You don’t need a degree in science to monitor backyard owls or measure trees. And anyone with a computer can help scientists track seal populations in Antarctica. Citizen science projects like these — which depend on crowdsourced data — are booming. And when faced with a planet scarred by industrialization and climate change, these efforts might be exactly what we need, environmental journalist Mary Ellen Hannibal argues in Citizen Scientist.
What we call “citizen science” was once just “science.” After all, many early conservationists and natural historians — people like John Muir — weren’t academics. As species disappear faster and faster, scientists can’t work alone. They need the eyes and ears of passionate people who are watching as flowers bloom earlier each year and butterflies become sparser.

Hannibal dips her toes into some of the citizen science projects happening within driving distance of her home in San Francisco. She chronicles efforts to count, track and save a variety of species, including sea otters and redwood trees.

Along the way, Hannibal discovers heroes both modern and historical: For instance, Rebecca Moore, who leads Google Earth Outreach, originally developed the mapping tool in the early 2000s to help stop logging in the Santa Cruz Mountains. And Alice Eastwood, botany curator at the California Academy of Sciences in the early 1900s, helped build the museum’s plant collection. Lacking a college degree, she collected specimens for nearly 60 years — and even saved part of the collection from the 1906 San Francisco earthquake.

While Hannibal is contemplating extinction and habitat destruction, her father is dying from cancer. Her field expeditions become a lens through which she processes her dad’s death. The parallels make Citizen Scientist part memoir, part science tale and part history book. Hannibal has a conversational writing style that moves quickly from topic to topic, punctuated with humorous and thoughtful asides.

Although centered in California, the book has a global message: Humans have much in common with the species we’re trying to save. Grizzlies and wolves, for instance, “leave their natal home, light out for a huge territory, find a mate, and establish a new base of operations,” Hannibal writes. The human heroes in our storybooks aren’t so different.

A genetic study of HIV viruses from the 1970s may finally clear the name of a man long identified as the source of the AIDS epidemic in the United States. HIV came to New York City between 1969 and 1973, long before the man known as Patient Zero became infected, researchers report October 26 in Nature.

Using techniques developed to decipher badly degraded ancient DNA from fossils, researchers reconstructed the genetic instruction books of eight HIV viruses from blood samples collected in 1978 and 1979 in New York City and San Francisco. The viral DNA was so genetically diverse that the viruses must have been circulating in the cities for years, picking up variations, says evolutionary biologist Michael Worobey of the University of Arizona in Tucson.
Worobey and colleagues calculate that the virus probably first jumped to the United States in 1970 or 1971. So HIV spread for about a decade before AIDS was recognized in 1981 and found to be caused by a retrovirus in 1983.
Examining the relationships between the New York City and San Francisco viruses with HIV strains from elsewhere let researchers trace the virus’s path. The eight American samples all came from the same branch of the HIV family tree as ones from the Caribbean. That suggests that HIV spread from Africa to the Caribbean before making its way to the United States. New York HIV samples were more diverse than those from California, indicating that New York City was probably the hub of early HIV spread and the virus arrived in San Francisco later.
Worobey and colleagues also examined HIV DNA from Patient Zero. Also known as Case 57, he was part a 1984 study of gay men with AIDS in Los Angeles who had either a rare cancer called Kaposi’s sarcoma or Pneumocystis carinii pneumonia, both complications of the disease. Researchers from the Centers for Disease Control and Prevention found that many of the men had had sexual contact with each other, helping to establish that HIV is sexually transmitted.
Later, in the book And the Band Played On, author Randy Shilts identified Patient Zero as an Air Canada flight attendant named Gaëtan Dugas. It was widely interpreted that Dugas was the first case of HIV in the United States, even though the CDC never claimed — and has repeatedly refuted — that, says epidemiologist James Curran, a coauthor of the 1984 study who is now at Emory University in Atlanta. Part of the confusion may have been that Patient Zero was supposed to be identified as Patient O (for “outside of California”).

Dugas became a flight attendant in 1974 and began traveling to the United States shortly after, says Richard McKay, coauthor of the new study and a medical historian at the University of Cambridge. Dugas estimated that he had about 250 male sexual partners each year between 1979 and 1981. Shilts and others contended that Dugas was intentionally spreading the virus to others, though he was diagnosed with Kaposi’s sarcoma in 1980 before anyone knew what AIDS was or that it was caused by a virus.

Now, the genetic analysis confirms that Dugas was not carrying the earliest version of the virus. “This individual was simply one of thousands infected before HIV/AIDS was recognized,” McKay says.

The new study is a cautionary tale against trying to pin the spread of an infectious disease on any one person, says Robert Remien, a behavioral scientist at Columbia University Medical Center. “There’s no blame or cause to be laid on any of those people in those early years.”

Editor’s note: This story was updated November 10, 2016, to fix the alignment of the timeline with the phylogenetic tree and to update the number of sequential diagnoses in the Patient Zero cluster of AIDS cases.

SAN DIEGO — A nerve-zapping headset caused people to shed fat in a small preliminary study.

Six people who had received the stimulation lost on average about 8 percent of the fat on their trunks in four months, scientists reported November 12 at the annual meeting of the Society for Neuroscience.

The headset stimulated the vestibular nerve, which runs just behind the ears. That nerve sends signals to the hypothalamus, a brain structure thought to control the body’s fat storage. By stimulating the nerve with an electrical current, the technique shifts the body away from storing fat toward burning it, scientists propose.
Six overweight and obese people received the treatment, consisting of up to four one-hour-long sessions of stimulation a week. Because it activates the vestibular system, the stimulation evoked the sensation of gently rocking on a boat or floating in a pool, said study coauthor Jason McKeown of the University of California, San Diego.

After four months, body scans measured the trunk body fat for the six people receiving the treatment and three people who received sham stimulation. All six in the treatment group lost some trunk fat, despite not having changed their activity or diet. In contrast, those in the sham group gained some fat. Researchers suspect that metabolic changes are behind the difference. “The results were a lot better than we thought they’d be,” McKeown said.

Earlier studies had found that vestibular nerve stimulation causes mice to drop fat and pack on muscle, resulting in what McKeown called Schwarzenegger mice. Though small, the current study suggests that the approach has promise in people. McKeown and colleagues have started a company based on the technology and plan to test it further, he said.

Building mountains in minutes requires deep rocks and a big bang.

Rings of mountainous peaks sit inside large impact craters, but scientists weren’t sure how these features formed. One explanation proposed that these mountains form from deep rocks jolted to the surface by the impact. Another theory suggested that uplift caused surface rocks to congregate in heaps around the crater.

Rocks extracted from ground zero of the impact that devastated the dinosaurs have now resolved this debate. That crater’s peak ring is made up of deep rocks, researchers report in the Nov. 18 Science.
Confirming this explanation of peak ring formation will help scientists study the depths of other planets, says study coauthor Sean Gulick, a geophysicist at the University of Texas at Austin. It will also help better estimate the environmental damage wrought by the dinosaur-killing impact.、
“Unlike tectonic mountains that take millions of years to form, these mountains are made in less than 10 minutes,” Gulick says. Knowing the forces involved in sculpting those mountains will allow scientists to better estimate the total energy released during the catastrophic crash.
The Chicxulub impactor whacked into Mexico’s Yucatán Peninsula around 66 million years ago, leaving behind a 200-kilometer-wide hole in the ground. Rising around 600 meters from the crater floor — though now buried under sediment – is the peak ring. While similar rings of mountains have been spotted inside large craters on other planetary bodies such as the moon and Mercury, Chicxulub is the only crater on Earth with an intact peak ring structure. And “it’s a lot cheaper to get to the one in Mexico,” Gulick says.

Last spring, Gulick and colleagues drilled into Chicxulub’s peak ring off the coast of Mexico using a special ship that can convert into a stable platform using three long legs. Rock samples, collected from about 750 to 1,300 meters below the seafloor, contained bits of granite and other minerals that would have been buried many kilometers belowground just before the impact. That means that the same process that built the peak ring must have churned those deep rocks to the surface, the researchers concluded.
That result does not mesh with the idea that the peak ring material instead came from much closer to the surface. Under that theory, after impact, surface material slides down the crater rim onto the floor. The middle of the floor then rebounds upward due to the removal of the weight of the overlying rock. That uplift shifts the fallen material, forming a peak ring.
Instead, the dynamic collapse theory of peak ring formation explains what happened at Chicxulub, researchers say. After the initial strike, churned-up material rushed in to fill the deep void left by the impact, like water when a stone is dropped into a pond. The flowing material met in the middle of the crater and surged upward into a towering central peak that then collapsed outward, dumping rocks previously buried several kilometers underground onto the crater’s surface.
These rocks became more porous and less dense during their dramatic rise, the researchers found. While typical deep rocks in the region have an average density of more than 2.6 grams per cubic centimeter, the peak ring rocks average just 2.41 grams per cubic centimeter and are heavily fractured.

“About 10 percent of the rock is pores, so there’s lots of space,” Gulick says. Microbes, he proposes, may have moved into those holes as life repopulated the impact site. Early life on Earth may have even gotten its first foothold in the porous rock inside similar impact craters, he speculates.

The high porosity of the Chicxulub rock could also explain why the moon’s crater-riddled crust is highly porous and help solve other planetary mysteries as well, says Ross Potter, a planetary scientist at Brown University.

“Impact craters are excavating material from depth, so they’re very good probes into the interior of planetary bodies,” he says. “You may be able to find very interesting samples that tell you a lot about not only the cratering process itself, but also the interior of the planet and how the planet formed.”

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.

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.