November 27, 2013
When we think of ants as builders, we normally imagine them digging intricate tunnel networks as part of underground colonies.
But David Hu, Nathan Mlot and a team of other researchers at Georgia Tech are studying a very different type of building behavior specific to one ant species: The ability of Solenopsis invicta to construct bridges, rafts and even temporary shelters using their own bodies as building material.
“Fire ants are capable of building what we call ‘self-aggregations,’” Hu says. “They can build little boats, little houses called bivouacs and even bridges to cross streams by being the building material, linking their bodies together and forming strong networks.”
The ants are now considered an invasive species in 25 states, Asia and Australia, but their unusual behavior is a survival strategy shaped by their native environment: a particular area of wetlands in western Brazil that are flooded frequently. “The ants live underground, but when it begins to flood, they have to gather the colony members, pull them out of the ground and build a floating raft,” Hu says.
When this raft hits land, the ants keep building. To cross small streams during their subsequent migration, they make living bridges that allow the entire colony to scramble to safety. Afterward, using their bodies, they construct a temporary aboveground encampment to provide shelter for the few days it takes to re-dig underground tunnels. All the while, the ants that form the temporary shelter are continuously moving, but still preserving the structure. “It’s really living architecture—it has well-constructed, organized tunnels, brooding rooms,” Hu says. At least for the ants in the inside, this provides protection against hostile weather or predators.
Hu, an engineer, is primarily interested in studying the swarming ants as a novel material with unprecedented characteristics. As part of his group’s recent research, presented yesterday at an annual meeting of the American Physical Society, he and colleagues considered the ants within the context of other “active materials”—substances that can respond to changing conditions, such as self-healing cements that can use the energy in sunlight to expand and fill their own fractures.
“We wanted to characterize what kind of material it is—is it a fluid, or is it a solid, and how does it respond to stress?” he says. “In nature, for instance, these rafts might float down a river and bump into rocks, or raindrops might hit them.”
To test these self-aggregations, Hu’s team used a few techniques, comparing live ant structures to clumped dead ants as a control. Using a rheometer—a device that can precisely measure the stress response and flow of a fluid, and is often applied in industrial situations (such as the development of a new shampoo)—they found that the ants continuously reorganize their structure to maintain stability.
Many materials behave like a solid when stressed by forces moving at certain speeds, and a fluid when stressed by slowed ones. Water, for instance, behaves like a fluid when you stick your hand in it, but a solid when hit by a human body jumping off a diving board—the reason that a belly flop hurts so much.
But the ant structures are a combination of solid and fluid when stressed by forces at all speeds, the researchers found. They actively deform their structure to accommodate a stress (like a fluid) but then bounce back into place afterward (like a solid). Check out what happens when one of their structures is compressed by a petri dish, for instance:
“This makes sense, based on their natural environment,” Hu says. “If they’re floating in a raft down a river, they have no control over where it floats, so if there’s something in the way—say, a twig—you see respond and flow around the twig, kind of like an amoeba.”
The ants’ sheer resiliency and buoyancy is also remarkable. When the researchers tried to push the floating rafts below the water’s surface, they found they could resist a significant amount of force and float back up:
This is enabled, in part, by the ants’ exoskeletons, which are naturally hydrophobic (i.e. they chemically repel water). When many ants clump together to form a structure, water doesn’t penetrate into the gaps between then, so when they’re forced underwater, the air that remains in these cavities helps them float.
Perhaps the biggest mystery of these ants’ remarkable living structures is how the creatures communicate to build them. Most ant communication is based on trails of pheromones left on the ground, but in such an interconnected form, that type of communication seems unlikely. Microscopic examination reveals that the ants grasp each other using both their jaws and little claws on the end of their legs. Noting this, Hu adds, ”We think they’re communicating through touch, but we really don’t understand it yet.”
November 25, 2013
Once upon a time, scientists thought that the human brain was a rigid, predictable organ, not tremendously different from the lungs or liver. Based on a person’s genetics, it developed in a predetermined way, endowing an individual with a particular level of learning capabilities, problem-solving abilities and baseline intelligence.
Now, though, as part of emerging research into brain plasticity, neuroscientists are recognizing that the brain is a responsive, constantly evolving organ that can change at both the cellular and large-scale levels due to environmental influences and experiences. Much of this research is hopeful: It’s shown how in people with impaired vision, for instance, areas of the brain normally devoted to processing sights can be repurposed to analyze sound.
Over the past few months, though, a series of studies have emphasized that the brain can change for worse, as well as for the better. A child’s brain, not surprisingly, is especially vulnerable to such effects—and this research has shown that growing up in difficult circumstances dictated by poverty can wreak damage to a child’s cognitive skills that last a lifetime.
An October study by researchers from the University of Michigan, for instance, used fMRI (functional magnetic resonance imaging)—which detects blood flow in various areas of the brain as a reflection of brain activity—to study the regulation of emotions in young adults who were part of a long-term study on poverty. They compared a participant’s family income at age 9 (based on survey data collected at the time) with his or her current neural activity in different brain regions, and found that those who grew up in poverty showed increased activity in the amygdala (believed to be involved in anxiety, fear and emotional disorders) and decreased activity in the prefrontal cortex (which limits the influence of the amygdala, putting long-term decision making over impulse) when the participants were shown emotionally-upsetting images.
It’s impossible to know for sure, but the researchers suspect that a range of chronic stresses that can accompany growing up in poverty—things like crowding, noise, violence, family turmoil or separation—impact the development of the brain in childhood and adolescence, potentially explaining this correlation.
Another October study, meanwhile, took a more basic approach, examining the relationship between nurturing during childhood and the growth of brain tissue in children between the ages of six and 12. In it, Washington University in St. Louis researchers found that among the 145 children studied, those whose parents had poor nurturing skills had slowed growth in white matter, grey matter and the volumes of several different areas of the brain involved with learning skills and coping with stress. Based on the differing growth rates between children who resembled each other in terms of other key factors, it seemed as though the experience of growing up with adults with less nurturing skills effectively set back their mental development a year or two. And impoverished parents, they found, were more likely to have poor nurturing skills.
Sure, attempting to objectively evaluate the parenting styles of the adults in this study might be a bit heavy-handed, but the study identified chronic stresses experienced by the children as a key element as well: Children who grew up in poverty but had fewer stressful life events (as part of a larger program, they’d gone through annual assessments from the age of three onward) demonstrated smaller reductions in neural development.
Others have even looked into very specific behavioral effects of poverty. A recent Northwestern University study found a link that children with lower socioeconomic status tended to have less efficient auditory processing abilities—that is, the area of their brains responsible for processing sound showed more response to distracting noise and less activity as a result of a speaker’s voice than control participants. This might be an effect, the researchers say, of the known correlation between low income and the amount of noise exposure in urban populations.
Of course, most of these are limited by the very nature of a longitudinal study in that they’re correlations, rather than causations—ethics aside, it’s impossible to actively alter a person’s childhood circumstances in a controlled manner and then check the results, so researchers are forced to observe what happens in the real world and draw conclusions. Additionally, in most of these cases, it’s unknown whether the effects are temporary or permanent—whether children exposed to poverty are permanently left behind their peers, or whether they’re able to catch up if given the chance.
But the fact that correlations between poverty and altered mental function when stressed has been repeatedly observed across a range of study designs, circumstances and research groups makes it likely that these effects aren’t aberrations. Additionally, even if they are temporary effects that can be resolved by changing a child’s environment, there’s other recent research that dishearteningly reveals a neurological mechanism that helps to perpetuate poverty, by making it difficult for parent to make choices that change these circumstances.
An August study in Science found that being preoccupied with the all-consuming concerns of poverty—struggling to pay medical bills, for instance—taxes the brain, leaving less extra bandwidth to solve complex cognitive problems and harming long-term decision making ability. In a pair of study groups (shoppers in a New Jersey mall and sugar cane farmers in rural India), simply getting the participants thinking about economic problems (asking them what they’d do if they had to pay $1500 to repair their car, for instance) caused them to perform more poorly on tests that measure IQ and impulse control than otherwise.
The bandwidth problem they identified is temporary, not permanent, but it does explain how making the difficult decisions that might allow someone to get ahead are harder for a person immersed in poverty. It also highlights yet another stressor for parents seeking to ensure that their children escape poverty—they might be inadvertently contributing to an environment that keeps their children from rising above their circumstances.
November 21, 2013
Over the course of 1700 miles, they sampled the water for small pieces of plastic more than 100 times. Every single time, they found a high concentration of tiny plastic particles. “It doesn’t look like a garbage dump. It looks like beautiful ocean,” Miriam Goldstein, the chief scientist of the vessel sent by Scripps Institution of Oceanography, said afterward. “But then when you put the nets in the water, you see all the little pieces.”
In the years since, a lot of public attention has been justifiably paid to the physical effects of this debris on animals’ bodies. Nearly all of the dead albatrosses sampled on Midway island, for instance, were found to have stomachs filled with plastic objects that likely killed them.
But surprisingly little attention has been paid to the more insidious chemical consequences of this plastic on food webs—including our own. “We’d look over the bow of the boat and try to count how many visible pieces of plastic were there, but eventually, we got to the point that there were so many pieces that we simply couldn’t count them,” says Chelsea Rochman, who was aboard the expedition’s Scripps vessel and is now a PhD student at San Diego State University. “And one time, I was standing there and thinking about how they’re small enough that many organisms can eat them, and the toxins in them, and at that point I suddenly got goosebumps and had to sit down.”
“This problem is completely different from how it’s portrayed,” she remembers thinking. “And, from my perspective, potentially much worse.”
In the years since, Rochman has shown how plastics can absorb dangerous water-borne toxins, such as industrial byproducts like PCB (a coolant) and PBDE (a flame retardant). Consequently, even plastics that contain no toxic substances themselves, such as polyethylene—the most widely used plastic, found in packaging and tons of other products—can serve as a medium for poisons to coalesce from the marine environment.
But what happens to these toxin-saturated plastics when they’re eaten by small fish? In a study published today in Scientific Reports, Rochman and colleagues fill in the picture, showing that the toxins readily transfer to small fish through plastics they ingest and cause liver stress.This is an unsettling development, given that we already know such pollutants concentrate further the more you move up the food chain, from these fish to the larger predatory fish that we eat on a regular basis.
In the study, researchers soaked small pellets of polyethylene in the waters of San Diego Bay for three months, then tested them and discovered that they’d absorbed toxins leached into the water from nearby industrial and military activities. Next, they put the pollution-soaked pellets in tanks (at concentrations lower than those found in the Great Pacific garbage patch) with a small, roughly one-inch-long species called Japanese rice fish. As a control, they also exposed some of the fish to virgin plastic pellets that hadn’t marinated in the Bay, and a third group of fish got no plastic in their tanks at all.
Researchers still aren’t sure why, but many small fish species will eat these sort of small plastic particles—perhaps because, when covered in bacteria, they resemble food, or perhaps because the fish simply aren’t very selective about what they put in their mouths. In either case, over the course of two months, the fish in the experiment consumed many plastic particles, and their health suffered as a result.
“We saw significantly greater concentrations of many toxic chemicals in the fish that were fed the plastic that had been in the ocean, compared to the fish that got either clean plastic or no plastic at all,” Rochman says. “So, is plastic a vector for these chemicals to transfer to fish or to our food chain? We’re now fairly confident that the answer is yes.”
These chemicals, of course, directly affected the fishes’ health. When the researchers examined the tiny creatures’ livers (which filter out toxins in the blood) they found that the animals exposed to the San Diego Bay-soaked plastic had significantly more indications of physiological stress: 74 percent showed severe depletion of glycogen, an energy store (compared to 46 percent of fish who’d eaten virgin plastic and zero percent of those not exposed to plastic), and 11 percent exhibited widespread death of individual liver cells. By contrast, the fish in the other treatments showed no widespread death of liver cells. One particular plastic-fed fish had even developed a liver tumor during the experimental period.
All this is bad news for the entire food webs that rest upon these small fish, which include us. “If these small fish are eating the plastic directly and getting exposed to these chemicals, and then a bigger fish comes up and eat five of them, they’re getting five times the dose, and then the next fish—say, a tuna—eats five of those and they have twenty-five times the dose,” Rochman explains. “This is called biomagnification, and it’s very well-known and well-understood.”
This is the same reason why the EPA advises people to limit their consumption of large predatory fish like tuna. Plastic pollution, whether found in high concentrations in the Great Pacific garbage patch or in the waters surrounding any coastal city, appears to be central to the problem, serving as a vehicle that carries toxins into the food chain in the first place.
November 20, 2013
About a month ago, I suffered my first-ever concussion, when I was (accidentally) kicked in the head playing ultimate frisbee. Over the next few weeks, I dutifully followed medical instructions to avoid intense physical activity. For a little while, I noticed a bit of mental fogginess—I had trouble remembering words and staying focused—but eventually, these symptoms faded away, and I now feel essentially the same as before.
Except, it turns out, that if doctors were to look inside my head using a type of brain scanning technology called diffusion MRI, there’s a good chance that they’d notice lingering abnormalities in the gray matter of my left prefrontal cortex. These abnormalities, in fact, could persist up to four months after the injury, even after my behavioral symptoms are long gone. This news, from a study published today in the journal Neurology, underlines just how much more prolonged and complex the healing process from even a mild concussion is than we’ve previously thought.
“These results suggest that there are potentially two different modes of recovery for concussion, with the memory, thinking and behavioral symptoms improving more quickly than the physiological injuries in the brain,” Andrew R. Mayer, a neuroscientist at the University of New Mexico and lead author of the study, explained in a press statement issued with the paper.
The abnormalities that Mayer’s team detected, they say, are so subtle that they can’t be detected by standard MRI or CT scans. Instead, they found them using the diffusion MRI technology, which measures the movement of molecules (mostly water) through different areas of the brain, reflecting the tissue’s underlying architecture and structure.
Mayer and colleagues performed these scans on 26 people who’d suffered mild concussions four months earlier, in addition to scanning them 14 days after the injuries. They also gave them behavioral and memory tests at both times, and then compared all the results to 26 healthy participants.
In the initial round, the people with concussions performed slightly worse than the healthy participants on tests that measure memory and attention, consistent with prior findings on concussions. Using the diffusion MRI, the researchers also found structural changes in the prefrontal cortex of both hemispheres of the subjects with recent concussions.
Four months later, the behavioral tests showed that the gap between the two groups had significantly narrowed, and the concussion patients’ self-reported symptoms were less significant too. But interestingly, when they averaged the scans of all 26 people, the neurological changes were still detectable in the left hemisphere of their brains.
What were these abnormalities? Specifically, their gray matter—the squishy outer layer of brain tissue in the cortex—showed ten percent more fractional anisotrophy (FA) than the controls’. This value is a measure of how likely water molecules located in this area are to travel in one direction, along the same axis, rather than scattering in all directions. It’s believed to reflect the density and thickness of neurons: the thicker and denser these brain cells are, the more likely water molecules are to flow in the direction of the cells’ fibers.
In other words, in this one particular area of the brain, people who’d suffered concussions four months earlier may have denser, thicker neurons than before. But it’s hard to say what these abnormalities reflect, and if they’re even a bad thing. As I found during my semi-obsessive post-concussion research, there are bigger gaps in scientists’ understanding of the brain than any other part of our bodies, and knowledge of the healing process after a concussion is no exception.
The scientists speculate that the increased FA could be a lingering effect of edema (the accumulation of fluid with the brain as a result of concussion) or gliosis (a change in the shape of the brain’s structural cells, rather than neurons).
But it’s even possible that this increased FA could be a sign of healing. A 2012 study found that in people who’d suffered mild concussions, higher FA scores right after the injury were correlated with fewer post-concussive symptoms, such as memory loss, a year after the injury. Similarly, a study published this past summer found a correlation between low FA scores and the incidence of severe symptoms right after a concussion. Interestingly, the researchers noted similar correlations in studies of Alzheimer’s—people with the disease tend to also demonstrate lower FA scores, in the same areas of the brain as those with most severe concussions, underscoring the link to memory performance.
If that’s the case, then the thicker, denser neurons in the brain of people with concussions might be something like the tough scabs that form after your skin gets burned, scabs that linger long after the pain has dissipated. As Mayer points out, during the recovery process after a burn “reported symptoms like pain are greatly reduced before the body is finished healing, when the tissue scabs.” In a similar way, the symptoms of a concussion—memory loss and difficulty maintaining attention, for instance—may disappear after a few weeks, while the nerve tissue continues forming its own type of scab four months later.
It’s possible that this scab, though, might be vulnerable. Scientific research is increasingly revealing just how devastating the impact of repeated concussions—the type suffered by football players—can be in the long term. “These findings may have important implications about when it is truly safe to resume physical activities that could produce a second concussion, potentially further injuring an already vulnerable brain,” Mayer said. The fact that the brain’s healing process is more prolonged than previously assumed could help explain why returning to the field a few weeks after a concussion and experiencing another is so dangerous.
November 15, 2013
There are plenty of ways to study history. You can conduct archaeological digs, examining the artifacts and structures buried under the ground to learn about past lifestyles. You can read historical texts, perusing the written record to better understand events that occurred long ago.
But an international group of medical researchers led by Andrés Moreno-Estrada and Carlos Bustamante of Stanford and Eden Martin of the University of Miami are looking instead at a decidedly unconventional historical record: human DNA.
Hidden in the microscopic genetic material of people from the Caribbean, they’ve found, is an indelible record of human history, stretching back centuries to the arrival of Europeans, the decimation of Native American populations and the trans-Atlantic slave trade. By analyzing these genetic samples and comparing them to the genes of people around the world, they’re able to pinpoint not only the geographic origin of various populations but even the timing of when great migrations occurred.
As part of a new project, documented in a study published yesterday in PLOS Genetics, the researchers sampled and studied the DNA of 251 people living in Florida who had ancestry from one of six countries and islands that border the Caribbean—Cuba, Haiti, Dominican Republic, Puerto Rico, Honduras and Colombia—along with 79 residents of Venezuela who belong to one of three Native American groups (the Yukpa, Warao and Bari tribes). Each study participant was part of a triad that included two parents and one of their children who were also surveyed, so the researchers could track which particular genetic markers were passed on from which parents.
The researchers sequenced the DNA of these participants, analyzing their entire genomes in search of particular genetic sequences—called single-nucleotide polymorphisms (SNPs)—that often differ between unrelated individuals and are passed down from parent to child. To provide context for the SNPs they found in people from these groups and areas, they compared them to existing databases of sequenced DNA from thousands of people globally, such as data from the HapMap Project.
Tracing a person’s DNA to a geographical area is relatively straightforward—it’s well-established that particular SNPs tend to occur in different frequencies in people with different ancestries. As a result, sequencing the DNA of someone living in Florida whose family came from Haiti can reveal what proportion of his or her ancestors originally came from Africa and even where in Africa those people lived.
But one of the most amazing things about the state of modern genetics is that it also allows scientists to draw chronological conclusions about human migration, because blocks of these SNPs shorten over time at a generally consistent rate. ”You can essentially break the genome up into European chunks, Native American chunks and African chunks,” Martin says. “If each of these regions are longer, it suggests they arrived in the gene pool more recently, because time tends to break up the genome. If these chunks are shorter, it suggests there’s been a lot of recombination and mixing up of the genome, which suggests the events were longer ago.”
Modeling their DNA data with these assumptions built in, the researchers created a portrait of Caribbean migration and population change that stretches back to before the arrival of Columbus. One of their most interesting findings was just how few Native Americans survived the arrival of Europeans, based on the DNA data. “There was an initial Native American genetic component on the islands,” Martin says, “but after colonization by the Europeans, they were almost decimated.”
This decimation was the result of European attacks and enslavement, as well as the disease and starvation that came in their wake. The DNA analysis showed that the native population collapse of Caribbean islands happened almost immediately after the arrival of Columbus, within one generation of his first visits and the appearance of other Europeans. The gene pool on the mainland, by contrast, shows a more significant Native American influence, indicating that they didn’t die off at the same rates.
What replaced the missing Native American genes in island populations? The answer reflects the conquering Europeans’ solution to diminishing populations available for labor: slaves kidnapped and imported from Africa. The DNA analysis showed a heavy influence from characteristically African SNPs, but notably, it revealed two separate phases in the trans-Atlantic slave trade. “There were two distinct pulses of African immigration,” Martin says. “The first pulse came from one part of West Africa—the Senegal region—and the second, larger pulse came from another part of it, near the Congo.”
This corresponds to written records and other historical sources, which show an initial phase of slave trade starting around 1550, in which slaves were mostly kidnapped from the Senegambia area of the Mali Empire, covering modern-day Senegal, Gambia and Mali (the orange area in the map at right). This first push accounted for somewhere between 3 and 16 percent of the total Atlantic slave trade. It was followed by a second, much heavier period that made up more than half of the trade and peaked during the late 1700s, in which slaves were largely taken from what is now Nigeria, Cameroon, Gabon and the Congo (the red and green areas).
The genetic analysis can also look at genes that are passed down on the X chromosome in particular, revealing the historical influence of different ancestries on both the female and male sides of the genome. They found that, in the populations studied, Native American SNPs were more prevalent on the X chromosome than the others, reflecting the history of both marriage and rape of Native American women by Spanish men who settled in the area.
As medical researchers, the scientists are primarily interested in using the findings to advance research into the role of genetics in diseases that disproportionately affect Hispanic populations. Similar research on genetics and ethnicity has revealed that, for instance, Europeans are much more likely to suffer from cystic fibrosis, or sickle-cell anemia tends to strike people of African ancestry.
“Hispanics are extremely diverse genetically—they originate from countries all over the world,” Martin says. “So that poses great challenges in genetic studies. We can’t just lump all Hispanics into a group and think of them as homogenous, so we’re trying to look more deeply into their genetic heritage and where it came from.”