A popular type of heartburn medicine could hasten wear and tear of blood vessels.

Proton pump inhibitors, or PPIs, gunk up cells that typically line the veins and arteries like a slick coat of Teflon, researchers report May 10 in Circulation Research. Excess cellular junk ages the cells, which could make blood vessels work less smoothly.

The results, though controversial, are the first inkling of evidence that might explain why PPIs have recently been linked to so many different health problems, from heart attacks to dementia.
“The authors present a compelling story,” says Ziyad Al-Aly, a nephrologist at the Veterans Affairs Saint Louis Health Care System in Missouri. It begins to outline how using PPIs could spell trouble later on, he says. But Al-Aly notes that the study has one big limitation: It was done in cells, not people.

Gastroenterologist Ian Forgacs from King’s College Hospital in London agrees. Drawing conclusions about humans from cells grown in the lab requires “a huge leap of faith,” he says. So far, scientists have found only correlations between PPIs and their alleged side effects. “We need to know whether these drugs really do cause dementia and coronary disease and renal disease,” he says.

In the last few decades, proton pump inhibitors have emerged as a kind of wonder drug for heartburn. The drugs switch off molecular machines that pump acid into the stomach. So less acid surges up to burn the esophagus.

In 2012, nearly 8 percent of U.S. adults were taking prescription PPIs, according to a survey published last year in JAMA. (Some PPIs are also available over-the-counter.) Many people use PPIs for longer than they’re supposed to, says study coauthor John Cooke, a cardiologist at Houston Methodist Research Institute in Texas. “These are very powerful drugs­ — they’re not Tums,” he says. “They have side effects.”

Several of these side effects are still under debate. And if PPIs do increase the risk of dementia, say, or kidney disease, no one knows how. So Cooke and colleagues explored what chronic exposure to the drugs, which travel through the bloodstream, does to cells lining the blood vessels.
Human cells treated with a PPI called esomeprazole (sold as Nexium) seemed to age faster than untreated cells, the researchers found. The cells lost their youthful shape and instead “looked kind of like a fried egg,” Cooke says. They also lost the ability to split into new cells, among other signs of aging.

Cooke traced the rapid aging to mishaps in acid-filled cellular chambers called lysosomes. These chambers act as tiny garbage disposals; they get rid of junk like broken-down proteins. But PPIs, which work so well at shutting down acid production in the stomach, also seemed to shut down the acidic garbage disposals, too, the researchers found. That caused proteins to pile up, forming “little heaps of rubbish,” Cooke says.

Mucking with blood vessels’ lining could trigger all sorts of problems. For instance, instead of gliding easily through, platelets and white blood cells could get hung up, sticking to vessel walls like Velcro. “That’s how hardening of the arteries starts,” Cooke says.

The next step is to see if similar damage occurs in people. Doctors and regulatory agencies should take a second look at the widespread use of PPIs, too, Cooke says. “There’s enough data now that we have to be very cautious in our use of these agents.”

But some researchers think PPIs are getting a bum rap. “Everybody and their mother now want to hammer PPIs,” says gastroenterologist David Metz of the University of Pennsylvania. “It’s unfortunate because they’re spectacular drugs and they save people’s lives.”

The real question, Al-Aly says, is whether the benefits outweigh the risks.

In the scorching heat of the Kalahari Desert, some birds still manage to keep their cool.

Thermal imaging reveals that the southern yellow-billed hornbill (Tockus leucomelas) vents heat from its beak, a phenomenon previously observed in toco toucans (Ramphastos toco). A team of South African researchers snapped infrared photos of 18 hornbills on a farm in the southern edge of the desert at temperatures from 15° to 45° Celsius.

When air temperatures hit 30.7° Celsius, the difference between beak surface temperature and air temperature spikes — indicating the birds were actively radiating heat through their beaks. At most, the birds lost about 25.1 watts per square meter through their beaks. Hornbills probably manage this cool trick by dilating the blood vessels to increase flow in their uninsulated beaks, the team writes May 18 in PLOS ONE.

Toucans lose about 60 percent of their total heat loss through their beaks, but hornbills only shed up to 20 percent of their heat loss through this method. The researchers chalk that difference up to larger beak-to-body-size in toucans.

A last-ditch weapon against drug-resistant bacteria has met its match in Pennsylvania.

A 49-year-old woman has tested positive for a strain of Escherichia coli resistant to the antibiotic colistin, researchers report May 26 in Antimicrobial Agents and Chemotherapy.

It’s the first time in the United States that scientists have found bacteria carrying a gene for colistin resistance known as mrc-1, write study coauthor Patrick McGann of Walter Reed Army Institute of Research in Silver Spring, Md., and colleagues.
But perhaps even more alarming is that the gene rides on a transferable loop of DNA called a plasmid.

“That means we now see a possibility of spread,” says physician and clinical microbiologist Robert Skov. And not just from mother cell to daughter cell, he says, but to neighboring strains of bacteria, too.

Bacteria carry most of their genetic information in a tangle of DNA contained in chromosomes inside the cell. But tiny loops of DNA called plasmids hang around outside of the tangle. These loops carry extra information that bacteria can use, like how to protect themselves from antibiotics. Bacteria can swap plasmids like trading cards, effectively spreading instructions for antibiotic resistance.

In December, Skov and colleagues discovered a Danish patient carrying bacteria with mcr-1 plasmid DNA, like the woman in Pennsylvania. And in November of 2015, researchers reported something similar in China.

Until then, all known colistin resistance was due to tweaks in chromosomal DNA (which, unlike plasmid DNA, isn’t easily spread among bacteria), says Skov, of the Statens Serum Institut in Copenhagen, who was not involved with the new work.

Colistin, a 50-year-old drug that doctors largely stopped prescribing in the 1970s because of its side effects, has made a comeback in the last five to 10 years. It’s used when other antibiotics fail; it’s a treatment option for people infected with multidrug-resistant bacteria. Now, with colistin-resistant bacteria, Skov says, antibiotic treatment options are becoming more and more limited.

The problem, scientists have been pointing out for years, is that people are taking antibiotics too frequently. More use means more opportunity for bacteria to develop resistance.

Still, even with colistin-resistant bacteria emerging all over the world, Skov says he doesn’t expect thousands of people to become infected.

“The scenario now is that once in a while, we’ll see a patient carrying bacteria that we don’t have any good antibiotics left for.” But that, he adds “is dreadful enough.”

Quasisatellite
KWAH-zee-SAT-ah-lite n.
A body that orbits the sun and appears to orbit Earth.

Asteroid 2016 HO3 appears to orbit Earth, but that’s just an illusion. As the space rock loops around the sun, it plays leapfrog with our planet, sometimes speeding ahead sometimes falling behind. The asteroid’s suncentric orbit keeps it from qualifying as a full-fledged moon of Earth, but its constant proximity to us is enough to make it the only known “quasisatellite” of our world.
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This temporary tagalong was discovered on April 27 in images from the Pan-STARRS observatory in Hawaii. The asteroid’s orbit around the sun is similar to Earth’s — one year on 2016 HO3 is just about 16 hours longer than an Earth year. Earth’s gravity keeps the asteroid from wandering; it never strays farther than about 400 million kilometers from Earth and never comes closer than about 14 million kilometers (38 times Earth’s distance to the moon).

The tiny rock — no more than about 100 meters across — has probably tagged along with Earth for about a century, and orbital calculations suggest that it will continue to do so for several centuries to come.

A remote galaxy might harbor a type of black hole that arises directly from a massive cloud of gas rather than forming after the death of a star. This rare specimen could explain how some galaxies built gargantuan black holes in the first billion years or so after the Big Bang.

The galaxy, known as CR7, is unusual (SN: 7/25/2015, p. 8). It blasts out more ultraviolet radiation than other galaxies that lived at the same time, roughly 13 billion years ago (about 800 million years after the Big Bang). The gas in CR7 also appears to lack elements such as carbon and oxygen, which are forged within stars and then ejected into space. One idea is that CR7 is giving birth to first-generation stars, similar to the first stars ever created in the universe. Another hypothesis is that CR7 harbors the first known “direct collapse” black hole, one that forms when a blob of interstellar gas collapses under its own weight without first forming stars.
A black hole is more likely, suggest Aaron Smith of the University of Texas at Austin and colleagues in the Aug. 11 Monthly Notices of the Royal Astronomical Society. The researchers developed computer simulations that explore how interstellar gas interacts with the harsh radiation from primordial stars or a large black hole. Smith and colleagues find that the light from a cache of hot, young stars can’t explain why a parcel of gas is racing away from CR7 at about 580,000 kilometers per hour. What can push the gas, they report, is radiation from a superheated disk of debris swirling around a black hole roughly 100,000 times as massive as the sun.

If CR7 does host a black hole, it would be the first evidence of one forming out of clouds that haven’t given birth to stars yet. Astronomers struggle to explain how some supermassive black holes could form in about 1 billion years out of just smaller black holes merging together. “There’s just not enough time to do that,” Smith says. A direct collapse black hole, however, creates a massive seed all in one go, jump-starting the growth of a behemoth that will eventually weigh as much as several billion suns.

“This is definitely a good step forward,” says David Sobral, an astrophysicist at Lancaster University in England who discovered CR7 in 2015. But it’s too early to say whether a black hole or a group of stars is powering CR7, he says. “I’ve tried to stay a bit away from it and argue that what we need is new observations instead of taking sides.”

With the data that are available, it’s hard to distinguish between stars or a black hole, says Sobral. That’s why he and colleagues have reserved time with the Hubble Space Telescope in January and are awaiting new data from the Atacama Large Millimeter/submillimeter Array in Chile. Data from both observatories will help researchers look for traces of heavy elements in CR7. If these more sensitive data still show no sign of atoms such as carbon, says Sobral, then CR7 probably hosts a nest of first-generation stars. A black hole, on the other hand, probably would have formed long enough ago that there would be enough time for stars to form and pollute CR7 with a smidgen of heavy elements, he says.

A growing census of similar locales will help as well. “We’re now finding that CR7 is not alone,” Sobral says. He and his colleagues have since found four other galaxies comparable to CR7 in the early universe, results presented June 27 at the National Astronomy Meeting in Nottingham, England. “We don’t have to discuss one single thing,” he says, “but we can put [CR7] into a broader picture.”

Training the brain could give paraplegics more control over their bodies.

After a year working with devices that link machine to brain, people paralyzed by spinal cord injuries were able to regain some movement and feeling in their legs, Miguel Nicolelis and colleagues report August 11 in Scientific Reports.

The training included an assortment of therapies with futuristic-looking gizmos, including virtual reality goggles and robotic exoskeletons that fasten over the body. All patients were better able to sense pain and touch, and half had their diagnosis upgraded from complete to partial paralysis.
“This is a very key milestone in the field of brain-machine interfaces,” Nicolelis said in a news briefing August 9.

But some scientists aren’t convinced that it’s such an advance.

Researchers have already proposed (and demonstrated) the benefits of brain-machine interface technology before, says Brendan Allison, a neuroscientist at the University of California, San Diego. While the new work is impressive and stands out for such long-term brain training, he says, “it’s simply not a breakthrough.”

Paralyzing spinal cord injuries can sever the bundle of nerves that carries messages from the brain to the body. So even if the brain tells the toes to move, the message dead-ends when it hits the injury site. For people with these severe injuries, there’s not much doctors can do to help, said Nicolelis, of Duke University. “They basically just try to get you adapted to life in a wheelchair.”

In 2012, he and colleagues started a project to help paraplegics walk, with assistance. With a stretchy cap placed over their heads to capture brain signals, patients would use their thoughts to control an exoskeleton, a robotic walker that held their bodies upright. The device would give paraplegics some mobility again — at least that was the goal. What the team found was far more exciting, Nicolelis said.
For one year, Nicolelis’ team worked with eight people who had been paralyzed for between three and 13 years. Twice a week for one hour, patients trained on a variety of rehabilitation tools. They learned how to control an avatar in virtual reality by imagining moving their legs, and later, how to use the brain-controlled exoskeleton. Patients also did hours of traditional physical therapy, including strengthening and stretching exercises.
About seven months into the project, the researchers noticed that all patients were beginning to regain control of one or more muscles below their spinal cord injury. And after 12 months, all patients experienced improvements in sensing touch and pain. One woman even gave birth to a child, and could feel the contractions during the delivery, Nicolelis said.

Though all patients had severe spinal cord injuries, he thinks some nerve cells must have survived and that the training rekindled their activity.

The amount of clinical recovery “is almost like a dream,” Nicolelis said. It may be enough to upgrade brain-machine interfaces, he said, from an assistive therapy (something that helps people walk — like crutches or a cane) to something that actually that helps people recover.

Again, that’s not a new idea, says Donatella Mattia, a neurophysiologist at the Institute for Research and Health Care in Rome. Other scientists working with paralyzed stroke patients have already shown improvements in arm mobility after using brain-machine interfaces.

What’s more, teasing out cause and effect in the new study isn’t easy, says University of Houston neural engineer José Contreras-Vidal. Patients underwent a complicated blend of therapies, with different lengths of training. Despite the caveats, though, he thinks the work is a step forward. And in clinical research, he says, “even incremental is good.”

Scientists have created giant molecules — the size of bacteria — that may be useful in future quantum computers.

The molecules of unusual size are formed from pairs of Rydberg atoms — atoms with an electron that has been boosted into a high-energy state. Such electrons orbit far from their atom’s nucleus and, as a result, can feel the influence of faraway atoms.

To create the molecules, researchers cooled cesium atoms nearly to absolute zero, hitting them with lasers to form Rydberg atoms that bound together in pairs. These molecules are about one thousandth of a millimeter in size — a thousand times the size of a typical molecule — scientists report August 19 in Physical Review Letters.
“I think it’s fundamentally interesting and important because it’s such a curious thing,” says physicist David Petrosyan of the Institute of Electronic Structure & Laser at the Foundation for Research and Technology–Hellas in Heraklion, Greece. “The size of these molecules is huge.”

This is not the first time such molecules have been created, but the previous evidence was not clear-cut. “Before, maybe it wasn’t clear if this is really a molecule in the sense that it’s vibrating and rotating. It could have been just two atoms sitting therewith very weak interactions or no interactions,” says Johannes Deiglmayr, a physicist at ETH Zürich and a coauthor of the study.

Deiglmayr and collaborators measured the molecules’ binding energies — the energy that holds the two atoms together. Additionally, the scientists made detailed calculations to predict the molecules’ properties. These calculations were “extensive and seemed to match really well with their measurements,” says physicist Phillip Gould of the University of Connecticut in Storrs.

The result has practical implications, Petrosyan notes. In quantum computers that use atoms as quantum bits, scientists perform computations by allowing atoms to interact. Rydberg atoms can interact with their neighbors over long distances, and when bound together, the atoms stay put at a consistent distance from one another — a feature that may improve the accuracy of calculations.

Previously, researchers have used rubidium atoms to make another type of large molecule, formed from Rydberg atoms bonded with normal atoms. But these wouldn’t be useful for quantum computation, Petrosyan says, as they rely on a different type of bonding mechanism.

Where you live and what you eat can rapidly affect the types of friendly bacteria inhabiting your body. To see how the microbes that inhabit the mouth and intestines change over time, Duke University computational biologist Lawrence David zealously chronicled his microbiome for an entire year. (For more on David and this experiment, see “Lawrence David’s gut check gets personal.”)

A stream plot (below, top graph) shows the ebb and flow of phyla of bacteria in his gut over time. The thickness of each stream indicates a bacterial group’s relative abundance in daily fecal samples.
David peered closer at the data in a horizon plot (above, bottom graph; colored squares at left indicate the phylum of the bacteria represented in each row). He first determined each type of bacteria’s normal abundance in his gut, then calculated how much they differed from the median abundance. Warmer colors (red, orange, yellow) indicate that bacteria in that group increased in abundance, and cooler colors (blue, green) indicate a decrease in abundance. Living abroad from day 71 to day 122 had a dramatic — but short-lived — effect on David’s microbiome.

Using records unearthed from library storage vaults, researchers recently revealed that the sugar industry paid nutrition experts from Harvard University to downplay studies linking sugar and heart disease. Although the incident happened in the 1960s, it appears to have helped redirect the scientific narrative for decades.

The documents — which include correspondence, symposium programs and annual reports — show that the Sugar Research Foundation (as it was named at the time) paid professors who wrote a two-part review in 1967 in the New England Journal of Medicine. That report was highly skeptical of the evidence linking sugar to cardiovascular problems but accepting of the role of fat. The now-deceased professors’ overall conclusion left “no doubt” that reducing the risk of heart disease was a matter of reducing saturated fat and cholesterol, according to researchers from the University of California, San Francisco, who published their report online September 12 in JAMA Internal Medicine.

“Why does it matter today? The sugar industry helped deflect the way the research was developing,” says study coauthor Cristin Kearns, a dentist at UCSF’s Institute for Health Policy Studies. The Harvard team’s scientific favoritism had a role in directing research and policy attention toward fat and cholesterol. And in fact, the first dietary guidelines published by the federal government in 1980 said there was no convincing evidence that sugar causes heart disease, stating “the major health hazard from too much sugar is tooth decay.”
Following the publication of the Harvard report, fat and cholesterol went on to hijack the scientific agenda for decades, and even led to a craze of low-fat foods that often added sugar. Kearns points out that it was only in 2015 that dietary guidelines finally made a strong statement to limit sugar. Researchers writing this year in Progress in Cardiovascular Diseases note that current studies estimate that diets high in added sugars carry a three times higher risk of death from cardiovascular disease. (For its part, the Sugar Association says in a statement on its website that “the last several decades of research have concluded that sugar does not have a unique role in heart disease.”)

The level at which the food industry continues to influence nutrition research is still a much-debated topic. The Sugar Association’s statement acknowledged the secret deal occurred, but pointed out that “when the studies in question were published, funding disclosures and transparency standards were not the norm they are today.” Journals now require all authors to list conflicts of interest, especially funding from a source has a vested interest in the outcome.

That doesn’t mean that trade groups and industry associations no longer have an influence on scientists, says Andy Bellatti, cofounder and strategic director of Dietitians for Professional Integrity, which has campaigned to push the Academy of Nutrition and Dietetics to sever its ties with industry, While a modern researcher could not take corporate money, even for speaking fees, without disclosure, the influences may be more subtle, he says. “We’re not talking about making up data, but perhaps influencing how a research question is framed.”

In a commentary published with the JAMA study, Marion Nestle, a nutrition researcher at New York University, wrote that industry influence has not disappeared. She cited recent New York Times investigations of Coca-Cola–sponsored research and Associated Press stories revealing that a candy trade group sponsored research attempting to show that children who eat sweets have a healthy body weight.

Bellatti says that researchers don’t necessarily want to be cozy with industry, but sometimes turn to commercial sources because non-biased research money is lacking. “The reason the food industry is able to do this is because there is such little public funding for nutrition and disease,” Bellatti says.
For that reason, the scientific community should not reject industry money wholesale, says John Sievenpiper, a physician and nutrition researcher at the University of Toronto. A study of his was once ridiculed on Nestle’s blog because the disclosures covered two full pages. He believes that any scientist who takes industry money should adhere to an even higher standard of openness, including releasing study protocols ahead of time so reviewers can make sure the research question was not changed midstream to favor a certain conclusion.

While many parallels have been made between the food and tobacco industries, Sievenpiper believes those comparisons miss the complicated nature of the human diet. Tobacco is always bad, never good. Sugar, fat, cholesterol and other components of diet are some of both, making research into their effects much more nuanced, he says. And unlike with tobacco, the solution can’t be to never eat them. He believes solutions won’t involve turning single nutrients like fat or sugar into villains, but promoting better overall patterns of eating, like the Mediterranean diet.

Kearns, who has spent the past 10 years looking into the sugar industry’s influence on science, isn’t finished yet. She says her curiosity first arose during a conference on gum disease and diabetes in 2007, when she noticed a lack of scientific discussion of sugar. She started out simply Googling industry influences. The trail eventually led her to scour library archives, until she came across dusty boxes of records from a closed sugar company in Colorado. “The first page I looked at in that archive had a confidential memo,” she says. “I knew I had something no one else had never talked about before.”

She doesn’t see the research going sour any time soon. “This was their 226th project in 1965,” she says. “There’s a lot more to the story.”

Editor’s note: Science has retracted the study described in this article. The May 3, 2019, issue of the journal notes that a panel of outside experts convened by Kyoto University in Japan concluded in March 2019 that the paper contained falsified data, manipulated images and instances of plagiarism, and that these were the responsibility of lead author Aiming Lin, a geophysicist at Kyoto University. In agreement with the investigation’s recommendation, the authors withdrew the report.

A titanic volcano stopped a mega-sized earthquake in its tracks.

In April, pent-up stress along the Futagawa-Hinagu Fault Zone in Japan began to unleash a magnitude 7.1 earthquake. The rupture traveled about 30 kilometers along the fault until it reached Mount Aso, one of Earth’s largest active volcanoes. That’s where the quake met its demise, geophysicist Aiming Lin of Kyoto University in Japan and colleagues report online October 20 in Science. The quake moved across the volcano’s caldronlike crater and abruptly stopped, the researchers found.

Geophysical evidence suggests that a region of rising magma lurks beneath the volcano. This magma chamber created upward pressure plus horizontal stresses that acted as an impassable roadblock for the seismic slip powering the quake, the researchers propose. This rare meetup, the researchers warn, may have undermined the structural integrity surrounding the magma chamber, increasing the likelihood of an eruption at Aso.