Category: Uncategorized

Bats, better known for their mousy looks, can have a colorful side. A new species, discovered when two bats were caught at an abandoned miners’ tunnel in western Africa, sports showy swathes of orange fur.

The new finds “are just gorgeous,” says mammalogist Nancy Simmons of the National Museum of Natural History in New York City. Orange fur on the bats’ backs contrasts with black sections of wing membranes.

But that’s not what sets this bat apart: Three other Myotis species from the continent are similarly flashy. Rather less visible traits, from details of hidden striping in its fur to its echolocation calls, peg Myotis nimbaensis as something unusual, Simmons and colleagues report online January 13 in American Museum Novitates.

The new species was discovered the old-fashioned way — out in a remote forest at night with keen eyes studying real animals. That’s not so common nowadays in the age of sensitive genetic tools, Simmons says. Many of the 20 or so new bat species typically named every year are detected through genetic analyses of museum specimen lookalikes. M. nimbaensis differs genetically from near kin — about as much as humans differ from gorillas. Differences also show up in teeth as well as other anatomy.

But when researchers collected the first bat, near the mouth of an abandoned tunnel for mineral exploration up in Guinea’s section of the Nimba Mountains, the flashy beast wasn’t obviously anything new. While most of the more than 1,400 known kinds of bats are various shades of brown, bats here and there around the world can be yellow, fluffball white or coppery red. And there was the matter of the three other orange Myotis species. (How, or whether, the colors matter in animals active at night, Simmons says, is “one of the mysteries.”)

One way to tell the new species apart is from the proportions of secret stripes on the individual hairs in orange fur patches. In the newly named bats, the bottom third of each orange hair is black. Then comes a creamy white middle third before the hair turns pumpkin at the tip.

Researchers named M. nimbaensis after its mountainous habitat. The Nimba Mountains shoot up abruptly from lowland forests, creating little “sky islands” of isolated habitat on peaks, says coauthor Eric Moïse Bakwo Fils, a bat specialist at the University of Maroua in Cameroon. M. nimbaensis probably eats insects, judging by its interlocking triangular teeth.

Bakwo Fils worries about the fragility of sky islands and the newfound bats’ future. Small animals flitting in the dark rarely get the conservation attention that large charismatic African wildlife does. Yet we depend on various little half-seen bats streaking in the dark to catch insects, pollinate plants, spread seeds and help with other chores that keep our ecosystems going.

In 2015, two Princeton economists published data showing that white people in their 40s and 50s in the United States were dying at much higher rates than expected — and that the death rates for that age group had been rising sharply for almost two decades. The big killers like cancer and heart disease weren’t to blame. Instead, alcohol misuse, drug overdoses and suicide caused these early deaths, which the economists, Anne Case and Angus Deaton, called “deaths of despair.”

I remember reading that paper and thinking it was a revelation — a dataset able to reveal something profound happening to our society that was largely hidden until this analysis. I was also moved by the phrase “deaths of despair,” which casts a vision of a person being ground down by years of disappointment and struggle. People without college degrees are most affected, the study and other research shows. The reasons for their struggles are many, including the evaporation of stable manufacturing jobs and health insurance, fractured families and a lack of social supports.

This trend toward more suffering and shorter lives shows no hint of waning. In 2015, U.S. life expectancy declined for the first time in decades. Other rich countries have not experienced similar declines.

In this issue, behavioral sciences writer Bruce Bower revisits the deaths of despair hypothesis, exploring Case and Deaton’s latest research connecting despair with reports of physical pain, as well as other scientists’ efforts to define despair to learn how to avoid despair-related deaths. It’s a fascinating exploration of how social scientists go about testing a new construct, seeking to learn if and how despair is different than depression and other mental health diagnoses. Bower also made illuminating connections between the demoralization, grief and anger that people feel during this pandemic, as they lose friends and family, jobs and social ties.

People who feel threatened, ignored and alone are more vulnerable to conspiracy theories and misinformation. The spread of misinformation has been disastrous for our country’s response to the coronavirus pandemic, with social media channels awash with misinformation about fake cures and questioning whether masks are useful (they are!). That misinformation has caused needless suffering and death. Anti-vaccine rhetoric, including false claims that the COVID-19 vaccine contains a microchip designed to track people’s movements, is pushing some people to avoid vaccines, which are our best shot to end the pandemic, along with masks and social distancing. As of November, 21 percent of adults in the United States said they do not intend to get the shot, and that more information would not change their minds.

Shared facts and common truth can shed light on the challenges we face, including the pandemic and attacks on our system of government. The “deaths of despair” research is a shining example of how science can illuminate the effects of complex social and economic trends on our lives. Science can help us understand what’s happening to us, and how we can build a better future. It’s time to listen.

For the first time, astronomers have definitively spotted a flaring magnetar in another galaxy.

These ultra-magnetic stellar corpses were thought to be responsible for some of the highest-energy explosions in the nearby universe. But until this burst, no one could prove it, astronomers reported January 13 at the virtual meeting of the American Astronomical Society and in papers in Nature and Nature Astronomy.

Astronomers have seen flaring magnetars in the Milky Way, but those are so bright that it’s impossible to get a good look at them. Possible glimpses of flaring magnetars in other galaxies may have been spotted before, too. But “the others were all a little circumstantial, and not as rock solid,” says astrophysicist Victoria Kaspi of the McGill Space Institute in Montreal, who was not involved in the new discovery. “Here you have something that is so incontrovertible, it’s like, okay, this is it. There’s no question anymore.”

The first sign of the magnetar arrived as a blast of X-rays and gamma rays on April 15. Five telescopes in space, including the Fermi Gamma-ray Space Telescope and the Mars Odyssey orbiter, observed the blast, giving scientists enough information to track down its source: the galaxy NGC 253, or the Sculptor galaxy, 11.4 million light-years away.

At first, astronomers thought that the blast was a type of cataclysmic explosion called a short gamma-ray burst, or GRB, which are typically caused by colliding neutron stars or other destructive cosmic events.

But the signal looked weird for a short GRB: It rose to peak brightness quickly, within two milliseconds, tailed off for another 50 milliseconds and appeared to be over by about 140 milliseconds. As the signal faded, some of the telescopes detected fluctuations in the light that changed faster than a millisecond.

Typical short GRBs that result from a neutron star collision don’t change like that, said astrophysicist Oliver Roberts of the Universities Space Research Association in Huntsville, Ala. But flaring magnetars in our own galaxy do, when the bright spot where the flare was emitted comes in and out of view as the magnetar spins.

Then, surprisingly, the Fermi telescope caught gamma rays with energies higher than a gigaelectronvolt arriving four minutes after the initial blast. There is no way for the known sources of short GRBs to do that.

“We’ve discovered a masquerading magnetar in a nearby galaxy, and we’ve unmasked it,” said astrophysicist Kevin Hurley of the University of California, Berkeley at a Jan. 13 news briefing.

The researchers think that the flare was triggered by a massive starquake, one thousand trillion trillion, or 10²⁷, times as large as the 9.5 magnitude earthquake recorded in Chile in 1960. “I’m from California, and out here we would definitely call that the Big One,” Hurley says. The quake led the magnetar to release a blob of plasma that sped away at nearly the speed of light, emitting gamma rays and X-rays as it went.

The discovery suggests that at least some signals that look like short GRBs are in fact from magnetar flares, as astronomers have long suspected (SN: 11/3/10). It also means that three earlier events that astronomers had flagged as possible magnetar flares probably were actually from the magnetized stellar corpses, giving astronomers a population of magnetar flares to compare to each other.

The finding could have exciting implications for fast radio bursts, another mysterious cosmic signal that has had astronomers scratching their heads for over a decade. Several lines of evidence connect fast radio bursts to magnetars, including another signal coming from within the Milky Way that coincidentally also arrived in April 2020 (SN: 6/4/20).

“That [discovery] leant extra credence to fast radio bursts being [from] magnetars,” Kaspi says, though there are still problems with that theory.

Kaspi has compared the apparent frequency of magnetar flares in other galaxies to the frequency of fast radio bursts and found that the rates are similar. “That argues that actually, most or all fast radio bursts could be magnetars…. I don’t think yet it’s the total solution,” but it’s a good step, she says.

Spiking COVID-19 cases, slow vaccine rollout and the emergence of more transmissible coronavirus variants in some countries have sparked debate among scientists over the best way to protect people with recently authorized vaccines. 

One idea involves delaying when people receive the second of two required vaccine doses, so that more people can receive the doses that are currently available. 

That’s happening in the United Kingdom, where researchers have raised concerns about a new coronavirus variant that appears to be more contagious than other versions. Officials there are opting to extend the time between each vaccine dose from three or four weeks to up to three months (SN: 12/22/20). 

In the United States, on the other hand, officials strongly recommend that states stick to the regimen that the U.S. Food and Drug Administration authorized in December — two shots spaced three weeks apart for Pfizer-BioNTech’s vaccine and four weeks apart for Moderna’s. 

On January 12, the Trump administration announced it was no longer holding back second shots of COVID-19 vaccines, several days after President-elect Joe Biden suggested he would release all the shots. While that may speed protection for more Americans, it also raises the possibility that people might not get their second doses on time, if manufacturing problems arise.  

The possibility that second doses could be delayed has some experts concerned because it might lead to millions of people walking around with only partial immunity to the coronavirus, a condition that could be ripe for harmful mutations of the virus to arise.

Delaying the second shot is a gamble, says Ramón Lorenzo-Redondo, a virologist at Northwestern University Feinberg School of Medicine in Chicago, particularly without a lot of evidence suggesting how well one dose works. Officials “shouldn’t gamble [their] best tools” to fight the pandemic, he says. “We don’t want to fuel [potential viral evolution] by doing suboptimal immunization of the population.”

How that fueling of virus evolution could happen comes down to the immune system. If people have full immunity as a result of vaccination, their immune response is likely to be robust, spawning large numbers of neutralizing antibodies, for example, that stop viruses from getting into cells and heading off harmful mutations before they arise. But if people have partial immunity, that immune response is likely to be weaker. 

It’s like when doctors encourage patients to finish a full course of antibiotics, Lorenzo-Redondo says. In that case, eliminating susceptible bacteria with a full course could help lower the chance that stragglers build up resistance.

For the COVID-19 vaccine, if people’s second doses are delayed long enough — akin to not finishing a full complement of antibiotics — it’s possible that low numbers of neutralizing antibodies triggered by only one dose may only partially fight an infection. That might provide more time for variants of the virus with immune-dodging mutations to arise and thrive and be transmitted to other people.

If immune-dodging variants do arise as a result of shot delays and spread to lots of people, that could deal a blow to vaccines’ effectiveness. For example, if mutations arose that prevented vaccine-induced antibodies from binding to the virus, or caused antibodies to bind less tightly, that virus variant may be more likely to infect cells than variants without the mutation and thus cause disease, Lorenzo-Redondo says. With cases surging in many places, including the United Kingdom and the United States, the coronavirus could have even more chances to accumulate vaccine-evading mutations than it would if case numbers were lower.

For now, it’s unclear how protected vaccinated people are after a single shot and for how long. Trial participants who received Pfizer-BioNTech’s vaccine had low levels of neutralizing antibodies 21 days after the first dose, researchers reported in the Dec. 17 New England Journal of Medicine. But clinical trial results from both the Pfizer-BioNTech and Moderna vaccines suggest that protection begins around two weeks after the first dose — Pfizer-BioNTech’s vaccine had an efficacy of around 50 percent after the first dose and Moderna’s had around 80 percent efficacy (SN: 12/18/20). It’s unknown how durable that protection might be, says Sarah Cobey, an epidemiologist and evolutionary biologist at the University of Chicago, but it would be weird to see it fade quickly. 

Cobey is one of the scientists who isn’t worried about the risk of a long delay between shots.  Instead, expanding how many people get the first dose could actually help control how much the coronavirus changes, she says. That’s because even the partial protection that people may get from a single dose “will almost certainly lower the prevalence of infection,” she says. Fewer infections overall would mean fewer coronavirus variants in general circulating among people. By virtue of numbers, the coronavirus then may not accumulate as many mutations that could help it evade immune systems.

And even if a virus accumulates mutations that help it dodge the immune response as a result of the dose delay, such changes might in turn damage essential viral functions like breaking into and hijacking a host cell. A virus that can escape immunity, for instance, might end up being less transmissible. For now, it’s unclear what might happen with the coronavirus, which in general mutates more slowly than other similar viruses thanks to a unique proofreading enzyme that acts as a spell-check for the letters that make up the coronavirus’s genetic blueprint (SN: 1/28/20).

What’s more, the immune responses that a person makes also don’t attack just one part of a virus. Antibodies, for instance, including those induced by vaccines, hit many different parts of viral proteins, making it harder for the virus to escape. And over time antibodies can get better at their job (SN: 11/24/20). So, most mutations are unlikely to render antibodies completely ineffective. 

“You put that all together and it’s a pretty high barrier” for virus evolution to work around, says Adam Lauring, an infectious disease physician and virologist at the University of Michigan Medical School in Ann Arbor. 

In lab experiments, for example, COVID-19 patient serum that harbors myriad coronavirus antibodies still stops the coronavirus from infecting cells in a dish, even if there are viral mutations, researchers reported in a preliminary study posted January 4 at bioRxiv.org. While a few mutations — including one present in a coronavirus variant now circulating in South Africa — made antibodies in the serum less effective at stopping viruses from infecting cells, the serum’s virus-halting activity didn’t outright disappear. 

Still, that doesn’t mean potentially risky viral evolution as a result of delaying doses is not going to happen. “I think this is something we need to study and we need to look at for sure,” Lauring says. For now, “I’m not sure we know enough that we can really confidently say what one or other [vaccine-dosing] strategy is going to do.”