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Buying a handgun in Connecticut means waiting — lots of waiting. First comes an eight-hour safety course. Then picking up an application at a local police department. Review of the application (which includes a background check and fingerprinting) can take up to eight weeks. If approved, the state issues a temporary permit, which the buyer trades in at state police headquarters for a permanent one. Then it’s back to the store for the gun.

Head west to Missouri, though, and buying a handgun is practically a cakewalk. Customers at Osage County Guns in Belle, Mo., for example, can walk into the store and walk out with a gun if they pass the FBI’s instant background check, says John Dawson, the store’s chief technical officer.
“If a person knew exactly what they wanted,” he says, the store could, “in theory, complete the transaction in about 15 minutes.”

Missouri and Connecticut have staked out opposite ends of the gun law spectrum. Connecticut didn’t require handgun buyers to get a permit until 1995. Missouri had a tough law on the books, but repealed it in 2007. The states’ laws have flip-flopped, making for a fascinating natural experiment on gun laws’ effects on gun violence.

The states “had mirror image policy changes, and mirror image results,” says Daniel Webster, a health policy researcher at Johns Hopkins University.

Flipping the laws was associated with 15 percent fewer gun suicides in Connecticut and 16 percent more in Missouri, a statistical analysis by Webster and colleagues, published last year in Preventive Medicine, estimated. Similar analyses by Webster in 2014 and 2015 indicated a 40 percent reduction in Connecticut gun homicide numbers, and an 18 percent rise in Missouri.
The evidence is very suggestive, says Harvard University researcher David Hemenway. But it’s not extensive enough to persuade everyone — or to move national policy.

In fact, questions loom about the impact of all sorts of policies, from background checks to assault weapons bans to gun buybacks. That’s partly because gun research faces roadblocks at every turn: Scientists have to deal with data shutouts, slashed funding and, occasionally, harassment.

For a few questions, however, researchers have come up with solid answers: There’s a convincing link between gun availability and gun suicide, for one. And studies from the United States and abroad suggest that some gun laws do rein in gun violence. To make firm conclusions, though, scientists are desperate for more data.

But the U.S. Centers for Disease Control and Prevention can’t collect gun data like it used to, and information about guns used in individual crimes is locked up tight. Under current federal laws, Hemenway says, “It’s almost impossible for researchers to get even the data that are available.”

Locked up
In a squat brick building tucked in the hills of Martinsburg, W. Va., gun data are overflowing.

Thousands of cardboard boxes, stacked high in tidy columns, line the hallways of the federal government’s National Tracing Center. In the parking lot, steel shipping containers hold even more boxes. Each box contains about 2,000 pages of gun purchase records. To trace a gun, the center’s employees often search through these records by hand.

That’s their job: tracking when and where guns used in crimes were originally purchased, and by whom. It’s a huge undertaking: In 2015, the center, part of the Bureau of Alcohol, Tobacco, Firearms and Explosives, or ATF, received more than 373,000 gun trace requests from law enforcement.
Such a mass of data is a researcher’s dream. But current laws keep gun traces secret. The agency shares traces only with law enforcement. The public can see just summaries or aggregate data.

Webster has used this data to paint a rough picture of how Missouri’s repeal affected the flow of guns to criminals. In 2006, when buying a handgun required a permit, 56.4 percent of guns recovered by police had been originally sold by a Missouri gun dealer. In 2012, five years after the state nixed the permit requirement, the number rose to 71.8 percent, Webster and colleagues reported in the Journal of Urban Health in 2014.

The findings suggest that it’s easier now for criminals in Missouri to get their hands on legally purchased guns. But Webster can’t say for certain whether more guns are moving to criminals — or whether legal gun owners are committing more crimes. For that, he’d need to see the individual gun traces.

About a decade ago, researchers who wanted such detailed data could get it. “We’d just hand them a DVD,” says ATF information specialist Neil Troppman. “Those days are long over.”

A handful of laws snarl the process, from how a gun trace begins to who can see the data.

One big hitch in the system: Police officers who find a gun at a crime scene can’t always look up the owner’s name on a computer. That’s because there is no national registry — no searchable database of guns and their owners. To set one up would be illegal. So police have to submit a request to the tracing center, which tracks the gun’s movement from manufacturer or importer to dealer. Then the ATF can ask the dealer who bought the gun. If the dealer has gone out of business, ATF employees dig for the answer themselves, in old gun purchase records stockpiled at the tracing center. The process takes an average of five days. And after law enforcement gets the data, federal law makes sure no one else can see it.

Federal constraints
In 2003, Congress unleashed a beast of a bill with an amendment that effectively tore out the ATF’s tongue. The Tiahrt amendment was the first in a series of provisions that drastically limited the agency’s ability to share its crime gun data — no giving it to researchers, no making it public, no handing it over under Freedom of Information Act requests (the public’s channel for tapping into information from the federal government).

Funding for gun control research had dried up a few years earlier. There’s no outright ban, but a 1996 amendment had nearly the same effect. It’s known as the Dickey amendment, and it barred the CDC from using funds to “advocate or promote gun control.” According to a 2013 commentary in JAMA, that meant almost any research on guns.
If the 1996 law’s language was vague, Congress made the message clear by cutting the CDC’s budget by $2.6 million — exactly the same amount the agency had spent the previous year on gun violence research. The funds were later reinstated, but earmarked for other things. So the CDC largely backed off, except for some basic tallying, says spokesperson Courtney Lenard, because of the funding cuts and because Congress “threatened to impose further cuts if that research continued.”

In 2011, Congress hit the National Institutes of Health with similar restrictions. About a year later, President Obama tried to ease the choke hold: He ordered the CDC to research the causes and prevention of gun violence, and called on Congress to provide $10 million in funding. Finally, 17 years after the CDC cuts, news reports proclaimed that the ban had been lifted and research could resume. But Congress never authorized the money, and the CDC remained on the sidelines. This April, nearly 150 health and science organizations, universities and other groups signed a letter urging Congress to restore the CDC’s funding.

Meanwhile, research on gun violence and gun control trudges forward: Researchers can sometimes convince law enforcement agencies to share data on guns linked to crimes, and grants can come from private foundations. Yet even with limits on research, the science in some cases is solid: A gun in the home, for example, increases the odds a person will commit suicide by about 3-to-1. Here, Hemenway says, “The weight of the evidence is overwhelming.”

But how to use laws to reduce gun violence remains hotly contested, and opinions among the public, and even scientists, are polarized.

Critics of gun control laws think the matter is clear: Again and again studies show that gun control policies just don’t work, says economist John Lott, who has written extensively on the subject. Take background checks, he says, “Given that these laws are costly, you’d like to believe there’s some evidence that they produce a benefit.”

Webster acknowledges the divisive split in opinions. “The vast majority of people are on one side of the fence or the other,” he says. “They’ll point to a study that is convenient to their political arguments and call it a day.”

Bad for your health
For researchers who manage to navigate the legal tangles and funding troubles of gun research, actually doing the research itself isn’t easy.

Unlike clinical trials in medicine, where scientists can give, for example, a cholesterol drug to half a study’s participants and then compare the effects between users and nonusers, scientists studying gun violence can’t dole out new handguns to one group and none to another and see what happens.

Instead, researchers turn to observational studies. That means looking at how — and if — suicides track with gun ownership in different groups of people and over time, for example. Finding a link between two observations doesn’t necessarily mean they’re connected. (People have linked the yearly number of Nicolas Cage movies to swimming pool drownings, after all.) But finding a lot of links can be telling.

For suicides, the link to gun access holds strong — among old people, young people, women, adolescents, “you name it,” Hemenway says. Lots of guns means lots of suicides by gun, he says.
In 2007, Hemenway and colleagues examined gun ownership rates and statewide suicide data from 2000 to 2002. People in states with a high percentage of gun owners (including Wyoming, South Dakota and Alaska) were almost four times as likely to kill themselves with guns as people living in states with relatively few gun owners (such as Hawaii, Massachusetts and Rhode Island), the researchers reported in the Journal of Trauma Injury, Infection and Critical Care.

More recently, a 2013 study in Switzerland compared suicide rates before and after an army reform that cut the number of Swiss soldiers by half. After the reform, fewer people had access to army-issued guns — and the suicide rate dipped down by about two per 100,000 men age 18–43. That’s about 30 men each year who didn’t die from suicide, the study’s authors estimated in the American Journal of Psychiatry.

A 2014 review of 16 such studies, published in the Annals of Internal Medicine, came to the same conclusion, again: Access to guns meant higher risk of suicide.

“The evidence is unassailable,” says Stanford University criminologist John Donohue. “It’s as strong as you can get.”

Mental illness factors into suicide too, says Jeffrey Swanson, a medical sociologist at Duke University. (Some 21 to 44 percent of suicides reported to the CDC are committed by people with mental health problems.) And federal laws aren’t particularly good at keeping guns away from mentally ill people. A 1968 law prohibits gun sales to a narrow slice of people with a history of mental illness, but it’s easy for others to slip through the cracks. Even people the law does target can end up with guns — because states don’t have to report mental health records to the FBI’s national background-check system.

“You’ve got tons of records that would disqualify people from buying guns,” Swanson says, but they don’t necessarily make it into the system.
Even if the United States had a perfect mental health care system and cured schizophrenia and bipolar disorder and depression, he says, the overall problem of gun violence would still exist. Mentally ill people just aren’t that violent toward others, Swanson noted in the Annals of Epidemiology in 2015. In fact, people with mental illness committed fewer than 5 percent of U.S. gun killings between 2001 and 2010, according to the CDC.

“People think that in order to fix gun violence, we need to fix the mental health care system,” Swanson says. That’s wrong, he argues. “It’s a diversion from talking about guns.”

Weak laws
After Sandy Hook, San Bernardino and other high-profile mass shootings, people have been talking about what gun control laws, if any, actually work.

Unfortunately, there’s just not enough evidence to make strong conclusions about most laws, Hemenway says. In 2005, for example, a federal task force reviewed 51 studies of gun laws, mostly in the United States, and came up empty-handed. The task force couldn’t say whether any one of the laws made much of a difference. The efficacy of U.S. gun laws is hard to pin down for two main reasons, Hemenway says: Gun laws aren’t typically very strong, and studies tend to look at overall effects on violence.

One major study published in JAMA in 2000 analyzed suicide and homicide data from 1985 to 1997 to evaluate the impact of the Brady Act, a 1994 federal law that requires background checks for people buying guns.

Eighteen states and the District of Columbia already followed the law. So researchers compared suicide and homicide rates with those in the 32 states new to the law. If Brady curbed gun violence, those 32 states should see dips in deaths.
That didn’t happen (with one exception: Gun suicides in those states dropped in people age 55 and older — by about 1 per 100,000 people).

“I don’t think anybody was really shocked,” Webster says. After all, Brady had a gaping hole: It didn’t require background checks for guns bought from private sellers (including those at gun shows). The loophole neutered Brady: People who didn’t want a background check could simply find a willing private seller. That’s just too easy, Webster says: It’s like letting people decide whether they want to go through the metal detector at the airport.

Like the Brady Act, the 1994 Federal Assault Weapons Ban didn’t seem to do much to prevent violence, criminologist Christopher Koper and colleagues concluded in a 2004 report to the U.S. Department of Justice. The law, which expired in 2004, imposed a 10-year ban on sales of military-style semiautomatic guns. These weapons fire one bullet per trigger squeeze and have features like threaded barrels (which can be used for screwing on silencers) or barrel mounts (for attaching bayonets). The 1994 law also banned most large-capacity magazines (storage devices that feed guns more than 10 rounds of ammo).

But like Brady, the ban came with a catch: It didn’t apply to weapons and magazines made before September 13, 1994. That’s a lot of exemptions. At the time, the United States had more than 1.5 million assault weapons and nearly 25 million guns with large-capacity magazines, reported Koper, of George Mason University in Fairfax, Va.

“The more complete the bans are, the better the effects seem to be,” Donohue says. Take Australia: In 1996, the country enacted strict laws and a gun buyback program after a mass shooting killed 35 people in Tasmania. The ban made certain long-barreled guns illegal (including semiautomatic rifles and pump-action shotguns — weapons that let people fire lots of rounds quickly), and the country bought back and destroyed more than 650,000 guns.

With the law, Donohue says, “Australia effectively ended the problem of mass shootings.”

And as economists Christine Neill and Andrew Leigh found, the law drastically cut down the number of gun suicides, too.
Tough laws
Eleven years after Australia launched its tough gun control legislation, Neill, of Wilfrid Laurier University in Canada, and Leigh, then at Australian National University in Canberra, announced that the law might actually be saving lives.

Critics attacked. One petitioned Neill’s university to reprimand her. Then they came for Leigh’s e-mails. He had to hand over any that mentioned firearms or guns. Had there been anything improper — any whiff that the researchers were biased — Neill believes gun advocates would have pounced.

Neill and Leigh, now an Australian politician, had uncovered telling changes in different regions’ suicide rates between 1990–1995 and 1998–2003. “Firearms suicides fell most in Tasmania, by a long shot,” Neill says, almost 70 percent, the team later reported in 2010 in the American Law and Economics Review.

Australia’s law, called the National Firearms Agreement, or NFA, applied to all of the country’s states and territories, but some had more guns than others. Tasmania, for example, had the most guns bought back, Neill says: 7,302 guns per 100,000 people. More guns bought back meant bigger drops in suicide rates, she says.
Instead, the United States goes for smaller laws, fashioned mostly state-by-state. Still, some may be effective. Blocking domestic violence offenders’ access to guns seems to cut down on homicides, for example. From 1982 to 2002, states with restraining order laws that bar offenders from buying guns had rates of intimate partner homicide that were 10 percent lower than in states lacking the laws, researchers reported in 2006 in Evaluation Review.It’s a stark result, and suggests that tough laws can have big impacts. Australia “did an outright ban and something akin to a confiscation of guns,” Webster says. “That’s never going to happen in the United States.”

In 2010, Webster and colleagues reported similar results at the city level. He and colleagues tracked intimate partner homicides from 1979 to 2003 in 46 U.S. cities. Those that made it hard for people with domestic violence restraining orders to get guns had 19 percent fewer intimate partner homicides compared with cities with less stringent laws, the team reported in Injury Prevention.

“These are pretty consistent findings,” Webster says. Those state policies seem to be working.

Conclusions about other, more well-known laws, such as “right-to-carry,” are less convincing. Such laws, which allow people to carry concealed handguns in public, could offer people a means of defense. Or they could make it easier for people in an argument to whip out a gun.
“The findings are all over the map,” Hemenway says. A report from the National Research Council in 2005 found no causal link between right-to-carry laws and crime. It also concluded that people do use guns to protect themselves (say, by threatening or shooting an attacker) but how often is hard to say. Estimates vary from 100,000 to 2.5 million times per year in the United States.

Economist Mark Gius of Quinnipiac University in Hamden, Conn., estimated that restricting people’s right to carry boosts a state’s murder rate by 10 percent, he reported in 2014 in Applied Economics Letters.

Donohue’s 2014 results lean a different way. The Stanford researcher updated the NRC analysis with more than a decade of new data and found that laws letting people carry concealed weapons boost violent crime — a bit. Based on data from 1979 to 2012, his statistical modeling showed that a state with a right-to-carry law would experience 8 percent more aggravated assaults than a state without such a law, for example.

“More and more evidence is amassing that these laws are harmful,” Donohue says, but he concedes that there’s still uncertainty. “I’m not quite ready to say that we’ve nailed it down.”

Less uncertainty would require more analyses and more data. But in this field, even that doesn’t guarantee consensus.

“The problem is that there are many ways to slice the data,” Donohue says. “Almost nothing is as clear as the advocates make it — on both sides.”

Shaken-but-not-stirred remnants of Earth’s earliest years still exist nearly 4.6 billion years later.

Researchers traced the shadowy footprints of an isotope that hasn’t existed for over 4.5 billion years to much younger lava rocks from the Pacific and Atlantic oceans. That suggests that reservoirs of the ancient mantle may be hidden deep inside the planet, geochemist Hanika Rizo and colleagues report May 13 in Science.

Earth formed about 4.6 billion to 4.5 billion years ago as planetary bodies collided, disintegrating and melting to accrete into one mass like a hot, rocky lint ball. Geologists have assumed that any relics of this bumpy beginning were mixed beyond recognition.
Instead, Rizo’s team found a surprise: Some modern flood basalts have unusually high concentrations of tungsten-182. That’s significant because that isotope forms only from radioactive decay of hafnium-182. And hafnium-182 only existed during Earth’s first 50 million years. “These isotopes had to be created early,” says Rizo, of the University of Quebec in Montreal.
It is “spectacular” that some of Earth’s earliest materials may still be preserved, says Matthias Willbold, a geochemist at the University of Manchester in England. “We may have to revise our view of the Earth’s internal structure.”

Rizo and colleagues measured the tungsten-182 in flood basalts from two locations: Canada’s Baffin Bay, part of the 60-million-year-old North Atlantic Igneous Province, and near the Solomon Islands, part of the 120-million-year-old Ontong Java Plateau in the Pacific Ocean. “Flood basalts are not normal eruptions,” Rizo says. “They are capable of tapping into the deep mantle.”
Her team found that levels of tungsten-182 in the lavas varied, suggesting that the deep sources of these younger rocks were different pieces of Earth’s oldest material, each with their own isotopic signature and history. These results also show that the ancient remnants have somehow escaped being mixed by convection currents.

Geophysicists have identified two large “blobs” in the deep mantle, called large low-shear velocity provinces. Those blobs “could be candidates” for the remnants of the ancient mantle, Rizo says.

What builds up can also tear down, a new study of bacteria suggests.

Bacteria build biofilms, communities of the microorganisms encased in a protective goo that shields the microbes from antibiotics and immune system attacks. But the very enzymes bacteria use to construct that shield can also destroy some of its molecules and strip away the protection, researchers report May 20 in Science Advances.

“We’re weaponizing the bacteria against themselves,” says P. Lynne Howell, a structural microbiologist at the Hospital for Sick Children in Toronto. Howell and colleagues studied Pseudomonas aeruginosa bacteria, which can cause pneumonia and other infections and is particularly problematic for people with the lung disease cystic fibrosis.
The researchers discovered that two enzymes, PelAh and PslGh, which the bacteria use to build two different sugar polymers, can degrade those same polymers. That delete function, supplied by parts of the enzymes known as glycoside hydrolase domains, normally helps correct mistakes or prevents buildup of the sugar chains inside bacterial cells, Howell says.

In laboratory tests, synthetic versions of the glycoside hydrolase domains applied to P. aeruginosa cultures stopped the bacteria from forming new biofilms and melted existing ones. Stripping away sugar polymers did not kill the bacteria but did make them more vulnerable to antibiotics and immune cells. Human lung cells grown in dishes containing the enzymes suffered no harm, suggesting the enzymes wouldn’t damage human tissues.

Animal tests are needed to determine whether the enzymes are safe and can fight biofilm infections in the body, Howell says. Similar enzymes from other bacteria and fungi may also fight biofilm infections caused by those organisms, she says.

Giant pandas have better ears than people — and polar bears. Pandas can hear surprisingly high frequencies, conservation biologist Megan Owen of the San Diego Zoo and colleagues report in the April Global Ecology and Conservation.

The scientists played a range of tones for five zoo pandas trained to nose a target in response to sound. Training, which took three to six months for each animal, demanded serious focus and patience, says Owen, who called the effort “a lot to ask of a bear.”

Both males and females heard into the range of a “silent” ultrasonic dog whistle. Polar bears, the only other bears scientists have tested, are less sensitive to sounds at or above 14 kilohertz. Researchers still don’t know why pandas have ultrasonic hearing. The bears are a vocal bunch, but their chirps and other calls have never been recorded at ultrasonic levels, Owen says. Great hearing may be a holdover from the bears’ ancient past.

Two newly discovered Triceratops relatives sported some peculiar headgear.

Researchers uncovered skull fragments of Machairoceratops cronusi in 77-million-year-old mudstone from the Wahweap Formation in southern Utah. Unlike other horned dinosaurs, the roughly 8-meter-long M. cronusi had two grooved horns with spatula-like tips bowed forward from the back of its neck shield. The grooves’ function baffles researchers.

A different research team found a younger cousin of M. cronusi in Montana’s Judith River Formation. Spiclypeus shipporum lived about 76 million years ago and had distinct brow horns that protruded sideways from its skull along with unusual spikes on its neck shield — some pointing outward, others bent forward. S. shipporum’s distinct horns and spikes may have allowed individuals of the species to recognize one another, says Jordan Mallon, a paleobiologist involved in the research at the Canadian Museum of Nature in Ottawa.

The new finds add to the diversity among the herbivorous horned dinosaurs that roamed North America during the Late Cretaceous period. “We thought we knew most things [about horned dinosaurs],” says Eric Lund, a paleontologist at Ohio University in Athens who analyzed M. cronusi. “But we’ve just scratched the surface.”

Papers detailing the new species were published May 18 in PLOS ONE.

Armor-plated marine microbes surprised scientists a few years ago by recovering their shell-building prowess in levels of ocean acidification expected under future climate change. But those gains were short-lived, new research shows.

For four years, marine ecologist Lothar Schlüter and colleagues steeped Emiliania huxleyi phytoplankton in seawater acidified by carbon dioxide. After an initial drop in shell calcification — a process that helps sequester CO2 from the atmosphere — the microbes mostly restored their calcification activities within a year, the researchers had reported.
But as the experiment continued, the phytoplankton began making less and less shell material. By the end of the experiment, the phytoplankton in the acidified water were calcifying less than a population that hadn’t been exposed to such harsh conditions, the researchers report July 8 in Science Advances.

In the future, the shell-making phytoplankton “may calcify even less than we assume today based on short-term experiments,” says study coauthor Thorsten Reusch, a marine ecologist who works with Schlüter at the GEOMAR Helmholtz Center for Ocean Research in Kiel, Germany. “One year just isn’t long enough to tell us something about how evolutionary adaptation will play out.”
While phytoplankton in the ocean may ultimately follow a different evolutionary path than those under lab conditions, the work shows that the evolutionary response to climate change is more complex than previously thought, Reusch says. There is a silver lining, though: When returned to present-day seawater conditions, the phytoplankton bounced back to their original calcification rates. So even if ocean acidification continues, the phytoplankton could quickly restart calcifying if conditions ever improved. “This isn’t a case of ‘use it or lose it,’” Reusch says.
Photosynthetic plankton produce about half of Earth’s oxygen and their sinking carcasses transport carbon from the ocean surface to the seafloor — both key steps in the temperature-regulating carbon cycle. The weight of E. huxleyi’s circular, shieldlike shells serves as ballast during the descent, accelerating the carbon drawdown.

The shell-making process requires E. huxleyi to lower its own acidity by pushing protons out through its cell wall. But as the ocean becomes more acidic, that proton pushing will require more energy to overcome an increasing acidity difference between the inside and outside of the cell. Many scientists worry that that energy cost could cause calcifying phytoplankton such as E. huxleyi to ultimately give up their shells. That would slow the CO2 drawdown and worsen climate change, the scientists fear.

Schlüter, Reusch and colleagues started their tests with a single cell of E. huxleyi collected off the coast of Norway in 2009. Populations grown from this cell lived in containers of acidified seawater about the size of soda cans. Around 2,100 generations later, at the end of the study, the acidity-acclimated phytoplankton population calcified about four-fifths as much shell material as a population that had been kept in regular seawater before being plopped into acidified water.

That calcification decline could be an evolutionary trade-off, Reusch says. The shells probably protect E. huxleyi from predators and pathogens. But in more acidic waters, the energy costs of building shells may outweigh their benefits. The researchers plan to conduct the same experiment again, this time introducing predators to see if the added hazard makes the phytoplankton hold on to their shells.

“There are a lot of surprises in store for us in terms of the kinds of evolutionary responses these organisms can have,” says Tatiana Rynearson, an oceanographer at the University of Rhode Island’s Narragansett campus who was not involved in the study. “Evolution continues.”

ORLANDO, Fla. — Weight gain may depend on how an individual’s genes react to certain diets, a new study in mice suggests.

Four strains of mice fared differently on four different diets, William Barrington of North Carolina State University in Raleigh reported July 15 at the Allied Genetics Conference.

One strain, the A/J mouse, was nearly impervious to dietary changes. Those mice didn’t gain much weight or have changes in insulin or cholesterol no matter what they ate: a fat-and-carbohydrate-laden Western diet, traditional Mediterranean or Japanese diet (usually considered healthy) or very low-carbohydrate, fat-rich fare known as the ketogenic diet.
In contrast, NOD/ShiLtJ mice gained weight on all but the Japanese diet. Those mice’s blood sugar shot up — a hallmark of diabetes — on a Mediterranean diet, but decreased on the Japanese diet.

FVB/NJ mice didn’t get fat on the Western diet, but became obese and developed high cholesterol and other health problems on the ketogenic diet. The opposite was true for C57BL/6J mice. They became obese and developed cholesterol and other problems linked to heart disease and diabetes in people on the Western diet, but not on the ketogenic diet. They also fattened up on the Mediterranean diet.

The results indicate that “there’s no universally healthy diet,” Barrington said. The findings echo results of a human study in which blood sugar rose in some people after eating some foods, even when the same food had no effect on other people (SN: 1/9/16, p. 8). Such individual reactions to food suggest that diets should be personalized.

Barrington and colleagues are working to find the genes that control the mouse strains’ varying responses to what they eat. There is still no way to predict how people will fare on a given diet, he said.

MANCHESTER, England — The human nose harbors not only a deadly enemy — Staphylococcus aureus — but also its natural foe. Scientists have now isolated a compound from that foe that might combat MRSA, the methicillin-resistant strain of S. aureus.

“We didn’t expect to find this. We were just trying to understand the ecology of the nose to understand how S. aureus causes problems,” bacteriologist Andreas Peschel of the University of Tübingen in Germany said at a news briefing July 26 during the EuroScience Open Forum. Investigating the intense interspecies competition in the nose — where microbes fight for space and access to scant sugars and amino acids — might offer a fertile alternative to searching for new drug candidates in soil microbes.
Antibiotic researcher Kim Lewis of Northeastern University in Boston agrees in general that the approach might produce new drug discovery leads. But so far the human microbiome has produced only a handful of potential new antibiotics (including lactocillin). If “the compound they found is membrane-acting, [it] will be useful for topical applications, but not as a systemic antibiotic,” he wrote in an e-mail. And new systemic antibiotics are needed most, he says.
Despite being a relatively nutrient-poor environment, the human nose is home to more than 50 species of bacteria. One of these is S. aureus, a dominant cause of hospital-acquired infections such as MRSA, as well as infections of the blood and heart. But there’s a huge variability in the nasal microbe scene between individuals: while S. aureus is present in the nasal passages of roughly 30 percent of people, the other 70 percent don’t have any sign of it.

Trying to explain this difference led Peschel and colleagues to study “the ecology of the nose.” They suspected that other nasal inhabitants, well-tuned to compete in that harsh niche, might be blocking S. aureus from colonizing the nose in those who don’t carry it.

From nasal secretion samples, the team isolated 90 strains of different Staphylococcus species. Of these, one bacterium, S. lugdunensis, killed S. aureus when the two were grown together in a dish. Introducing a variety of mutations into S. lugdunensis produced a strain that didn’t kill. The missing gene, the team showed, normally produced an antibiotic, which the researchers named lugdunin; it represents the first example of a new class of antibiotic.

Lugdunin was able to fend off MRSA as well as a strain of Enterococcus resistant to the antibiotic vancomycin. Neither bacteria developed resistance. The team also pitted S. lugdunensis against S. aureus in test tube and mouse studies, with S. lugdunensis besting S. aureus. Only 5.9 percent of 187 hospital patients had S. aureus in their noses if they also carried S. lugdunensis, the team found, while S. aureus was present in 34.7 percent of those without S. lugdunensis. Peschel and colleagues also reported the results July 28 in Nature.
Lugdunin cleared up a staph skin infection in mice, but it’s unclear how the compound works. Researchers could not rule out that it damages the cell membrane, which could limit its use in humans to a topical antibiotic. Peschel and coauthor Bernhard Krismer also suggest that the bacterium itself might be a good probiotic, applied nasally, to fend off staph infections in vulnerable hospital patients.

For the first time in the United States, free-flying genetically modified mosquitoes have federal approval to take wing in Florida. But when, and if, that will happen is still up in the air. Local officials will make the final decision — possibly not until after the November elections.

The World Health Organization has recognized these mosquitoes as possible tools for fighting the spread of mosquito-borne Zika virus. But the U.S. Food and Drug Administration’s decision, announced August 5, covers only a specific, preliminary test release of GM mosquitoes on Key Haven in the Florida Keys, where no locally transmitted Zika cases have been reported.
This trial of OX513A mosquitoes, genetically engineered by the British company Oxitec, “would be unlikely to result in adverse effects on the environment or human health,” the FDA ruled. If Key West commissioners approve it, the trial would release abundant GM male Aedes aegypti species carrying a gene that will cause their offspring to die. In tests in Brazil, Panama and the Cayman Islands, months of releasing these mosquitoes has reduced the wild populations of Ae. aegypti mosquitoes by 90 percent or more. As a result, a Brazil neighborhood has seen mosquito-borne dengue cases plummet (SNOnline: 7/15/16).

To see whether OX513A could work in the United States, too, the test release would now need approval from the Florida Keys Mosquito Control District Board of Commissioners. Opponents of GM organisms have protested the idea, so the five commissioners have arranged for a nonbinding referendum question to appear on the November ballot. Commissioners plan to wait until the community has weighed in before making their final decision, says mosquito control district spokeswoman Beth Ranson.

If the mosquito plan gets a thumbs up, Oxitec could release mosquitoes in December, said Hadyn Parry, the company’s chief executive officer. Monitoring and testing could take six months and results would go back to the FDA with an application to allow the mosquitoes to be released commercially — and more broadly — in the United States for mosquito control.

As Zika rages in Puerto Rico, and with Miami reporting the first locally mosquito-transmitted cases on the U.S. mainland, debate over the controversial mosquito has taken on new urgency. Tom Frieden, director of the U.S. Centers for Disease Control and Prevention, has noted that efforts to eradicate mosquitoes in an area in Miami have fallen short (SNOnline: 8/1/16).

Ae. aegypti mosquitoes resist many pesticides, bite during the day, love human houses, and can breed in plant saucers and other small pools of water. Virtually a domestic animal, this species bites people almost exclusively. It’s suspected to be the main spreader of Zika virus, and also does a fine job of infecting people with dengue, chikungunya and yellow fever viruses.
Oxitec GM mosquitoes, developed in 2002, would target Floridian pests via a new twist in the decades-old strategy of male sterilization. Mid-20th century entomologists sterilized screwworms by irradiating them and releasing the decoy males in overwhelming clouds. So many wild females mated with these sterile males that eventually the gruesome screwworm pests of livestock disappeared from the United States.

OX513A, with their mix of old-fashioned strategy and newfangled genetic tinkering, has kicked up anti-GMO feeling, even though it’s not the first U.S. approval of testing a GM insect in pest control. That honor goes to pink bollworms in the Southwest in 2009, though their release passed largely unnoticed outside the pest-control community. But when the FDA released a favorable draft opinion in March, saying the GM-mosquito test would probably have “no significant impact” on people or the environment, more than 2,000 people typed comments on the public FDA site. Many were vehemently opposed to the plan, peppering their comments with multiple exclamation points and the occasional “OMG!!!”

Some commenters worried about blood contact from the bite of a GM organism, possible allergies should someone accidentally swallow one and unknown consequences to the environment.

Oxitec posted explanations responding to those fears: Almost all mosquitoes released would be males, which don’t bite; males will die three or four days after release; their offspring are engineered to die without unnatural amounts of tetracycline — a lab-provided supplement — in their diets. Angry public comments, however, largely dismissed these reassurances as corporate-funded research.

Another commenter wondered whether a successful test, driving down the Ae. aegypti population on the Keys, could make room for some other insect menace. That’s a reasonable question, says Phil Lounibos of the University of Florida in Vero Beach. He has studied competition between Ae. aegypti and the relentlessly biting Asian tiger mosquito, Aedes albopictus. These tiger mosquitoes were once rare on the Keys, but he has found that they can take over from Ae. aegypti, in part by sexual deception. Tigers that mate with Ae. aegypti females render the females sterile and have thus conquered other parts of Florida. Even though Ae. aegypti is recognized as a more potent vector for human disease, the tigers can carry many of the same viruses (including Zika), Lounibos warns (SNOnline: 5/16/16).

As far as ecological concerns go, entomologist Bruce Tabashnik of the University of Arizona in Tucson, has no problem with eradicating Ae. aegypti from the Florida Keys or anywhere else in the Americas. “It’s an invasive species,” he says. “There are no ecological ethics violated.”

Tabashnik was part of the research team monitoring the first GM insect release in the United States: sterile male pink bollworms. Males of this invasive pest species that prey on cotton in the Southwest were sterilized by radiation. However, Oxitec had inserted a gene that made them fluoresce red so monitors could tell the friendlies from the wild targets. Tabashnik recalls no particular public outcry over the experiment. It took place in a sparsely populated area and, instead of mosquitoes, involved a kind of moth only a cotton farmer could hate.

So far outrage, or even interest, in other tweaked pest-control animals seems minimal compared with GM-mosquito fever. A proposed test of Oxitec’s GM diamondback moth in New York has inspired fewer comments. Tests of a non-GM but still tinkered-with mosquito — Ae. albopictus developed to carry Wolbachia bacteria that interfere with mating — were first approved in 2012 for release in American Samoa. Later tests have released these bacteria-carrying mosquitoes in California and other sites in the mainland United States.

WASHINGTON — When bacteria lose genes needed to make enzymes for important chemical reactions, defeat isn’t inevitable. Sometimes other enzymes will take on new roles to patch together a work-around chain of reactions that does the job, biologist Shelley Copley reported August 4 at the 2nd American Society for Microbiology Conference on Experimental Microbial Evolution.

Bacteria that can adapt in this way are more likely to survive when living conditions change, passing along these new tricks to their descendants. So studying these biochemical gymnastics is helping scientists to understand how evolution works on a molecular level.
Working with different strains of Escherichia coli bacteria, Copley and colleagues deleted genes responsible for making crucial enzymes. The team then watched the microbes replicate for many generations to see how they worked around those limitations.

Most enzymes are highly specialized: They only work well to speed up one type of reaction, the way a key fits only one lock. But some enzymes are more like master keys — they can boost multiple reactions, though they tend to specialize in one. These so-called “promiscuous” enzymes can switch away from their specialty if conditions change.

Copley’s team found that new enzymes would sub in to replace the missing ones. For instance, E. coli missing an enzyme needed to make vitamin B6 synthesized the vitamin using a different set of enzymes. But surprisingly, the promiscuous enzymes didn’t end up directly triggering the same reaction as the enzymes they replaced. Instead, the replacement enzymes cobbled together a different (often longer) work-around series of reactions that ultimately achieved the same function.

“We were rerouting metabolism,” said Copley, of the University of Colorado Boulder.

By modifying the bacteria’s genes and forcing the microbes to survive with a more limited chemical toolkit, Copley’s work gives a more detailed look at the biochemistry underlying evolution, says biologist Gavin Sherlock of Stanford University, who was not involved in the research.
Betul Kacar, a synthetic biologist at Harvard University, says promiscuity could also be a window into the past, giving hints about enzymes’ previous roles earlier in evolutionary history. The role that an enzyme jumps in to play in a pinch could have once been its main job. “Trying to understand how novel pathways arise, what kind of mechanistic underlying forces shape those trajectories, is quite essential,” she says.

Bacteria can piece together all sorts of alternative routes in response to missing enzymes, depending on specific environmental conditions, Copley said. The ones that are most successful are more efficient —they have fewer steps, or they yield more of the desired reaction product.