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.”

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.

Growing planets carve rings and spiral arms out of the gas and dust surrounding their young stars, researchers report in three papers to be published in Astronomy & Astrophysics. And dark streaks radiating away from the star in one of the planet nurseries appear to be shadows cast onto the disk by the clumps of planet-building material close to the star. This isn’t the first time that astronomers have spied rings around young stars, but the new images provide a peek at what goes into building diverse planetary systems.

The three stars — HD 97048, HD 135344B and RX J1615.3-3255 — are all youthful locals in our galaxy. They sit between 460 and 600 light-years away; the oldest is roughly a mere 8 million years old. All the stars have been studied before. But now three teams of researchers have used a new instrument at the Very Large Telescope in Chile to see extra-sharp details in the planet construction zone around each star.

The new instrument, named SPHERE, was designed to record images, spectra and polarimetry (the orientations of light waves) of young exoplanet families. Flexible mirrors within the instrument adapt to atmospheric turbulence above the telescope, and a tiny disk blocks light from the star, allowing faint details around the star to come into view.

SAN FRANCISCO — Cell biologists are learning more about how the Zika virus disrupts brain cells to cause the birth defect microcephaly, in which a baby’s brain and head are smaller than usual. Meantime, several strategies to combat the virus show preliminary promise, researchers reported at the American Society for Cell Biology’s annual meeting. Among the findings:

Brain cell die-off
Zika causes fetal brain cells neighboring an infected cell to commit suicide, David Doobin of Columbia University Medical Center reported December 6. In work with mice and rats, Doobin and colleagues found suggestions that the cells’ death might be the body’s attempt to limit spread of the virus.

The researchers applied techniques they had previously used to investigate a genetic cause of microcephaly to narrow when in pregnancy the virus is most likely to cause the brain to shrink. Timing of the virus’s effect varied by strain. For one from Puerto Rico, brain cell die-off happened in mice only in the first two trimesters. But a strain from Honduras could kill developing brain cells later into pregnancy. Microcephaly can lead to seizures, mental impairment, delays in speech and movement and other problems.

Enzyme stopper
Disrupting a Zika enzyme could help stop the virus. The enzyme, NS3, causes problems when it gloms on to centrioles, a pair of structures inside cells needed to divvy up chromosomes when cells divide, Andrew Kodani, a cell biologist at Boston Children’s Hospital reported December 6.

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

A chemical called an anthracene can help fend off dengue, so Kodani and colleagues tested anthracene on Zika as well. Small amounts of the chemical can prevent NS3 from tinkering with the centrioles, the researchers found. So far the work has only been done in lab dishes.
Protein face-off
Another virulent virus could disable Zika. Work with cells grown in lab dishes suggests a bit of protein, or peptide, from the hepatitis C virus, could muck up Zika’s proteins.

The peptide interferes with HSP70, a protein that helps assemble complexes of other proteins, including ones involved in protein production. That peptide and other compounds were already known to inhibit hepatitis C replication, UCLA virologist Ronik Khachatoorian and colleagues had previously discovered. The hepatitis C virus peptide stops Zika virus proteins from being made and hampers assembly of the virus, Khachatoorian reported December 5.

The peptide has not been tested in animals yet.

Earth was momentarily ripe for the evolution of animals hundreds of millions of years before they first appeared, researchers propose.

Chemical clues in ancient rocks suggest that 2.32 billion to 2.1 billion years ago, shallow coastal waters held enough oxygen to support oxygen-hungry life-forms including some animals, researchers report the week of January 16 in the Proceedings of the National Academy of Sciences. But the first animal fossils, sponges, don’t appear until around 650 million years ago, following a period of scant oxygen known as the boring billion (SN: 11/14/15, p. 18).
“As far as environmental conditions were concerned, things were favorable for this evolutionary step to happen,” says study coauthor Andrey Bekker, a sedimentary geologist at the University of California, Riverside. Something else must have stalled the rise of animals, he says.

Microbes began flooding Earth with oxygen around 2.3 billion years ago during the Great Oxidation Event. This breath of oxygen enabled the eventual emergence of complex, oxygen-dependent life-forms called eukaryotes, an evolutionary line that would later include animals and plants. Scientists have proposed that the Great Oxidation Event wasn’t a smooth rise, but contained an “overshoot” during which oxygen concentrations momentarily peaked before dropping to a lower, stable level during the boring billion. Whether that overshoot was enough to support animals was unclear, though.

Bekker and colleagues tackled this question using a relatively new way to measure ancient oxygen. Rock weathering can wash the element selenium into the oceans. In oxygen-free waters, all of the selenium settles onto the seafloor. But in water with at least some oxygen, only a fraction of the selenium is deposited. And the selenium that is laid down is disproportionately that of a lighter isotope of the element, leaving atoms of a heavier isotope to be deposited elsewhere.
If ancient coasts contained relatively abundant oxygen, the researchers expected to find more light selenium close to shore and more heavy selenium in deeper, oxygen-deprived waters. Analyzing shales formed under deep waters around the world, the researchers found just such an isotope segregation. These shales had an abundance of the heavier selenium, leading researchers to infer that the lighter version of the element was concentrated closer to shore.

Oxygen concentrations in coastal waters were at least nearly one percent of present-day levels and “were flirting with the limits of what complex life can survive,” proposes study coauthor Michael Kipp, a geochemist at the University of Washington in Seattle. While the environment was probably suitable for eukaryotes, life hadn’t evolved enough by this point to take advantage of the situation, Kipp proposes. The appearance of eukaryotes in the fossil record would take hundreds of millions of years of more evolution (SN Online: 5/18/16), he says, and the first animals even longer.
Tracking selenium is such a new technique, though, that “interpretations could change as we better understand how it works,” says Philip Pogge von Strandmann, a geochemist at University College London. Currently the method is “tricky,” he says, especially for precisely estimating oxygen concentrations.