A mysterious new disease may be to blame for severe, unexplained inflammation in older men. Now, researchers have their first good look at who the disease strikes, and how often.

VEXAS syndrome, an illness discovered just two years ago, affects nearly 1 in 4,000 men over 50 years old, scientists estimate January 24 in JAMA. The disease also occurs in older women, though less frequently. Altogether, more than 15,000 people in the United States may be suffering from the syndrome, says study coauthor David Beck, a clinical geneticist at NYU Langone Health in New York City. Those numbers indicate that physicians should be on the lookout for VEXAS, Beck says. “It’s underrecognized and underdiagnosed. A lot of physicians aren’t yet aware of it.”
Beck’s team reported discovering VEXAS syndrome in 2020, linking mutations in a gene called UBA1 to a suite of symptoms including fever, low blood cell count and inflammation. His team’s new study is the first to estimate how often VEXAS occurs in the general population — and the results are surprising. “It’s more prevalent than we suspected,” says Emma Groarke, a hematologist at the National Institutes of Health in Bethesda, Md., who was not involved with the study.
VEXAS tends to show up later in life ­­— after people somehow acquire UBA1 mutations in their blood cells. Patients may feel overwhelming fatigue, lethargy and have skin rashes, Beck says. “The disease is progressive, and it’s severe.” VEXAS can also be deadly. Once a person’s symptoms begin, the median survival time is about 10 years, his team has found.

Until late 2020, no one knew that there was a genetic thread connecting VEXAS syndrome’s otherwise unexplained symptoms. In fact, individuals may be diagnosed with other conditions, including polyarteritis nodosa, an inflammatory blood disease, and relapsing polychondritis, a connective tissue disorder, before being diagnosed with VEXAS.

To ballpark the number of VEXAS-affected individuals, Beck’s team combed through electronic health records of more than 160,000 people in Pennsylvania, in a collaboration with the NIH and Geisinger Health. In people over 50, the disease-causing UBA1 mutations showed up in roughly 1 in 4,000 men. Among women in that age bracket, about 1 in 26,000 had the mutations.

A genetic test of the blood can help doctors diagnose VEXAS, and treatments like steroids and other immunosuppressive drugs, which tamp down inflammation, can ease symptoms. Groarke and her NIH colleagues have also started a small phase II clinical trial testing bone marrow transplants as a way to swap patients’ diseased blood cells for healthy ones.

Beck says he hopes to raise awareness about the disease, though he recognizes that there’s much more work to do. In his team’s study, for instance, the vast majority of participants were white Pennsylvanians, so scientists don’t know how the disease affects other populations. Researchers also don’t know what spurs the blood cell mutations, nor how they spark an inflammatory frenzy in the body.

“The more patients that are diagnosed, the more we’ll learn about the disease,” Beck says. “This is just one step in the process of finding more effective therapies.”

For nearly 650 years, the fortress walls in the Chinese city of Xi’an have served as a formidable barrier around the central city. At 12 meters high and up to 18 meters thick, they are impervious to almost everything — except subatomic particles called muons.

Now, thanks to their penetrating abilities, muons may be key to ensuring that the walls that once protected the treasures of the first Ming Dynasty — and are now a national architectural treasure in their own right — stand for centuries more.

A refined detection method has provided the highest-resolution muon scans yet produced of any archaeological structure, researchers report in the Jan. 7 Journal of Applied Physics. The scans revealed interior density fluctuations as small as a meter across inside one section of the Xi’an ramparts. The fluctuations could be signs of dangerous flaws or “hidden structures archaeologically interesting for discovery and investigation,” says nuclear physicist Zhiyi Liu of Lanzhou University in China.
Muons are like electrons, only heavier. They rain down all over the planet, produced when charged particles called cosmic rays hit the atmosphere. Although muons can travel deep into earth and stone, they are scattered or absorbed depending on the material they encounter. Counting the ones that pass through makes them useful for studying volcano interiors, scanning pyramids for hidden chambers and even searching for contraband stashed in containers impervious to X-rays (SN: 4/22/22).

Though muons stream down continuously, their numbers are small enough that the researchers had to deploy six detectors for a week at a time to collect enough data for 3-D scans of the rampart.

It’s now up to conservationists to determine how to address any density fluctuations that might indicate dangerous flaws, or historical surprises, inside the Xi’an walls.

A type of bacteria that’s overabundant in the nasal passages of people with hay fever may worsen symptoms. Targeting that bacteria may provide a way to rein in ever-running noses.

Hay fever occurs when allergens, such as pollen or mold, trigger an inflammatory reaction in the nasal passages, leading to itchiness, sneezing and overflowing mucus. Researchers analyzed the composition of the microbial population in the noses of 55 people who have hay fever and those of 105 people who don’t. There was less diversity in the nasal microbiome of people who have hay fever and a whole lot more of a bacterial species called Streptococcus salivarius, the team reports online January 12 in Nature Microbiology.
S. salivarius was 17 times more abundant in the noses of allergy sufferers than the noses of those without allergies, says Michael Otto, a molecular microbiologist at the National Institute of Allergy and Infectious Diseases in Bethesda, Md. That imbalance appears to play a part in further provoking allergy symptoms. In laboratory experiments with allergen-exposed cells that line the airways, S. salivarius boosted the cells’ production of proteins that promote inflammation.

And it turns out that S. salivarius really likes runny noses. One prominent, unpleasant symptom of hay fever is the overproduction of nasal discharge. The researchers found that S. salivarius binds very well to airway-lining cells exposed to an allergen and slathered in mucus — better than a comparison bacteria that also resides in the nose.

The close contact appears to be what makes the difference. It means that substances on S. salivarius’ surface that can drive inflammation — common among many bacteria — are close enough to exert their effect on cells, Otto says.

Hay fever, which disrupts daily activities and disturbs sleep, is estimated to affect as many as 30 percent of adults in the United States. The new research opens the door “to future studies targeting this bacteria” as a potential treatment for hay fever, says Mahboobeh Mahdavinia, a physician scientist who studies immunology and allergies at Rush University Medical Center in Chicago.

But any treatment would need to avoid harming the “good” bacteria that live in the nose, says Mahdavinia, who was not involved in the research.

The proteins on S. salivarius’ surface that are important to its ability to attach to mucus-covered cells might provide a target, says Otto. The bacteria bind to proteins called mucins found in the slimy, runny mucus. By learning more about S. salivarius’ surface proteins, Otto says, it may be possible to come up with “specific methods to block that adhesion.”

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.

SEATTLE — Luke Skywalker’s home planet in Star Wars is the stuff of science fiction. But Tatooine-like planets in orbit around pairs of stars might be our best bet in the search for habitable planets beyond our solar system.

Many stars in the universe come in pairs. And lots of those should have planets orbiting them (SN: 10/25/21). That means there could be many more planets orbiting around binaries than around solitary stars like ours. But until now, no one had a clear idea about whether those planets’ environments could be conducive to life. New computer simulations suggest that, in many cases, life could imitate art.
Earthlike planets orbiting some configurations of binary stars can stay in stable orbits for at least a billion years, researchers reported January 11 at the American Astronomical Society meeting. That sort of stability, the researchers propose, would be enough to potentially allow life to develop, provided the planets aren’t too hot or cold.

Of the planets that stuck around, about 15 percent stayed in their habitable zone — a temperate region around their stars where water could stay liquid — most or even all of the time.

The researchers ran simulations of 4,000 configurations of binary stars, each with an Earthlike planet in orbit around them. The team varied things like the relative masses of the stars, the sizes and shapes of the stars’ orbits around each other, and the size of the planet’s orbit around the binary pair.

The scientists then tracked the motion of the planets for up to a billion years of simulated time to see if the planets would stay in orbit over the sorts of timescales that might allow life to emerge.

A planet orbiting binary stars can get kicked out of the star system due to complicated interactions between the planet and stars. In the new study, the researchers found that, for planets with large orbits around star pairs, only about 1 out of 8 were kicked out of the system. The rest were stable enough to continue to orbit for the full billion years. About 1 in 10 settled in their habitable zones and stayed there.

Of the 4,000 planets that the team simulated, roughly 500 maintained stable orbits that kept them in their habitable zones at least 80 percent of the time.

“The habitable zone . . . as I’ve characterized it so far, spans from freezing to boiling,” said Michael Pedowitz, an undergraduate student at the College of New Jersey in Ewing who presented the research. Their definition is overly strict, he said, because they chose to model Earthlike planets without atmospheres or oceans. That’s simpler to simulate, but it also allows temperatures to fluctuate wildly on a planet as it orbits.
“An atmosphere and oceans would smooth over temperature variations fairly well,” says study coauthor Mariah MacDonald, an astrobiologist also at the College of New Jersey. An abundance of air and water would potentially allow a planet to maintain habitable conditions, even if it spent more of its time outside of the nominal habitable zone around a binary star system.

The number of potentially habitable planets “will increase once we add atmospheres,” MacDonald says, “but I can’t yet say by how much.”

She and Pedowitz hope to build more sophisticated models in the coming months, as well as extend their simulations beyond a billion years and include changes in the stars that can affect conditions in a solar system as it ages.

The possibility of stable and habitable planets in binary star systems is a timely issue says Penn State astrophysicist Jason Wright, who was not involved in the study.

“At the time Star Wars came out,” he says, “we didn’t know of any planets outside the solar system, and wouldn’t for 15 years. Now we know that there are many and that they orbit these binary stars.”

These simulations of planets orbiting binaries could serve as a guide for future experiments, Wright says. “This is an under-explored population of planets. There’s no reason we can’t go after them, and studies like this are presumably showing us that it’s worthwhile to try.”

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.