospital and Harvard Medical School in Boston.
Here’s what we know so far about the treatments used to treat the president.
How do the treatments work?
In a news release on October 2, the White House announced that Trump had received a single dose of Regeneron’s antibody cocktail shortly after his diagnosis. (Regeneron, in Tarrytown, N.Y, is a major financial supporter of Society for Science & the Public, which publishes Science News.)
That cocktail includes a pair of monoclonal antibodies that each target a different part of the coronavirus’s spike protein. The virus uses the spike protein to pick a cellular lock, called ACE2, to break into cells and begin replicating. By binding to the spike, antibodies can neutralize the virus and curb the infection. Such monoclonal antibodies have been tested early in infection, in people who are not severely ill with COVID-19.
Later that day, physicians moved Trump to Walter Reed National Military Medical Center in Bethesda, Md., where he began a five-day course of remdesivir, a drug developed by biopharmaceutical company Gilead Sciences, which is based in Foster City, Calif. Remdesivir, which is given intravenously, mimics a building block of the coronavirus’s genetic material. It tricks the virus into incorporating the faux compound into the virus’s genetic blueprint, instead of incorporating a real building block, bringing viral replication to a halt.
Then, on October 3, the president also received dexamethasone, his medical team said in a news conference on October 4. The steroid, administered through a muscle injection or intravenously, is typically reserved for patients who require supplemental oxygen or are on a ventilator. The drug suppresses inflammation, an immune response that is behind some severe COVID-19 cases.
What do the data say so far about these drugs?
Some monoclonal antibodies, such as those from Indianapolis-based pharmaceutical company Eli Lilly and Regeneron have shown early hints of success, although the results are still preliminary (SN 9/22/20). The treatments appear to reduce levels of the virus in the body.
Such antibodies are likely best used early on, while the virus is still replicating in a patient’s body, Gandhi says.
Later during disease, viral replication wanes but severely ill patients may have massive amounts of inflammation from an overactive immune response. Without lots of virus circulating in the body, antibodies that dampen viral growth are less effective at making patients better.
So far, studies suggest that remdesivir and dexamethasone can help people who end up in the hospital, Gandhi says. Remdesivir may be best used early, before patients require hospital care, but it hasn’t yet been tested in mildly ill patients. The company is working on developing an inhaled version that could be administered earlier in an infection outside of a hospital setting.
Remdesivir was the first drug shown to curb viral replication and potentially speed recovery in hospitalized COVID-19 patients (SN: 4/29/20). Dexamethasone has been used for decades to treat a variety of ailments and was the first drug shown to reduce COVID-19 deaths among people who need supplemental oxygen (SN: 6/16/20). In September, the World Health Organization confirmed that steroids are beneficial for COVID-19 patients — specifically those who were severely or critically ill (SN: 9/2/20).
The WHO and U.S. National Institutes of Health do not recommend steroid use in people who are less sick, as the drugs can suppress their immune system’s response to the coronavirus and might make the disease worse, says Gandhi, who has helped write COVID-19 treatment guidelines for NIH as well as the Infectious Diseases Society of America.
Trump received remdesivir and dexamethasone within a day or two, respectively, of his diagnosis. Such treatment may be a sign that Trump’s condition is more severe than reported, or it could be a preemptive measure to ensure his symptoms don’t become severe. Initially, his symptoms were described as mild, but his physicians have said that since his diagnosis, Trump had a high fever and has received supplemental oxygen when his blood oxygen level dipped.
What we know about how the drugs might work when combined?
“We don’t yet know how they work together,” Gandhi says.
Researchers have made strides in uncovering potential treatments, and trials for a wide variety of drugs are ongoing. But, so far, the use of remdesivir, monoclonal antibodies and dexamethasone in combination hasn’t been studied. Some efforts are under way to find answers. Participants in the treatment arm of one clinical trial for a monoclonal antibody, for instance, are receiving both the antibody and remdesivir to compare their use together with remdesivir alone.
“There are theoretical reasons to think that it would make sense to combine them,” Gandhi says. For instance, an antiviral drug like remdesivir should “shut down virus replication and then dexamethasone would mop up the inflammation.”
Inflammation is part of the body’s natural response to viral infection and normal levels help clear the virus from the body. If a patient is suffering from high amounts of inflammation and requires steroid treatments to suppress the response, it might be beneficial to have an antiviral on hand to help snuff out the infection.
Because antivirals target the virus while the steroids dampen a potentially harmful immune response, such combination therapies shouldn’t overstimulate a patient’s immune system, he says. It’s unknown whether using the drugs together might help or hinder their effectiveness.
“Sometimes we in medicine end up making decisions without perfect data,” Gandhi says. “Unfortunately, that’s the situation [in a pandemic], and then we use our best judgment.”
That judgment is under a bright spotlight thanks to Trump’s high profile. Saying that Trump “may not be entirely out of the woods yet,” White House physician Sean Conley on October 5 reported in a news conference that the president’s condition had improved enough that he was cleared to leave the hospital and return to the White House. “If we can get through [another week] to Monday with him remaining the same — or improving, better yet — then we will all take the final deep sigh of relief.”
