SAN ANTONIO — Early Christian monks’ vows of silence may have attracted not only the devout but also a fair number of hearing-impaired men with a sacred calling.

A team led by bioarchaeologist Margaret Judd of the University of Pittsburgh found that a substantial minority of Byzantine-era monks buried in a communal crypt at Jordan’s Mount Nebo monastery display skeletal signs of hearing impairments. Judd presented these results November 19 at the annual meeting of the American Schools of Oriental Research.
Judd has directed excavations at Mount Nebo since 2007. Her new results focus on a two-chambered crypt containing skeletons of at least 57 men presumed to have been monks. Oil lamps found in the crypt date to the 700s.

About 16 percent of these men displayed damage to middle ear bones caused by infections known as otitis media. This condition frequently occurs in childhood and can lead to lasting hearing problems even if the infection clears up quickly (SN Online: 3/10/10). Monks showing signs of otitis media probably suffered mild to moderate hearing loss.

Damage to one middle ear bone, the stapes, in two other individuals likely caused severe hearing loss in one ear each. In another case, a fracture above the left eye could have damaged middle ear bones, Judd proposed. Finally, one skull’s thickened bone may have resulted from Paget’s disease, a viral infection in adulthood that can impair hearing.

Hearing loss would have had little effect on monks’ daily lives, since they communicated with hand signals, nods and other gestures, Judd said. Even if some developed hearing ailments after joining the monastery, those conditions must have largely gone undetected by affected monks and their peers who rarely or never spoke, she suggested.

Without light, we cannot see. That’s why “dark galaxies” have eluded astronomers for so long. Two years ago, these star-starved entities were virtually unknown. But scientists now have better ways of seeing, even in dim conditions. New telescopes that can detect the faint light from these mysterious galaxies have enabled scientists to chalk up a considerable list: Dark galaxies seem to be much more common than anyone had thought. One rivals the Milky Way in size but holds only a hundredth as many stars.

Cataloging these dark galaxies, as Christopher Crockett reports (SN: 12/10/16, p. 18), is just the beginning. Scientists still don’t know how such galaxies might have formed or how their small populations of stars can fend off the gravitational grabs of other galaxies. Understanding dark galaxies will take more time and more intense study of their faint light.
Cleverly built telescopes may allow us to examine the cosmic darkness, but a different type of cleverness entirely is required to delve into the minds of animals. Specifically, researchers trying to understand the evolutionary roots of mathematics must resort to complex tests for evaluating how animals judge quantities, Susan Milius reports in “Animals give clues to the origins of human number crunching.” (SN: 12/10/16, p. 22).

Counting seems an all-too-human concept, and yet many creatures can reliably pick out a greater number of treats. Figuring out how animals are making such a choice (is it surface area? volume? number?) has frustrated researchers and occasionally triggered disagreements. But the latest studies show signs that many animals do have some quantitative sense, even if it’s far less sophisticated than our own.

Much less illuminating are the results that supposedly would have provided the final answer about heart health risks posed by the anti-inflammatory pain medicine Celebrex. Like Vioxx, which was taken off the market years ago after it was linked to heart problems, Celebrex (generic name celecoxib) is what’s known as a COX-2 inhibitor. Many experts were concerned that the problems with Vioxx might also show up in people who took Celebrex. But there were little data, so the U.S. Food and Drug Administration asked for a large study to clear up the question. When the results were reported in November at a meeting of the American Heart Association, they brought little resolution, Laura Beil reports in “Popular painkiller doesn’t have more heart risks than others, study claims” (SN: 12/10/16, p. 6). Despite finding no elevated heart risk from Celebrex use, and fewer gastrointestinal side effects compared with ibuprofen and naproxen, the study was not done as cleverly as it needed to be. It enrolled people already at low risk of heart problems, for one. Dosages of medicines shifted during the long study. Many taking Celebrex dropped out before the study was completed. Far from settling the issue, the research leaves many questions unanswered.

In so many areas, science succeeds — seeing into the darkness, exploring the unknown and investigating fantastical ideas. But sometimes the signal is faint, the tools we use too crude, the logic shaky, the deeper understanding still elusive. That’s when scientists need to be more clever, more persistent, more wedded to reason and committed to revealing whatever truths can be found out there in the light.

Brilliant births and destructive deaths of stars might take a runt of a galaxy and stretch it to become a ghostly behemoth, new computer simulations show. This process could explain the origin of recently discovered dark galaxies, which can be as wide as the Milky Way but host roughly 1 percent as many stars.

Since 2015, astronomers have found hundreds of these shadowy systems lurking in and around several clusters of galaxies (SN: 12/10/16, p. 18). How these dark galaxies form is a puzzle. But prolific star formation and blast waves from exploding stars could be responsible, researchers suggest in a paper to appear in Monthly Notices of the Royal Astronomical Society Letters.
“The mystery is: Are these galaxies like the Milky Way, or are they dwarf galaxies?” says study coauthor Arianna Di Cintio, an astrophysicist at the University of Copenhagen in Denmark. “Our mechanism could be a nice formation scenario for these galaxies and prove that they are dwarfs.”

Di Cintio and colleagues ran computer simulations of galaxy evolution and found that some runts can be inflated by stellar energy. Radiation from young massive stars heats up interstellar gas, preventing it from forming more stars. And a flurry of supernova explosions can toss that gas out of the galaxy. The gravity of the galaxy drops, and so does its ability to hold on to stars and dark matter, an enigmatic substance thought to help hold galaxies together. “Dark matter particles fly outward and start the expansion,” says Di Cintio. “This happens to the stellar population as well.”

Those galaxies that remain as runts in the simulations go through this process just once, whereas giant dark galaxies regurgitate their gas multiple times. And that provides a way to test this idea, says Di Cintio. First astronomers need to find dark entities far away from galaxy clusters where the environment can also take its toll. Then researchers can estimate the ages of stars in the galaxy to see if there have been multiple bursts of star formation. If this hypothesis is correct, dark galaxies might also be loaded up with lots of hydrogen gas that allows them to sustain several rounds of gas purging.

“It is very interesting to see that, in some cases, [supernovas] can be efficient enough to expand dwarf galaxies,” says Nicola Amorisco, also at the University of Copenhagen. He helped put forth an idea that dark galaxies start as runts that get stretched because of rapid rotation. Recent observations also show that some dark systems have masses that are similar to dwarf galaxies (though one is as hefty as the Milky Way). “It is even possible that a combination of — or the interplay between — a few different mechanisms could be responsible,” says Amorisco. “It will be very exciting to understand whether that is the case.”

SAN FRANCISCO — Mostly dead is still partly alive, even for cells on the brink of suicide, new research suggests.

Near-death experiences may play a role in embryo development and help cancer cells that survive chemotherapy spread throughout the body, Denise Montell, a cell biologist at the University of California, Santa Barbara, reported December 6 at the annual meeting of the American Society for Cell Biology.

Montell described a recently discovered process called anastasis that saves cells in the midst of committing a type of cellular suicide known as apoptosis. She and others are only beginning to unravel how the process works. Preliminary results indicate that cells simultaneously kill themselves and hold on to a lifeline in case conditions improve, she said.
Scientists had thought that once a cell going through apoptosis activated an executioner molecule known as a caspase, the cell would surely die, said Claire Walczak, a cell biologist at Indiana University in Bloomington. But cells sometimes call off their attempted suicides at the last moment, even after the executioner starts working, cell biologist Ho Lam Tang discovered in 2008 while a graduate student at the Chinese University of Hong Kong. Tang, now at Johns Hopkins University, named the process anastasis, which in Greek means “rising to life.”

Tang’s discovery that apoptosis is reversible “was really shocking,” said Walczak. “It’s a really nice illustration of how adaptable cells are.”

Tang initially made the discovery by treating an immortal type of cancer cells, called HeLa cells, with a drug that stimulates apoptosis. Once the cells were dying, Tang washed away the drug and some of the cells recovered.

“That experiment is essentially what we do to patients” undergoing chemotherapy treatment, said J. Marie Hardwick, a cell and molecular biologist at Johns Hopkins. She reported with Tang last year in Scientific Reports that fruit fly egg cells can come back from apoptosis and even produce an adult fly.

Cancer patients are given a dose of chemotherapy drugs or radiation that causes cells to commit apoptosis. Then the treatments are stopped for a short time to allow the patient to recover. If cancer cells can come back through anastasis, they may cause a resurgence of the disease, Hardwick suggests. Many of the cells brought back by anastasis have genetic defects. “If you’ve already attempted to die, you’ve got problems,” Hardwick says.
Some cells that survive apoptosis brought on by stresses such as heat or irradiation can go on to divide and “do basically anything a normal cell can do,” Montell said. But unpublished work from her lab indicates that cells brought back to life by anastasis may never go back to their untreated state and may carry permanent memories of their near-death experiences, she said at the cell biology meeting.

Montell and colleagues compared gene activity in untreated cells and ones taken to the brink of death and allowed to recover for varying amounts of time. Cell survival genes are already being made while the cell is preparing to kill itself, her team discovered.

“Dying cells are actually hedging their bets. They’re on the brink of death. They don’t know if things are going to get better or get worse,” Montell said. After recovery, the reanimated cells begin to move and to stimulate blood vessel production. Those are things cells do when healing a wound, but they are also actions taken by tumor cells.

“This would be an extremely unbeneficial response if the cells in question happen to be cancer cells,” Montell said. The findings suggest that stopping anastasis may lead to more effective cancer treatments.

In some other cases, stimulating anastasis may benefit patients, Montell said, such as by saving heart cells after a heart attack or brain cells after a stroke. Those cells don’t divide much so there’s less risk of cancer and recovered cells could restore heart and brain function.

Scientists don’t know exactly how anastasis works — few researchers are even aware it happens — so it may take some time before anyone is able to start or stop anastasis at will, Hardwick said.

SAN FRANCISCO — Disrupting the Zika enzyme NS3 could help stop the virus. NS3 causes problems when it gloms on to centrioles, structures inside cells needed to divvy up chromosomes when cells divide, Andrew Kodani, a cell biologist at Boston Children’s Hospital, reported December 6 at the American Society for Cell Biology’s annual meeting.

Zika, dengue and other related viruses, known as flaviviruses, all use a version of NS3 to chop joined proteins apart so they can do their jobs. (Before chopping, Zika’s 10 proteins are made as one long protein.) But once NS3 finishes slicing virus proteins, it moves to the centrioles and can interfere with their assembly, Kodani and colleagues found. Something similar happens in some genetic forms of microcephaly.

Kodani and colleagues found that small amounts of a chemical called anthracene can prevent NS3 from tinkering with the centrioles. So far the work has been done only in lab dishes.

At first glance, the stories taking the top two spots in Science News’ review of 2016 have little in common. Scientists began searching decades ago for gravitational waves. Discussions of these subtle signals from dramatic and distant phenomena appear dozens of times in the SN archive starting as early as the 1950s. Their long-awaited discovery, our No. 1 story of the year, touched off celebration of a new era in astronomy.

Less expected, and far from subtle, was the sudden rise in Brazil of microcephaly cases, linked this year to Zika virus infections — our No. 2 story. Little was known about Zika before the outbreak, which delivered devastation and fear across the Americas. In fact, only a single previous mention of Zika exists in the SN archive, in a book review from the 1990s.
But the stories have at least one thing in common: Both highlight the power of scientific discoveries to trigger our deepest human emotions. Pure elation as well as overwhelming dread can accompany research advances.

2016 brought many more sentiments, too. There was enthusiasm for the discovery of the exoplanet Proxima b, concern for the prospects of three-parent babies and feelings of potential but also impending peril in the openings of Arctic passageways.

The editors and writers at Science News also recognize that some of the best and most moving stories are those that are still unfolding. So, in addition to the discoveries of 2016, we review milestones, setbacks and other tales of unsteady progress. Sonia Shah writes about a new wave of infectious diseases; Tom Siegfried explores convergent failures in the field of particle physics; and Laurel Hamers covers key challenges for self-driving cars. Then, Science News writers share what science news they’re most excited about in the year to come. — Elizabeth Quill

Four proteins that can transform adult cells into embryonic-like ones can also turn back the aging clock, a new study in mice suggests.

Partial reprogramming of cells within prematurely aging mice’s bodies extended the rodents’ average life span from 18 weeks to 24 weeks, researchers report December 15 in Cell. Normal mice saw benefits, too: Muscles and pancreas cells healed better in middle-aged mice that got rejuvenation treatments than in mice that did not. The experiment could be evidence that epigenetic marks — chemical tags on DNA and proteins that change with age, experience, disease and environmental exposures — are a driving factor of aging. Some marks accumulate with age while others are lost.
“It’s an inspiring paper,” says Jan van Deursen, a biologist at the Mayo Clinic in Rochester, Minn., who studies diseases of aging. He gives the paper an “A” for sparking imagination, but lower marks for practical applications to human aging because it would involve gene therapy and could be risky. “It’s all cool, but I don’t see that it could ever be applied in medicine,” he says. “We could be terribly wrong. Hopefully we are.”

Researchers reset the mice’s aging clock by genetically engineering the animals to make four proteins when the rodents were treated with the antibiotic doxycycline. Those four proteins — Oct4, Sox2, Klf4 and c-Myc — are known as “Yamanaka factors” after Shinya Yamanaka. The Nobel Prize‒winning scientist demonstrated in 2006 that the proteins could turn an adult cell into an embryonic-like cell known as an induced pluripotent stem cell, or iPS cell (SN: 11/3/12, p. 13; SN: 7/14/07, p. 29).
The factors help strip away epigenetic marks that enable cells to know whether they are heart, brain, muscle or kidney cells, for example. As a result, stripped cells revert to the ultraflexible pluripotent state and are capable of becoming nearly any type of cell. Other researchers have used the Yamanaka factors to reprogram cells within living mice before, but those attempts resulted in the growth of tumors. (Cancer cells resemble stem cells in that they don’t have a specific identity and are “undifferentiated.”)
Those tumors indicated to Alejandro Ocampo and colleagues that the proteins were rewriting epigenetic programming to take cells back to an undifferentiated state. But “you don’t need to go all the way back to pluripotency” to erase the marks associated with aging, says Ocampo, a stem cell biologist at the Salk Institute for Biological Studies in La Jolla, Calif. A milder reprogramming treatment might reverse aging without stripping away cells’ identity, leading to cancer, Ocampo and colleagues thought.

The researchers put genetically engineered mice with a premature aging disease called progeria on a regimen in which the animals were treated with doxycycline two days per week to turn on the Yamanaka factors. Mice that made the reprogramming proteins lived six weeks longer on average than mice that didn’t get the treatment. The mice didn’t get cancer, but still died prematurely (lab mice usually live two to three years on average). “We are far away from perfection,” Ocampo says.

Normally aging mice also got benefits from the treatment. When the animals were 1 year old (roughly middle-aged), the researchers treated them with doxycycline two days per week for three weeks. Treated mice were better able to repair muscles and replace insulin-producing cells in the pancreas than untreated mice. Not all organs fared as well, Ocampo says, citing preliminary evidence. Ongoing experiments will determine whether the epigenetic reprogramming can make the mice live any longer or healthier.
People probably won’t be genetically engineered the way mice are. But chemicals and small molecules might also be able to wipe away epigenetic residue that builds up with aging and restore marks that were lost over time, returning to a pattern seen in youth, Ocampo suggests.

Researchers still don’t know whether all cells are rejuvenated by the treatment. Yamanaka factors may breathe new life into aging stem cells, allowing them to replenish damaged tissues. Or the factors may wake up senescent cells — cells that have shut down normal functions and cease to divide, but may send signals to neighboring cells that cause them to age (SN: 3/5/16, p. 8). Reviving senescent cells could be dangerous, says van Deursen; the body shuts cells down to prevent them from becoming cancerous.

Plenty of evidence indicates that resetting epigenetic programming can extend life, says Ocampo. He points to a recent report that Dolly the Sheep’s cloned sisters are aging normally (SN: 8/20/16, p. 6) as a hopeful sign that reprogramming probably isn’t dangerous, and might one day safely prevent many of the diseases associated with aging in people, if not lengthening life spans.

An experimental Ebola vaccine has triumphed in West Africa.

Of 5,837 people in Guinea who received a single shot of the vaccine, rVSV-ZEBOV, in the shoulder, none became infected with the virus 10 to 84 days after vaccination. That’s “100% protection,” researchers report December 22 in the Lancet.

World Health Organization researcher Ana Maria Henao-Restrepo and colleagues tested a “ring vaccination” approach, by immediately vaccinating family members and other contacts of people infected with Ebola. This strategy seemed to staunch the virus’s spread. Among 4,507 people never vaccinated or who got a delayed vaccine, 23 contracted Ebola.

The findings echo preliminary results reported in 2015, and offer a promising line of defense for future outbreaks. But scientists still do not know how long-lasting the vaccine’s protection would be.

In late 2013, West Africa saw the beginning of what would become the largest Ebola outbreak in history, with more than 11,300 deaths reported, and 28,616 cases in Guinea, Sierra Leone and Liberia. Since then, scientists have been racing to create a safe and effective vaccine.

A molecule originally proposed more than 40 years ago breaks the rules about how carbon connects to other atoms, scientists have confirmed. In this unusual instance, a carbon atom bonds to six other carbon atoms. That structure, mapped for the first time using X-rays, is an exception to carbon’s textbook four-friend limit, researchers report in the Jan. 2 Angewandte Chemie.

Although the idea for the structure isn’t new, “I think it has a larger impact when someone can see a picture of the molecule,” says Dean Tantillo, a chemist at the University of California, Davis who wasn’t part of the study. “It’s super important that people realize that although we’re taught carbon can only have four friends, carbon can be associated with more than four atoms.”
Atoms bond by sharing electrons. In a typical bond two electrons are shared, one from each of the atoms involved. Carbon has four such sharable electrons of its own, so it tends to form four bonds to other atoms.

But that rule doesn’t always hold. In the 1970s, scientists made an unusual discovery about a molecule called hexamethylbenzene. This molecule has a flat hexagonal ring made of six carbon atoms. An extra carbon atom sticks off each vertex of the ring, like six tiny arms. Hydrogen atoms attach to the ring’s arms. And leftover electrons zip around the middle of the ring, strengthening the bonds and making the molecule more stable.
When the scientists removed two electrons from the molecule, leaving it with a positive charge, some evidence suggested it might dramatically change its shape. It seemed to rearrange so that one carbon atom was bonded to six other carbons. But the researchers didn’t experimentally confirm that structure.
Now, a different lab has revisited the question. Making this charged version of hexamethylbenzene is a challenge because it’s stable only in extremely strong acid, says study coauthor Moritz Malischewski, a chemist at the Free University of Berlin. And the experimental details in the old study were a bit fuzzy. But after a bit of tinkering, he managed to create the charged molecule. He and coauthor Konrad Seppelt crystallized it with some other molecules, and then used X-rays to get a three-dimensional map of the crystal structure.

The X-ray experiment confirmed what other scientists had suggested in the 1970s: When hexamethylbenzene lost two electrons, it reordered itself. One carbon atom jumped out of the ring and took a new position on top, turning the flat hexagonal ring into a five-sided carbon pyramid. And the carbon on top of the pyramid was indeed bonded to six other carbons — five in the ring below, and one above.

“This molecule is very exceptional,” says Malischewski. Though scientists have found other exceptions to carbon’s four-bond limit, this is the first time carbon has been shown associating with this many other carbon atoms.

When Malischewski measured the length of the molecule’s chemical bonds, the top carbon’s six bonds were each a bit longer than an ordinary carbon-carbon bond. A longer bond is generally less strong. So by picking more partners, that carbon has a slightly weaker connection to each one.

“The carbon isn’t making six bonds in the sense that we usually think of a carbon-carbon bond as a two-electron bond,” Tantillo says. That’s because the carbon atom still has only four electrons to share. As a result, it spreads itself a bit thin by sharing electrons among the six bonds.

Hyoliths are evolutionary misfits no more.

This class of ancient marine invertebrates has now been firmly pegged as lophophorates, a group whose living members include horseshoe worms and lamp shells, concludes an analysis of more than 1,500 fossils, including preserved soft tissue.

The soft-bodied creatures, encased in conical shells, concealed U-shaped guts and rings of tentacles called lophophores that surrounded their mouths. Fossil analysis suggests that hyoliths used those tentacles and spines, called helens, to trawl the seafloor more than 500 million years ago, researchers report online January 11 in Nature.

For years, paleontologists have argued over where on the tree of life these bottom-feeders belonged. Some scientists thought hyoliths were closely related to mollusks, while others thought the odd-looking creatures deserved a branch all their own. This new insight into hyolith anatomy “settles a long-standing paleontological debate,” the researchers write.