Olympic swimmers shave their bodies before a big race to break records. Swordfish use a different trick, a new study suggests: They grease their heads. The fish (Xiphias gladius) are among the fastest in the ocean — their streamlined bodies can cut through the water at about 90 kilometers per hour.

A newly discovered oil-producing organ in the fish’s head gives it slick skin that could boost its speed, scientists report in the July 6 Journal of Experimental Biology. MRI scans show that the organ links to tiny pores on the head that ooze the oil, creating a thin layer of lubrication on the skin’s surface.
Tiny ridged structures called denticles surround the pores. Denticles look like scales but are made of dentine and enamel, like teeth. The scientists, a team from the Netherlands, think the lubrication and the textured denticles might work together, making a water-repelling surface that lets swordfish glide through the water with minimal drag.

If you’ve ever watched a baby purse her lips to hoot for the first time, or flash a big, gummy grin when she sees you, or surprise herself by rolling over, you’ve glimpsed the developing brain in action. A baby’s brain constructs itself into something that controls the body, learns and connects socially.

Spending time with an older person, you may notice signs of slippage. An elderly man might forget why he went into the kitchen, or fail to anticipate the cyclist crossing the road, or muddle medications with awkward and unfamiliar names. These are the signs of the gentle yet unrelenting neural erosion that comes with normal aging.
These two seemingly distinct processes — development and aging — may actually be linked. Hidden in the brain-building process, some scientists now suspect, are the blueprints for the brain’s demise. The way the brain is built, recent research suggests, informs how it will decline in old age.
That the end can be traced to the beginning sounds absurd: A sturdily constructed brain stays strong for decades. During childhood, neural pathways make connections in a carefully choreographed order. But in old age, this sequence plays in reverse, brain scans reveal. In both appearance and behavior, old brains seem to drift backward toward earlier stages of development. What’s more, some of the same cellular tools are involved in both processes.

Probing the connections between growing and aging may reveal how time affects the brain. And with a deeper understanding of brain aging, and the tools involved, scientists might be able to slow — or even stop — mental decline.
That’s a lofty goal, made even more challenging by the multitude of theories from a diversity of researchers that aim to explain why and how the brain ages. Everybody focuses on a different aspect of the aging brain, leaving no one with a sense of the whole process, says epigeneticist Art Petronis of the Center for Addiction and Mental Health in Toronto. It’s like people trying to put together a giant jigsaw puzzle from separate rooms, each with only a few pieces in hand. So far, people studying how the brain ages have found only the evidence they can grab.

Petronis and others are intrigued by the idea that the brain’s early life holds clues to its end. “You see blips here and blips there,” he says. “This critical mass is accumulating.”

Other scientists, including Caleb Finch of the University of Southern California, in Los Angeles, caution against falling for appealing but overly simple explanations for aging. As a gerontologist who has been thinking about aging for 50 years, he has seen aging theories come and go, a perspective that makes him skeptical that the complex process can be reduced to the notion that it’s just development in reverse. “The more we poke into biology, the more wondrously complex it is,” he says.

Nonetheless, there’s something to the notion that aging starts early. “We are born dying,” Finch says. And poking at that idea just might lead somewhere.

Head start
When the human brain makes its first appearance in the third week of gestation, it is no more than a minuscule smear of indistinct cells. This glob then grows at a furious rate up through the preschool years. At the same time, these accumulating brain cells begin to take on specific jobs, changing from generalists to specialists. Nerve cells are born and migrate to their final destinations, linking up in precise order to form the high-speed neural connections that enable memory, emotion and thought. And scientists now realize that the way the brain is built has lifelong effects.
In 1932 and 1947, nearly every Scottish 11-year-old sat down to take an intelligence test. Decades later, their scores have matured into academic gold, offering scientists a rare opportunity to see how intelligence fares with age. In 1999, scientists led by Ian Deary of the University of Edinburgh got back in touch with as many of the long-ago test takers as possible, forming a group of more than 1,000 people — ranging in age from 80 to 95 — called the Lothian Birth Cohort. Deary and colleagues have studied the group in detail, and one factor rises above the rest: People with higher intelligence scores at age 11 were more likely to have better thinking skills in old age.

Childhood intelligence wasn’t the only factor, though. From the start, Deary and his colleagues cast a wide net, imaging participants’ brains and examining genetics, lifestyles, health and social factors. “We were right to do so, because there is a large range of mostly small influences on people’s cognitive aging,” he says. But the fact that intelligence at age 11 can partially predict who will be sharp into their 90s suggests that a long-lasting brain must be solidly constructed.

One way in which the brain is built well involves its white matter — tracts of tissue that connect distant brain regions, allowing for quick communication. And in fact, members of the Lothian Birth Cohort with healthier white matter in old age, measured by an MRI-based brain scan method called diffusion tensor imaging, performed better on tests of brain function, Deary and colleagues found.

Mature neural highways take decades to develop. Brain areas are still solidifying into a person’s thirties. The later-blooming brain regions oversee jobs like impulse control and judgment, two well-known weak spots among teenagers.

These slow-to-grow brain networks are the first to go in old age, neuroscientist Gwenaëlle Douaud of the University of Oxford and colleagues found. Networks of nerve cells (the gray matter) are guided by a “last in, first out” rule, brain scans of 484 people from 8 to 85 years of age indicate. “What we show is a precise mirroring for these regions,” she says.

These networks, which reach their peak around age 39 for men and age 41 for women, handle sophisticated jobs, like merging multiple kinds of information together, she says. And sure enough, people with seemingly healthier neural connections had better memories, Douaud’s team reported in the Proceedings of the National Academy of Sciences in 2014.

Special no more
As neural connections come and go with age, brain cells themselves change in a way that harkens to the brain’s early days. Human brain cells are a dazzlingly diverse crew that handle a variety of jobs, from sending crucial signals to clearing out clutter. Yet these workers come from common ancestors that eventually specialize as the brain matures. In old age, some of these specialists seem to revert, becoming more similar to one another once again.
Cells are controlled by genes, but those genes don’t always behave the same way across a life span. Markers on cells’ DNA can dial activity up or down, controlling how much protein is made from a particular gene. In the case of brain cells, these epigenetic marks, many of which are laid down early in life in response to the environment, are one of the things that make nerve cells distinct from one another. So a nerve cell in the hippocampus, a structure important for memory, has an epigenetic fingerprint that’s distinct from that of a nerve cell in the cerebellum, a part of the brain important for movement.

But with age, these marks become less distinct, both between regions in a single brain and even among different people, Petronis says. After age 75, brain cells become more similar to one another, both in their epigenetic marks and their genes’ behaviors, he and colleagues reported April 28 in Genome Biology.

That was a big surprise, he says. It contradicts a popular concept called epigenetic drift, which says that with time, epigenetic stamps accumulate on cells, making the cells more distinct. But Petronis’ results suggest that once nerve cells hit a certain age, they begin to experience a different kind of drift, back toward sameness.

Petronis cautions that his results are preliminary and need to be reproduced. But he says they point to the link between development and aging. “Developmental epigenetic marks and aging epigenetic marks seem to be overlapping to some extent,” he says.

It’s not just nerve cells that show tendencies toward conformity in old age. Microglia do too, researchers recently found. These brain cells have multiple job descriptions, including fighting off pathogens, snipping unnecessary neural connections and hoovering up cellular debris. Microglia in different parts of the brain use their genes in specific ways — making more or fewer proteins as needed. This protein customization helps the microglia do their diverse jobs.

But this specificity diminishes with age. Microglia in the hippocampus actually become less diverse as mice get older, neuroscientist Barry McColl of the University of Edinburgh and colleagues reported in the March Nature Neuroscience. “It wasn’t something we were looking for at all,” McColl says.

The unexpected results hint that a slow loss of specialization might cause trouble during aging by hindering cells as they try to do their particular jobs, McColl says. “That’s the overriding — but quite speculative — theory we’ve got at the moment.”

Loss of specialization with age may happen not just in single brain cells, but in the networks they form. Any time a person sees, hears or feels something, the brain fires off a pattern of highly specific neural responses. Cognitive neuroscientist Bradley Buchsbaum of Baycrest Health Sciences in Toronto and colleagues wondered if elderly brains might lose the ability to form these sharp neural reflexes.

For Buchsbaum’s study, 28 adults — half young and half old — watched video clips while undergoing functional MRI brain scans, which detect changes in blood flow that represent the activity of big collections of nerve cells. As participants watched snippets of President Barack Obama giving a speech, a skateboarding dog and a meat slicer in action, their brains responded to the sights and sounds. Later, they were asked to remember the videos.

In people ages 21 to 32, each type of video evoked a specific and sharp neural fingerprint, both as people saw the videos for the first time and remembered them later. The sharper the fingerprint, the better the memory, the researchers reported in 2014 in the Journal of Neuroscience.

But in people 64 to 78, the neural signatures became fuzzy and less distinct, particularly when participants tried to remember the videos. Buchsbaum calls this fuzziness dedifferentiation. “In the beginning, you’ve got this blank slate,” he says. But along the way, brain areas diversify and connect in intricate ways. Dedifferentiation is an about-face toward that blank slate.
Other observations of the old brain seem to fit this idea. Language, for instance, is handled by the left side of the young adult brain. But in elderly people, both hemispheres are required to handle the job. And in older people, remembering can activate both sides of the frontal cortex, instead of just one as in younger people.

Some cognitive psychologists caution against making too much of these signs of generalization. Understanding spoken language is one of the tasks that scientists thought might become hazier in the brain with age. But when psychologist Karen Campbell of Harvard University and colleagues asked old people to simply listen to language while in a scanner, without any additional tests, the task elicited brain responses that looked similar to the specialized responses of younger people.

Campbell’s results, published May 11 in the Journal of Neuroscience, suggest that the extra work of experimental tests — and not the task itself — may take more brainpower in older people, an addition that may confound simple interpretations. Her results are “a challenge to other scientists,” she says. “Try a more natural approach.”

Snip early and snip late
Although scientists are still probing the relationship between brain construction and deconstruction, it’s becoming clear that the brain relies on some of the same tools for both jobs.

One of the most tantalizing finds has to do with microglia. The synaptic pruning that these cells do is crucial for a growing brain, shaping the tangle of new nerve cells into an efficient, elegantly connected information processor.

This snipping may happen late in life, too, and that may not be a good thing. Synapses in the hippocampi of mice and humans become sparser with age. But when mice were engineered to lack a protein that helps mark synapses for destruction, old mice no longer showed synapse thinning, neuro-scientist Cynthia Lemere of Brigham and Women’s Hospital in Boston and colleagues reported last year in the Journal of Neuroscience. These lucky mice with an abundance of synapses performed better on memory tests and learning, too.
Other recent results from neuroscientist Beth Stevens’ lab at Harvard hint that excessive synapse pruning may play a role in Alzheimer’s disease (SN: 4/30/16, p. 6) and schizophrenia, though what kicks off the pruning is a mystery. “One of the really big questions is what turns this pathway on in aging, or in Alzheimer’s or other diseases?” she says. “Are they the same kind of signals that we’ve identified in development, or could they be completely different?”

Finding those signals and other molecules in the body that could stall some of the brain’s aging processes might lead to better treatments for Alzheimer’s, schizophrenia or even the mental decline that comes with healthy aging.

But just because things appear to be similar doesn’t mean that they are the same thing, cautions neurologist Tony Wyss-Coray of Stanford University. Finding a developmental process that’s also at work during aging “doesn’t mean that we are triggering a developmental program,” he says. A protein that becomes active again later in life is not necessarily trying to restart development.

A lack of clarity on brain aging hasn’t stopped scientists from floating ideas for delaying the mental trouble that comes with age. One notion is to wipe out age-related epigenetic changes on brain cells, a concept called “epigenetic rejuvenation.” Scientists might be able to overwrite epigenetic changes using the same cellular tools that manage those marks.

Other researchers are looking to the blood for answers. Wyss-Coray and others have turned up tantalizing evidence that some mysterious contents in young blood can rejuvenate the older brain. Young blood spurred more neural connections and stimulated the birth of newborn nerve cells in mice. The brain changes came with better memory and a sharpened sense of smell (SN: 5/31/14, p. 8). The researchers are trying to figure out which blood components led to the improvements, described in Nature Medicine in 2014, and are testing whether plasma from young people can help the brains of older people with Alzheimer’s disease.

Given the parallels emerging between development and aging, these approaches that borrow from youth to stave off decrepitude start to make sense. “Sometimes things start converging,” Petronis says, “and it’s very interesting to see that process.”

It now appears that women can pass Zika virus to men through sex.

U.S. health officials have reported the first known case of female-to-male sexual transmission of Zika virus. The woman, who was not pregnant, had traveled to a Zika-afflicted region, the U.S. Centers of Disease Control and Prevention reports July 15. On the day of her return to New York City, she had vaginal intercourse with a male partner, who wasn’t wearing a condom.

Three days later, after developing a rash, fever and other symptoms, doctors detected Zika virus RNA in her blood and urine. A week after sex, the woman’s partner, who had not recently traveled outside the United States and had not noticed any mosquito bites, developed similar symptoms. Tests revealed that he also had Zika RNA in his urine.

Scientists knew that men could transmit Zika to women through sex, and had hints that reverse was true as well. Earlier this month, researchers detected Zika RNA in the genital tract of an infected woman.

Clones don’t age prematurely, new research on Dolly the Sheep’s sisters suggests.

Researchers and animal welfare activists have been concerned that cloning, or somatic cell nuclear transfer, could cause health problems in cloned animals. Instead, a study of 13 cloned sheep found no signs of early aging or other health problems, researchers report July 26 in Nature Communications.

“These animals were remarkably healthy and fall within the normal range that we’d expect in animals of this age,” said developmental biologist Kevin Sinclair of the University of Nottingham in Leicestershire, England. Sinclair spoke July 25 during a news conference at the EuroScience Open Forum in Manchester, England.
The cloning technique places the DNA-containing nucleus of an adult cell into an egg where the DNA is reprogrammed to an embryonic state. Dolly the Sheep, born in 1996, was the first mammal ever cloned. Since then, researchers have cloned a wide variety of animals. The technique doesn’t always work and many potential clones die before birth or shortly after. Surviving animals might have problems because of incomplete reprogramming of the DNA.

Dolly herself gave rise to the idea that clones age fast. Compared with other animals her age, Dolly had shorter telomeres, the caps that protect the ends of chromosomes from unraveling. Short telomeres have been associated with aging. Plus, Dolly had severe arthritis. She died at age 6, although not of old age. Dolly and other sheep in her flock were infected with a virus that killed them (SN: 3/1/03, p. 141).

Her untimely death, arthritis and short telomeres “were mushed together in people’s perception,” leading to the idea that clones age prematurely, said Katrin Hinrichs, a reproductive physiologist at Texas A&M University College of Veterinary Medicine and Biomedical Sciences in College Station. Hinrichs and other researchers not involved in the study hope the new report corrects the record on cloning and aging. “Now we have a reference to say what is and what is not a result of cloning,” she says.

How fast animals age varies, even among nonclones, says reproductive biologist Mark Westhusin, also of Texas A&M. Westhusin was on the team that produced cc (short for Carbon Copy), the first cloned cat (SN: 3/23/02, p. 189). She is now 15 and doing fine, says Westhusin. “This is a nice paper to confirm in a more formal scientific setting what most people involved with cloning have believed for a long time,” he says. Some studies have even hinted that clones may live longer than conventionally bred animals (SN: 4/29/00, p. 279).

In the study, Sinclair and colleagues examined 13 cloned sheep from 7 to 9 years old (roughly equivalent to people in their 50s to 70s). Four of the sheep — Debbie, Denise, Dianna and Daisy — were cloned in 2007 from the same mammary gland tissue that produced Dolly. “We had four almost identical sisters to Dolly and thought this would be a great chance to revisit this,” Sinclair said. He and colleagues compared the Dolly the Sheep sisters and nine clones of other sheep with 5- to 6-year-old sheep bred by traditional means.
Cloned sheep had normal blood sugar, insulin levels and blood pressure. A few had mild arthritis. One of Dolly’s sister clones had moderate arthritis. The researchers have not yet measured the clones’ telomeres.

Sheep in this study were cloned with modifications to the original technique that may have produced a better outcome. But Dolly’s problems didn’t necessarily stem from being a clone. She may have developed arthritis as a result of trauma to her joints. It’s also not clear whether her short telomeres were really an indicator of premature aging. Certainly her death had nothing to do with being a clone; noncloned animals in her flock also died, researchers say. Overall, Sinclair said, “perhaps Dolly was a little less lucky.”

Cloning today is done mostly in South America and Asia, and infrequently in the United States, says Hinrichs. Polo ponies and cattle are among the most-cloned animals. “Cloning is so costly and inefficient that your animal has to be very special for a cloning to be worth it,” she says. As a result, most cloned animals are prized breeding stock or performance animals. Some animals that are genetically resistant to diseases are also cloned for veterinary and medical research.

When the brain runs low on oxygen, red blood cells sense the deficit and hurl themselves through capillaries to deliver their cargo. That reaction, described online August 4 in Neuron, suggests that red blood cells can both detect and remedy low oxygen.

When researchers stimulated the feet of mice, nerve cells fired off signals in the corresponding part of the brain, depleting that area’s oxygen. Red blood cells in capillaries picked up their speed in response. And in artificial capillaries, the lower the oxygen, the faster the red blood cells moved, Jiandi Wan of the Rochester Institute of Technology in New York and colleagues found. That swiftness was caused by the cells becoming more flexible, a bendiness that let them squeeze through narrow capillaries faster. When researchers stiffened red blood cells with a chemical, the effect of low oxygen on speed disappeared.

The results reinforce the complex and important role of blood in the brain. The findings might ultimately be relevant for disorders in which the link between neural activity and blood flow is damaged, including Alzheimer’s disease, says study coauthor Maiken Nedergaard of the University of Rochester Medical Center.

The annual Perseid meteor shower, which peaks on the morning of August 12, might be more dazzling than usual this year. Researchers predict that up to 200 meteors per hour could race across the sky — roughly double the typical rate — as Earth plows through debris left behind by comet 109P/Swift-Tuttle.

Earth usually grazes the edge of the debris stream, home to pieces that flake off the comet during its 133-year journey around the sun. But this year Jupiter’s gravity might have nudged the debris so that Earth passes closer to the center of the swarm.

While the shower peaks tonight, Perseid meteors will be visible for at least two more nights. No special equipment is needed to watch the shower. Just find a dark sky, away from lights, get comfortable and look up. The best time to watch the storm will be between midnight and dawn.

When someone uses the phrase “sleeping like a baby,” it’s obvious that they don’t really know how babies sleep. Many babies, especially newborns, are lousy sleepers, waking up every few hours to rustle around, cry and eat. For creatures who sleep up to 18 hours per 24-hour period, newborns are exhausting.

That means that bone-tired parents are often desperate to get their babies to sleep so they can rest too. A study published in the September Pediatrics captured this nightly struggle in the homes of 162 Pennsylvanian families. And the results revealed something disturbing: Despite knowing that they were being videotaped, many parents didn’t put their babies into a safe sleeping spot.

The risk of sleep-related infant deaths, including those caused by strangulation or sudden infant death syndrome, goes up when babies are put in unsafe sleeping positions or near suffocation hazards. Babies should be on their back on a firm mattress free of any objects. But that wasn’t the case for the majority of babies in the study, says Ian Paul, a pediatrician at Penn State.

As a parent to three, Paul is sympathetic to the difficulties of soothing babies to sleep. “The first few months are really exhausting,” he says. But as a pediatrician, he also sees the risks of ignoring safe sleep guidelines. “Parents need to realize that these risks are real and might happen to them.”

The videos taken for the study revealed that at 1 month of age, nearly all of the babies were put onto a sleep surface that had a loose or ill-advised item. Some of those objects aren’t surprising: Loose blankets, pillows, stuffed animals, crib bumpers and a SIDS monitor turned up in babies’ sleep areas. “The fact that almost every baby had loose bedding in the crib was disturbing,” Paul says. Stranger objects, such as cords, electrical wires and even a pet, were also observed.

Some of these items, such as sleep positioners and the soft bumpers that run around crib rails, are sold at baby stores. “If they’re selling it, parents think it is safe,” Paul says. “That’s just not the case.” Despite public health messages, babies are still suffocating on bumpers or getting trapped between bumpers and their mattress. There are no federal rules against crib bumpers, but several areas have banned them.

The study also spotted lots of bed hopping. Often, babies would start the night in a safe crib, but by the morning, they’d be in a more dangerous place, such as a bed full of pillows with a parent. The nightly shifts usually went from safe to unsafe as tired parents moved their babies around, Paul and colleagues found.

Paul recommends that parents create a safe place right next to their own beds for their babies to sleep, such as a bassinet or playpen. By designing their environment to encourage good habits at night, tired parents may be more likely to put the baby into a safe spot.

In a macabre twist, the hominid evolutionary tree’s most famous fossil star, Lucy, tumbled to her death from high up in a tree, a controversial new study suggests.

Some of the damage to Lucy’s 3.2-million-year-old partial skeleton most likely occurred when she fell from a height of 13 meters or more, say paleoanthropologist John Kappelman of the University of Texas at Austin and his colleagues. Lucy, an ancient ambassador of a prehuman species called Australopithecus afarensis, must have accidentally plunged from a tree while climbing or sleeping, the scientists propose online August 29 in Nature.
Bone breaks from head to ankle fit a scenario in which Lucy dropped the equivalent of least four to five stories, landing feet first before thrusting her arms out in an attempt to break her fall, Kappelman says. Tellingly, the ancient female’s right shoulder blade slammed into the top of her upper arm bone, Kappelman says. The shoulder end of Lucy’s arm bone displays sharp breaks, as well as bone fragments and slivers forcibly driven into the shaft.
Such damage frequently appears in present-day people who fall from great heights or are in serious car accidents, Kappelman says. Massive internal bleeding typically follows a body slam as hard as Lucy’s, he adds.

“Lucy probably bled out pretty fast after falling,” Kappelman says.
Nonsense, responds paleoanthropologist Tim White of the University of California, Berkeley. He calls the new paper “a classic example of paleoanthropological storytelling being used as clickbait for a commercial journal eager for media coverage.”

Cracks and breaks throughout Lucy’s skeleton occurred after her death, White asserts. Bone cracking was caused by fossilization and by pressure on fossils embedded in eroding sandstone. Fossilization-related breakage much like Lucy’s — including extensive shoulder-joint damage — appears on the bones of a variety of nonclimbing animals, including gazelles, hippos and rhinos, White says.
When people accidentally fall from heights between two and 21 meters, he adds, physicians have documented frequent fractures of the spine, head, elbows, wrists, ankles and feet — but not the shoulders.

Scientists have been unable to decipher how Lucy died since her 1974 discovery in Ethiopia by anthropologist Donald Johanson of Arizona State University in Tempe and his graduate student at that time, Tom Gray. A Johanson-led team, which included White, attributed Lucy’s bone damage primarily to fossilization in a 1982 report.

Intrigued by extensive crushing and breakage at Lucy’s right shoulder joint, Kappelman consulted orthopedic surgeon and study coauthor Stephen Pearce of the Austin Bone and Joint Clinic. When shown a 3-D printed model of Lucy’s skeleton enlarged to the size of a modern human adult (Lucy stood only about 107 centimeters tall, or 3 feet, 6 inches), Pearce said the arm damage looked like that caused by an individual extending an arm to break a steep fall.

Kappelman and colleagues then scoured high-resolution CT scans of Lucy’s bones obtained in 2008, when the ancient skeleton was brought to the University of Texas during a U.S. museum tour.

Along with the upper right arm bone and shoulder blade, damage consistent with hitting the ground after a long fall appeared in bones from an ankle, legs, pelvis, lower back, ribs, jaw and braincase, the researchers say. Fossilization and geological forces caused additional cracking and breaks on Lucy’s remains, as described in the 1982 report, they add.
Although initially skeptical that cause of death could be discerned in a fossil individual as old as Lucy, paleoanthropologist William Jungers of the Stony Brook University Medical Center in New York says the evidence indeed points to a fatal fall. No other explanation can account for Lucy’s pattern of bone damage, he says.

If Lucy toppled out of a tree while climbing or snoozing in a nest, her kind must have split time between life on the ground and in trees, Kappelman says. Some researchers have long argued that A. afarensis was built mainly for walking (SN: 12/1/12, p. 16).

Even today, Jungers says, deaths from accidental falls out of trees occur among some African hunter-gatherers, especially when raiding bee’s nests for honey (SN: 8/20/16, p. 10), and in wild chimps, animals more adept at tree climbing than Lucy was.

Lucy’s species could climb trees, White says, but “we do not know how often, or whether for shelter or food.”

For bacteria, practice makes perfect: Adjusting to ever higher levels of antibiotics preps them to morph into super resistant strains, and scientists can now watch it happen. A new device — a huge petri dish coated with different concentrations of antibiotics — makes this normally hidden process visible, microbiologist Michael Baym and colleagues report in the Sept. 9 Science. The setup gives a step-by-step picture of how garden-variety microbes become antibiotic-resistant superbugs.

“As someone who’s studied evolutionary biology for a long time, I think it has a real wow factor,” says Sam Brown, a microbiologist at the Georgia Institute of Technology in Atlanta who wasn’t involved in the study. The bacteria are “climbing this impossible mountain of antibiotics.”
Scientists often study microbial evolution in flasks where everything is mixed together. “Inside that flask, in order for a new strain to evolve, the new mutant has to be more fit than everything around it,” says Baym, of Harvard Medical School. “But in nature, we see a second dynamic: You don’t necessarily need to be more fit than everything around you. You just need to make it into a new environment.”

Baym and colleagues modeled those spatial dynamics using a giant dish more than a meter long instead of a standard palm-sized petri dish. That gave the bacteria more room to diversify and also let the researchers create a gradient of antibiotics on the plate. Low concentrations of trimethoprim or ciprofloxacin antibiotics at the edges ramped up to much higher levels in the middle. Then, the team put Escherichia coli bacteria on each end of the plate and watched the microbes multiply over the next week and a half.

In general, as the E. coli mutated in ways that let them handle higher and higher levels of antibiotics, their descendants could press into new territory on the plate. The bacteria that made it to the middle could tolerate doses of antibiotics a thousand times higher than what was necessary to kill the original bacteria.

But antibiotic resistance didn’t always make bacteria competitive colonizers. Highly resistant bacteria sometimes spread more slowly. Trapped in the back by faster-moving bacteria at the forefront, the stragglers’ descendants formed pockets of super-resistance at lower antibiotic concentrations.
Baym and his colleagues think the experimental setup could be used to study microbial evolution under other environmental and spatial constraints, like the availability of particular nutrients.

As chief scientist for a voyage of the research vessel Endeavor, oceanographer Melissa Omand oversaw everything from the deployment of robotic submarines to crew-member bunk assignments. The November 2015 expedition 150 kilometers off Rhode Island’s coast was collecting data for Omand’s ongoing investigations of the fate of carbon dioxide soaked up by the ocean.

But Omand, an assistant professor at the University of Rhode Island’s campus in Narragansett, wasn’t on the ship. Instead of riding the waves with her crew, she was working, sometimes 16-hour days, inside a dark room at the university’s Inner Space Center — staring at computer monitors in a sort of NASA mission control for oceanographers. When she submitted the trip proposal a year earlier, she hadn’t foreseen that she’d be eight months pregnant with her first child when the ship set sail.
Still, missing the trip was unthinkable, she says. The Inner Space Center, she realized, offered a way to direct the mission from shore via satellite. After proposing the solution to her higher-ups, and a lot of meetings that followed, she got permission to be the first chief scientist to remotely lead an Endeavor cruise.

“She doesn’t let many obstacles get in her way,” says Colleen Durkin, an oceanographer at Moss Landing Marine Laboratories in California, who participated in the cruise. “That’s one of the fun things about working with her. She’s willing to try new things.”
Her commitment to her science and her drive to find creative solutions are helping Omand tackle a big problem in oceanography. For a decade, she has been studying the mechanisms — such as currents and the dining and dying of microorganisms — that move carbon and nutrients through the ocean. In a breakout paper, published last year in Science, she reported the discovery that eddies can pull carbon from phytoplankton deep into the ocean, a previously undescribed phenomenon. Studying the fate of that carbon isn’t just interesting, she says, it’s vital to predicting the fate of our climate. “The ocean has a huge capacity to absorb excess carbon dioxide in our atmosphere,” Omand says. But as the planet warms, atmosphere and ocean might interact differently. Scientists need all the information they can get to figure out how to adapt to those changing conditions and mitigate the effects of climate change.

Omand, 36, first got her feet wet on the rivers and lakes surrounding her hometown of Toronto. In her teens, she worked as a canoe guide, exploring the region’s waterways. “That was absolutely the root of my interest in earth science and environmental issues,” she says. “I’m essentially doing the same thing now, just on a much bigger boat.”

After starting off as a premed student at the University of Guelph in Canada, she was ultimately drawn to the university’s physics program. “I found it very satisfying that all these problems boiled down to a few underlying rules and equations,” she says. During her undergraduate studies, her focus was millions and millions of kilometers away from Earth’s oceans. She coded software used to help calibrate X-ray instruments on NASA’s Mars Exploration Rovers, which identified the makeup of Martian rocks.
While considering areas of physics for her graduate studies, Omand received an email that altered her heading. Chris Garrett, a professor (now emeritus) at Canada’s University of Victoria, introduced her to physical oceanography. “He showed me demonstrations of what happens to dye in a rotating water tank,” she recalls. “I was hooked by that.” The churning of water appealed to Omand for the same reason the field of physics did: Whether in tanks or oceans, the water’s movements can be expressed by a set of specific equations, called the Navier-Stokes equations.

Omand has applied these equations in much of her work. During a Ph.D. at the Scripps Institution of Oceanography in La Jolla, Calif., she and colleagues studied the origins of a red tide off California’s coast. The team found that the red tide, fertilized by a layer of nutrients, had been festering under the ocean surface for a week before being drawn upward. Omand and her colleagues used a Jet Ski modified with a GPS system and scientific instruments to collect data. Later, as a postdoctoral researcher at Woods Hole Oceanographic Institution in Massachusetts, she and mentor Amala Mahadevan investigated mechanisms to explain how nitrogen, an important nutrient for phytoplankton, moves around below the sunlit layer of the sea.

During her time at Woods Hole, Omand also started tracking the journey of CO2 taken in by springtime algae blooms in the North Atlantic.
When the phytoplankton in these colossal blooms, which can stretch hundreds of kilometers across, die or are digested by other marine life, particles containing organic carbon are released into the water. The heavier of these particles sink, quarantining the carbon from the atmosphere. About 30 percent of all CO2 emitted by human activities has ended up in the oceans, thanks in part to these sinking particles.

Scientists had believed that smaller particles would remain near the surface. But with robotic submarines called gliders that cruised up and down the water column sensing light scattered by the particles, Omand and colleagues found a surprisingly large amount of small carbon particles. These particles were around 100 to 350 meters deep, in the ocean’s “twilight zone,” where phytoplankton rarely live.
Omand combined measurements such as temperature and salinity from several gliders to explain how the particles got pulled so far down. By analyzing those measurements alongside computer simulations and satellite data — an innovative mix of sources that provided finer details and the bigger picture — she showed that the carbon-rich particles were carried down by spiraling ocean currents called eddies. Water escaping these bowl-shaped depressions can become sandwiched between deeper ocean layers, remaining trapped along with any particles even once an eddy subsides.

The accompanying carbon drain cools the Earth, says Eric D’Asaro, an oceanographer at the University of Washington in Seattle who collaborated with Omand on the research. Though the finding doesn’t change the total amount of carbon known to be taken in, the study identifies a new mechanism that could account for as much as half of all carbon known to be pulled into the deep North Atlantic during spring. The mechanism could also play a role elsewhere in the world’s oceans, D’Asaro, Omand and colleagues reported in April 2015 in Science.

“Her work sets the table for the next decade in terms of understanding the interaction between the turbulence of the ocean and how carbon is injected down to depth,” says David Siegel, an oceanographer from the University of California, Santa Barbara. “She’s going to be one of the new leaders of this field.”

Now a mother — her daughter was born a few weeks after the cruise — and an assistant professor at the University of Rhode Island, Omand continues her creative problem-solving, often by calling on unexpected technology. On a research trip in June (she was on the ship this time), Omand used an iPhone in a waterproof case to automatically snap pictures every half hour of particles raining down from the ocean’s top layer. Scientists previously measured the rates of sinking particles with traps that provided no information about how the rates changed throughout the day. Omand got the idea to affix her old iPhone to the traps after being offered only $40 for the used phone. “There’s got to be something really amazing I can do with this,” she thought.

Next spring, Omand will harness the same telepresence software she used for the 2015 Endeavor trip to virtually take undergraduate students on board. Omand’s ability to harness technology to solve tricky scientific challenges is a big reason why she can identify new truths about our oceans, says Mahadevan. “Every problem she touches,” Mahadevan says, “something beautiful comes out.”