High-tech shrink art may be the key to making tiny electronics, 3-D nanostructures or even holograms for hiding secret messages.
A new approach to making tiny structures relies on shrinking them down after building them, rather than making them small to begin with, researchers report in the Dec. 23 Science.
The key is spongelike hydrogel materials that expand or contract in response to surrounding chemicals (SN: 1/20/10). By inscribing patterns in hydrogels with a laser and then shrinking the gels down to about one-thirteenth their original size, the researchers created patterns with details as small as 25 billionths of a meter across. At that level of precision, the researchers could create letters small enough to easily write this entire article along the circumference of a typical human hair.
Biological scientist Yongxin Zhao and colleagues deposited a variety of materials in the patterns to create nanoscopic images of Chinese zodiac animals. By shrinking the hydrogels after laser etching, several of the images ended up roughly the size of a red blood cell. They included a monkey made of silver, a gold-silver alloy pig, a titanium dioxide snake, an iron oxide dog and a rabbit made of luminescent nanoparticles. Because the hydrogels can be repeatedly shrunk and expanded with chemical baths, the researchers were also able to create holograms in layers inside a chunk of hydrogel to encode secret information. Shrinking a hydrogel hologram makes it unreadable. “If you want to read it, you have to expand the sample,” says Zhao, of Carnegie Mellon University in Pittsburgh. “But you need to expand it to exactly the same extent” as the original. In effect, knowing how much to expand the hydrogel serves as a key to unlock the information hidden inside.
But the most exciting aspect of the research, Zhao says, is the wide range of materials that researchers can use on such minute scales. “We will be able to combine different types of materials together and make truly functional nanodevices.”
Today’s red jungle fowl — the wild forebears of the domesticated chicken — are becoming more chickenlike. New research suggests that a large proportion of the wild fowl’s DNA has been inherited from chickens, and relatively recently.
Ongoing interbreeding between the two birds may threaten wild jungle fowl populations’ future, and even hobble humans’ ability to breed better chickens, researchers report January 19 in PLOS Genetics.
Red jungle fowl (Gallus gallus) are forest birds native to Southeast Asia and parts of South Asia. Thousands of years ago, humans domesticated the fowl, possibly in the region’s rice fields (SN: 6/6/22). “Chickens are arguably the most important domestic animal on Earth,” says Frank Rheindt, an evolutionary biologist at the National University of Singapore. He points to their global ubiquity and abundance. Chicken is also one of the cheapest sources of animal protein that humans have.
Domesticated chickens (G. gallus domesticus) were known to be interbreeding with jungle fowl near human settlements in Southeast Asia. Given the unknown impacts on jungle fowl and the importance of chickens to humankind, Rheindt and his team wanted to gather more details. Wild jungle fowl contain a store of genetic diversity that could serve as a crucial resource for breeding chickens resistant to diseases or other threats.
The researchers analyzed and compared the genomes — the full complement of an organism’s DNA — of 63 jungle fowl and 51 chickens from across Southeast Asia. Some of the jungle fowl samples came from museum specimens collected from 1874 through 1939, letting the team see how the genetic makeup of jungle fowl has changed over time.
Over the last century or so, wild jungle fowl’s genomes have become increasingly similar to chickens’. Between about 20 and 50 percent of the genomes of modern jungle fowl originated in chickens, the team found. In contrast, many of the roughly 100-year-old jungle fowl had a chicken-ancestry share in the range of a few percent.
The rapid change probably comes from human communities expanding into the region’s wilderness, Rheindt says. Most modern jungle fowl live in close vicinity to humans’ free-ranging chickens, with which they frequently interbreed.
Such interbreeding has become “almost the norm now” for any globally domesticated species, Rheindt says, such as dogs hybridizing with wolves and house cats crossing with wildcats. Pigs, meanwhile, are mixing with wild boars and ferrets with polecats. Wild populations that interbreed with their domesticated counterparts could pick up physical or behavioral traits that change how the hybrids function in their ecosystem, says Claudio Quilodrán, a conservation geneticist at the University of Geneva not involved with this research.
The effect is likely to be negative, Quilodrán says, since some of the traits coming into the wild population have been honed for human uses, not for survival in the local environment.
Wild jungle fowl have lost their genetic diversity as they’ve interbred too. The birds’ heterozygosity — a measure of a population’s genetic diversity — is now just a tenth of what it was a century ago.
“This result is initially counterintuitive,” Rheindt says. “If you mix one population with another, you would generally expect a higher genetic diversity.”
But domesticated chickens have such low genetic diversity that certain versions of jungle fowl genes are being swept out of the population by a tsunami of genetic homogeneity. The whittling down of these animals’ genetic toolkit may leave them vulnerable to conservation threats.
“Having lots of genetic diversity within a species increases the chance that certain individuals contain the genetic background to adapt to a varied range of different environmental changes and diseases,” says Graham Etherington, a computational biologist at the Earlham Institute in Norwich, England, who was not involved with this research.
A shallower jungle fowl gene pool could also mean diminished resources for breeding better chickens. The genetics of wild relatives are sometimes used to bolster the disease or pest resistance of domesticated crop plants. Jungle fowl genomes could be similarly valuable for this reason.
“If this trend continues unabated, future human generations may only be able to access the entirety of ancestral genetic diversity of chickens in the form of museum specimens,” Rheindt says, which could hamper chicken breeding efforts using the wild fowl genes.
Some countries such as Singapore, Rheindt says, have started managing jungle fowl populations to reduce interbreeding with chickens.
A 120-million-year-old fossil bird found in China could offer some new clues about how landbound dinosaurs evolved into today’s flying birds. The dove-sized Cratonavis zhui sported a dinosaur-like head atop a body similar to those of today’s birds, researchers report in the January Nature Ecology & Evolution.
The flattened specimen came from the Jiufotang Formation, an ancient body of rock in northeastern China that is a hotbed for preserved feathered dinosaurs and archaic birds. CT scans revealed that Cratonavis had a skull that was nearly identical (albeit smaller) as those of theropod dinosaurs like Tyrannosaurus rex, paleontologist Li Zhiheng of the Chinese Academy of Sciences in Beijing and colleagues report. This means that Cratonavis still hadn’t evolved the mobile upper jaw found in modern birds (SN: 5/2/18). It’s among just a handful of specimens that belong to a recently identified group of intermediate birds known as the jinguofortisids, says Luis Chiappe, a paleontologist at the Natural History Museum of Los Angeles County who was not involved in the study. Its dino-bird mishmash “is not unexpected.” Most birds discovered from the Age of Dinosaurs exhibited more primitive, toothed heads than today’s birds, he says. But the new find “builds on our understanding of this primitive group of birds that are at the base of the tree of birds.”
Cratonavis also had an unusually elongated scapula and hallux, or backward-facing toe. Rarely seen in Cretaceous birds, enlarged shoulder blades might have compensated for the bird’s otherwise underwhelming flight mechanics, the researchers say. And that hefty big toe? It bucks the trend of shrinking metatarsals seen as birds continued to evolve. Cratonavis might have used this impressive digit to hunt like today’s birds of prey, Li’s team says.
Filling those shoes may have been too big of a job for Cratonavis, though. Given its size, Chiappe says, the dino-headed bird would have most likely been a petite hunter, taking down the likes of beetles, grasshoppers and the occasional lizard rather than terrorizing the skies.
The worst procrastinators probably won’t be able to read this story. It’ll remind them of what they’re trying to avoid, psychologist Piers Steel says.
Maybe they’re dragging their feet going to the gym. Maybe they haven’t gotten around to their New Year’s resolutions. Maybe they’re waiting just one more day to study for that test.
Procrastination is “putting off to later what you know you should be doing now,” even if you’ll be worse off, says Steel, of the University of Calgary in Canada. But all those tasks pushed to tomorrow seem to wedge themselves into the mind — and it may be harming people’s health. In a study of thousands of university students, scientists linked procrastination to a panoply of poor outcomes, including depression, anxiety and even disabling arm pain. “I was surprised when I saw that one,” says Fred Johansson, a clinical psychologist at Sophiahemmet University in Stockholm. His team reported the results January 4 in JAMA Network Open.
The study is one of the largest yet to tackle procrastination’s ties to health. Its results echo findings from earlier studies that have gone largely ignored, says Fuschia Sirois, a behavioral scientist at Durham University in England, who was not involved with the new research.
For years, scientists didn’t seem to view procrastination as something serious, she says. The new study could change that. “It’s that kind of big splash that’s … going to get attention,” Sirois says. “I’m hoping that it will raise awareness of the physical health consequences of procrastination.”
Procrastinating may be bad for the mind and body Whether procrastination harms health can seem like a chicken-and-egg situation.
It can be hard to tell if certain health problems make people more likely to procrastinate — or the other way around, Johansson says. (It may be a bit of both.) And controlled experiments on procrastination aren’t easy to do: You can’t just tell a study participant to become a procrastinator and wait and see if their health changes, he says. Many previous studies have relied on self-reported surveys taken at a single time point. But a snapshot of someone makes it tricky to untangle cause and effect. Instead, in the new study, about 3,500 students were followed over nine months, so researchers could track whether procrastinating students later developed health issues.
On average, these students tended to fare worse over time than their prompter peers. They were slightly more stressed, anxious, depressed and sleep-deprived, among other issues, Johansson and colleagues found. “People who score higher on procrastination to begin with … are at greater risk of developing both physical and psychological problems later on,” says study coauthor Alexander Rozental, a clinical psychologist at Uppsala University in Sweden. “There is a relationship between procrastination at one time point and having these negative outcomes at the later point.”
The study was observational, so the team can’t say for sure that procrastination causes poor health. But results from other researchers also seem to point in this direction. A 2021 study tied procrastinating at bedtime to depression. And a 2015 study from Sirois’ lab linked procrastinating to poor heart health.
Stress may be to blame for procrastination’s ill effects, data from Sirois’ lab and other studies suggest. She thinks that the effects of chronic procrastinating could build up over time. And though procrastination alone may not cause disease, Sirois says, it could be “one extra factor that can tip the scales.”
No, procrastinators are not lazy Some 20 percent of adults are estimated to be chronic procrastinators. Everyone might put off a task or two, but chronic procrastinators make it their lifestyle, says Joseph Ferrari, a psychologist at DePaul University in Chicago, who has been studying procrastination for decades. “They do it at home, at school, at work and in their relationships.” These are the people, he says, who “you know are going to RSVP late.”
Though procrastinators may think they perform better under pressure, Ferrari has reported the opposite. They actually worked more slowly and made more errors than non-procrastinators, his experiments have shown. And when deadlines are slippery, procrastinators tend to let their work slide, Steel’s team reported last year in Frontiers in Psychology.
For years, researchers have focused on the personalities of people who procrastinate. Findings vary, but some scientists suggest procrastinators may be impulsive, worriers and have trouble regulating their emotions. One thing procrastinators are not, Ferrari emphasizes, is lazy. They’re actually “very busy doing other things than what they’re supposed to be doing,” he says.
In fact, Rozental adds, most research today suggests procrastination is a behavioral pattern.
And if procrastination is a behavior, he says, that means it’s something you can change, regardless of whether you’re impulsive.
Why procrastinators should be kind to themselves When people put off a tough task, they feel good — in the moment. Procrastinating is a way to sidestep the negative emotions linked to the task, Sirois says. “We’re sort of hardwired to avoid anything painful or difficult,” she says. “When you procrastinate, you get immediate relief.” A backdrop of stressful circumstances — say, a worldwide pandemic — can strain people’s ability to cope, making procrastinating even easier. But the relief it provides is only temporary, and many seek out ways to stop dawdling.
Researchers have experimented with procrastination treatments that run the gamut from the logistical to the psychological. What works best is still under investigation. Some scientists have reported success with time-management interventions. But the evidence for that “is all over the map,” Sirois says. That’s because “poor time management is a symptom not a cause of procrastination,” she adds.
For some procrastinators, seemingly obvious tips can work. In his clinical practice, Rozental advises students to simply put down their smartphones. Silencing notifications or studying in the library rather than at home can quash distractions and keep people on task. But that won’t be enough for many people, he says.
Hard-core procrastinators may benefit from cognitive behavioral therapy. In a 2018 review of procrastination treatments, Rozental found that this type of therapy, which involves managing thoughts and emotions and trying to change behavior, seemed to be the most helpful. Still, not many studies have examined treatments, and there’s room for improvement, he says.
Sirois also favors an emotion-centered approach. Procrastinators can fall into a shame spiral where they feel uneasy about a task, put the task off, feel ashamed for putting it off and then feel even worse than when they started. People need to short-circuit that loop, she says. Self-forgiveness may help, scientists suggested in one 2020 study. So could mindfulness training.
In a small trial of university students, eight weekly mindfulness sessions reduced procrastination, Sirois and colleagues reported in the January Learning and Individual Differences. Students practiced focusing on the body, meditating during unpleasant activities and discussed the best way to take care of themselves. A little self-compassion may snap people out of their spiral, Sirois says.
“You made a mistake and procrastinated. It’s not the end of the world,” she says. “What can you do to move forward?”
Supercooled water is two of a kind, a new study shows.
Scientists have long suspected that water at subfreezing temperatures comes in two distinct varieties: a high-density liquid that appears at very high pressures and a low-density liquid at lower pressures. Now, ultrafast measurements have caught water morphing from one type of liquid to the other, confirming that hunch. The discovery, reported in the Nov. 20 Science, could help explain some of water’s quirks.
The experiment “adds more and more evidence to the idea that water really is two components … and that that is the reason that underlies why water is so weird,” says physicist Greg Kimmel of Pacific Northwest National Laboratory in Richland, Wash., who was not involved in the study.
When free from impurities, water can remain liquid below its typical freezing point of zero degrees Celsius, forming what’s called a supercooled liquid. But the dual nature of supercooled water was expected to appear in a temperature realm so difficult to study that it’s been dubbed “no-man’s-land.” Below around –40° C, water remains liquid for mere instants before it crystallizes into ice. Making the task even more daunting, the high-density phase appears only at very high pressures. Still, “people have dreamt about how to do an experiment,” says Anders Nilsson of Stockholm University. Thanks to speedy experimental maneuvers, Nilsson and colleagues have infiltrated that no-man’s-land by monitoring water’s properties on a scale of nanoseconds. “This is one of the major accomplishments of this paper,” says computational chemist Gül Zerze of Princeton University. “I’m impressed with their work.”
The scientists started by creating a type of high-density ice. Then, a pulse from an infrared laser heated the ice, forming liquid water under high pressure. That water then expanded, and the pressure rapidly dropped. Meanwhile, the researchers used an X-ray laser to investigate how the structure of the water changed, based on how the X-rays scattered. As the pressure decreased, the water transitioned from a high-density to low-density fluid before crystallizing into ice.
Previous studies have used ultrafast techniques to find hints of water’s two-faced demeanor, but those have been done mainly at atmospheric pressure (SN: 9/28/20). In the new work, the water was observed at about 3,000 times atmospheric pressure and –68° C. “It’s the first time we have real experimental data at these pressures and temperatures,” says physicist Loni Kringle of Pacific Northwest National Laboratory, who was not involved with the experiment.
The result could indicate that supercooled water has a “critical point” — a certain pressure and temperature at which two distinct phases merge into one. In the future, Nilsson hopes to pinpoint that spot.
Such a critical point could explain why water is an oddball liquid. For most liquids, cooling makes them become denser and more difficult to compress. Water gets denser as it is cooled to 4° C, but becomes less dense as it is cooled further. Likewise, its compressibility increases as it’s cooled.
If supercooled water has a critical point, that could indicate that the water experienced in daily life is strange because, under typical pressures and temperatures, it is a supercritical liquid — a weird state that occurs beyond a critical point. Such a liquid would not be the high-density or low-density form, but would consist of some regions with a high-density arrangement of water molecules and other pockets of low density. The relative amounts of those two structures, which result from different arrangements of hydrogen bonds between the molecules, would change as the temperature changes, explaining why water behaves strangely as it is cooled.
So despite the fact that the experiment involved extreme pressures and temperatures, Nilsson says, “it influences water in our ordinary life.”
2022 was the year many people decided the coronavirus pandemic had ended.
President Joe Biden said as much in an interview with 60 Minutes in September. “The pandemic is over,” he said while strolling around the Detroit Auto Show. “We still have a problem with COVID. We’re still doing a lot of work on it. But the pandemic is over.”
His evidence? “No one’s wearing masks. Everybody seems to be in pretty good shape.”
But the week Biden’s remarks aired, about 360 people were still dying each day from COVID-19 in the United States. Globally, about 10,000 deaths were recorded every week. That’s “10,000 too many, when most of these deaths could be prevented,” the World Health Organization Director-General Tedros Adhanom Ghebreyesus said in a news briefing at the time. Then, of course, there are the millions who are still dealing with lingering symptoms long after an infection. Those staggering numbers have stopped alarming people, maybe because those stats came on the heels of two years of mind-boggling death counts (SN Online: 5/18/22). Indifference to the mounting death toll may reflect pandemic fatigue that settled deep within the public psyche, leaving many feeling over and done with safety precautions.
“We didn’t warn people about fatigue,” says Theresa Chapple-McGruder, an epidemiologist in the Chicago area. “We didn’t warn people about the fact that pandemics can last long and that we still need people to be willing to care about yourselves, your neighbors, your community.”
Public health agencies around the world, including in Singapore and the United Kingdom, reinforced the idea that we could “return to normal” by learning to “live with COVID.” The U.S. Centers for Disease Control and Prevention’s guidelines raised the threshold for case counts that would trigger masking (SN Online: 3/3/22). The agency also shortened suggested isolation times for infected people to five days, even though most people still test positive for the virus and are potentially infectious to others for several days longer (SN Online: 8/19/22).
The shifting guidelines bred confusion and put the onus for deciding when to mask, test and stay home on individuals. In essence, the strategy shifted from public health — protecting your community — to individual health — protecting yourself. Doing your part can be exhausting, says Eric Kennedy, a sociologist specializing in disaster management at York University in Toronto. “Public health is saying, ‘Hey, you have to make the right choices every single moment of your life.’ Of course, people are going to get tired with that.”
Doing the right thing — from getting vaccinated to wearing masks indoors — didn’t always feel like it paid off on a personal level. As good as the vaccines are at keeping people from becoming severely ill or dying of COVID-19, they were not as effective at protecting against infection. This year, many people who tried hard to make safe choices and had avoided COVID-19 got infected by wily omicron variants (SN Online: 4/22/22). People sometimes got reinfected — some more than once (SN: 7/16/22 & 7/30/22, p. 8). Those infections may have contributed to a sense of futility. “Like, ‘I did my best. And even with all of that work, I still got it. So why should I try?’ ” says Kennedy, head of a Canadian project monitoring the sociological effects of the COVID-19 pandemic.
Getting vaccinated, masking and getting drugs or antibody treatments can reduce the severity of infection and may cut the chances of infecting others. “We should have been talking about this as a community health issue and not a personal health issue,” Chapple-McGruder says. “We also don’t talk about the fact that our uptake [of these tools] is nowhere near what we need” to avoid the hundreds of daily deaths.
A lack of data about how widely the coronavirus is still circulating makes it difficult to say whether the pandemic is ending. In the United States, the influx of home tests was “a blessing and a curse,” says Beth Blauer, data lead for the Johns Hopkins University Coronavirus Resource Center. The tests gave an instant readout that told people whether they were infected and should isolate. But because those results were rarely reported to public health officials, true numbers of cases became difficult to gauge, creating a big data gap (SN Online: 5/27/22). The flow of COVID-19 data from many state and local agencies also slowed to a trickle. In October, even the CDC began reporting cases and deaths weekly instead of daily. Altogether, undercounting of the coronavirus’s reach became worse than ever.
“We’re being told, ‘it’s up to you now to decide what to do,’ ” Blauer says, “but the data is not in place to be able to inform real-time decision making.”
With COVID-19 fatigue so widespread, businesses, governments and other institutions have to find ways to step up and do their part, Kennedy says. For instance, requiring better ventilation and filtration in public buildings could clean up indoor air and reduce the chance of spreading many respiratory infections, along with COVID-19. That’s a behind-the-scenes intervention that individuals don’t have to waste mental energy worrying about, he says.
The bottom line: People may have stopped worrying about COVID-19, but the virus isn’t done with us yet. “We have spent two-and-a-half years in a long, dark tunnel, and we are just beginning to glimpse the light at the end of that tunnel. But it is still a long way off,” WHO’s Tedros said. “The tunnel is still dark, with many obstacles that could trip us up if we don’t take care.” If the virus makes a resurgence, will we see it coming and will we have the energy to combat it again?
A group at the National Bureau of Standards at Boulder, Colo., now reports an extremely accurate [speed of light] measurement using the wavelength and frequency of a helium-neon laser.… The result gives the speed of light as 299,792.4562 kilometers per second.
Update That 1972 experiment measured the two-way speed of light, or the average speed of photons that traveled from their source to a reflective surface and back. The result, which still holds up, helped scientists redefine the standard length of the meter (SN: 10/22/83, p. 263). But they weren’t done putting light through its paces. In the late 1990s and early 2000s, photons set a record for slowest measured speed of light at 17 meters per second and froze in their tracks for one-thousandth of a second (SN: 1/27/01, p. 52). For all that success, one major hurdle remains: directly testing the one-way speed of light. The measurement, which many scientists say is impossible to make, could resolve the long-standing question of whether the speed of light is uniform in all directions.
Some immune defenses of the brain may have their roots in the gut.
A new study in mice finds that immune cells are first trained in the gut to recognize and launch attacks on pathogens, and then migrate to the brain’s surface to protect it, researchers report online November 4 in Nature. These cells were also found in surgically removed parts of human brains.
Every minute, around 750 milliliters of blood flow through the brain, giving bacteria, viruses or other blood-borne pathogens an opportunity to infect the organ. For the most part, the invaders are kept out by three membrane layers, called the meninges, which wrap around the brain and spinal cord and act as a physical barrier. If a pathogen does manage to breach that barrier, the researchers say, the immune cells trained in the gut are ready to attack by producing a battalion of antibodies.
The most common route for a pathogen to end up in the bloodstream is from the gut. “So, it makes perfect sense for these [immune cells] to be educated, trained and selected to recognize things that are present in the gut,” says Menna Clatworthy, an immunologist at the University of Cambridge.
Clatworthy’s team found antibody-producing plasma cells in the leathery meninges, which lie between the brain and skull, in both mice and humans. These immune cells produced a class of antibodies called immunoglobulin A, or IgA.
These cells and antibodies are mainly found in the inner lining of the gut and lungs, so the scientists wondered if the cells on the brain had any link to the gut. It turned out that there was: Germ-free mice, which had no microbes in their guts, didn’t have any plasma cells in their meninges either. However, when bacteria from the poop of other mice and humans were transplanted into the mice’s intestines, their gut microbiomes were restored, and the plasma cells then appeared in the meninges.
“This was a powerful demonstration of how important the gut could be at determining what is found in the meninges,” Clatworthy says.
Researchers captured microscope images of an attack in the meninges of mice that was led by plasma cells that had likely been trained in the guts. When the team implanted a pathogenic fungus, commonly found in the intestine, into the mice’s bloodstream, the fungus attempted to enter the brain through the walls of blood vessels in the meninges. However, plasma cells in the membranes formed a mesh made of IgA antibodies around the pathogen, blocking its entry. The plasma cells are found along the blood vessels, Clatworthy says, where they can quickly launch an attack on pathogens.
“To my knowledge, this is the first time anyone has shown the presence of plasma cells in the meninges. The study has rewritten the paradigm of what we know about these plasma cells and how they play a critical role in keeping our brain healthy,” says Matthew Hepworth, an immunologist at the University of Manchester in England who was not involved with the study. More research is needed to classify how many of the plasma cells in the meninges come from the gut, he says.
The finding adds to growing evidence that gut microbes can play a role in brain diseases. A previous study, for instance, suggested that in mice, boosting a specific gut bacterium could help fight amyotrophic lateral sclerosis, or ALS, a fatal neurological disease that results in paralysis (SN: 7/22/19). And while the new study found the plasma cells in the brains of healthy mice, previous research has found other gut-trained cells in the brains of mice with multiple sclerosis, an autoimmune disease of the brain and the spinal cord.
For now, the researchers want to understand what cues plasma cells follow in the guts to know it is time for them to embark on a journey to the brain.
It’s official: 2020 now has the most named storms ever recorded in the Atlantic in a single year.
On November 9, a tropical disturbance brewing in the northeastern Atlantic Ocean gained enough strength to become a subtropical storm. With that, Theta became the year’s 29th named storm, topping the 28 that formed in 2005.
With maximum sustained winds near 110 kilometers per hour as of November 10, Theta is expected to churn over the open ocean for several days. It’s too early to predict Theta’s ultimate strength and trajectory, but forecasters with the National Oceanic and Atmospheric Administration say they expect the storm to weaken later in the week.
If so, like most of the storms this year, Theta likely won’t become a major hurricane. That track record might be the most surprising thing about this season — there’s been a record-breaking number of storms, but overall they’ve been relatively weak. Only five — Laura, Teddy, Delta, Epsilon and Eta — have become major hurricanes with winds topping 178 kilometers per hour, although only Laura and Eta made landfall near the peak of their strength as Category 4 storms.
Even so, the 2020 hurricane season started fast, with the first nine storms arriving earlier than ever before (SN: 9/7/20). And the season has turned out to be the most active since naming began in 1953, thanks to warmer-than-usual water in the Atlantic and the arrival of La Niña, a regularly-occurring period of cooling in the Pacific, which affects winds in the Atlantic and helps hurricanes form (SN: 9/21/19). If a swirling storm reaches wind speeds of 63 kilometers per hour, it gets a name from a list of 21 predetermined names. When that list runs out, the storm gets a Greek letter.
While the wind patterns and warm Atlantic water temperatures set the stage for the string of storms, it’s unclear if climate change is playing a role in the number of storms. As the climate warms, though, you would expect to see more of the destructive, high-category storms, says Kerry Emanuel, an atmospheric scientist at MIT. “And this year is not a poster child for that.” So far, no storm in 2020 has been stronger than a Category 4. The 2005 season had multiple Category 5 storms, including Hurricane Katrina (SN: 12/20/05).
There’s a lot amount of energy in the ocean and atmosphere this year, including the unusually warm water, says Emanuel. “The fuel supply could make a much stronger storm than we’ve seen,” says Emanuel, “so the question is: What prevents a lot of storms from living up to their potential?” A major factor is wind shear, a change in the speed or direction of wind at different altitudes. Wind shear “doesn’t seem to have stopped a lot of storms from forming this year,” Emanuel says, “but it inhibits them from getting too intense.” Hurricanes can also create their own wind shear, so when multiple hurricanes form in close proximity, they can weaken each other, Emanuel says. And at times this year, several storms did occupy the Atlantic simultaneously — on September 14, five storms swirled at once.
It’s not clear if seeing hurricane season run into the Greek alphabet is a “new normal,” says Emanuel. The historical record, especially before the 1950s is spotty, he says, so it’s hard to put this year’s record-setting season into context. It’s possible that there were just as many storms before naming began in the ‘50s, but that only the big, destructive ones were recorded or noticed. Now, of course, forecasters have the technology to detect all of them, “so I wouldn’t get too bent out of shape about this season,” Emanuel says.
Some experts are hesitant to even use the term “new normal.”
“People talk about the ‘new normal,’ and I don’t think that is a good phrase,” says James Done, an atmospheric scientist at the National Center for Atmospheric Research in Boulder, Colo. “It implies some new stable state. We’re certainly not in a stable state — things are always changing.”
When some bacteria manage to escape being killed by a virus, the microbes end up hamstringing themselves. And that could be useful in the fight to treat infections.
The bacterium Shigella flexneri — one cause of the infectious disease shigellosis — can spread within cells that line the gut by propelling itself through the cells’ barriers. That causes tissue damage that can lead to symptoms like bloody diarrhea. But when S. flexneri in lab dishes evolved to elude a type of bacteria-killing virus, the bacteria couldn’t spread cell to cell anymore, making it less virulent, researchers report November 17 in Applied and Environmental Microbiology.
The research is a hopeful sign for what’s known as phage therapy (SN: 11/20/02). With antibiotic-resistant microbes on the rise, some researchers see viruses that infect and kill only bacteria, known as bacteriophages or just phages, as a potential option to treat antibiotic-resistant infections (SN: 11/13/19). With phage therapy, infected people are given doses of a particular phage, which kill off the problematic bacteria. The problem, though, is that over time those bacteria can evolve to be resistant against the phage, too.
“We’re kind of expecting phage therapy to fail, in a sense,” says Paul Turner, an evolutionary biologist and virologist at Yale University. “Bacteria are very good at evolving resistance to phages.” But that doesn’t mean the bacteria emerge unscathed. Some phages attack and enter bacteria by latching onto bacterial proteins crucial for a microbe’s function. If phage therapy treatments relied on such a virus, that could push the bacteria to evolve in such a way that not only helps them escape the virus but also impairs their abilities and makes them less deadly. People infected with these altered bacteria might have less severe symptoms or may not show symptoms at all.
Previous studies with the bacteria Pseudomonas aeruginosa, for instance, have found that phage and bacteria can engage in evolutionary battles that drive the bacteria to be more sensitive to antibiotics. The new study hints that researchers could leverage the arms race between S. flexneri and the newly identified phage, which was dubbed A1-1 after being found in Mexican wastewater, to treat shigellosis.
S. flexneri in contaminated water is a huge problem in parts of the world where clean water isn’t always available, such as sub-Saharan Africa and southern Asia, says Kaitlyn Kortright, a microbiologist also at Yale University. Every year, approximately 1.3 million people die from shigellosis, which is caused by four Shigella species. More than half of those deaths are in children younger than 5 years old. What’s more, antibiotics to treat shigellosis can be expensive and hard to access in those places. And S. flexneri is becoming resistant to many antibiotics. Phage therapy could be a cheaper, more accessible option to treat the infection.
The blow to S. flexneri’s cellular spread comes because to enter cells, A1-1 targets a protein called OmpA, which is crucial for the bacteria to rupture host cell membranes. The researchers found two types of mutations that made S. flexneri resistant to A1-1. Some bacteria had mutations in the gene that produces OmpA, damaging the protein’s ability to help the microbes spread from cell to cell. Others had changes to a structural component of bacterial cells called lipopolysaccharide.
The mutations in lipopolysaccharide were surprising, Kortright says, because the relationship between that structural component and OmpA isn’t fully worked out. One possibility is that those mutations distort OmpA’s structure in a way that the phage no longer recognizes it and can’t enter bacterial cells.
One lingering question is whether S. flexneri evolves in the same way outside a lab dish, says Saima Aslam, an infectious diseases physician at the University of California, San Diego who was not involved in the work. Still, the findings show that it’s “not always a bad thing” when bacteria become phage-resistant, she says.
