While searching for shipwreck remains near Oman in the Arabian Sea in 2014, divers discovered an unusual metal disk that has since proven to be the world’s oldest known mariner’s astrolabe, British researchers report.
The navigational device came from the wreckage of a ship in the Portuguese armada that had been part of explorer Vasco da Gama’s second voyage to India from 1502 to 1503. Historical decorations on the artifact led the researchers to suggest that the disk was used as early as 1496. A bit wider than a dollar bill, the astrolabe contains carvings of Portugal’s royal coat of arms and a depiction of a ringed Earth that was associated with a Portuguese king who ruled from late 1495 to 1521. Laser imaging of the disk revealed 18 scale marks separated at 5-degree intervals.
The device, used to take altitudes at sea, could have measured from 0 degrees — when the sun is at the horizon — to 90 degrees — when the sun is directly overhead, the team reports in a study published online March 16 in the International Journal of Nautical Archaeology. Only one other solid disk, mariner’s astrolabe has been found, and its authenticity and age are uncertain, say oceanographer David Mearns and colleagues. Mearns directs Blue Water Recoveries in Midhurst, England, a company that locates and studies shipwrecks.
Of 104 artifacts known to have been used as mariner’s astrolabes, the new find is not only the oldest, but also the only one decorated with a national symbol, the researchers say. By the early 1500s, most navigators had adopted more precise, open-wheeled astrolabes.
Since people in the United States began dying in the fentanyl-related drug overdose epidemic, whites have been hit the hardest. But new data released March 21 by the Centers for Disease Control and Prevention show that African-Americans and Hispanics are catching up.
Non-Hispanic whites still experience the majority of deaths involving fentanyl, a synthetic opioid. But among African-Americans and Hispanics, death rates rose faster from 2011 to 2016. Whites experienced a 61 percent annual increase, on average, while the rate rose 140.6 percent annually for blacks and 118.3 percent per year for Hispanics. No reliable data were available for other racial groups. Overall, the number of U.S. fentanyl-related deaths in 2011 and 2012 hovered just above 1,600. A sharp increase began in 2013, reaching 18,335 deaths in 2016. That’s up from 0.5 deaths per 100,000 people in 2011 to 5.9 per 100,000 in 2016.
In the first three years of the data, men and women died from fentanyl-related overdoses at similar rates, around 0.5 per 100,000. But in 2013, those paths diverged, and by 2016, the death rate among men was 8.6 per 100,000; for women it was 3.1 per 100,000. Overdose death rates rose most sharply along the East Coast, including in New England and the middle Atlantic, and in the Great Lakes region.
One of the most powerful opioids, fentanyl has been around for decades and is still prescribed to fight pain. But it has emerged as a street drug that is cheap to make and is found mixed into other drugs. In 2013, fentanyl was the ninth most common drug involved in overdose deaths, according to the CDC report; in 2016, it was number one. Just a little bit can do a lot of damage: The drug can quickly kill a person by overwhelming several systems in the body (SN: 9/3/2016, p. 14).
Viruses, which cannot reproduce on their own, infect cells and usurp their genetic machinery for use in making new viruses…. But just how viruses use the cell machinery is unknown.… Some answers may come from work with an unusual virus, called M13, that has a particularly compatible relationship with … [E. coli] bacteria. — Science News, April 5, 1969
Update M13 did help unlock secrets of viral replication. Some bacteria-infecting viruses, called bacteriophages or simply phages, kill the host cell after hijacking the cell’s machinery to make copies of themselves. Other phages, including M13, leave the cell intact. Scientists are using phage replication to develop drugs and technologies, such as virus-powered batteries (SN: 4/25/09, p. 12). Adding genetic instructions to phage DNA for making certain molecules lets some phages produce antibodies against diseases such as lupus and cancer. The technique, called phage display, garnered an American-British duo the 2018 Nobel Prize in chemistry (SN: 10/27/18, p. 16).
There are no teensy cups. But a urine test for wild mosquitoes has for the first time proved it can give an early warning that local pests are spreading diseases.
Mosquito traps remodeled with a pee-collecting card picked up telltale genetic traces of West Nile and two other worrisome viruses circulating in the wild, researchers in Australia report April 4 in the Journal of Medical Entomology.
The tests were based on an innovative saliva monitoring system unveiled in 2010: traps that lure mosquitoes into tasting honey-coated cards. Among its advantages, this card-based medical testing doesn’t need the constant refrigeration that checking whole mosquitoes does. And it’s not as labor intensive as monitoring sentinel chickens or pigs for signs of infection. But testing traces of mosquito saliva left on these cards comes close to the limits of current molecular methods for detecting viruses. In part, it’s an issue of volume. A mosquito drools fewer than five nanoliters of saliva when it tastes a card. In comparison, mosquitoes excrete about 1.5 microliters of liquid per pee, offering a veritable flood of material. So Dagmar Meyer of James Cook University in Cairns, Australia and her colleagues created urine collectors using standard overnight light traps and longer-standing traps that exhale delicious carbon dioxide, a mosquito come-hither.
The team set out 29 urine traps in two insect-rich spots in Queensland along with traps equipped to catch mosquito saliva. When mosquitoes fell for the trick and entered a urine trap, their excretions dripped through a mesh floor onto a collecting card. Adding a moist wick of water kept trapped mosquitoes alive and peeing longer, thus improving the sample. Pee traps picked up three viruses — West Nile, Ross River and Murray Valley encephalitis — while the saliva ones detected two, the researchers report.
My youngest child, now just over a year old, has started to talk. Even though I’ve experienced this process with my older two, it’s absolutely thrilling. He is putting words to the thoughts that swirl around in his sweet little head, making his mind a little less mysterious to the rest of us.
But these early words may not mean what we think they mean, a new study hints. Unsurprisingly, when 2-year-olds were asked a series of “this or that” questions, the toddlers showed strong preferences — but not for the reasons you’d think. Overwhelmingly, the toddlers answered the questions with the last choice given. That bias, described in PLOS ONE on June 12, suggests that young children’s answers to these sorts of questions don’t actually reflect their desires. Instead, kids may simply be echoing the last thing they heard.
This verbal quirk can be used by parents to great effect, as the researchers point out in the title of their paper: “Cake or broccoli?” More fundamentally, the results raise questions about what sort of information a verbal answer actually pulls out of a young child’s mind. This murkiness is especially troublesome when it comes to questions whose answers call for adult action, such as: “Did you hit your sister on purpose or on accident?”
In the first series of experiments, researchers led by Emily Sumner at the University of California, Irvine, asked 24 1- and 2-year-olds a bunch of two-choice questions, some of which involved a polar bear named Rori or a grizzly bear named Quinn. One question, for example, was, “Does Rori live in an igloo or a tepee?” Later, the researchers switched the bear and the order of the options, asking, for example, “Does Quinn live in a tepee or an igloo?”
The toddlers could answer either verbally or, for reluctant speakers, by pointing at one of two stickers that showed the choices. When the children answered the questions by pointing, they chose the second option about half the time, right around chance. But when the toddlers spoke their answers, they chose the second option 85 percent of the time, regardless of the bear. SECOND BEST A toddler taking part in a study selects the second option in three either-or questions. This tendency, called the recency bias, may reflect kids’ inability to juggle several choices in their minds simultaneously. Credit: E. Sumner et al/PLOS ONE 2019
This abundance of second options selected — a habit known as the recency bias — might be due to the fact that young children have trouble holding the first option in mind, the researchers suspect. Other experiments showed that children’s tendency toward the second option got stronger when the words got longer.
Adults actually have the opposite tendency: We’re more inclined to choose the first option we’re given (the primacy bias). To see when this shift from last to first occurs, the researchers studied transcripts of conversations held between adults and children ages 1.5 to 4. In these natural conversations, 2-year-olds were more likely to choose the second option. But 3- and 4-year-olds didn’t show this bias, suggesting that the window closes around then.
The results hold a multitude of delightful parenting hacks: “Would you like to jump on the bed all night, or go to sleep?” But more importantly, the study serves as a reminder that the utterances of small children, while fascinating, may not carry the same meanings as those that come from more mature speakers. If you really want a straight answer, consider showing the two options to the toddler. But if you go that route, be prepared to hand over the cake.
No one should have to sleep with the fishes, but new research on zebrafish suggests that we sleep like them.
Sleeping zebrafish have brain activity similar to both deep slow-wave sleep and rapid eye movement, or REM, sleep that’s found in mammals, researchers report July 10 in Nature. And the team may have tracked down the cells that kick off REM sleep.
The findings suggest that the basics of sleep evolved at least 450 million years ago in zebrafish ancestors, before the evolution of animals that give birth to live young instead of laying eggs. That’s 150 million years earlier than scientists thought when they discovered that lizards sleep like mammals and birds (SN: 5/28/16, p. 9).
What’s more, sleep may have evolved underwater, says Louis C. Leung, a neuroscientist at Stanford University School of Medicine. “These signatures [of sleep] really have important functions — even though we may not know what they are — that have survived hundreds of millions of years of evolution.” In mammals, birds and lizards, sleep has several stages characterized by specific electrical signals. During slow-wave sleep, the brain is mostly quiet except for synchronized waves of electrical activity. The heart rate decreases and muscles relax. During REM or paradoxical sleep, the brain lights up with activity almost like it’s awake. But the muscles are paralyzed (except for rapid twitching of the eyes) and the heart beats erratically.
For many years, scientists have known that fruit flies, nematodes, fish, octopuses and other creatures have rest periods reminiscent of sleep. But until now, no one could measure the electrical activity of those animals’ brains to see if that rest is the same as mammals’ snoozing.
Leung and colleagues developed a system to do just that in zebrafish by genetically engineering them to make a fluorescent molecule that lights up when it encounters calcium, which is released when nerve cells and muscles are active. By following the flashes of light using a light sheet microscope, the researchers tracked brain and muscle activity in the naturally transparent fish larvae.
The next task was to lull fish asleep under the microscope. In some experiments, the team added drugs that trigger either slow-wave or REM sleep in mammals to the fish’s water. In others, researchers deprived fish of sleep for a night or tuckered the fish out with lots of activity during the day. Results from all the snooze-inducing methods were the same.
Sleeping fish have two distinct types of brain activity while sleeping, the team found. One, similar to slow-wave sleep, was characterized by short bursts of activity in some nerve cells in the brain. The researchers call that state slow-bursting sleep. REM-like sleep, which the researchers dubbed “propagating-wave sleep,” was characterized by frenzied brain activity that spreads like a wave through the brain. The researchers aren’t calling the sleep phases REM or slow-wave sleep because there are some minor differences between the way fish and mammals sleep. A group of cells that line hollow spaces called ventricles deep in the brain seems to trigger that wave of REM-like brain activity. These ependymal cells dip fingerlike cilia into the cerebral spinal fluid that bathes the ventricles and the central nervous system. The cells appear to beat their cilia faster as amounts of a well-known, sleep-promoting hormone called melanin-concentrating hormone in the fluid increases, the researchers discovered. It’s unclear how the ependymal cells communicate with the rest of the brain to set off REM-like activity. Such cells are also present in mammals, but no one has yet been able to see that deeply into the brains of sleeping mammals to determine whether the cells play a role in sleep. But knowing about these cells may help researchers develop better sleep aids, Leung says.
Just as in mammals, zebrafish’s whole bodies are affected during sleep. Their muscles relax during sleep and their hearts slow from about 200 beats per minute when awake to about 110 to 120 beats per minute while asleep during the slow-wave–like sleep. During the REM-like sleep, the heart slows even more to about 90 beats per minute and loses its regular rhythm. And the fish’s muscles also go completely slack. The one characteristic that the fish lack is rapid eye movement. Instead, the eyes roll back into their sockets, says study coauthor Philippe Mourrain, a biologist at Stanford University School of Medicine.
Lack of eye movement could indicate that emotion-processing parts of the brain, such as the amygdala, aren’t as active in zebrafish as they are in mammals, says sleep researcher Allan Pack of the University of Pennsylvania Perelman School of Medicine. With their brain-activity monitoring, the researchers have taken sleep research “to the next level,” says Pack, and “they present pretty compelling evidence” of slow-wave and REM-like sleep in the fish.
The whole-body involvement that the researchers documented solidifies the argument that fish sleep is similar to mammals, says neuroscientist Paul Shaw of Washington University School of Medicine in St. Louis. In all organisms known to snooze, “sleep is manifest everywhere” in the body, he says.
Future experiments may show why poor sleep or a lack of Zs contributes to health problems in people, such as obesity, heart disease and diabetes.
Ice sheets expanded across much of northern Europe from around 25,000 to 19,000 years ago, making a huge expanse of land unlivable. That harsh event set in motion a previously unrecognized tale of two human populations that played out at opposite ends of the continent.
Western European hunter-gatherers outlasted the icy blast in the past. Easterners got replaced by migrations of newcomers.
That’s the implication of the largest study to date of ancient Europeans’ DNA, covering a period before, during and after what’s known as the Last Glacial Maximum, paleogeneticist Cosimo Posth and colleagues report March 1 in Nature. As researchers have long thought, southwestern Europe provided refuge from the last Ice Age’s big chill for hunter-gatherers based in and near that region, the scientists say. But it turns out that southeastern Europe, where Italy is now located, did not offer lasting respite from the cold for nearby groups, as previously assumed.
Instead, those people were replaced by genetically distinct hunter-gatherers who presumably had lived just to the east along the Balkan Peninsula. Those people, who carried ancestry from parts of southwestern Asia, began trekking into what’s now northern Italy by about 17,000 years ago, as the Ice Age began to wane.
“If local [Ice Age] populations in Italy did not survive and were replaced by groups from the Balkans, this completely changes our interpretation of the archaeological record,” says Posth, of the University of Tübingen in Germany.
Posth and colleagues’ conclusions rest on analyses of DNA from 356 ancient hunter-gatherers, including new molecular evidence for 116 individuals from 14 countries in Europe and Asia. Excavated human remains that yielded DNA dated to between about 45,000 and 5,000 years ago (SN: 4/7/21).
Comparisons of sets of gene variants inherited by these hunter-gatherers from common ancestors enabled the researchers to reconstruct population movements and replacements that shaped ancient Europeans’ genetic makeup. For the first time, ancient DNA evidence included individuals from what’s known as the Gravettian culture, which dates from about 33,000 to 26,000 years ago in central and southern Europe, and from southwestern Europe’s Solutrean culture, which dates to between about 24,000 and 19,000 years ago. Contrary to expectations, makers of Gravettian tools came from two genetically distinct groups that populated western and eastern Europe for roughly 10,000 years before the Ice Age reached its peak, Posth says. Researchers have traditionally regarded Gravettian implements as products of a biologically uniform population that occupied much of Europe.
“What we previously thought was one genetic ancestry in Europe turned out to be two,” says paleogeneticist Mateja Hajdinjak of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, who did not participate in the new study. And “it seems that western and southwestern Europe served as a [refuge from glaciation] more than southeastern Europe and Italy.”
Descendants of the western Gravettian population, who are associated with Solutrean artifacts and remnants of another ancient culture in western Europe that ran from about 19,000 to 14,000 years ago, outlasted the Ice Age before spreading northeastward across Europe, the researchers say.
Further support for southwestern Europe as an Ice Age refuge comes from DNA extracted from a pair of fossil teeth that belonged to an individual linked to the Solutrean culture in southern Spain. That roughly 23,000-year-old adult was genetically similar to western European hunter-gatherers who lived before and after the Last Glacial Maximum, Max Planck paleogeneticist Vanessa Villalba-Mouco and colleagues, including Posth, report March 1 in Nature Ecology & Evolution.
Meanwhile, the genetic evidence suggests that hunter-gatherers in what’s now Italy were replaced by people from farther east, probably based in the Balkan region. Those newcomers must have brought with them a distinctive brand of stone artifacts, previously excavated at Italian sites and elsewhere in eastern Europe, known as Epigravettian tools, Posth says. Many archaeologists have suspected that Epigravettian items were products of hunter-gatherers who clustered in Italy during the Ice Age’s peak freeze.
But, Hajdinjak says, analyses of DNA from fossils of Ice Age Balkan people are needed to clarify what groups moved through Italy, and when those migrations occurred.
Ultimately, descendants of Ice Age migrants into Italy reached southern Italy and then western Europe by around 14,000 years ago, Posth and colleagues say. Ancient DNA evidence indicates that, during those travels, they left a major genetic mark on hunter-gatherers across Europe.
Like so many others, I’ve been watching the HBO series The Last of Us. It’s a classic zombie apocalypse drama following Joel (played by Pedro Pascal) and Ellie (Bella Ramsey) as they make their way across the former United States (now run by a fascist government called Fedra).
I’m a big fan of zombie and other post-apocalyptic fiction. And my husband had told me how good the storyline is in the video game that inspired the series, so I was prepared for interesting storytelling. What I didn’t expect was to be so intrigued by the science behind the sci-fi. In the opening minutes of the series, two scientists on a fictional 1968 talk show discuss the microbes that give them pandemic nightmares. One says it’s fungi — not viruses or bacteria — that keep him awake. Especially worrisome, he says, are the fungi that control rather than kill their hosts. He gives the example of fungi that turns ants into living zombies, puppeteering the insects by flooding their brains with hallucinogens.
He goes on to warn that even though human body temperature keeps us fungus-free, that might not be true if the world got a little bit warmer. He predicts that as the thermostat climbs, a fungus that hijacks insects could mutate a gene allowing it to burrow into human brains and take control of our minds. Such a fungus could induce its human puppets to spread the fungus “by any means necessary,” he says. What’s worse, there are no preventatives, treatments or cures, nor any way to make them.
It’s a brief segment, but it had me hooked. It all sounded so chilling and … plausible. After all, fungi like ones that cause nail infections, yeast infections and ringworm already infect people.
So I consulted some experts on fungal infections to find out whether this could actually happen.
I’ve got good news and bad news.
First, the bad news.
Bad news: Climate change has already helped one fungus mutate to infect humans I wanted to know if warming has spurred any fungi to mutate and become infectious. So I called Arturo Casadevall. He has been thinking about fungi and heat for a long time. He’s proposed that the need to avoid fungal infections may have provided the evolutionary pressure that drove mammals and birds to evolve warm-bloodedness (SN: 12/3/10).
Most fungal species simply can’t reproduce at human body temperature (37° Celsius, or 98.6° Fahrenheit). But as the world warms, “these strains either have to die or adapt,” says Casadevall, a microbiologist who specializes in fungal infections at Johns Hopkins Bloomberg School of Public Health. That raises the possibility that fungi that now infect insects or reptiles could evolve to grow at temperatures closer to human body temperature.
At the same time, humans’ average body temperature has been falling since the 19th century, at least in high-income countries, researchers reported in eLife in 2020. One study from the United Kingdom pegs average body temperature at 36.6° C (97.9° F). And some of us are even cooler.
Fungi’s possible adaptation to higher heat and humans’ cooling body temperature are on a collision course, Casadevall says. He and colleagues presented evidence of one such crash. Climate change may have allowed a deadly fungus called Candida auris to acclimate to human body temperatures (SN: 7/26/19). A version of the fungus that could infect humans independently emerged on three continents from 2012 to 2015. “It’s not like someone took a plane a spread it. These things came out of nowhere simultaneously,” Casadevall says.
Some people argue that the planet hasn’t warmed enough to make fungi a problem, he says. “But you have to think about all the really hot days [that come with climate change]. Every really hot day is a selection event,” in which many fungi will die. But some of those fungi will have mutations that help them handle the heat. Those will survive. Their offspring may be able to survive future even hotter heat waves until human body temperature is no challenge.
Fungi that infect people are usually not picky about their hosts, Casadevall says. They will grow in soil or — if given an opportunity — in people, pets or in other animals. The reason fungi don’t infect people more often is that “the world is much colder than we are, and they have no need of us,” he says.
When people do get infected, the immune system usually keeps the fungi in check. But fungal infections can cause serious illness or be deadly, particularly to people with weakened immune systems (SN: 11/29/21; SN: 1/10/23).
The second episode of The Last of Us reveals that the zombie-creating fungi initially spread through people eating contaminated flour. Then, the infected people attack and bite others, spreading the fungus.
In real life, most human infections arise from breathing in spores. But Casadevall says it’s “not implausible” that people could get infected by eating spores or by being bitten.
Also bad: Fungal genes can adapt to higher heat I also wondered exactly how a fungus could evolve in response to heat. Asiya Gusa, a fungal researcher at Duke University School of Medicine, has published one possibility.
In 2020, she and colleagues reported in the Proceedings of the National Academy of Sciences on how one fungus mutated at elevated temperature to become harder to fight.
Cryptococcus deneoformans, which already infects humans (though it’s no zombie-maker), became resistant to some antifungal drugs when grown at human body temperature. The resistance was born when mobile bits of DNA called transposons (often called jumping genes) hopped into a few genes needed for the antifungals to work.
In a follow-up study, Gusa and colleagues grew C. deneoformans at either 30° C or 37° C for 800 generations, long enough to detect multiple changes in their DNA. Fungi had no problem growing at the balmy 30° C (86° F), the temperature at which researchers typically grow fungi in the lab. But their growth slowed at the higher temperature, a sign that the fungi were under stress from the heat.
In C. deneoformans, that heat stress really got things jumping. One type of transposon accumulated a median of 12 extra copies of itself in fungi grown at body temperature. By contrast, fungi grown at 30° C tended to pick up a median of only one extra copy of the transposon. The team reported those results January 20 in PNAS. The researchers don’t yet know the effect the transposon hops might have on the fungi’s ability to infect people, cause disease or resist fungus-fighting drugs.
So yeah, the bad news is not great. Fungi are mutating in the heat and at least one species has gained the ability to infect people thanks to climate change. Other fungi that infect people are more widespread than they were in the 1950s and 1960s, also thanks to a warming world (SN: 1/4/23).
But I promised good news. And here it is.
Good news: Human brains may resist zombification It may not be our body temperature, but our brain chemistry, that protects us from being hijacked by zombifying fungi.
I consulted Charissa de Bekker and Jui-Yu Chou, two researchers who study the Ophiocordyceps fungi that are the model for the TV show’s fungal menace. These fungi infect ants, flooding the insects with a cocktail of chemicals that steer the ants to climb plants. Once in position, the ants chomp down and the chemicals keep the jaw muscles locked in place (SN: 7/17/19).
Unlike most fictional zombies, the ants are alive during this process. “A lot of people get the misconception that we work on undead ants,” says de Bekker, a microbiologist at Utrecht University in the Netherlands. She’s glad to see the show “stick to the story of the host being very much alive while its behaviors change.” The fungi even help preserve the ant, keeping it alive even while feeding on it. But eventually the ant dies. Then a mushroom rises from the corpse, showering spores onto the ground where other ants may become infected.
Related species of Ophiocordyceps infect various species of ants and other insects. But each fungal species is very specific to the host it infects. That’s because the fungi had to individualize the chemicals they use to control the particular species they infect. The ability to manipulate behavior comes at the cost of not being able to infect multiple species. A fungus that specializes in infecting ants probably can’t get past humans’ immune systems, says Chou, a fungal researcher at the National Changhua University of Education in Taiwan. “Think of a key that fits into a specific lock. It is only this unique combination that will trigger the lock to open,” he says.
Even if the fungi evolved to withstand human body temperature and immune system attacks, they probably couldn’t take control of our minds, de Bekker says. “Manipulation is like a whole different ballgame. You need a ton of additional tools to get there.” It took millions of years of coevolution for the fungi to master piloting ants, after all.
While fungi do make mind-altering chemicals that can affect human behavior (LSD and psilocybin, for instance), Casadevall agrees that fungi that mind control insects probably won’t turn humans into zombies. “It’s not one of my worries,” he says.
Infected ants don’t turn into vicious, biting zombies either, de Bekker says. “If anything, we actually see the healthy ants being aggressive toward infected individuals, once they figure out that they’re infected, to basically get rid of them.” That “social immunity” helps protect the rest of the nest from infection.
Also good: Humans are innovative enough to develop treatments The fictional scientist’s assertion that we couldn’t prevent, treat or cure these fungal infections is also a stretch.
Antifungal drugs exist and they cure many fungal infections, though some infections may persist. Some that spread to the brain may be particularly difficult to clear.Some fungi are also evolving resistance to the drugs. And a few fungal vaccines are in the works, although they may not be ready for years.
The experts I talked to say they hope the show will bring attention to real fungal diseases.
Gusa was especially glad to see fungi in the limelight. And she shares my fondness for that retro series opening in which the scientist predicts climate change could spawn mind-controlling fungi bent on infecting every person on the planet.
“I was pretty much yelling at the TV when I watched the [show’s] intro,” in an excited kind of way, she says. “This is the foundation of a lot of my grant funding … the threat of thermal adaptation of fungi.… To see it played out on the screen was something kind of fun.”
For the first time, researchers have harnessed the body’s own chemistry to “grow” electrodes inside the tissues of living fish, blurring the boundary between biology and machines.
The technique uses the body’s sugars to turn an injected gel into a flexible electrode without damaging tissues, experiments show. Zebrafish with these electrodes grown in their brains, hearts and tail fins showed no signs of ill effects, and ones tested in leeches successfully stimulated a nerve, researchers report in the Feb. 24 Science. Someday, these electrodes could be useful for applications ranging from studying how biological systems work to improving human-machine interfaces. They also could be used in “bioelectronic medicine,” such as brain stimulation therapies for depression, Parkinson’s disease and other conditions (SN: 2/10/19).
Soft electronics aim to bridge the gap between soft, curvy biology and electronic hardware. But these electronics typically still must carry certain parts that can be prone to cracks and other issues, and inserting these devices inevitably causes damage to tissues.
“All the devices we have made, even though we have made them flexible, to make them more soft, when we introduce them, there will still be a scar. It’s like sticking a knife into the organ,” says Magnus Berggren, a materials scientist at Linköping University in Sweden. That scarring and inflammation can degrade electrode performance over time.
Previous efforts to grow soft electronics inside tissues have drawbacks. One approach uses electrical or chemical signals to power the transformation from chemical soup to conducting electrodes, but these zaps also cause damage. A 2020 study got around this problem by genetically modifying cells in worms to produce an engineered enzyme that does the job, but the new method achieves its results without genetic alterations.
Berggren and colleagues’ electrodes instead exploit a natural energy source already present in the body: sugars. The gel cocktail contains molecules called oxidases that react with the sugars — glucose or lactate — to produce hydrogen peroxide. That then activates another ingredient in the cocktail, an enzyme called hydrogen peroxidase, which is the catalyst needed to transform the gel into a conducting electrode.
“The approach leverages elegant chemistry to overcome many of the technical challenges,” says biomedical engineer Christopher Bettinger of Carnegie Mellon University in Pittsburgh, who was not involved in the study.
To test the technique, the researchers injected the cocktail into the brains, hearts and tail fins of transparent zebrafish. The gel turns blue when it becomes conductive, giving a visual readout of its success. “The beautiful thing is you can see it: The zebrafishes’ tail changes color, and we know that blue indicates a conducting polymer,” says materials scientist Xenofon Strakosas, also of Linköping University. “The first time I saw it, I thought ‘Wow, it’s really working!’”
The fish appeared to suffer no ill effects, and the researchers saw no evidence of tissue damage. In partially dissected leeches, the team showed that delivering a current to a nerve via a soft electrode could induce muscle contractions. Ultimately, devices like this could be paired with various wireless technologies in development.
Long-term implant performance remains to be determined, however. “The demonstrations are impressive,” Bettinger says. “What remains to be seen is the stability of the electrode.” Over time, substances in the body could react with the electrode materials, degrading it or even producing toxic substances.
The team still needs to refine how precisely the electrodes can stimulate nerves, says chemical engineer Zhenan Bao of Stanford University, who was not involved in the work. She and colleagues developed the way to “grow” electrical components using genetic modifications. Ensuring stimulation is concentrated where it’s needed for a treatment, while preventing the leakage of current to unwanted regions will be important, she says.
In the new study, the relative abundance of different sugars in different tissues determines exactly where electrodes form. But in the future, a component of the main ingredient could be swapped out for elements that attach to specific bits of biology to make targeting much more precise, Berggren says. “We’re conducting experiments right now where we’re trying to bind these materials directly on individual cells.” Notes Strakosas: “There are some applications where precision is really important; that’s where we have to invest effort.”
The best shot we have at minimizing the future impacts of climate change is to limit global warming to 1.5 degrees Celsius. Since the Industrial Revolution began, humankind has already raised the average global temperature by about 1.1 degrees. If we continue to emit greenhouse gases at the current rate, the world will probably surpass the 1.5-degree threshold by the end of the decade.
That sobering fact makes clear that climate change isn’t just a problem to solve someday soon; it’s an emergency to respond to now. And yet, most people don’t act like we’re in the midst of the greatest crisis humans have ever faced — not politicians, not the media, not your neighbor, not myself, if I’m honest. That’s what I realized after finishing The Climate Book by Greta Thunberg.
The urgency to act now, to kick the addiction to fossil fuels, practically jumps off the page to punch you in the gut. So while not a pleasant read — it’s quite stressful — it’s a book I can’t recommend enough. The book’s aim is not to convince skeptics that climate change is real. We’re well past that. Instead, it’s a wake-up call for anyone concerned about the future.
A collection of bite-size essays, The Climate Book provides an encyclopedic overview of all aspects of the climate crisis, including the basic science, the history of denialism and inaction, and what to do next. Thunberg, who became the face of climate activism after starting the Fridays For Future protests as a teenager (SN: 12/16/19), assembles an all-star roster of experts to write the essays.
The first two sections of the book lay out how a small amount of warming can have major, far-reaching effects. For some readers, this will be familiar territory. But as each essay builds on the next, it becomes clear just how delicate Earth’s climate system is. What also becomes clear is the significance of 1.5 degrees (SN: 12/17/18). Beyond this point, scientists fear, various aspects of the natural world might reach tipping points that usher in irreversible changes, even if greenhouse gas emissions are later brought under control. Ice sheets could melt, raise sea levels and drown coastal areas. The Amazon rainforest could become a dry grassland.
The cumulative effect would be a complete transformation of the climate. Our health and the livelihood of other species and entire ecosystems would be in danger, the book shows. Not surprisingly, essay after essay ends with the same message: We must cut greenhouse gas emissions, now and quickly.
Repetition is found elsewhere in the book. Numerous essays offer overlapping scientific explanations, stats about emissions, historical notes and thoughts about the future. Rather than being tedious, the repetition reinforces the message that we know what the climate change threat is, we know how to tackle it and we’ve known for a long time. Thunberg’s anger and frustration over the decades of inaction, false starts and broken pledges are palpable in her own essays that run throughout the book. The world has known about human-caused climate change for decades, yet about half of all human-related carbon dioxide emissions ever released have occurred since 1990. That’s the year the Intergovernmental Panel on Climate Change released its first report and just two years before world leaders met in Rio de Janeiro in 1992 to sign the first international treaty to curb emissions (SN: 6/23/90).
Perversely, the people who will bear the brunt of the extreme storms, heat waves, rising seas and other impacts of climate change are those who are least culpable. The richest 10 percent of the world’s population accounts for half of all carbon dioxide emissions while the top 1 percent emits more than twice as much as the bottom half. But because of a lack of resources, poorer populations are the least equipped to deal with the fallout. “Humankind has not created this crisis,” Thunberg writes, “it was created by those in power.”
That injustice must be confronted and accounted for as the world addresses climate change, perhaps even through reparations, Olúfẹ́mi O. Táíwò, a philosopher at Georgetown University, argues in one essay.
So what is the path forward? Thunberg and many of her coauthors are generally skeptical that new tech alone will be our savior. Carbon capture and storage, or CCS, for example, has been heralded as one way to curb emissions. But less than a third of the roughly 150 planned CCS projects that were supposed to be operational by 2020 are up and running.
Progress has been impeded by expenses and technology fails, science writer Ketan Joshi explains. An alternative might be “rewilding,” restoring damaged mangrove forests, seagrass meadows and other ecosystems that naturally suck CO2 out of the air (SN: 9/14/22), suggest environmental activists George Monbiot and Rebecca Wrigley.
Fixing the climate problem will not only require transforming our energy and transportation systems, which often get the most attention, but also our economies (endless growth is not sustainable), political systems and connection to nature and with each other, the book’s authors argue.
The last fifth of the book lays out how we could meet this daunting challenge. What’s needed is a critical mass of individuals who are willing to make lifestyle changes and be heard. This could trigger a social movement strong enough to force politicians to listen and create systemic and structural change. In other words, it’s time to start acting like we’re in a crisis. Thunberg doesn’t end the book by offering hope. Instead, she argues we each have to make our own hope.
“To me, hope is not something that is given to you, it is something you have to earn, to create,” she writes. “It cannot be gained passively, through standing by and waiting for someone else to do something. Hope is taking action.”
