It was one of the flashiest mysteries in the news about a decade ago — honeybee workers were vanishing fast for no clear reason. To this day, that puzzle has never been entirely solved, researchers acknowledge.

And maybe it never will be. Colony collapse disorder, or CCD, as the sudden mass honeybee losses were called, has faded in recent years as mysteriously as it began. It’s possible the disappearances could start up again, but meanwhile bees are facing other problems.
CCD probably peaked around 2007 and faded since, says Jeff Pettis, who during the heights of national curiosity was running the Beltsville, Md., honeybee lab for the U.S. Department of Agriculture’s research wing. And five years have passed since Dennis vanEngelsdorp, who studies bee health at the University of Maryland in College Park, has seen a “credible case” of colony collapse.

Beekeepers still report some cases, but Pettis and vanEngelsdorp aren’t convinced such cases really are colony collapse disorder, a term that now gets used for a slew of things that are bad for bees. To specialists, colony collapse is a specific phenomenon. An apparently healthy colony over the course of days or a few weeks loses much of its workforce, while eggs and larvae, and often the queen herself, remain alive. Also food stores in collapsing colonies don’t get raided by other bees as a failing colony’s treasures usually do.

“I think I know what happened,” says Pettis, now in Salisbury, Md., consulting on pollinator health. His proposed scenario for CCD, like those of some other veterans of the furor, is complex and doesn’t rest on a single exotic killer. But so far, no experiment has nailed the proof.
Looking back, Pettis realizes he had heard about what might have been early cases of CCD, described as colonies “just falling apart,” for several years before the phenomenon made headlines. Then in November 2006, Pennsylvania beekeeper David Hackenberg, as usual, sent his colonies to Florida for the winter. They arrived in fine shape. Soon after, however, many buzzing colonies had shrunk to stragglers. Yet there were no dire parasite infestations and no dead bee bodies in sight.

“It was, ‘OK, something weird just happened,’ ” remembers Jay Evans of the USDA’s honeybee lab in Beltsville. “It looked like a ‘flu,’ something that kind of swept through miraculously fast.”

No single menace, however, could be tightly linked to every sick colony, or only to sick colonies. Varroa mites, small hive beetles, Nosema fungi, deformed wing virus, unusual signs of pesticide exposure, for instance —screening techniques at the time just weren’t picking up a clear pattern in any of these bee bedevilments.

“People were following this story like crazy,” Pettis says. The bees’ unexplained plight prompted a national outbreak of amateur entomology. “There were people saying, ‘Why aren’t you doing more with jet contrails?’ There were ‘alien abductions.’ And the rapture — the bees were being called home.”

Entomologists were hounded by the press, not to mention leaned on by politicians and pursued by would-be entrepreneurs. “For me, what made it rewarding,” Pettis says, “was that people were learning about the value of pollination.”
A Columbia University researcher who had identified pathogens in mysterious human disease outbreaks took a crack at the problem. Ian Lipkin had never worked with bees, but he and his lab collaborated with entomologists and other bee specialists to search for any genetic signature of a pathogen appearing only in collapsing colonies. The approach of searching through mass samples, with their messy traces of gut microbes and random parasites, is now familiar as metagenomics. At the time, this way of searching for pathogens was groundbreaking, says collaborator Diana Cox-Foster, then at Penn State. The resulting paper, in Science , pointed to several viruses, especially the previously obscure Israeli Acute Paralysis Virus , or IAPV ( SN: 9/8/07, p. 147 ).
That emphasis on IAPV, which got a lot of attention at the time, hasn’t held up well. “It’s not 100 percent ruled out,” Evans says. But the explanation’s main problem is shared by other threats proposed as a single cause of CCD. After finding IAPV or another presumed single menace in sick bees in one place, he says, “you could go to other apiaries that were collapsing and not find it, or you could find it in healthier colonies.”

As an apiary inspector for Pennsylvania at the time, vanEngelsdorp monitored for signs of collapse in over 200 hives. “We tried to watch it happen but we couldn’t,” he says. None collapsed. Even finding the sickest bees in collapsing colonies was a challenge. Doomed bees presumably flew off in multiple directions, and birds or other scavengers usually found the bees before scientists could.

A gang of killers
Pettis now sees the disaster as a two-step process. Various stressors such as poor nutrition and pesticide exposure weakened bees so much that a virus, maybe IAPV, could quickly kill them in droves. Evans, too, sees various stressors mixing and matching. When pressed for his best guess, he says “all of the above.”

Cox-Foster has managed to re-create part of the process, the vanishing effect that marked the end for stressed bees. When she infected honeybee colonies in a greenhouse with a virus, the sick bees left the hive but were trapped by the greenhouse walls before dispersing too far to be found. (Of course, this experiment doesn’t demonstrate how colonies with no sign of a virus died.)

That tendency for sick bees to leave hives, vanEngelsdorp proposes, could have developed as a hygiene benefit. “Altruistic suicide,” as social-insect biologists call it. Flying away from the colony could minimize a sick bee’s tendency to pass disease to the rest of the family.
Today, hive losses remain high even with CCD waning or gone, according to national surveys by the Bee Informed Partnership, a nonprofit bee health collaboration. Beekeepers typically note that they either expect or can tolerate annual losses between 15 and 20 percent of their total number of colonies. Yet from April 2016 until March 2017, losses across the United States ran at about a third of hives. And that was a so-called good year, the second-lowest loss in the seven years with data on annual losses.

Classic CCD may not be much threat these days, but the “four p’s” — poor nutrition, pesticides, pathogens and parasites — are, says Cox-Foster, now at a USDA lab for pollinating insects in Logan, Utah. While honeybees aren’t likely to go extinct, these threats to the beekeeping industry boost pollination costs, which could affect food prices.

Coping with the four p’s may not fire the imaginations of armchair entomologists. But it’s more than enough of a challenge for the bees.

With the Eastern Conference Semifinals tied at 2-2 heading back to Boston for a "Pivotal Game 5," the Celtics were completely routed by the 76ers on their home floor.

It was clear from the opening tip that Philadelphia simply wanted it more. Boston had no answer for Philadelphia's star duo, as Joel Embiid and James Harden pick-and-rolled the Celtics' defense to death while Tyrese Maxey delivered dagger after dagger whenever his number was called.

Embiid finished with a game-high 33 points, torturing Boston's drop coverage with a barrage of midrange jumpers. The MVP didn't score a single point at the rim — all 10 of his made field goals came in the soft spots of the Celtics' defensive gameplan.

Harden teed him up perfectly, dishing out 10 assists, while Maxey poured in 30 points with six 3-pointers.
Star forward Jayson Tatum finally found his groove after another field-goalless first quarter, catching fire in the second and third quarters to keep Boston in it. He finished with 36 points, 10 rebounds and five assists, and Jaylen Brown chipped in 24 points, but the Celtics couldn't overcome poor shooting nights from Al Horford (0-7 3PT), Marcus Smart (2-7 FG), Malcolm Brogdon (3-9 FG) and Derrick White (2-6 FG).

MORE: Breaking down Celtics' major clutch problems in NBA Playoffs

Now, trailing 3-2 in the series and in need of a road win to keep their season alive, the Celtics find themselves in the exact same position as their NBA Finals run a season ago.

Celtics in familiar territory after dropping Game 5 to 76ers
In the 2022 Eastern Conference Semifinals, the Celtics had a complete meltdown in the final minutes of Game 5, losing to the Bucks on the TD Garden parquet to fall into a 3-2 hole.

With their backs against the wall as the series shifted to Milwaukee, Tatum delivered his signature performance of the postseason, erupting for 46 points to force a Game 7 in Boston.
The Celtics carried that momentum back onto their home floor, destroying the Bucks by 28 points to advance to the Eastern Conference Finals.

After falling into the exact same position against the 76ers, Boston's leaders all gave their spin on how last year's experience prepared them for Game 6 on Thursday.

"It's easy, we've been there before," Smart began. "It's one game at a time. So you know they're feeling good. We got to go to a hostile environment and we got to go take it. it's not gonna be easy. It's gonna be a dog fight."

Smart elaborated further, specifically comparing this situation to Game 6 in Milwaukee last year.

"The brutality of it. It's a true dogfight, scratching and clawing, biting, blood, everything," he told the media. "And if you're not willing to pretty much get dirty, if you're not willing to bleed… If you’re not willing to break something, willing to tear something, going hard, then you shouldn’t be on that court because that's what it is.

"That's what the playoffs are about. Hopefully, you stay safe but that's the mentality. You gotta go, you gotta be willing to risk it all for these games. And that's the mentality we got to have.”
Tatum wasn't as intense as Smart, but he offered some musings as to how Boston can approach Game 6 differently than Game 5.

"I think we were a little tight today, so go out there and relax. There's no secret answer. Go out there and play how we know we're capable of, and we'll see."

Brown, on the other hand, elected to keep last year in the past.

"Last year's over with. This year, we gotta come out and be better than we were tonight or we'll have a different ending. Obviously, we are still in this series and we gotta muster up what we got left to win Game 6," he told the media.

The Celtics will look to keep their championship hopes alive when they travel to Philadelphia to take on the Sixers in a win-or-go-home Game 6 on Thursday, May 11 at 7:30 p.m. ET on ESPN.

Meet Zhong Zhong and Hua Hua, the first primates cloned by reprogramming adult cells.

Two decades after Dolly the Sheep was successfully cloned (SN: 3/1/97, p. 132), Chinese researchers have used the same technique — somatic cell nuclear transfer — to clone two healthy baby macaque monkeys. The results, reported January 24 in Cell, could lead to more efficient cloning and a better way to study genetic diseases in primates.

“This could be it — the next step in cloning,” says Jose Cibelli, a geneticist at Michigan State University in East Lansing not involved with the study.
Over 20 species of mammals have been cloned via somatic cell nuclear transfer — including cats, dogs, rats and even a camel (SN: 3/23/02, p. 189). This cloning technology has improved since Dolly’s birth in 1996. Back then, she was the only sheep born from 277 attempts. By 2014, the cloning technique had an 80 percent success rate in pigs. Despite these gradual advances (SN: 3/8/14, p. 7), cloning of nonhuman primates has long eluded researchers.

A rhesus monkey “clone” was created through embryo splitting, a technique that divides a single embryo into genetically identical embryos, in 1999. But this type of cloning has little in common with somatic cell nuclear transfer.
In somatic cell nuclear transfer, a nucleus from a mature body cell is transplanted into an egg cell without a nucleus. The egg cell must then reprogram the nucleus’s DNA, basically stripping the body cell of its identity and returning it to an embryonic state. With no set identity, it can become any kind of cell in the body.

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Previous failures in reprogramming primate cells probably happened because the egg ran into roadblocks — portions of the body cell’s DNA known as reprogramming-resistant regions, say study coauthor Mu-ming Poo, director of the Institute of Neuroscience at the Chinese Academy of Sciences in Shanghai, and his colleagues. In these regions, DNA is so tightly wrapped around proteins called histones that the egg can’t reprogram those bits. So the researchers added two molecules aimed at loosening the DNA’s packaging.

The team tried this method with two types of body cells: ovarian cells from an adult and connective tissue cells from a fetus. Although 22 out of 42 monkeys became pregnant with embryos cloned from ovarian cells, only two babies were born and neither survived long past birth. Efforts with embryos made with the fetal cells resulted in six pregnancies among 21 surrogate monkey moms and two healthy babies.

“After 20 years of trying from the most talented groups, and nothing working, finally this works,” Cibelli says. “This research is going to help cloning of all species.”

Cloned primates could help researchers better understand diseases in humans. Macaques are close genetic relatives to humans, making the monkeys better analogs than other lab animals. And clones make it easier to weed out the complications of different genetics when studying diseases or testing drugs.

The sisters are just a few weeks old, but they hold a lifetime of promise for researchers. Poo says the scientists will watch for any abnormalities as Zhong Zhong and Hua Hua grow and play.

“The monkeys are in good health and very active,” he says. “There are no signs they are unhealthy.”

More than 100 days after two neutron stars slammed together, merging into one, new telescope images have revealed that the collision’s lingering X-ray light show has gotten brighter. And scientists don’t fully understand why.

NASA’s orbiting X-ray telescope, Chandra, previously picked up the X-rays 15 days after gravitational waves from the cataclysm reached Earth on August 17, 2017 (SN: 11/11/17, p. 6). The merged remnant then spent several months too close to the sun for its X-rays to be seen.

When the remnant reemerged from the sun’s veil on December 4, it was about four times brighter than when it was last spotted, Daryl Haggard of McGill University in Montreal and her colleagues report January 18 in Astrophysical Journal Letters.

The glow may be tapering off. The XMM-Newton space telescope found on December 29 that the X-ray signal may be starting to weaken, according to a paper published January 18 at arXiv.org.

“The plot is about to thicken,” says Haggard. Chandra has collected new data to look for a drop in brightness.

Scientists are debating how to explain the enduring X-rays. Neutron star collisions are expected to emit bright jets of material, creating X-rays that fade quickly. The long-lasting X-rays might be explained by a “cocoon” of debris (SN Online: 12/20/17), among other possibilities.

Though they be but little, they are fierce.

Airborne particles smaller than 50 nanometers across can intensify storms, particularly over relatively pristine regions such as the Amazon rainforest or the oceans, new research suggests. In a simulation, a plume of these tiny particles increased a storm’s intensity by as much as 50 percent.

Called ultrafine aerosols, the particles are found in everything from auto emissions to wildfire smoke to printer toner. These aerosols were thought to be too small to affect cloud formation. But the new work suggests they can play a role in the water cycle of the Amazon Basin — which, in turn, has a profound effect on the planet’s hydrologic cycle, researchers report in the Jan. 26 Science.
“I have studied aerosol interactions with storms for a decade,” says Jiwen Fan, an atmospheric scientist at the Pacific Northwest National Laboratory in Richland, Wash., who led the new study. “This is the first time I’ve seen such a huge impact” from these minute aerosols.

Larger aerosol particles greater than 100 nanometers, such as soot or black carbon, are known to help seed clouds. Water vapor in the atmosphere condenses onto these particles, called cloud condensation nuclei, and forms tiny droplets. But water vapor doesn’t condense easily around the tinier particles. For that to be possible, the air must contain even more water vapor than is usually required to form clouds, reaching a very high state of supersaturation.

Such a state is rare — larger aerosols are usually also present to form water droplets, removing that extra water from the atmosphere, Fan says. But in humid places with relatively low background air pollution levels, such as over the Amazon, supersaturation is common, she says.
From 2014 to 2015, Brazilian and U.S. research agencies collaborated on a field experiment to collect data on weather and pollution conditions in the Amazon Basin. As part of the experiment, several observation sites tracked plumes of air pollution traveling from the city of Manaus out across the rainforest. During the warm, wet season, there is little difference day to day in most meteorological conditions over the rainforest, such as temperature, humidity and wind direction, Fan says. So a passing pollution plume represents a distinct, detectable perturbation to the system.

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The international team examined vertical wind motion, or updrafts, and aerosol concentration data from one of these stations from March to May 2014. When a large plume of aerosols with an abundance of ultrafine particles passed by an observation station, the researchers observed a corresponding, more powerful vertical wind motion and heavier rain. Such updrafts intensify storms, helping to drive stronger circulation.

Next, the researchers conducted simulations of an actual storm that occurred on March 17, 2014, matching its temperature, wind and water vapor conditions, as well as a low level of background aerosols in the atmosphere. Then, the team introduced several pollution scenarios to interact with the storm, including no plume and a typical plume from the Manaus metropolis. The results suggested that the ultrafine aerosol particles, in particular, were not only acting as cloud condensation nuclei over the Amazon Basin, but also that the water droplets the aerosols created significantly strengthened the gathering storm.

If the conditions are right, the sheer abundance of the ultrafine particles in such a plume would rapidly create a very large number of cloud droplets. The formation of those droplets would also suddenly release a lot of latent heat — released from a substance as it changes from a vapor to a liquid — into the atmosphere. The heat would rise, creating updrafts and quickly strengthening the storm.

Aside from the Amazon, Fan notes that such pristine, humid conditions can also exist over large swaths of the oceans. One recent study in Geophysical Research Letters that she points to found a link between well-traveled shipping lanes, which would contain abundant exhaust including ultrafine aerosols, and an increase in lightning strikes. “This mechanism may have been at play there,” she says.

Atmospheric scientist Joel Thornton of the University of Washington in Seattle, who led the study on the shipping exhaust, says it’s possible that ultrafine particles play a role in that scenario. “What this paper does is raise the stakes in needing to develop a deeper, more accurate understanding of the sources and fates of atmospheric ultrafine particles,” Thornton says.

Meteorologist Johannes Quaas of the University of Leipzig in Germany, who was not involved in either study, agrees. “It’s a very interesting hypothesis.”

But the observations described in the new study don’t definitively demonstrate that ultrafine aerosols alone drive updrafts, Quaas adds. The weather conditions may appear highly consistent from day to day, but such systems are still highly chaotic. Everything from wind to temperature to how the land surface interacts with incoming solar radiation may be variable, he notes. “In reality, it’s not just the aerosols that change.”