Magnetic poles are seemingly inseparable: Slice a magnet in half, and you get two smaller magnets, each with its own north and south poles. But exotic magnetic particles that flout this rule may be lurking undetected, some physicists suspect.

The hunt is in full swing for these hypothetical particles known as magnetic monopoles — which possess a lone north or south pole. Now, two groups of researchers have further winnowed down the particles’ possible masses and characteristics, using data from particle accelerators and the corpses of stars.
There’s good reason to suspect magnetic monopoles are out there, some physicists suggest. The particles’ existence would explain why electric charge is quantized — why it always seems to come in integer multiples of the charge of an electron instead of a continuous range of values. As a result, magnetic monopoles are popular. “A lot of people think they should exist,” says James Pinfold, a particle physicist at the University of Alberta in Edmonton, Canada.

If even a single magnetic monopole were detected, the discovery would rejigger the foundations of physics. The equations governing electricity and magnetism are mirror images of one another, but there’s one major difference between the two phenomena. Protons and electrons carry positive and negative electric charges, respectively, but no known particle has a magnetic charge. A magnetic monopole would be the first, and if one were discovered, electricity and magnetism would finally be on equal footing.

For decades, scientists have searched fruitlessly for magnetic monopoles. Recent work at the Large Hadron Collider, located at the particle physics lab CERN in Geneva, has reinvigorated the search. Magnetic monopoles might be produced there as protons slam together at record-high energies of 13 trillion electron volts.

Unfortunately, the latest search by Pinfold and collaborators with the Monopole and Exotics Detector at the LHC, or MoEDAL (pronounced “medal”), found no magnetic monopoles, despite analyzing six times the data as the project’s previous pursuits. Still, the new research has set some of the most stringent constraints yet on how easily the hypothetical particles may interact with matter, the MoEDAL collaboration reports December 28 at arXiv.org.
Magnetic monopoles may also dwell where magnetic fields are extraordinarily strong and temperatures are high. Under these conditions, pairs of monopoles might form spontaneously. Such extreme environments can be found around a special kind of dead star known as a magnetar, and in the aftermath of collisions of heavy atomic nuclei in particle accelerators. By studying these two scenarios, physicists Arttu Rajantie and Oliver Gould, both of Imperial College London, put new constraints on monopoles’ masses, the researchers report in the Dec. 15 Physical Review Letters.

If magnetic monopoles had relatively small masses, the particles would sap the strength of magnetars’ magnetic fields. That fact suggests that the particles must be more massive than about 0.3 billion electron volts — about a third the mass of a proton — the researchers calculate. That estimate depends on another unknown property of monopoles, the strength of their magnetic charge. The particles have a minimum possible magnetic charge. A magnetic charge larger than this baseline value would correspond to a minimum mass greater than 0.3 billion electron volts.

For a monopole with twice the minimum charge, Rajantie and Gould determined that magnetic monopoles must be more massive than about 10 billion electron volts, going by data from collisions of lead nuclei in the Super Proton Synchrotron, a smaller accelerator at CERN. Studying similar collisions of lead nuclei in the LHC could improve this estimate, due to the LHC’s higher collision energies.

While other experiments have set higher monopole mass limits than the new estimates, those analyses relied on questionable theoretical assumptions, Rajantie says. “These are currently the strongest bounds on the masses of magnetic monopoles that don’t rely on assumptions” about how the particles are created, he says.

The results are “very exciting,” says theoretical physicist Kimball Milton of the University of Oklahoma in Norman, who was not involved with the research. Of course, he adds, it’s “not as exciting as if somebody actually found a magnetic monopole.”

Even if monopoles do exist, the particles might be so heavy that they can’t be produced by accelerators or cosmic processes. The only magnetic monopoles in the universe might be remnants of the Big Bang. A future incarnation of MoEDAL, located on a mountaintop instead of in an accelerator’s cavern, could look for such magnetic monopoles that sprinkle down on Earth from space, Pinfold says.

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.

A new blood test might reveal whether someone is at risk of getting Alzheimer’s disease.

The test measures blood plasma levels of a sticky protein called amyloid-beta. This protein can start building up in the brains of Alzheimer’s patients decades before there’s any outward signs of the disease. Typically, it takes a brain scan or spinal tap to discover these A-beta clumps, or plaques, in the brain. But evidence is growing that A-beta levels in the blood can be used to predict whether or not a person has these brain plaques, researchers report online January 31 in Nature.
These new results mirror those of a smaller 2017 study by a different team of scientists. “It’s a fantastic confirmation of the findings,” says Randall Bateman, an Alzheimer’s researcher at Washington University School of Medicine in St. Louis, who led the earlier study. “What this tells us is that we can move forward with this [test] approach with fairly high confidence that this is going to pan out.”

There’s currently no treatment for Alzheimer’s that can slow or stop the disease’s progression, so catching it early can’t currently improve a patient’s outcome. But a blood test could help researchers more easily identify people who might be good candidates for clinical trials of early interventions, says Steven Kiddle, a biostatistician at the University of Cambridge, who wasn’t part of either study.

Creating such a test has been challenging: Relatively little A-beta floats in the bloodstream compared with how much accumulates in the brain. And many past studies haven’t found a consistent correlation between the two.

In the new study, researchers used mass spectrometry, a more sensitive measuring technique than used in most previous tests, which allowed the detection of smaller amounts of the protein. And instead of looking at the total level of the protein in the blood, the team calculated the ratios between different types of A-beta, says coauthor Katsuhiko Yanagisawa, a gerontologist at the National Center for Geriatrics and Gerontology in Obu, Japan.
He and his colleagues analyzed brain scans and blood samples from a group of 121 Japanese patients and a group of 252 Australian patients. Some participants had Alzheimer’s, some didn’t, and some had mild cognitive impairments that weren’t related to Alzheimer’s.

Using the ratios, the researchers found that they could discriminate between people who had A-beta plaques in the brain and those who didn’t. A composite biomarker score, created by combining two different ratios, predicted the presence or absence of A-beta plaques in the brain with about 90 percent accuracy in both groups of patients, the researchers found.

The new results are promising, Kiddle says, but the test still needs more refining before it can be used in the clinic. Another wild card: the cost. It’s still not clear whether the blood test will be more affordable than a brain scan or a spinal tap.

Controlled thermonuclear fusion is moving so well that full-scale development could begin within five years, says Dr. David J. Rose….It might take 20 to 30 years beyond that before fusion could move into the power grid, though, he predicts. — Science News, February 17, 1968

Update
Governments and private-sector start-ups are still trying to wrangle thermonuclear fusion — the process that lights up stars and ignites hydrogen bombs — for clean energy, with limited progress (SN: 2/6/16, p. 18). One of the biggest ongoing projects is ITER in France, an international effort to build the first magnetic fusion reactor that pumps out more energy than it consumes. ITER plans to flip on the machine in 2025. Optimistic estimates put the first fusion power plants on the grid no sooner than 2040.

AUSTIN, Texas — To reduce your impact on air quality, you might expect to trade in your gas-guzzling clunker of a car — but you can also unplug those air fresheners.

In urban areas, emissions from consumer goods such as paint, cleaning supplies and personal care products now contribute as much to ozone and fine particulate matter in the atmosphere as do emissions from burning gasoline or diesel fuel.

The finding is largely a sign of success, study coauthor Brian McDonald said February 15 during a news conference at the annual meeting of the American Association for the Advancement of Science. Steps taken to clean up car exhaust over the past few decades have had a huge effect, and as a result, “the sources of air pollution are now becoming more diverse in cities,” said McDonald, a chemist at Cooperative Institute for Research in Environmental Sciences in Boulder, Colo.
“When you have a big mountain in front of you, it’s difficult to know what lies behind it,” says Spyros Pandis, a chemical engineer at Carnegie Mellon University in Pittsburgh who wasn’t part of the study. Now, other sources of air pollution are becoming more visible.

The new study, also published in the Feb. 16 Science, focused on volatile organic compounds, or VOCs, that are derived from petroleum. These are a diverse array of hundreds of chemicals that easily vaporize and make their way into the atmosphere. Some VOCs can be harmful when directly inhaled — molecules released by bleach and paint make people lightheaded, for example.

Beyond their immediate effects, VOCs react with other molecules in the air, such as oxygen and nitrogen oxides, to generate ozone as well as fine particulate matter. (Those nitrogen oxides come, in large part, from vehicle exhaust.) High levels of fine particulate matter make it hard to breathe and contribute to chronic lung problems (SN: 9/30/17, p. 18). And while ozone high in the atmosphere helps shield Earth from the sun’s ultraviolet radiation, at ground level, it mixes with fine particulates to form breath-choking smog.

Over a period of six weeks, the researchers collected air samples in Pasadena, located in the notoriously smoggy Los Angeles valley. They also evaluated indoor air quality measurements made by other scientists. The team traced the molecules found in these air samples to their original sources using databases that show the specific volatile organic compounds released by specific products.

Consumer products that emit VOCs have an outsized effect on air pollution, the team found. About 15 times as much oil and natural gas is used as fuel than ends up in consumer products ranging from soaps, shampoos and deodorants to air fresheners, glues and cleaning sprays. And yet these everyday products were responsible for 38 percent of the VOC emissions, the researchers found, while gasoline and diesel emissions accounted for only 33 percent. Consumer products also contributed just as much as fuels to chemical reactions that lead to ozone and fine particulate matter. The emissions from consumer products also dwarfed those from the production of oil and gas, called upstream emissions.
Regulations on VOCs vary by state, but most consumer products are regulated only for their potential contribution to ground-level ozone, not fine particulate matter. This study makes it clear that even though most volatile emissions from consumer products happen indoors, that air eventually gets vented outside, where it can contribute to larger-scale atmospheric pollution in multiple ways, McDonald said.

More work needs to be done to see whether other cities show the same pattern, the researchers add, as well as to figure out which kinds of VOCs might be particularly problematic. Because there are so many VOCs and they all react differently in the atmosphere, there’s still a lot to learn about which might be most likely to form fine particles and therefore be the best targets for reduction.

Part of the challenge with many these volatile-emitting products is that they’re specifically designed to evaporate as part of their job, says study coauthor Jessica Gilman, an atmospheric chemist at the National Oceanic and Atmospheric Administration in Boulder. For some products, like paints, there are low-VOC formulations available. But finding replacements for key ingredients in other products can be hard. Picking unscented versions of personal care products when possible and using the minimum amount necessary can help reduce the impact on air quality.

To play good defense against the next viral pandemic, it helps to know the other team’s offense. But the 263 known viruses that circulate in humans represent less than 0.1 percent of the viruses suspected to be lurking out there that could infect people, researchers report in the Feb. 23 Science.

The Global Virome Project, to be launched in 2018, aims to close that gap. The international collaboration will survey viruses harbored by birds and mammals to identify candidates that might be zoonotic, or able to jump to humans. Based on the viral diversity in two species known to host emerging human diseases — Indian flying foxes and rhesus macaques — the team estimates there are about 1.67 million unknown viruses still to be discovered in the 25 virus families surveyed. Of those, between 631,000 and 827,000 might be able to infect humans.
The $1.2 billion project aims to identify roughly 70 percent of these potential threats within the next 10 years, focusing on animals in places known to be hot spots for the emergence of human-infecting viruses. That data will be made publicly available to help scientists prepare for future virus outbreaks — or, ideally, to quash threats as they emerge.

“It’s ambitious,” says Peter Daszak, president of EcoHealth Alliance in New York City and a member of the Global Virome Project’s steering committee. But it’s more cost effective to head off pandemics than to deal with the aftermath, he says. “We believe we’re going to get ahead of this pandemic threat.”