A star that mysteriously disappeared might be the first confirmed case of a failed supernova, a star that tried to explode but couldn’t finish the job. A newborn black hole appears to have been left behind to snack on the star’s remains.

In 2009, a star in the galaxy NGC 6946 flared up over several months to become over 1 million times as bright as the sun. Then, it seemed to vanish. While the star could just be hiding behind a wall of dust, new observations with the Hubble Space Telescope, reported online September 6 at arXiv.org, strongly suggest that the star did not survive. A faint trickle of infrared light, however, emanates from where the star used to be. The remnant glow probably comes from debris falling onto a black hole that formed when the star died, write Caltech astronomer Scott Adams and colleagues.
Black holes are typically thought to form in the aftermath of a supernova, the explosive death of a massive star. But multiple lines of evidence have recently hinted that not all heavyweights go out with a bang. Some stars might skip the supernova and collapse into a black hole. Until now, though, evidence that this happens has been either spotty or indirect.

“This is the first really solid observational evidence for a failed supernova,” says Elizabeth Lovegrove, an astronomer at the University of California, Santa Cruz. “Some supernovas really do fail and this is what they look like.”

This attempt at a supernova, first observed with the Large Binocular Telescope in Arizona, occurred about 19 million light-years away in the constellation Cygnus. Only one other known star — a yellow supergiant that faded away in 2010 — is suspected to be a failed supernova, though there’s not enough data to say for certain.

When a star at least eight times as heavy as the sun runs out of thermonuclear fuel, it can no longer support its own weight. Gas crashes down on the star’s core, bounces and sends a shock wave racing back toward the surface that tears the star apart. Some stars might be so massive that the shock wave doesn’t have enough oomph to push against the onrush of collapsing star stuff. The shock fizzles, the supernova fails and the core gathers enough mass to collapse into a black hole, possibly taking the rest of the star down with it.

If the dying star is a red supergiant — a ruddy orb that can be over 1,000 times as wide as the sun — it might give a signal before vanishing. As the core collapses, it releases an enormous amount of gravitational energy. A second shock wave ripples up through the star — not powerful enough for an explosion, but enough to burp off the loosely held outer layers of the supergiant and expose the feeding black hole.
That’s exactly what Adams and colleagues think they saw. Hubble images from before 2009 reveal a star about 25 to 30 times as massive as the sun sitting where the flash of light came from. The star doesn’t show up in images taken since the eruption. Neither the brightness of the flash, the rate at which the brightness evolved nor the amount of light coming from there now fully matches other types of stellar incidents, such as a collision between a pair of stars or the violent outbursts that accompany some aging supermassive stars.

If the star did give birth to a black hole, X-rays may be radiating from debris spiraling down its gravitational throat. Adams and collaborators are waiting on observations from the space-based Chandra X-ray Observatory to check that idea. They also continue to monitor what’s left of the star. The star might still be there, hiding within a shell of dust expelled during the 2009 eruption. If that’s the case, it should become visible again in the coming years as the cloak dissipates.

A satellite of Saturn joins the club of moons with possible oceans. A subsurface sea of water might hide beneath the icy crust of Dione, one of Saturn’s moons, researchers report online October 9 in Geophysical Research Letters. That puts Dione in good company alongside Enceladus (another moon of Saturn) and several moons of Jupiter, as well as possibly Pluto (SN Online: 9/23/16).

Dione’s ocean is about 100 kilometers below the surface and roughly 65 kilometers deep, Mikael Beuthe, a planetary scientist at the Royal Observatory of Belgium in Brussels, and colleagues report. They inferred the ocean’s presence from measurements of Dione’s gravity made by the Cassini spacecraft.

A child mummy buried in a church crypt in Lithuania could hold the oldest genetic evidence of smallpox.

Traces of the disease-causing variola virus linger in the mummy, which dates to about 1654, evolutionary geneticist Ana Duggan and colleagues report December 8 in Current Biology. Previously, a team of researchers had reported variola DNA in a roughly 300-year-old Siberian mummy.

Some Egyptian mummies, dating back more than 3,000 years, have pockmarks that scientists have interpreted as signs of smallpox, indicating the disease may have tormented humans for millennia. “The definitive feature of smallpox is a pustular rash,” says Duggan of McMaster University in Hamilton, Canada. “But it isn’t easy to say whether a rash comes from smallpox or chicken pox or measles.”
Duggan’s team analyzed skin from the mummy, believed to be a boy who died between ages 2 and 4. They found DNA from an ancient strain of variola, and compared it with dozens of strains from the 20th century. The ancient and modern strains weren’t all that different, the researchers found. They shared a common ancestor that dates to around the late 16th century, not long before the boy died.

“It’s a little bit curious,” Duggan says. More diversity might be expected of a virus that had been kicking around since ancient Egyptian times. The find could suggest that “the timeline of smallpox existing in humans isn’t that deep at all.”

In fact, historical mortality records suggest that around the late 16th century, smallpox seemed to go “from something that occasionally caused infection to more of an epidemic disease,” Duggan says.

But researchers can’t say for sure when smallpox started affecting humans on a large-scale, she cautions. Whether or not those ancient Egyptian mummies had smallpox is still an open question, she says. “We haven’t closed it.”

One hundred and ninety-two atoms have tied the knot.

Chains of carbon, hydrogen, oxygen and nitrogen atoms, woven together in a triple braid, form the most complex molecular knot ever described, chemists from the University of Manchester in England report in the Jan. 13 Science.

Learning how to tie such knots could one day help researchers weave molecular fabrics with all sorts of snazzy properties. “We might get the strength of Kevlar with a lighter and more flexible material,” says study coauthor David Leigh.
That’s still a long way away, but molecular knot tying has an appeal that’s purely intellectual, too, says University of Cambridge chemist Jeremy Sanders. “It’s like the answer to why you climb Everest,” he says. “It’s a challenge.”

Mathematicians know of more than six billion types of prime knots, which, like prime numbers, cannot be broken down into simpler components. “Prime knots can’t be built up by sticking other knots together,” Leigh explains. For years, chemists were able to synthesize just one type of prime knot out of small molecules. “We thought that was pretty ridiculous,” says Leigh.

That molecular knot was a trefoil, like a three-leaf clover. Jean-Pierre Sauvage and colleagues wove it from chemical strands in 1989. Sauvage won a Nobel Prize in 2016 for earlier work that used the same principles explored in his knots (SN: 10/29/16, p. 6).

In the decades since Sauvage’s trefoil, chemists have tried to synthesize other types of molecular knots, but “they’ve always found it incredibly difficult,” says chemist Sophie Jackson, also at the University of Cambridge.

Persuading nanoscale strands to interlock together in an orderly fashion isn’t simple. “You can’t just grab the ends and tie them like you would a shoelace,” Leigh says. Instead, scientists choose molecular ingredients that assemble themselves.
In 2012, Leigh and colleagues used the self-assembly technique to make a molecular pentafoil knot, a star-shaped structure made up of 160 atoms and with strands that cross five times (SN: 1/28/12, p. 12). This latest knot, with eight crossing points, is even more intricate.

Leigh’s team mixed together building blocks containing carbon, hydrogen, oxygen and nitrogen atoms with iron ions and chloride ions. “You dump them all in, heat them all up and they self-assemble,” he says. Sticky metal ions hold the building blocks in the correct position, and a single chloride ion sitting in the middle of the structure anchors it all together. Then, a chemical catalyst links the building blocks, forming the completed knot. The new knot is the tightest ever created, Leigh says, with just 24 atoms between each crossing point.

It’s beautiful, Sanders says. “It’s a string of atoms rolled up in a spherical shape, with an astonishing amount of symmetry.” Sanders is reluctant to speculate how such a knot might be used, but it’s round and very dense, he says. That could give it some interesting materials properties.

Leigh suspects that different molecular knots might behave differently, like the various knots used by fishermen and sailors. “We want to make specific knots, see what they do and then figure out how to best exploit that,” he says.

A big coconut crab snaps its outsized left claw as hard as a lion can bite, new measurements suggest. So what does a land crab the size of a small house cat do with all that pinch power?

For starters, it protests having its claw-force measured, says Shin-ichiro Oka of the Okinawa Churashima Foundation in Motobu, Japan. “The coconut crab is very shy,” he says. It doesn’t attack people unprovoked. But wrangling 29 wild Birgus latro crabs on Okinawa and getting them to grip a measurement probe inspired much snapping at scientists. Oka’s hand got pinched twice (no broken bones). “Although it was just a few minutes,” he says, “I felt eternal hell.”
The strongest claw grip the researchers measured squeezed with a force of about 1,765 newtons, worse than crushing a toe under the force of the full weight of a fridge. For comparison, a lion’s canines bite with 1,315 newtons and some of its molars can crunch with 2,024 newtons, a 2007 study calculated. Because grip strength increases with body size, crabs bigger than those measured in the study might surpass the bite force of most land predators, Oka and colleagues proposed last year in PLOS ONE.
Coconut crabs, however, start life about as scary as a soggy grain of rice. Fertilized eggs hatch in seawater and bob around planktonlike in the western Pacific and Indian oceans. The crabs eventually return to land, where they spend most of their long lives, up to 50 (or maybe 100) years, as landlubbers that will drown if forced back into water for too long. Yet females have to risk the ocean’s edge each time they lay the next generation of eggs.
Both moms and dads grow a powerful left claw, handy for dismembering whatever the omnivorous scavengers find: roadkill and other dead stuff, innards of palm trees and nuts. The crabs can break open coconuts, but the job “takes hours,” says Jakob Krieger of the University of Greifswald in Germany. Cracking open a red crab, however, takes seconds.

Coconut crabs not only scavenge red crabs but also hunt them on Christmas Island in the Indian Ocean, Krieger says. Only the strictest vegetarian would ignore the 44 million or so red crabs scuttling around, and even small coconut crabs get a taste. Krieger watched an underpowered coconut crab grab hold of and wrestle its prey. The red crab abandoned its trapped limb and fled. But the little coconut crab scored a crab-leg dinner.

A record-breaking quantum satellite has again blown away the competition, achieving two new milestones in long-distance quantum communications through space.

In June, Chinese researchers demonstrated that the satellite Micius could send entangled quantum particles to far-flung locations on Earth, their properties remaining intertwined despite being separated by more than 1,200 kilometers (SN Online: 6/15/17). Now researchers have used the satellite to teleport particles’ properties and transmit quantum encryption keys. The result, reported in two papers published online July 3 and July 4 at arXiv.org, marks the first time the two techniques have been demonstrated in space.
In quantum teleportation, the properties of one particle are transferred to another. The scientists first sent particles of light, or photons, from the ground to the satellite — a distance of up to 1,400 kilometers. When the researchers made particular measurements of other photons on the ground, the spacefaring particles took on the properties of the landlubbers, thanks to quantum entanglement between the earthbound and satellite-based particles. Although it’s a far cry from the Star Trek variety of teleportation, the process is an important ingredient of quantum communication.

Quantum key distribution is a method of creating a secret string of random numbers that can be used to encrypt communications. The researchers beamed photons from the satellite to Earth over distances of up to 1,200 kilometers, using the photons’ polarization, the orientation of their electromagnetic waves, to transmit a string of random numbers with utmost security.

Quantum communication via satellite can reach greater distances than land-based transmission, because in space, particles don’t get absorbed by the atmosphere. The new results pave the way for a global quantum internet that would provide for ultrasecure communications and allow quantum computers to work together.

A common blood sugar medication or an extra dose of a thyroid hormone can reverse signs of cognitive damage in rats exposed in utero to alcohol. Both affect an enzyme that controls memory-related genes in the hippocampus, researchers report July 18 in Molecular Psychiatry.

That insight might someday help scientists find an effective human treatment for fetal alcohol spectrum disorders, which can cause lifelong problems with concentration, learning and memory. “At this moment, there’s really no pharmaceutical therapy,” says R. Thomas Zoeller, a neurobiologist at the University of Massachusetts Amherst.
Fetal alcohol syndrome disorders may affect up to 5 percent of U.S. kids, according to estimates from the U.S. Centers for Disease Control and Prevention. Scientists don’t know exactly why alcohol has such a strong effect on developing brains. But the lower thyroid hormone levels commonly induced by alcohol exposure might be one explanation, suggests study coauthor Eva Redei, a psychiatrist at Northwestern University Feinberg School of Medicine in Chicago.

“The mother has to supply the thyroid hormones for brain development,” says Redei. So, pregnant women who drink might not be providing their fetuses with enough hormones for normal brain development. That could disrupt the developing hippocampus, a brain region involved in learning and memory.

To counter alcohol’s effects, Redei and her colleagues gave doses of thyroxine, a thyroid hormone, to newborn rats that had been exposed to alcohol before birth. (That timing coincides developmentally with the third trimester of pregnancy in humans.) The amount of alcohol fed to the rat moms corresponded roughly to a woman drinking a glass or two of wine a day.

The treatment helped, the team found. Healthy rats will freeze in place when they’re put in a room where they’ve previously experienced a mild electrical shock. Adult rats exposed to alcohol during development freeze for a shorter period of time, suggesting that they might not learn the association between the shock and the room as effectively. Thyroxine treatment after birth made rats freeze about 30 percent longer than rats that didn’t get the treatment — almost on par with rats born to nondrinking moms.

Surprisingly, treatment with a blood sugar drug called metformin also had a similar effect. While seemingly unrelated, the two treatments work in similar ways, Redei says. Alcohol makes the hippocampus produce less of an enzyme called Dnmt1. That enzyme regulates the way key learning and memory-related genes turn on and off during development. Disruptions in that process can harm hippocampus function. “Both treatments normalize those enzyme levels,” Redei says.
Whether this treatment will work in people is far from a guarantee: Many promising treatments shown in rats don’t pan out in humans. Plus, fetal alcohol syndrome includes a complex suite of physical, cognitive and behavioral symptoms, which probably aren’t all controlled by thyroid hormone levels.

“Kids with fetal alcohol effects don’t look like kids with congenital hypothyroidism,” a condition resulting in low thyroid hormone levels, says Zoeller. Alcohol exposure during development affects other systems, too, like the immune system.

Still, Redei eventually hopes to test thyroxine and metformin in pregnant drinkers during their third trimester to see if the drugs might improve their kids’ outcomes. (Both are generally recognized as safe for pregnant women at standard doses.)

If treatment works, it might be particularly helpful for women who drank heavily in their first trimester before realizing they were pregnant, says Joanne Rovet, who studies fetal alcohol syndrome at the Hospital for Sick Children in Toronto.

Scientists have created the largest map of dark matter yet, part of a slew of new measurements that help pin down the universe’s dark contents. Covering about a thirtieth of the sky, the map (above) charts the density of both normal matter — the stuff that’s visible — and dark matter, an unidentified but far more abundant substance that pervades the cosmos.

Matter of both types is gravitationally attracted to other matter. That coupling organizes the universe into more empty regions of space (No. 1 below and blue in the map above) surrounded by dense cosmic neighborhoods (No. 2 below and red in the map above).
Researchers from the Dark Energy Survey used the Victor Blanco telescope in Chile to survey 26 million galaxies in a section of the southern sky for subtle distortions caused by the gravitational heft of both dark and normal matter. Scientists unveiled the new results August 3 at Fermilab in Batavia, Ill., during a meeting of the American Physical Society.

Dark matter is also accompanied by a stealthy companion, dark energy, an unseen force that is driving the universe to expand at an increasing clip. According to the new inventory, the universe is about 21 percent dark matter and 5 percent ordinary matter. The remainder, 74 percent, is dark energy.

The new measurements differ slightly from previous estimates based on the cosmic microwave background, light that dates back to 380,000 years after the Big Bang (SN: 3/21/15, p. 7). But the figures are consistent when measurement errors are taken into account, the researchers say.
“The fact that it’s really close, we think is pretty remarkable,” says cosmologist Josh Frieman of Fermilab, who directs the Dark Energy Survey. But if the estimates don’t continue to align as the survey collects more data, something might be missing in cosmologists’ theories of the universe.

A new genetics study adds fuel to the debate about muscle aches that have been reported by many people taking popular cholesterol-lowering drugs called statins.

About 60 percent of people of European descent carry a genetic variant that may make them more susceptible to muscle aches in general. But counterintuitively, these people had a lower risk of muscle pain when they took statins compared with placebos, researchers report August 29 in the European Heart Journal.
Millions of people take statins to lower cholesterol and fend off the hardening of arteries. But up to 78 percent of patients stop taking the medicine. One common reason for ceasing the drugs’ use is side effects, especially muscle pain, says John Guyton, a clinical lipidologist at Duke University School of Medicine.

It has been unclear, however, whether statins are to blame for the pain. In one study, 43 percent of patients who had muscle aches while taking at least one type of statin were also pained by other types of statin (SN: 5/13/17, p. 22). But 37 percent of muscle-ache sufferers in that study had pain not related to statin use. Other clinical trials have found no difference in muscle aches between people taking statins and those not taking the drugs.

The new study hints that genetic factors, especially ones involved in the immune system’s maintenance and repair of muscles, may affect people’s reactions to statins. “This is a major advance in our understanding about myalgia,” or muscle pain, says Guyton, who was not involved in the study.

People with two copies of the common form of the gene LILRB5 tend to have higher-than-usual blood levels of two proteins released by injured muscles, creatine phosphokinase and lactate dehydrogenase. Higher levels of those proteins may predispose people to more aches and pains. In an examination of data from several studies involving white Europeans, people with dual copies of the common variant were nearly twice as likely to have achy muscles while taking statins as people with a less common variant, Moneeza Siddiqui of the University of Dundee School of Medicine in Scotland and colleagues discovered.

But when researchers examined who had pain when taking statins versus placebos, those with two copies of the common variant seemed to be protected from getting statin-associated muscle pain. Why is not clear.
People with double copies of the common form of the gene who experience muscle pain may stop taking statins because they erroneously think the drugs are causing the pain, study coauthor Colin Palmer of the University of Dundee said in a news release.

The less common version of the gene is linked to reduced levels of the muscle-damage proteins, and should protect against myalgia. Yet people with this version of the gene were the ones more likely to develop muscle pain specifically linked to taking statins during the trials.

The finding suggests that when people with the less common variant develop muscle pain while taking statins, the effect really is from the drugs, the researchers say.

But researchers still don’t know the nitty-gritty details of how the genetic variants promote or protect against myalgia while on statins. Neither version of the gene guarantees that a patient will develop side effects — or that they won’t. The team proposes further clinical trials to unravel interactions between the gene and the drugs.

More study is needed before doctors can add the gene to the list of tests patients get, Guyton says. “I don’t think we’re ready to put this genetic screen into clinical practice at all,” he says. For now, “it’s much easier just to give the patient the statin” and see what happens.

A vaccine to fight Lyme disease, decades in the making, has received a temporary green light from the U.S. Department of Agriculture. But it’s not for people — it’s for mice.

The vaccine isn’t a rodent-sized injection, which wouldn’t work for targeting large populations quickly. Instead, it’s coated onto edible, nutrition-free pellets that mice gobble up.

The vaccine makes mice develop antibodies that neutralize Borrelia burgdorferi, the bacterium that causes most U.S. cases of Lyme disease. When ticks imbibe the blood of a vaccinated mouse, the idea goes, they won’t get an active infection and so can’t transmit the bacteria to people or other animals.
“Mice are probably one of the most important reservoir hosts for Lyme disease,” especially in the Eastern United States where Lyme disease is rampant, says Jean Tsao, a disease ecologist at Michigan State University in East Lansing who was not involved in developing the new vaccine. Reservoir hosts are animals with B. burgdorferi in their blood (SN: 2/5/21).

The vaccine has a conditional license, granted on May 9. That means it is available on request by groups such as federal and state health agencies under certain conditions for roughly one year, with the possibility of renewal.

The first well-documented case of Lyme disease in a person in the United States was in 1970. A vaccine for humans was available from 1998 to 2002, but it was taken off the market due to low consumer demand, likely related to fears over the vaccine’s safety. Some vaccinated people reported developing arthritis, but the U.S. Food and Drug Administration found no meaningful difference in joint problems in vaccinated versus control groups.

Both the mouse and human vaccines use a protein called OspA, found on the surface of B. burgdorferi, to spur antibody production and prevent infection.

Biologist Maria Gomes-Solecki co-led the early development of the new mouse vaccine. Her team distributed an early version of the vaccine to areas in upstate New York from 2007 to 2011. B. burgdorferi has a two-year life cycle in ticks. This and other factors mean it takes time to see meaningful reductions in infections, says Gomes-Solecki, of the University of Tennessee Health Science Center in Memphis. After two and five years of vaccination, the researchers found that tick infections were reduced by 23 and 76 percent, respectively, compared with control sites.

That early vaccine used live Escherichia coli bacteria to deliver the OspA protein. But the current, green-lighted version of the vaccine uses inactive E. coli. A 2020 study of the new vaccine found a 30 percent reduction in the proportion of infected ticks in residential areas after two years, compared with control sites. Several coauthors on that study work for US Biologic, the company Gomes-Solecki cofounded to develop the vaccine.
“The vaccine they have works, but it’s not spectacular” in terms of the rate of reducing B. burgdorferi–infected ticks, says Sam Telford III, an epidemiologist at Tufts University in Medford, Mass., who was involved in the development of the human vaccine and led research in the 1990s for vaccinating mice.

Edible vaccines targeted at hosts have worked well for other diseases and species. For instance, vaccinating prairie dogs against the plague has decreased levels of the disease. For now, it remains to be seen whether vaccinating mice will result in lower Lyme risks for humans. “With additional studies as the product rolls out … we’ll see more data on how well it does,” Telford says. “It’s certainly a step in the right direction.”

Researchers are studying many approaches to controlling Lyme disease, including genetically engineered mice that produce B. burgdorferi antibodies without the need for vaccination (SN: 8/9/17). Tsao and Telford are studying how to limit tick populations by controlling deer numbers. And a new vaccine for humans is in late-phase testing in several thousand people.

Vaccines that target wildlife hosts will remain one tool among many for managing exposure to Lyme disease, the researchers say. Showering after being in areas with ticks, wearing long sleeves and pants and doing tick checks will still be important.

“We have to continue to be vigilant,” Gomes-Solecki says.