Male mammoths really had to watch their steps. More than two-thirds of woolly mammoth specimens recovered from several types of natural traps in Siberia came from males, researchers report November 2 in Current Biology.

Paleogenomicist Patrícia Pečnerová of the Swedish Museum of Natural History in Stockholm and her colleagues examined genomic data recovered from 98 mammoth bone, tooth, tusk and hair shaft specimens and found that 69 percent of their owners were male. Sex biases in fossil preservation are rare, and the sexes were almost certainly balanced at birth. So the researchers considered whether social and behavioral patterns might have meant that male mammoths more often died in such a way that their remains were buried and preserved, such as becoming trapped in a bog or falling through thin ice.

In modern elephants, herds of females and young live together, led by an experienced female, whereas males are more likely to live in bachelor groups or alone. That could result in more risk-taking behavior for those males. Woolly mammoths, the distant cousins of modern elephants, may have had the same social structures, the researchers suggest.

The study, the authors say, highlights how fossil genomic data can help illuminate the past social structures and behavior of extinct animals — and how existing fossils may not fully represent the original population.

Hard-boiled eggs are a dish best served cold.

When quickly reheated in a microwave and then pierced, the picnic staple can explode with a loud bang in a shower of hot, rubbery shrapnel. But this blast is far more likely to make a hot mess than hurt your hearing, according to research presented December 6 at the Acoustical Society of America meeting in New Orleans.

That distinction isn’t as odd as it might sound. In a lawsuit, a man claimed to have suffered burns and hearing damage after a microwaved, hard-boiled egg exploded in his mouth at a restaurant. Researchers from Charles M. Salter Associates, Inc. in San Francisco called as expert witnesses couldn’t find scientific papers backing up the claim that an egg could burst with enough vigor to cause hearing loss — just a lot of YouTube videos documenting eggsplosions.
So the researchers microwaved peeled hard-boiled eggs in water on high power for three minutes.

The eggs were “uncooperative,” study coauthor Anthony Nash said in a news conference. Some exploded in the microwave, while others wouldn’t explode at all. But of nearly 100 eggs tested, 28 exploded outside of the microwave after being poked with a meat thermometer. From 30 centimeters away, the sound pressure from those explosions ranged from 86 to 133 decibels.

The median sound pressure level recorded, 108 decibels, is about the same as that at an average rock concert. Continuous exposure to that noise level could damage hair cells inside ears that respond to sound. The National Institute for Occupational Safety and Health sets recommended exposure limits for sound pressures above 85 decibels, says William Murphy, a researcher at NIOSH who wasn’t part of the study. But those limits are based on daily exposure over years, he says.
A burst egg’s boom, on the other hand, lasts just milliseconds — not long enough to do much harm. “The likelihood for hearing damage from a single exploding egg was very low,” Nash said.

The lawsuit was settled out of court before Nash and his colleagues conducted the second phase of the study – considering how sound hits your ears when it’s coming from inside your mouth. An in-mouth explosion might send slightly more sound pressure to the ears, Nash says, but still probably not enough to cause lasting damage as a one-time accident.

A peeled egg probably explodes when pockets of water trapped in the yolk become superheated — hotter than the boiling temperature of water without actually bubbling, Nash suggested. When disrupted, say by a fork or a tooth, the water pockets spontaneously boil, bursting through the squishy egg white and sending bits flying. (It’s the same phenomenon that can occasionally make microwaved coffee spurt out of the mug onto your clean work clothes.)

A bigger risk than the noise might be the heat. Nash and his colleagues measured the temperature of yolks in eggs that didn’t burst. Those temperatures were, on average, 12 degrees Celsius above the surrounding water bath, which was often close to boiling.

This year, gene therapy finally became a clinical reality. The U.S. Food and Drug Administration approved two personalized treatments that engineer a patient’s own immune system to hunt down and kill cancer cells. The treatments, the first gene therapies ever approved by the FDA, work in people with certain blood cancers, even patients whose cancers haven’t responded to other treatments.

Called CAR-T cell immunotherapy (for chimeric antigen receptor T cell), one is for kids and young adults with B cell acute lymphoblastic leukemia, or ALL, approved in August (SN Online: 8/30/17). The other is for adults with non-Hodgkin lymphoma, approved in October. Other CAR-T cell therapies are in testing, including a treatment for multiple myeloma.
“It’s a completely different way of treating cancer,” says pediatric oncologist Stephan Grupp, who directs the Cancer Immunotherapy Program at the Children’s Hospital of Philadelphia. Grupp spearheaded the clinical trials of the newly approved ALL therapy, called Kymriah.

Researchers are developing many different versions of CAR-T cell therapies, but the basic premise is the same: Doctors remove a patient’s T cells (immune system cells that attack invaders) from a blood sample and genetically modify them to produce artificial proteins on their surfaces. Those proteins, called chimeric antigen receptors, recognize the cancer cells in the patient’s body. After the modified T cells make many copies of themselves in the lab, they’re unleashed in the patient’s bloodstream to find and kill cancer cells.
CAR-T cell therapy is particularly exciting because it works well in people whose cancers haven’t responded to other available treatments, says Renier Brentjens, an oncologist at Memorial Sloan Kettering Cancer Center in New York City. Of the 63 kids and young adults treated in a clinical trial of Kymriah, 83 percent had their cancers go into remission within three months.
Now that these therapies have been clinically approved, there’s been an “explosion of interest” in the approach, says Dario Campano, an immunopathologist at the National University Cancer Institute in Singapore. Going forward, he expects to see even more rapid progress in the technology. Fifteen years ago, Campana helped develop the chimeric antigen receptor that’s used in Kymriah today. For now, the treatments are approved for use only when other treatments have failed, but someday CAR-T cell therapy could be the first treatment doctors try, he says.

One drawback is the price. Kymriah costs $475,000 for a onetime treatment, according to Novartis, which makes Kymriah. The non-Hodgkin lymphoma treatment made by Gilead Sciences, called Yescarta, is listed at $373,000. The total price tag for treatment could be higher when the costs of dealing with side effects and complications are factored in.

The approach is approved only for blood cancers. Using CAR-T cell therapy on solid tumors will require finding ways to get the T cells past additional cellular roadblocks, Grupp says.

Have you fallen behind on your reading this year? Or maybe you’ve plowed through your must-reads and are ready for more. Science News has got you covered. Here are the staff’s picks for some of the best science books of 2017. Find detailed reviews from previous issues in the links below or in our Editors pick: Favorite books of 2017.

Against the Grain
James C. Scott

Armed with the latest archaeological research, a political anthropologist argues that the rise of civilization came at a big cost. The initial switch from hunting and gathering to agricultural states brought poor diets, labor-intensive work, outbreaks of infectious diseases and other hardships (SN: 10/14/17, p. 28). Yale Univ., $26

The Great Quake
Henry Fountain

Historical records and interviews with survivors flesh out this tale of how a massive earthquake in Alaska in 1964 provided geologists with key evidence needed to verify the theory of plate tectonics (SN: 9/16/17, p. 32). Crown, $28

Eclipse
Frank Close

More than just a primer on the science of solar eclipses, this memoir chronicles a physicist’s lifetime fascination with the celestial phenomenon and introduces readers to the quirky world of eclipse chasers (SN: 5/13/17, p. 28). Oxford Univ., $21.95

Rise of the Necrofauna
Britt Wray

Resurrecting woolly mammoths, passenger pigeons and other extinct creatures isn’t just a technological problem, as this book explains. “De-extinction” is also rife with ethical dilemmas (SN: 10/28/17, p. 28). Greystone Books, $26.95

Big Chicken
Maryn McKenna

Antibiotics transformed chicken farming, to the detriment of the birds and of human health, a journalist contends. Widespread use of the drugs fueled the industrialization of poultry production and the rise of antibiotic-resistant bacteria (SN: 9/30/17, p. 30). National Geographic, $27

Inferior
Angela Saini

A science writer makes a persuasive case that centuries of biased thinking and flawed scientific research have reinforced sexist stereotypes about women (SN: 9/2/17, p. 27). Beacon Press, $25.95

Caesar’s Last Breath
Sam Kean

Through fun historical anecdotes and lesser-known backstories of scientific greats, this entertaining book profiles the chemical elements that make up the air we breathe and traces the history of Earth’s atmosphere (SN: 7/8/17 & 7/22/17, p. 38). Little, Brown and Co., $28

Cannibalism
Bill Schutt

The grisly practice of eating your own kind turns out to be widespread in the animal kingdom, a zoologist explains in this captivating look at cannibalism (SN: 2/18/17, p. 29). Algonquin Books, $26.95

The Lost City of the Monkey God
Douglas Preston

A journalist tags along on an archaeological expedition to search for the real-life remains of a mythological city in this rainforest adventure tale that morphs into a medical mystery (SN: 2/4/17, p. 28). Grand Central Publishing, $28

The Death and Life of the Great Lakes
Dan Egan

Invasive species, urbanization and other threats have wreaked havoc on the Great Lakes, but this book still finds some glimmers of hope in the scientists who are making headway in resuscitating the ecosystem (SN: 3/18/17, p. 30). W.W. Norton & Co., $27.95

How to Tame a Fox
Lee Alan Dugatkin and Lyudmila Trut

An experiment to replay animal domestication by selectively breeding wild silver foxes is lovingly retold, including by the researcher who has kept the project alive for nearly 60 years (SN: 5/13/17, p. 29). Univ. of Chicago, $26

Making Contact
Sarah Scoles

In the face of numerous obstacles, Jill Tarter still managed to spearhead the search for extraterrestrial intelligence for decades, as this biography recounts (SN: 8/5/17, p. 26). Pegasus Books, $27.95

A Crack in Creation
Jennifer A. Doudna and Samuel H. Sternberg

Two experts, including one of the pioneers of CRISPR/Cas9, discuss the science and ethics of gene editing. Houghton Mifflin Harcourt, $28

These book reviews contain links to Amazon.com. Science News is a participant in the Amazon Services LLC Associates Program. Please see our FAQ for more details.

Life expectancy in the United States has decreased for the second year in a row, the first back-to-back drops in more than 50 years, the U.S. Centers for Disease Control and Prevention reports.

In 2016, life expectancy at birth was 78.6 years for the U.S. population as a whole. That’s 0.1 year less than in 2015. For men, life expectancy decreased from 76.3 years in 2015 to 76.1 years in 2016, while in women it remained the same, at 81.1 years. The new data, from CDC’s National Center for Health Statistics, are published online December 21.
Heart disease was the leading cause of death for 2016, followed by cancer, unintentional injuries such as drug overdoses and car crashes, chronic lower respiratory diseases including asthma, and stroke. Rounding out the top 10 causes of death were Alzheimer’s disease, diabetes, influenza and pneumonia, kidney disease and suicide.

The overall drop in life expectancy is largely a result of an uptick in the age-adjusted death rates for unintentional injuries, Alzheimer’s disease and suicide, the report’s authors say.

The driving force behind Yellowstone’s long and explosive volcanic history may not be as deep as once thought. A new study suggests that instead of a plume of hot mantle that extends down to Earth’s core, the real culprit is a subducting tectonic plate that began sinking beneath North America hundreds of millions of years ago.

Computer simulations show that movement of broken-up remnants of the ancient Farallon Plate could be stirring the mantle in a way that fuels Yellowstone, researchers report December 18 in Nature Geoscience. “The fit is so good,” says study coauthor Lijun Liu, a geodynamicist at the University of Illinois at Urbana-Champaign.
The giant supervolcano now beneath Yellowstone National Park, located mostly in Wyoming, has a 17-million-year history — much of it on the move. In that time, the locus of volcanism has moved northeastward from southwestern Idaho to its current location, where it most recently explosively erupted about 640,000 years ago. These shifting eruptions have created a track of volcanic craters resembling those created by the hot spot that formed the Hawaiian island chain. As a result, scientists have long suspected that a deep plume of magma originating from the core-mantle boundary, similar to the one that fuels Hawaii’s volcanoes, is the source of Yellowstone’s fury.

But the nature of the Yellowstone plume has been the subject of debate. “Usually with plumes, we can trace them to the core-mantle boundary,” says Robert Porritt, a seismologist at the University of Texas at Austin, who was not involved in the new work. To “see” Earth’s structure, seismologists use a technique called seismic tomography, which maps the interior using seismic waves generated by earthquakes. Particularly hot or liquid parts of the mantle slow some seismic waves known as shear waves. Tomographic images of mantle plumes such as the one beneath Hawaii show a low-velocity region that extends all the way down to the boundary between mantle and core, about 2,900 kilometers below Earth’s surface. Such deep plumes are thought to be necessary to provide sufficient heat for the volcanism.

“But at Yellowstone, we don’t have that large low-shear velocity thing at the core-mantle boundary,” Porritt says. Current images suggest a region of low-velocity material extending at least 1,000 kilometers deep — but whether there is a deeper plume is uncertain.

And the region is tectonically complex. About 200 million years ago, a tectonic plate to the west, known as the Farallon Plate, began to slide eastward beneath the North American Plate. The current Juan de Fuca Plate off the Pacific Northwest coast, one of the last remnants of the Farallon Plate, continues to slide beneath the western United States. Some researchers have suggested that, instead of a deep mantle plume, the flexing and melting of the subducting Juan de Fuca Plate are responsible for Yellowstone’s volcanism.
Liu and his colleagues have yet another idea. In 2016, Liu published research suggesting that the sinking ancient Farallon slab was acting like a lid on a deep mantle plume, preventing the plume from rising to the surface (SN Online: 2/3/16). “But we kept in mind that the problem was not solved,” Liu says. “The heat source [for Yellowstone] was still missing.”

The researchers created a sophisticated, supercomputer-driven series of simulations to try to find the best scenario that matches the three known knowns: the current tomographic images of the subsurface beneath the western United States; the volcanic history at Yellowstone as well as in the nearby Basin and Range regions; and the movements of the subducting slab since about 20 million years ago.

Yellowstone’s volcanism is linked not just to the currently subducting young Juan de Fuca Plate, but also to the remnants of its older incarnation, the Farallon Plate, the simulations suggest. Those remnants have continued to slide deeper and now lie beneath the eastern United States. This downward dive dragged hot mantle eastward along with it. As the Juan de Fuca Plate began to break up beneath the western United States, the hot mantle rose through the cracks. Some of that hot mantle circulated back to the west across the top of the Juan de Fuca Plate, fueling volcanism in the Basin and Range region. And some of it flowed eastward, adding heat to Yellowstone’s fire. The study doesn’t rule out the presence of a deep magma plume, but it suggests that such a plume plays little role in Yellowstone’s volcanism.

Porritt says he’s intrigued by the idea that the sinking Farallon slab beneath the central and eastern United States could be driving mantle circulation on such a large scale. However, he says, he isn’t convinced that the authors have truly solved the larger mystery of Yellowstone’s volcanism — or that a yet-to-be-found deep plume still isn’t playing a major role. “It’s an interesting debate that’s going to be raging, hopefully for decades.”

Fracking wells should not go to 11. Instead, turning down the volume — that is, of water pumped underground to help retrieve oil and gas — may reduce the number of earthquakes related to hydraulic fracturing.

The amount of water pumped into fracking wells is the No. 1 factor related to earthquake occurrence at Fox Creek, a large oil and gas production site in central Canada, researchers report January 19 in Science. An injection of 10,000 cubic meters of fluid or more at a well appears to trigger a quake.
Fox Creek sits atop the Duvernay Formation, a sedimentary layer rich in oil and gas. Before December 2013, the area was earthquake-free. Since then, hundreds of earthquakes have shaken the region; most were below magnitude 4, but a magnitude 4.8 quake in 2016 temporarily shut down operations.

Previous investigations revealed that fracking well injections at the site were triggering earthquakes on an underlying fault system. But mysteries remained: For example, why didn’t the quakes didn’t start until almost three years after fracking activities began in 2010?

Ryan Schultz of the Alberta Geological Survey in Edmonton and his colleagues compared the timing and location of the earthquakes with fracking activity at 300 wells in the region.

An analysis of rates of injection, fluid pressure and fluid volume for the wells closest in proximity to the quakes revealed that, at this site, only volume was linked to the quakes. A previous study has linked the rate of wastewater disposal injections to seismic slip (SN: 7/11/15, p. 10).
As for the three-year delay, the authors say, fracking well injections tend to increase in volume over time as operations mature. So once the injection volumes reached that 10,000-cubic- meter threshold, the earthquakes began.

Three days after Bronny James revealed that he had committed to USC, the Trojans have landed another son of an NBA great.

DJ Rodman, the son of five-time NBA champion Dennis Rodman, announced on Tuesday that he will transfer to USC for the 2023-24 season.

Rodman played four seasons at Washington State. He will use his extra year of eligibility to join a USC team that is loading up on talent.

Just how good is Rodman? And what role could he play for the Trojans?

How good is DJ Rodman?
Rodman was a reliable starter in 30 out of 31 games for Washington State this past season. He is coming off his most impactful year, posting 9.6 points, 5.8 rebounds, 1.4 assists and 0.7 steals while shooting 38.1 percent from beyond the arc in 2022-23.

Rodman scored in double figures in 12 contests this past year, including a 23-point performance against Eastern Washington in the NIT. He corralled double-digit rebounds in four games and snagged at least two steals in eight games.

Rodman plays on the wing, but he competes on the defensive end and on the glass — just like his father. He's a versatile defender who will take on perimeter assignments and battle big men in the post.

He'll create second-chance opportunities with a nose for the ball as an offensive rebounder, and he's capable of stretching the floor with an improved 3-point shot.

Rodman will add depth to a reloaded USC roster that should compete for a Pac-12 championship next season.

DJ Rodman college stats
Rodman played 111 games over four seasons at Washington State. He served as a role player over his first three seasons before being promoted to the starting lineup for his senior season.

You can find his career averages below:

21.7 minutes per game
5.5 points per game
4.0 rebounds per game
0.9 assists per game
0.4 steals per game
0.2 blocks per game
39.8 percent FG
35.2 percent 3PT
77.6 percent FT
USC roster for 2023, including DJ Rodman and Bronny James
Name Height Position Class Hometown High School
Isaiah Collier 6-4 G FR Marietta, Ga. Wheeler HS
Bronny James 6-3 G FR Los Angeles, Calif. Sierra Canyon HS
Arrinten Page 6-9 F FR Marrieta, Ga. Wheeler HS
Kobe Johnson 6-6 F JR Milwaukee, Wis. Nicolet HS
Vincent Iwuchukwu 7-1 F SO San Antonio, Texas Southern Calif. Academy
Oziyah Sellers 6-5 G SO Hayward, Calif. Southern Calif. Academy
Boogie Ellis 6-3 G SR San Diego, Calif. Mission Bay HS
Zach Brooker 6-0 G SR Calabasas, Calif. Sierra Canyon HS
Joshua Morgan 6-11 F SR Sacramento, Calif. Sheldon HS
Harrison Hornery 6-10 F JR Toowoomba, Australia Mater Dei HS
Kijani Wright 6-9 F SO Los Angeles, Calif. Sierra Canyon HS
DJ Rodman 6-6 F SR Newport Beach, Calif. JSerra Catholic HS
Did LeBron James and Dennis Rodman play together?
No, they did not.

Rodman retired after the 1999-00 season. James was drafted in 2003, making his NBA debut at the start of the 2003-04 season.

Since long before it gained fame as a precise gene-editing tool, CRISPR has had another job defending bacteria against viral invaders. And it’s far from alone. Ten sets of bacterial genes have similar, newly discovered defense roles, researchers report online January 25 in Science.

The discovery “probably more than doubles the number of immune systems known in bacteria,” says Joseph Bondy-Denomy, a microbiologist at the University of California, San Francisco, who wasn’t involved in the study.
Bacteria are vulnerable to deadly viruses called phages, which can hijack bacteria’s genetic machinery and force them to produce viral DNA instead. Some bacteria protect themselves against phage attacks with a system called CRISPR, which stores pieces of past invaders’ DNA so bacteria can recognize and fend off those phages in the future (SN: 4/15/17, p. 22). But only about 40 percent of bacteria have CRISPR, says study coauthor Rotem Sorek, a microbial genomicist at the Weizmann Institute of Science in Rehovot, Israel. That’s why he and his colleagues are hunting for other defense mechanisms.

Defense-related genes tend to cluster together in the genome, Sorek says. So his team sifted through genetic information from 45,000 microbes, flagging groups of genes with unknown functions that were located near known defense-related genes.

Many of the bacteria with these gene families hail from far-flung locations like the bottom of the ocean. So the researchers used the genomic data to synthesize the relevant bits of DNA and inserted them into Escherichia coli and Bacillus subtilis, which can both be grown and studied in the lab. Then, the researchers tracked how well the bacteria resisted phage attacks when various genes in a family were deleted. If getting rid of some of the genes affected the bacteria’s ability to fight off phages, that result suggested the group of genes was a defense system.

Nine groups of bacterial genes turned out to be antiphage defense systems, and one system protected against plasmids, another source of foreign DNA, the researchers found.
Previously discovered antiphage protective systems, such as CRISPR, have been described with acronyms, but, Sorek jokes, “we ran out of acronyms.” So the new systems are named after protective deities — like the Zorya, a pair of goddesses from Slavic mythology.

The data also reveal a possible shared origin between bacterial immune systems and similar defenses in more complex organisms, Sorek says. Some of the genes contained fragments of DNA that are also known to be an important part of the innate immune system in plants, mammals and invertebrates.

It’s likely the research will unleash a flurry of new studies to figure out how these new defense systems work and whether they, like CRISPR, might also be useful biotechnology tools, Bondy-Denomy predicts.

Zika virus may not be the black sheep of the family. Infections with either of two related viruses also cause fetal defects in mice, researchers find.

Some scientists have speculated that Zika’s capacity to harm a fetus might be unique among its kind, perhaps due to a recent change in the virus’s genetic material (SN: 10/28/17, p. 9). Others have argued that perhaps this dangerous ability was always there. It just wasn’t until the 2015–2016 epidemic in the Western Hemisphere that enough pregnant women were affected for public health researchers to identify the association with fetal defects (SN: 12/24/16, p. 19).
But new work suggests this capacity is not Zika’s alone. Pregnant mice infected with West Nile or Powassan virus — both flaviviruses, like Zika — also showed fetal harm. Over 40 percent of these infected fetuses died. But among pregnant mice infected with one of two other mosquito-borne viruses unrelated to Zika, all of the fetuses survived, scientists report online January 31 in Science Translational Medicine.

The research underscores that “many viruses, including some similar to Zika, can infect the placenta and the cells of the baby,” says George Saade, an obstetrician-gynecologist and cell biologist at the University of Texas Medical Branch at Galveston. “This list keeps growing and highlights the risks from viruses that we are not very familiar with.”

Like Zika, West Nile virus and Powassan virus are neurotropic, meaning these pathogens target nerve cells. Both viruses can cause inflammation of the brain or of the membranes that surround the brain. West Nile is transmitted to humans by mosquitoes that have bitten infected birds. From 1999 to 2016, there were more than 46,000 cases reported to the U.S. Centers for Disease Control and Prevention. Powassan, spread by ticks who have fed on infected rodents, is less widespread; only 98 cases were reported from 2007 to 2016, mostly in the Northeast and Great Lakes area.

Jonathan Miner, a virologist at the Washington University School of Medicine in St. Louis, and his colleagues conducted some of the initial work in mice that demonstrated that Zika could harm fetuses (SN: 6/11/16, p. 15). The new study tests the effects of four other viruses: the two flaviviruses and two alphaviruses, chikungunya and Mayaro, which also have led to outbreaks in Zika-affected areas.
The researchers infected 14 mice early in their pregnancies with one of the four viruses. By late pregnancy, 12 out of 30 fetuses from West Nile–infected mice had died, and half of the 16 fetuses from Powassan-infected mice had died. All of the fetuses from mice infected with chikungunya and Mayaro virus survived. West Nile virus and Powassan virus also replicated, or multiplied, more efficiently than the alphaviruses in lab samples of human placental tissue.

Zika, West Nile and Powassan share similarities in their genetic information, Miner says. “So there may be certain features of those virus genes and proteins in that particular family that confers this ability to infect certain cell types.” But scientists don’t understand fully what those features are yet, he says.

While this is the first study comparing the effects in mice of these mosquito-transmitted and tick-transmitted viruses in parallel, Miner says, past studies have raised the possibility of fetal infections with other flaviviruses besides Zika. A 2006 study of 77 pregnant women infected with West Nile virus reported that two had infants with microcephaly, the birth defect lately associated with Zika that results in unusually small and damaged brains.

In general, examining the potential effects of other flaviviruses on pregnant women and their developing fetuses is difficult, because outbreaks have been sporadic and less widespread than with Zika. It’s possible that cases in humans “could go largely unnoticed if we don’t look for them,” Miner says.