Why the coronavirus’s delta variant dominated 2021

2021 was a year of coronavirus variants.

Alpha and beta kicked off the year, and several worrisome variants later, omicron is closing it out. How omicron may come to define the pandemic’s future remains uncertain. But even as omicron comes on strong, one variant, which rose to global dominance midyear in a way variants like alpha and beta never did, continues to largely define the pandemic right now: delta.

Things had actually seemed to be looking up in some parts of the world in the late spring and early summer of 2021, a year and a half into the COVID-19 pandemic. In the United States, for instance, millions of people were vaccinated, cases of the disease were falling, and people were beginning to socialize and resume normal activities.

But then delta hit hard. First spotted in India in October 2020, this variant of SARS-CoV-2, the coronavirus that causes COVID-19, quickly swept around the world, supplanting other versions of the virus in 2021 (SN: 7/2/21). Delta overwhelmed health care systems, tore through unvaccinated populations and showed that even the vaccinated were vulnerable, causing some breakthrough cases.
It soon became clear why delta wreaks so much havoc. People infected with delta make more of the virus and spread it for longer than people infected with other variants, researchers reported in Clinical Infectious Diseases in August. As a result, delta infections are more contagious. Consider two scenarios in a community where no one has immunity to the coronavirus: A person infected with an earlier version of the virus — the one first identified in Wuhan, China, that set off the pandemic — might spread it to two or three others. But a person infected with delta may transmit it to five or six people.

Delta owes its success to mutations in some of its proteins. Take, for instance, a mutation called R203M in the coronavirus’s nucleocapsid, or N protein, located inside the virus. This mutation may increase the amount of viral RNA that can be made or make it easier for the N protein to do its job, packing RNA into newly assembled viral particles, researchers reported in Science in November.
Mutations similar to delta’s have appeared here and there in other variants that proved themselves capable of spreading more easily or better evading the body’s immune defenses than the original virus. That includes alpha, first spotted in the United Kingdom; beta, first characterized in South Africa; and gamma, first noted in Brazil. The recently discovered omicron variant, first described in South Africa and Botswana, also shares some of the same mutations (SN: 12/1/21).

Some of delta’s grab bag of mutations are identical to those found in other variants, while others change the same protein building block, or amino acid, in a different way or pop up in the same part of the virus. For instance, alpha and omicron also have the same mutation of the 203rd amino acid in the N protein, but it is a different amino acid change than seen in delta. And some mutations are entirely new to delta.
Scientists don’t yet know the effect that all those changes have on delta’s ability to replicate or spread to others. What’s more, delta continues to evolve, picking up additional changes over time. But studies have zeroed in on the unique constellation of mutations decorating the virus’ spike protein. It’s the knobby protein studding each coronavirus that helps the virus latch onto and invade human cells. What looks like an individual knob is in fact composed of three identical pieces that fit together, each carrying the same set of mutations.

Some of delta’s spike protein mutations may help the virus more easily break into cells, where it turns cell machinery into virus-making factories. Two of those, dubbed T478K and L452R, are advantageously located on the receptor-binding domain. This is the part of the spike protein that attaches to ACE2, a protein on the surface of host cells.

Other mutations show up in a region of the spike protein called the N-terminal domain, which is a known target of the immune system’s neutralizing antibodies. These mutations may help the virus evade those antibodies, which can stop the virus from infecting cells.

And yet two other mutations, P681R and D614G, may help prep newly made viruses to go out and conquer. Those mutations are nestled near the dividing line for two parts of the spike protein, S1 and S2. Those parts need to be split apart to allow the coronavirus to engage in the gymnastics needed to help it fuse with the membrane of its prospective human host cell.
Human cells actually aid in this process: Inside infected cells a human protein called furin nicks the spike protein between the S1 and S2 segments, opening the receptor-binding domain so it can better grab ACE2. The P681R and D614G mutations may make the spike protein easier for furin to cut. Once snipped, newly-made viruses are primed to infect other cells.

Taken together, these mutations help delta break into cells more quickly and perform several tasks better than other variants do. As a result, in 2021, delta was able to become the dominant variant in the world.

Here’s how specific delta spike protein mutations may aid in a cell take-over:

  1. Some mutations allow the spike protein to get a better grip on cells.
    The coronavirus begins its cellular break-in by latching onto a protein called ACE2 that studs the surface of many types of human cells. Three mutations may make delta grabbier than other variants.

D614G interrupts some molecular interactions in the spike protein near a hinge that controls whether the receptor binding domain is in a closed position where it is protected from antibodies, or in an open position so that it can grab ACE2. With the D614G mutation, it’s more likely that one or more of ACE2-snagging portions of the protein will be open for action.

L452R may strengthen the interaction between ACE2 and the spike protein, making the virus more likely to infect cells. The change switches the charge on a protein building block in a key part of the spike protein from neutral to positive. So, like a magnet attracted to metal, the mutation seems to make the spike protein bind more tightly to a part of ACE2 that has a negative charge.

T478K is unique to the delta variant. It’s so far unclear what it does, but like L452R, it may also help strengthen the spike protein’s hold on ACE2.

  1. Some mutations allow delta to better fuse with the cell’s membrane, paving the way for the coronavirus to dump its genetic material into the cell.
    Once delta latches onto ACE2, a human protein called TMPRSS2 cuts away a part of the spike protein. As a result, the S1 portion of the protein is discarded, freeing up the S2 portion of the protein to twist into shape for the next step in the process: fusing to the cell. Some evidence suggests delta may be better at letting go of S1, making breaking into cells easier.

L452R may help the virus fuse with the membrane on the outside of the cell it’s trying to infect. That allows the virus to release its genetic material and begin hijacking the cell’s machinery to begin making more copies of itself.

P681R may create a stretch of basic amino acids that could help the virus fuse better with the cell membrane, helping more viruses get inside more cells.

As a result of these and other changes, delta can fuse with cells faster and can enter cells that have lower levels of ACE2 studding their surfaces than other variants can, researchers reported in Science in October.

After the virus fuses to the cell, it sets loose its RNA and turns its new lair into a virus factory: Viral RNA is copied, human ribosomes make viral proteins and the cell churns out nearly identical copies of the coronavirus. As the virus makes copies of its RNA, it can make typos. Sometimes, the genetic errors help the virus, which can give rise to variants like delta. But not all changes are good for the virus. Some genetic typos cause damage to viral proteins, meaning the viruses with those mutations can’t infect new cells. Other changes don’t have any effect on the virus at all.

  1. Some delta mutations may better prime newly made viruses to more easily infect cells.
    Before newly made viruses are released from the cell, the human protein furin snips the spike protein between S1 and S2. That lets the spike protein adopt the right shape to snag human cells and sets the protein up to allow for better membrane fusion.

Delta may be snippier than other variants.

Mutations D614G and P681R may increase the number of spike proteins cut by furin on each newly made virus, better prepping the viruses to enter other cells.

D614G makes it easier for furin to make its snips. This preliminary cut happens in a different location than the TMPRSS2 cut. The mutation may also increase the number of spike proteins on each copy of the virus.

Like D614G, P681R may also boost the number of spike proteins cut by the human cell protein furin, priming the newly made viruses to infect new cells.

  1. Some mutations may help newly released viruses evade antibodies as the viruses seek out other cells to infect.
    The immune systems of people who have recovered from an infection or those who got vaccinated make antibodies to the coronavirus. Several of delta’s mutations may help the virus evade these antibodies, which would otherwise block viral entry into other cells.

T19R, G142D, R158G and two spots — called E156del and F157del — where amino acids are missing from the protein may hide parts of the virus from antibodies, helping it slip past those immune system defenses.

T478K, the mutation unique to the delta variant, is close to the same spot as E484K, a mutation that was implicated in the antibody-evasion tactics of the beta variant.

How a warming climate may make winter tornadoes stronger

Though tornadoes can occur in any season, the United States logs the greatest number of powerful twisters in the warmer months from March to July. Devastating winter tornadoes like the one that killed at least 88 people across Kentucky and four other states beginning on December 10 are less common.

But climate change could increase tornado intensity in cooler months by many orders of magnitude beyond what was previously expected, researchers report December 13 in a poster at the American Geophysical Union’s fall meeting.

Tornadoes typically form during thunderstorms when warm, humid airstreams get trapped beneath cooler, drier winds. As the fast-moving air currents move past each other, they create rotating vortices that can transform into vertical, spinning twisters (SN: 12/14/18). Many tornadoes are short-lived, sometimes lasting mere minutes and with a width of only 100 yards, says Jeff Trapp, an atmospheric scientist at the University of Illinois at Urbana-Champaign.
Over the last 20 years, tornado patterns have shifted so that these severe weather events occur later in the season and across a broader range in the United States than before, Trapp says (SN: 10/18/18). But scientists have struggled to pin down a direct link between the twister changes and human-caused climate change.

Unlike hurricanes and other severe storm systems, tornadoes happen at such a small scale that most global climate simulations don’t include the storms, says Kevin Reed, an atmospheric scientist at Stony Brook University in New York who was not involved in the new research.

To see how climate change may affect tornadoes, Trapp and colleagues started with atmospheric measurements of two historical tornadoes and simulated how those storm systems might play out in a warmer future.

The first historical tornado took place in the cool season on February 10, 2013, near Hattiesburg, Miss., and the second occurred in the warm season on May 20, 2013, in Moore, Okla. The researchers used a global warming simulation to predict how the twisters’ wind speeds, width and intensity could change in a series of alternative climate scenarios.

Both twisters would likely become more intense in futures affected by climate change, the team found. But the simulated winter storm was more than eightfold as powerful as its historical counterpart, in part due to a predicted 15 percent increase in wind speeds. Climate change is expected to increase the availability of warm, humid air systems during cooler months, providing an important ingredient for violent tempests.

“This is exactly what we saw on Friday night,” Trapp says. The unseasonably warm weather in the Midwest on the evening of December 10 and in the early morning of December 11 probably contributed to the devastation of the tornado that traveled hundreds of miles from Arkansas to Kentucky, he speculates.

Simulating how historical tornados could intensify in future climate scenarios is a “clever way” to address the knowledge gap around the effects of climate change on these severe weather systems, says Daniel Chavas, an atmospheric scientist at Purdue University in West Lafayette, Ind., who was not involved in the new research.

But Chavas notes that this research is only one piece of a larger puzzle as researchers investigate how tornados might impact communities in the future.

One drawback of this type of simulation is it often requires direct measurements from a historical event, Reed says. That limits its prediction power to re-creating documented tornadoes rather than broadly forecasting shifts in large-scale weather systems.

Though the team based its predictions on only two previous tornados, Trapp says he hopes that adding more historical twisters to the analysis could provide more data for policy makers as well as residents of communities that may have to bear the force of intensifying tornadoes.

Why it matters that health agencies finally said the coronavirus is airborne

This year, health experts around the world revised their views about how the coronavirus spreads. Aerosol scientists, virologists and other researchers had determined in 2020 that the virus spreads through the air, but it took until 2021 for prominent public health agencies to acknowledge the fact. The admission could have wide-ranging consequences for everything from public health recommendations and building codes to marching band practices (SN: 8/14/21, p. 24).

For decades, doctors and many researchers have thought that respiratory viruses such as cold and flu viruses spread mainly by people touching surfaces contaminated by mucus droplets and then touching their faces. That’s why, in the early days of the pandemic, disinfectant wipes flew off store shelves.

Surface-to-face transfer is still a probable route of infection for some cold-causing viruses, such as respiratory syncytial virus, or RSV. But it turns out that the coronavirus spreads mainly through fine aerosol particles that may hang in the air for hours, particularly indoors.

People spread such aerosols when coughing or sneezing, but also when talking, singing, shouting and even quietly breathing, allowing infected people to spread the disease even before they know they’re sick. Some evidence suggests that the coronavirus may be evolving to spread more easily through the air (SN: 9/25/21, p. 6).

It took collecting reams of data and more than 200 scientists pushing the World Health Organization and other public health agencies to acknowledge airborne spread of the coronavirus. In April 2021, both the WHO and U.S. Centers for Disease Control and Prevention updated their recommendations to note that airborne spread is a major route of infection (SN Online: 5/18/21).

That recognition was vital to public understanding of why wearing well-fitting masks is necessary in public indoor places (SN: 3/13/21, p. 14; SN Online: 7/27/21). Masking, social distancing and other measures to guard against the coronavirus are also credited with nearly wiping out flu last winter (SN Online: 2/2/21). Experts fear a resurgence of cold and flu this winter if those measures aren’t continued (SN Online: 8/12/21).

Knowledge that COVID-19 is an airborne disease has led to such measures as rearranging seating in orchestras (SN Online: 6/23/21) and updating recommendations for proper ventilation and filtration in buildings. Some scientists and activists have also suggested that the safety of indoor air should be regulated to reduce the spread of diseases, much like safety standards for food and drinking water.

A custom brain implant lifted a woman’s severe depression

A personalized brain implant eased the crushing symptoms of a woman’s severe depression, allowing her to once again see the beauty of the world. “It’s like my lens on the world changed,” said Sarah, the research volunteer who requested to be identified by her first name only.

The technology, described October 4 in Nature Medicine, brings researchers closer to understanding how to detect and change brain activity in ultraprecise ways (SN: 2/10/19).

The device was bespoke; it was built specifically for Sarah’s brain. The details of the new system may not work as a treatment for many other people, says Alik Widge, a psychiatrist and neural engineer at the University of Minnesota in Minneapolis. Still, the research is “a really significant piece of work,” he says, because it points out a way to study how brain activity goes awry in depression.

Researchers at the University of California, San Francisco implanted temporary thin wire electrodes into Sarah’s brain. The 36-year-old woman had suffered from severe depression for years. These electrodes allowed researchers to monitor the brain activity that corresponded to Sarah’s depression symptoms — a pattern that the researchers could use as a biomarker, a signpost of trouble to come. In Sarah’s case, a particular sign emerged: a fast brain wave called a gamma wave in her amygdala, a brain structure known to be involved in emotions.
With this biomarker in hand, the researchers then figured out where to stimulate the brain to interrupt Sarah’s distressing symptoms. A region called the ventral capsule/ventral striatum, or VC/VS, seemed to be the key. That’s not surprising; previous research suggests the region is involved with feeling good and other emotions. When researchers applied tiny jolts of electrical current to this region, Sarah’s mood improved. “We could learn the road map of Sarah’s brain in a way that we could really improve her depression symptoms,” Katherine Scangos of UCSF said in a Sept. 30 news briefing.

During this mapping phase of the experiment, Sarah felt joy when the right spot was stimulated. “I laughed out loud,” she said in the briefing. “This was the first time I had spontaneously laughed and smiled where it wasn’t faked or forced in five years.”

Surgeons then implanted a more permanent device into Sarah’s brain last June. Scientists programmed the device to detect when gamma signals were high in Sarah’s amygdala, and respond with a tiny jolt to her VC/VS. This happened about 300 times a day. The stimulation was calibrated so Sarah didn’t feel any zaps, but she said they left her feeling a little more energetic.

The research paper describes Sarah’s improvements as the technology did its work in her head over two months; it’s unclear how long the benefits might last, though she’s now had the device implanted for over a year. “As time has gone on, it’s been this virtuous cycle, a spiral upwards,” Sarah said. “Everything has gotten easier and easier and easier.”

The approach used by the UCSF researchers required a lot of sophisticated imaging and machine learning technology. That complexity may prevent it from being a wider treatment, cautions Helen Mayberg, a neurologist at Icahn School of Medicine at Mount Sinai in New York City.

Still, the results — which add to a variety of ways to detect and change problematic brain activity — contain valuable information about how depression takes hold of a brain, and how brain stimulation can change that, says Mayberg, whose research has helped build and refine the field of deep brain stimulation for mood disorders. “What we all want to know is, ‘How does this work?’”

A new particle accelerator aims to unlock secrets of bizarre atomic nuclei

Inscribed on an Italian family’s 15th century coat of arms and decorating an ancient Japanese shrine, the Borromean rings are symbolically potent. Remove one ring from the trio of linked circles and the other two fall apart. It’s only when all three are entwined that the structure holds. The rings have represented the concepts of unity, the Christian Holy Trinity and even certain exotic atomic nuclei.

A rare variety, or isotope, of lithium has a nucleus that is made of three conjoined parts. Lithium-11’s nucleus is separated into a main cluster of protons and neutrons flanked by two neutrons, which form a halo around the core. Remove any one piece and the trio disbands, much like the Borromean rings.

Not only that, lithium-11’s nucleus is enormous. With its wide halo, it is the same size as a lead nucleus, despite having nearly 200 fewer protons and neutrons. The discovery of lithium-11’s expansive halo in the mid-1980s shocked scientists (SN: 8/20/88, p. 124), as did its Borromean nature. “There wasn’t a prediction of this,” says nuclear theorist Filomena Nunes of Michigan State University in East Lansing. “This was one of those discoveries that was like, ‘What? What’s going on?’ ”
Lithium-11 is just one example of what happens when nuclei get weird. Such nuclei, Nunes says, “have properties that are mind-blowing.” They can become distorted into unusual shapes, such as a pear (SN: 6/15/13, p. 14). Or they can be sheathed in a skin of neutrons — like a peel on an inedible nuclear fruit (SN: 6/5/21, p. 5).

A new tool will soon help scientists pluck these peculiar fruits from the atomic vine. Researchers are queuing up to use a particle accelerator at Michigan State to study some of the rarest atomic nuclei. When it opens in early 2022, the Facility for Rare Isotope Beams, or FRIB (pronounced “eff-rib”), will strip electrons off of atoms to make ions, rev them up to high speeds and then send them crashing into a target to make the special nuclei that scientists want to study.

Experiments at FRIB will probe the limits of nuclei, examining how many neutrons can be crammed into a given nucleus, and studying what happens when nuclei stray far from the stable configurations found in everyday matter. With FRIB data, scientists aim to piece together a theory that explains the properties of all nuclei, even the oddballs. Another central target: pinning down the origin story for chemical elements birthed in the extreme environments of space.

And if scientists are lucky, new mind-blowing nuclear enigmas, perhaps even weirder than lithium-11, will emerge. “We’re going to have a new look into an unexplored territory,” says nuclear physicist Brad Sherrill, scientific director of FRIB. “We think we know what we’ll find, but it’s unlikely that things are going to be as we expect.”
Exploring instability
Atomic nuclei come in a dizzying number of varieties. Scientists have discovered 118 chemical elements, distinguished by the number of protons in their nuclei (SN: 1/19/19, p. 18). Each of those elements has a variety of isotopes, different versions of the element formed by switching up the number of neutrons inside the nucleus. Scientists have predicted the existence of about 8,000 isotopes of known elements, but only about 3,300 have made an appearance in detectors. Researchers expect FRIB will make a sizable dent in the missing isotopes. It may identify 80 percent of possible isotopes for all the elements up through uranium, including many never seen before.

The most familiar nuclei are those of the roughly 250 isotopes that are stable: They don’t decay to other types of atoms. The ranks of stable isotopes include the nitrogen-14 and oxygen-16 in the air we breathe and the carbon-12 found in all known living things. The number following the element’s name indicates the total number of protons and neutrons in the nucleus.

Stable nuclei have just the right combination of protons and neutrons. Too many or too few neutrons causes a nucleus to decay, sometimes slowly over billions of years, other times in mere fractions of a second (SN: 3/2/19, p. 32). To understand what goes on inside these unstable nuclei, scientists study them before they decay. In general, as the proton-neutron balance gets more and more off-kilter, a nucleus gets further from stability, and its properties tend to get stranger.

Such exotic specimens test the limits of scientists’ theories of the atomic nucleus. While a given theory might correctly explain nuclei that are near stability, it may fail for more unusual nuclei. But physicists want a theory that can explain the most unusual to the most banal.

“We would like to understand how the atomic nucleus is built, how it works,” says theoretical nuclear physicist Witold Nazarewicz, FRIB’s chief scientist.
A fast clip
Accelerating beams of ions in FRIB is like herding cats.

In the beginning, “it’s just a gaggle of cats,” says Thomas Glasmacher, FRIB’s laboratory director. The cats meander this way or that, but if you can nudge the unruly bunch in a particular direction — maybe you open a can of cat food — then the cats start moving together, despite their natural tendency to wander. “Pretty soon, it’s a stream of cats,” he says.

In FRIB’s case, the cats are ions — atoms with some or all of their electrons stripped off. And rather than cat food, electromagnetic forces get them moving en masse.

The journey starts in one of FRIB’s two ion sources, where elements are vaporized and ionized. After some initial acceleration to get the ions moving, the beam enters the linear accelerator, which is what sets the particles really cruising. The linear accelerator looks like a scaled-down freight train — a line of 46 boxes the color of pistachio ice cream, each about 2.5 meters tall, of varying lengths. But the accelerator sends the beam moving much faster than a cargo-filled train — up to about half the speed of light.

Within the green boxes, called cryomodules, superconducting cavities are cooled to just a few kelvins, a smidge above absolute zero. At those temperatures, the cavities can accelerate the ions using rapidly oscillating electromagnetic fields. The chain of pistachio modules wends around the facility in the shape of a paper clip, a contortion necessary so that the approximately 450-meter-long accelerator fits in the 150-meter-long tunnel that houses it.

When the beam is fully accelerated, it’s slammed into a graphite target. That hard hit knocks protons and neutrons off the nuclei of the incoming ions, forming new, rarer isotopes. Then, the specific one that a scientist wants to study is separated from the riffraff by magnets that redirect particles based on their mass and electric charge. The particles of interest are then sent to the experimental area, where scientists can use various detectors to study how the particles decay, measure their properties or determine what reactions they undergo.
The energy of FRIB’s beam is carefully selected for producing rare isotopes. Too much energy would blow the nuclei apart when they collide with the target. So FRIB is designed to reach less than a hundredth the energy of the Large Hadron Collider at CERN near Geneva, the world’s most energetic accelerator.

Instead, the new accelerator’s potential rests on its juiced-up intensity: Essentially, it has lots and lots of particles in its beam. For example, FRIB will be able to slam 50 trillion uranium ions per second into its target. As a result, it will produce more intense streams of rare isotopes than its predecessors could.

For isotopes that are relatively easily produced, FRIB will churn out about a trillion per second; plenty to study. That opens prospects for scrutinizing isotopes that are more difficult to make. Those isotopes might pop up once a week in FRIB, but that’s still much more often than in a weaker beam. It’s like a case of low water pressure in the bathroom: “You can’t have a shower if it’s just trickling,” says Nunes, who is one of the leaders of a coalition of theoretical physicists supporting research at FRIB. Now, “FRIB is going to come in with a fire hose.”
Dripping with neutrons
That fire hose will also come in handy for pinpointing a crucial boundary known as the neutron drip line.

Try to stuff too many neutrons in a nucleus, and it will decay almost immediately by spitting out a neutron. Imagine a greedy chipmunk with its cheeks so full of nuts that when it tries to shove in one more, another nut pops right back out. The threshold at which nuclei decay in this way marks the ultimate limits for bound nuclei. On a chart of the known elements and their isotopes, this boundary traces out a line, the neutron drip line. So far, scientists know the location of this crucial demarcation up through, at most, the 10th element on the periodic table, neon.

“FRIB is going to be the only way to go heavier and far enough out to define that drip line,” says nuclear physicist Heather Crawford of Lawrence Berkeley National Laboratory in California. FRIB is expected to determine the neutron drip line up to the 30th element, zinc, and maybe even farther.
Near that drip line, where neutrons greatly outnumber protons, is where nuclei get especially strange. Lithium-11, with its capacious halo, sits right next to the drip line. Crawford focuses on magnesium isotopes that are close to the drip line. The most common stable magnesium isotope has 12 protons and 12 neutrons. Crawford’s main target, magnesium-40, has 12 protons and more than double that number of neutrons — 28 — in its nucleus.

“That’s right out at the limits of existence,” Crawford says. Out there, theories that predict the properties of nuclei are no longer reliable. Theoretical physicists can’t always be sure what size and shape a given nucleus in this realm might be, or even whether it qualifies as a bound nucleus. A given theory might also fall short when predicting how much energy is needed to bump the nucleus into its various energized states. The spacing of these energy levels acts as a kind of fingerprint of an atomic nucleus, one that’s highly sensitive to the details of the nucleus’ shape and other properties.

Sure enough, magnesium-40 behaves unexpectedly, Crawford and colleagues reported in 2019 in Physical Review Letters. While theories predicted its energy levels would match those of magnesium isotopes with slightly fewer neutrons, magnesium-40’s energy levels were significantly lower than its neighbors’.

In August, Crawford learned that she will be one of the first scientists to use FRIB. Two experiments she and colleagues proposed were selected for the first round of about 30 experiments to take place over FRIB’s first two years. She’ll take a closer look at magnesium-40, which, like lithium-11, has a Borromean nucleus. Crawford now aims to determine if her chosen isotope also has a haloed nucleus. That’s one possible explanation for magnesium-40’s oddness. Despite the fact that nuclei with halos have been known for decades, theories still can’t reliably predict which nuclei will be festooned with them. Understanding magnesium-40 could help scientists firm up their accounting of nuclei’s neutron adornments.
Elemental origins
Physicists want to be able to poke around, like mechanics under the hood, to understand the cosmic nuclear reactions that make the universe go. “Nuclear physics is like the engine of a sports car. It’s what happens in the engine that determines how well the car performs,” says nuclear physicist Ani Aprahamian of the University of Notre Dame in Indiana.

The cosmos powered by that engine can be a violent place for nuclei, punctuated with dramatic stellar explosions and extreme conditions, including matter crammed into ultratight quarters by crushing gravity. These environments beget wonders of nuclear physics unlike those normally seen on Earth. FRIB will let scientists get a glimpse at some of those processes.

For example, physicists think that certain neutron-rich environments are the cauldron where many of the universe’s chemical elements are cooked. This cosmic connection allowed nuclear physicist Jolie Cizewski to make good on a childhood dream.

When Cizewski was a little girl, she caught the astronomy bug, she says. “I decided I was going to become an astronomer so I could go into space.” It might seem that she took a left turn from her childhood obsession. She never made it to orbit and she didn’t become an astronomer.

But echoes of that childhood dream now anchor her research. Instead of peering at the stars with a telescope, she’ll soon be using FRIB to reveal secrets of the cosmos.

Cizewski, of Rutgers University in New Brunswick, N.J., is working to unveil details of the cosmic nuclear reactions responsible for the nuclei that surround us. “I’m trying to understand how the elements, in particular those heavier than iron, have been synthesized,” she says.

Many of the elements around us — and in us — formed within stars. As large stars age, they fuse progressively larger atomic nuclei together in their cores, creating elements farther along the periodic table — oxygen, carbon, neon and others. But the process halts at iron. The rest of the elements must be born another way.

A process called the rapid neutron capture process, or r-process, is responsible for many of those other elements found in nature. In the r-process, atomic nuclei quickly soak up neutrons and bulk up to large masses. The neutronfest is interspersed with radioactive decays that form new elements. The sighting of two neutron stars merging in 2017 revealed that such collisions are one place where the r-process occurs (SN: 11/11/17, p. 6). But scientists suspect it might happen in other cosmic locales as well (SN: 6/8/19, p. 10).

Cizewski and colleagues are studying an abbreviated form of the r-process that might thrive in supernovas, which may not have enough oomph for the full r-process. The team has zeroed in on germanium-80, which plays a pivotal role in the weak r-process. Physicists want to know how likely this nucleus is to capture another neutron to become germanium-81. At FRIB, Cizewski will slam a beam of germanium-80 into deuterium, which has one proton and one neutron in its nucleus. Knowing how often germanium-80 captures the neutron will help scientists nail down the neutron-slurping chain of the weak r-process, wherever it might crop up.
A Borromean bent
Like the interlinked Borromean rings, different facets of nuclear physics are closely entwined, from mysteries of the cosmos to the inner workings of nuclei. The exotic nuclei that FRIB cooks up could also allow physicists to tap into the very bedrock of physics by testing certain fundamental laws of nature. And there’s a practical side to the facility as well. Scientists could collect some of the isotopes FRIB produces for use in medical procedures, for example.

Physicists are ready for surprises. “Every time we build such a facility, new discoveries come and breakthroughs in science come,” Nazarewicz says. Like the 1980s discovery of lithium-11’s Borromean nucleus, scientists may find something totally unexpected.

Earth is reflecting less light. It’s not clear if that’s a trend

The amount of sunlight that Earth reflects back into space — measured by the dim glow seen on the dark portions of a crescent moon’s face — has decreased measurably in recent years. Whether the decline in earthshine is a short-term blip or yet another ominous sign for Earth’s climate is up in the air, scientists suggest.

Our planet, on average, typically reflects about 30 percent of the sunlight that shines on it. But a new analysis bolsters previous studies suggesting that Earth’s reflectance has been declining in recent years, says Philip Goode, an astrophysicist at Big Bear Solar Observatory in California. From 1998 to 2017, Earth’s reflectance declined about 0.5 percent, the team reported in the Sept. 8 Geophysical Research Letters.

Using ground-based instruments at Big Bear, Goode and his colleagues measured earthshine — the light that reflects off our planet, to the moon and then back to Earth — from 1998 to 2017. Because earthshine is most easily gauged when the moon is a slim crescent and the weather is clear, the team collected a mere 801 data points during those 20 years, Goode and his colleagues report.

Much of the decrease in reflectance occurred during the last three years of the two-decade period the team studied, Goode says. Previous analyses of satellite data, he and his colleagues note, hint that the drop in reflectance stems from warmer temperatures along the Pacific coasts of North and South America, which in turn reduced low-altitude cloud cover and exposed the underlying, much darker and less reflective seas.
“Whether or not this is a long-term trend [in Earth’s reflectance] is yet to be seen,” says Edward Schwieterman, a planetary scientist at University of California, Riverside, who was not involved in the new analysis. “This strengthens the argument for collecting more data,” he says.

Decreased cloudiness over the eastern Pacific isn’t the only thing trimming Earth’s reflectance, or albedo, says Shiv Priyam Raghuraman, an atmospheric scientist at Princeton University. Many studies point to a long-term decline in sea ice (especially in the Arctic), ice on land, and tiny pollutants called aerosols — all of which scatter sunlight back into space to cool Earth.

With ice cover declining, Earth is absorbing more radiation. The extra radiation absorbed by Earth in recent decades goes toward warming the oceans and melting more ice, which can contribute to even more warming via a vicious feedback loop, says Schwieterman.

Altogether, Goode and his colleagues estimate, the decline in Earth’s reflectance from 1998 to 2017 means that each square meter of our planet’s surface is absorbing, on average, an extra 0.5 watts of energy. For comparison, the researchers note in their study, planet-warming greenhouse gases and other human activity over the same period boosted energy input to Earth’s surface by an estimated 0.6 watts of energy per square meter. That means the decline in Earth’s reflectance has, over that 20-year period, almost doubled the warming effect our planet experienced.