Particles of twisted light that have been entangled using quantum mechanics offer a new approach to dense and secure data storage.
Holograms that produce 3-D images and serve as security features on credit cards are usually made with patterns laid down with beams of laser light. In recent years, physicists have found ways to create holograms with entangled photons instead. Now there is, literally, a new twist to the technology.
Entangled photons that travel in corkscrew paths have resulted in holograms that offer the possibility of dense and ultrasecure data encryption, researchers report in a study to appear in Physical Review Letters. Light can move in a variety of ways, including the up-and-down and side-to-side patterns of polarized light. But when it carries a type of rotation known as orbital angular momentum, it can also propagate in spirals that resemble twisted rotini pasta.
Like any other photons, the twisted versions can be entangled so that they essentially act as one entity. Something that affects one of an entangled photon pair instantly affects the other, even if they are very far apart.
In previous experiments, researchers have sent data through the air in entangled pairs of twisted photons (SN: 8/5/15). The approach should allow high-speed data transmission because light can come with different amounts of twist, with each twist serving as a different channel of communication.
Now the same approach has been applied to record data in holograms. Instead of transmitting information on multiple, twisted light channels, photon pairs with different amounts of twist create distinct sets of data in a single hologram. The more orbital angular momentum states involved, each with different amounts of twist, the more data researchers can pack into a hologram.
In addition to cramming more data into holograms, increasing the variety of twists used to record the data boosts security. Anyone who wants to read the information out needs to know, or guess, how the light that recorded it was twisted.
For a hologram relying on two types of twist, says physicist Xiangdong Zhang of the Beijing Institute of Technology, you would have to pick the right combination of the twists from about 80 possibilities to decode the data. Bumping that up to combinations of seven distinct twists leads to millions of possibilities. That, Zhang says, “should be enough to ensure our quantum holographic encryption system has enough security level.” The researchers demonstrated their technique by encoding words and letters in holograms and reading the data back out again with twisted light. Although the researchers produced images from the holographic data, says physicist Hugo Defienne of the Paris Institute of Nanosciences, the storage itself should not be confused with holographic images.
Defienne, who was not involved with the new research, says that other quantum holography schemes, such as his efforts with polarized photons, produce direct images of objects including microscopic structures.
“[Their] idea there is very different . . . from our approach in this sense,” Defrienne says. “They’re using holography to store information,” rather than creating the familiar 3-D images that most people associate with holograms.
The twisted light data storage that Zhang and his colleagues demonstrated is slow, requiring nearly 20 minutes to decode an image of the acronym “BIT,” for the Beijing Institute of Technology where the experiments were performed. And the security that the researchers have demonstrated is still relatively low because they included only up to six forms of twisted light in their experiments.
Zhang is confident that both limitations can be overcome with technical improvements. “We think that our technology has potential application in quantum information encryption,” he says, “especially quantum image encryption.”
The existing boundaries of national parks and other habitat preserves aren’t enough to protect more than three-quarters of the world’s well-studied insects.
The finding, reported February 1 in One Earth, shows that people who design nature preserves “don’t really think about insects that much,” says coauthor Shawan Chowdhury, an ecologist at the German Centre for Integrative Biodiversity Research in Leipzig.
That’s a problem because insect populations around the globe are plummeting, a growing body of research suggests, probably due to climate change and human development (SN: 4/26/22). For instance, insect abundance in Puerto Rico has dropped by up to 98 percent over the last 35 years. Threats to insect survival could have ripple effects on plants and other animals. Insects help form the foundation for many ecosystems: They pollinate around 80 percent of all plant species and serve as a staple in the diets of hundreds of thousands of animals (and the occasional carnivorous plant).
One way to avert insect extinctions is to set aside the land they need to survive. But scientists know the ranges for only about 100,000 of the estimated 5.5 million insect species. To determine how well existing protected areas may be aiding insect conservation, Chowdhury and colleagues mapped the known habitats of about 89,000 of those species and compared the ranges with the boundaries of preserves from the World Database on Protected Areas.
Overall, these spaces don’t safeguard enough habitat for 67,384 insect species — about 76 percent of the species included in the study — the team found. Roughly 2 percent of species do not overlap with protected areas at all.
Conserving insects, Chowdhury says, will mean setting aside more insect-friendly spaces in the years ahead.
Earth’s inner core may have temporarily stopped rotating relative to the mantle and surface, researchers report in the January 23 Nature Geoscience. Now, the direction of the inner core’s rotation may be reversing — part of what could be a roughly 70-year-long cycle that may influence the length of Earth’s days and its magnetic field — though some researchers are skeptical.
“We see strong evidence that the inner core has been rotating faster than the surface, [but] by around 2009 it nearly stopped,” says geophysicist Xiaodong Song of Peking University in Beijing. “Now it is gradually mov[ing] in the opposite direction.” Such a profound turnaround might sound bizarre, but Earth is volatile (SN: 1/13/21). Bore through the ever-shifting crust and you’ll enter the titanic mantle, where behemoth masses of rock flow viscously over spans of millions of years, sometimes upwelling to excoriate the overlying crust (SN: 1/11/17, SN: 3/2/17, SN: 2/4/21). Delve deeper and you’ll reach Earth’s liquid outer core. Here, circulating currents of molten metals conjure our planet’s magnetic field (SN: 9/4/15). And at the heart of that melt, you’ll find a revolving, solid metal ball about 70 percent as wide as the moon.
This is the inner core (SN: 1/28/19). Studies have suggested that this solid heart may rotate within the liquid outer core, compelled by the outer core’s magnetic torque. Researchers have also argued the mantle’s immense gravitational pull may apply an erratic brake on the inner core’s rotation, causing it to oscillate.
Evidence for the inner core’s fluctuating rotation first emerged in 1996. Geophysicist Paul Richards of Columbia University’s Lamont-Doherty Earth Observatory in Palisades, N.Y., and Song, then also at Lamont-Doherty, reported that over a span of three decades, seismic waves from earthquakes took different amounts of time to traverse Earth’s solid heart.
The researchers inferred that the inner core rotates at a different speed than the mantle and crust, causing the time differences. The planet spins roughly 360 degrees in a day. Based on their calculations, the researchers estimated that the inner core, on average, rotates about 1 degree per year faster than the rest of Earth.
But other researchers have questioned that conclusion, some suggesting that the core spins slower than Song and Richards’ estimate or doesn’t spin differently at all.
In the new study, while analyzing global seismic data stretching back to the 1990s, Song and geophysicist Yi Yang — also at Peking University — made a surprising observation. Before 2009, seismic waves generated by sequences and pairs of repeating earthquakes — known as multiplets and doublets — traveled at different rates through the inner core. This indicated the waves from recurring quakes were crossing different parts of the inner core, and that the inner core was rotating at a different pace than the rest of Earth, aligning with Song’s previous research.
But around 2009, the differences in travel times vanished. That suggested the inner core had ceased rotating with respect to the mantle and crust, Yang says. After 2009, these differences returned, but the researchers inferred that the waves were crossing parts of the inner core that suggested it was now rotating in the opposite direction relative to the rest of Earth.
The researchers then pored over records of Alaskan earthquake doublets dating to 1964. While the inner core appeared to rotate steadily for most of that time, it seems to have made another reversal in rotation in the early 1970s, the researchers say.
Song and Yang infer that the inner core may oscillate with a roughly 70-year periodicity — switching directions every 35 years or so. Because the inner core is gravitationally linked to the mantle and magnetically linked to the outer core, the researchers say these oscillations could explain known 60- to 70-year variations in the length of Earth’s days and the behavior of the planet’s magnetic field. However, more work is needed to pin down what mechanisms might be responsible.
But not all researchers are on board. Yang and Song “identif[y] this recent 10-year period [that] has less activity than before, and I think that’s probably reliable,” says geophysicist John Vidale of the University of Southern California in Los Angeles, who was not involved in the research. But beyond that, Vidale says, things get contentious.
In 2022, he and a colleague reported that seismic waves from nuclear tests show the inner core may reverse its rotation every three years or so. Meanwhile, other researchers have proposed that the inner core isn’t moving at all. Instead, they say, changes to the shape of the inner core’s surface could explain the differences in wave travel times.
Future observations will probably help disentangle the discrepancies between these studies, Vidale says. For now, he’s unruffled by the purported chthonic standstill. “In all likelihood, it’s irrelevant to life on the surface, but we don’t actually know what’s happening,” he says. “It’s incumbent on us to figure it out.”
For some ant queens, the secret to long life might be a self-produced insulin blocker.
Ant queens are famously long-lived, even though they shouldn’t be. Generally, animals that put lots of energy into reproduction sacrifice some time off their life. But ant queens produce millions of eggs and live an extraordinarily long time compared with worker ants that don’t reproduce.
Now, researchers have shown how one ant species pulls off this anti-aging feat. When queens and wannabe queens of the species Harpegnathos saltator gear up to reproduce, a part of what’s called the insulin signaling pathway gets blocked, slowing aging, the researchers report in the Sept. 2 Science. That molecular pathway has long been implicated in aging in mammals, including humans. “There’s been a need to understand why queens, or reproductives, in social insects can live for so amazingly long,” says Marc Tatar, a biologist at Brown University in Providence, R.I., who was not involved with the study. Some ant species have queens that survive 30 times as long as their workers. Other social insects such as bees and termites also have long-lived queens.
In a rare behavior for ants, when a queen H. saltator dies, some female workers begin competing in duels for the chance to replace her (SN: 1/17/14). These hopeful royals develop ovaries, start laying eggs and transition into queenlike forms called gamergates. When a worker transitions to a gamergate, her life span becomes five times as long as it was. But if she doesn’t end up becoming queen and reverts back to a worker, her life span shortens again.
The researchers exploited this behavior to investigate the molecular underpinnings of anti-aging in these ants. H. saltator gamergates, it turns out, extend their life spans by taking advantage of a split in the insulin signaling pathway, the chain of chemical reactions that drive insulin’s effects on the body. One branch of this pathway is involved with reproduction, while the other is implicated in aging.
“Insulin comes with our life — [after] we eat, we have high insulin,” says Hua Yan, a biologist at the University of Florida in Gainesville. “But a constant high level of insulin is bad for longevity.”
Examining patterns of gene activity, Yan and colleagues found that gamergates have more active insulin genes than regular worker ants and, as a result, have increased metabolic activity and ovary development. But the secret sauce protecting the ants from the insulin’s aging effects appears to be a molecule called Imp-L2, which blocks the branch of the insulin pathway linked to aging, experiments showed. The branch involved in reproduction, however, remains active.
“What we don’t understand is how Imp-L2 can act on one aspect of the pathway and not on the other,” says study coauthor Claude Desplan, a developmental biologist at New York University.
These results represent a leap forward in our understanding of extreme social insect longevity, the researchers say, while also showcasing an anti-aging evolutionary adaptation that hasn’t been seen in the wild before.
For some ant queens, the secret to long life might be a self-produced insulin blocker.
Ant queens are famously long-lived, even though they shouldn’t be. Generally, animals that put lots of energy into reproduction sacrifice some time off their life. But ant queens produce millions of eggs and live an extraordinarily long time compared with worker ants that don’t reproduce.
Now, researchers have shown how one ant species pulls off this anti-aging feat. When queens and wannabe queens of the species Harpegnathos saltator gear up to reproduce, a part of what’s called the insulin signaling pathway gets blocked, slowing aging, the researchers report in the Sept. 2 Science. That molecular pathway has long been implicated in aging in mammals, including humans. “There’s been a need to understand why queens, or reproductives, in social insects can live for so amazingly long,” says Marc Tatar, a biologist at Brown University in Providence, R.I., who was not involved with the study. Some ant species have queens that survive 30 times as long as their workers. Other social insects such as bees and termites also have long-lived queens.
In a rare behavior for ants, when a queen H. saltator dies, some female workers begin competing in duels for the chance to replace her (SN: 1/17/14). These hopeful royals develop ovaries, start laying eggs and transition into queenlike forms called gamergates. When a worker transitions to a gamergate, her life span becomes five times as long as it was. But if she doesn’t end up becoming queen and reverts back to a worker, her life span shortens again.
The researchers exploited this behavior to investigate the molecular underpinnings of anti-aging in these ants. H. saltator gamergates, it turns out, extend their life spans by taking advantage of a split in the insulin signaling pathway, the chain of chemical reactions that drive insulin’s effects on the body. One branch of this pathway is involved with reproduction, while the other is implicated in aging.
“Insulin comes with our life — [after] we eat, we have high insulin,” says Hua Yan, a biologist at the University of Florida in Gainesville. “But a constant high level of insulin is bad for longevity.”
Examining patterns of gene activity, Yan and colleagues found that gamergates have more active insulin genes than regular worker ants and, as a result, have increased metabolic activity and ovary development. But the secret sauce protecting the ants from the insulin’s aging effects appears to be a molecule called Imp-L2, which blocks the branch of the insulin pathway linked to aging, experiments showed. The branch involved in reproduction, however, remains active.
“What we don’t understand is how Imp-L2 can act on one aspect of the pathway and not on the other,” says study coauthor Claude Desplan, a developmental biologist at New York University.
These results represent a leap forward in our understanding of extreme social insect longevity, the researchers say, while also showcasing an anti-aging evolutionary adaptation that hasn’t been seen in the wild before.
The Milky Way: An Autobiography of Our Galaxy takes a tour of our home in the cosmos from an unexpected perspective. Astrophysicist and folklorist Moiya McTier presents herself not as the author, but as the lucky human vessel through which the Milky Way has chosen to tell its story. Then she lets the galaxy take it away, with humor, heart and a huge dose of snark.
The book alternates chapters between science and mythology, reflecting McTier’s dual specialties (her bio says she was the first student in Harvard University’s history to study both). “Many of you don’t realize this, but myths were some of your species’ first attempt at scientific inquiry,” the Milky Way tells us.
The Milky Way is telling its story now because it’s sick of being ignored. Once upon a time, humans looked to the glittering smudge of stars in the sky for insight into when to plant crops or avoid floods. We told stories about the Milky Way’s importance in the origin and fate of the world.
Our galaxy ate it up: For an entity that spends most of its time ripping up smaller galaxies and watching its own stars die, “your stories made me feel loved and needed and, perhaps for the first time in my long existence, more helpful than I was ruinous.” But in the last few centuries, technology and light pollution have pulled humankind away. “At first, I thought it was just a phase,” the Milky Way says. “Then I remembered … that several hundred years is actually a long time for humans.” So the Milky Way decided to remind us why it’s so important. Its autobiography covers big-picture scientific questions about galaxies, like where they come from (“When a gas cloud loves itself very much,” the Milky Way explains, “it hugs itself extra tight, and after a few hundred million years, a baby galaxy is born. Leave the storks out of it, please.”). It also gets into what galaxies are made of, how they interact with other galaxies, and how they live and die. The book then zooms out to cover the origins and possible ends of the universe, mysteries like dark matter and dark energy, and even humankind’s search for other intelligent life (SN: 8/4/20).
The author takes pains to explain scientific jargon and the technical tools that astronomers use to study the sky. A lot of popular astronomy writing glosses over how astronomers think about cosmic distance or exactly what a spectrum is, but not this book. If you’ve ever been curious about these insider details, The Milky Way has you covered.
McTier’s version of our home galaxy is heavily anthropomorphized. The Milky Way is brash, vain and arrogant in a way that may hide a secret insecurity. Its central black hole is characterized as the physical embodiment of the galaxy’s shame and regrets, a source of deep existential angst. And its relationship with the Andromeda galaxy is like a long-term, long-distance romance, with each galaxy sending stars back and forth as love notes until the two can eventually merge (SN: 3/05/21).
This could have felt gimmicky. But McTier’s efforts to make the metaphors work while keeping the science accurate and up-to-date made the premise endearing and entertaining.
I laughed twice on Page 1. I learned a new word on Page 2. I dog-eared the endnotes early on because it became instantly clear I would want to read every one. I read this book while traveling in rural upstate New York, where the sky is much clearer than at my home outside of Boston. The Milky Way reminded me to look up and appreciate my home in the universe, just like its narrator wanted.
For millions of people, COVID-19 doesn’t end with a negative test. Weeks or months after traces of the virus disappear from noses and throats, symptoms can persist or come back. New ones might pop up and stick around for months. People suffering from long COVID are unwillingly in it for the long haul — and it’s still unclear who’s at the highest risk for the condition.
Researchers don’t yet have an official definition for long COVID, and its symptoms are wide-ranging (SN: 7/29/22). Some people struggle with extreme fatigue that interferes with their daily lives. Others can’t concentrate or struggle with memory amid thick brain fog. Still others have organ damage or a persistent cough and difficulty breathing. “There are a variety of different kinds of ways that people can have long COVID. It’s not just the one thing,” says Leora Horwitz, an internal medicine physician at New York University Langone Health. “That’s what makes it so hard to study.”
This spectrum of symptoms makes pinning down who’s at high risk for long-term health problems from the disease especially hard. Some post-COVID conditions may stem from virus-induced damage or from the stress of being hospitalized with severe disease. In other cases, the body’s own immune response to the virus could drive the damage. Or the virus may be hiding somewhere in the body, possibly the gut, helping symptoms to persist (SN: 11/24/20). Different causes may have different risk groups, says Hannah Davis, cofounder of the Patient-Led Research Collaborative, a research and advocacy group studying long COVID.
There are some broad hints about who’s at risk. Studies suggest that women are more likely than men to have lingering symptoms. COVID-19 patients with more than five symptoms in the first week of infection or preexisting health conditions such as asthma may be more likely to develop long COVID. Age also appears to be a risk factor, though results are mixed regarding whether the burden falls on older people or middle-aged people. Populations that were disproportionally hit by COVID-19 overall — including Black and Hispanic people — may similarly face disparities for long COVID. And while vaccination seems to protect people from developing long COVID, Horwitz says, it’s still unclear by how much.
Age is a risk factor for severe COVID-19, and the U.S. Centers for Disease Control and Prevention lists more than 30 health problems, including cancer and lung disease, that also raise the risk. “So many researchers assume that those [risk factors] will be the same for long COVID and there’s no scientific basis for that,” Davis says. There are many more that researchers could be missing when it comes to long COVID.
Using health records and exams, and knowledge of ailments with symptoms similar to long COVID, experts are on the hunt for those risk factors.
Examining health When it comes to getting a better handle on who’s at risk for long COVID — which also goes by the wonky alias Post-Acute Sequelae of SARS-CoV-2 infection — electronic health records may hold important clues.
Horwitz is part of the U.S. National Institutes of Health’s RECOVER initiative that aims to understand the long-term impacts of COVID-19. One arm of the study involves mining millions of electronic health records to find potential patterns.
Studying millions of these records should pinpoint potential risk factors that are rare in the population overall but perhaps more common for people with long COVID, Horwitz says. “That’s hard even in a cohort study of thousands.”
But health records aren’t perfect: They depend on physicians logging that patients are having trouble sleeping or focusing, or that they’re exhausted. “The things people are complaining about, we’re really bad at writing down those diagnoses on the record,” Horwitz says. “So we miss that.” To account for health records’ deficiencies, Horwitz and colleagues are also directly studying thousands of people. Participants answer a questionnaire every three months so that the team can identify what kinds of symptoms people have and whether they’re getting better or worse.
Then blood, urine, stool and saliva samples can reveal what’s happening in the body. Tests on those samples can uncover if the coronavirus is still around and causing trouble, or if the immune system has learned to attack the body itself. Participants with abnormal test results will undergo additional, targeted testing.
“Unlike electronic health records where it’s hit or miss, like somebody might have had a CAT scan or might not, here we say, ‘OK, you have trouble breathing. We will take a look at your lungs,’” Horwitz says.
The study includes a range of participants: adults and kids, pregnant people, those currently with COVID-19 and people who died after having the disease.
Some of the potential risk factors that the team is looking for include autoimmune diseases and other viral infections. The list may grow as more people join the study. “We’re trying to balance the fishing versus making sure that we’re at least fishing for things that could be in the water,” Horwitz says.
Among short supply, though, are people who never caught the virus — important “controls” to highlight what’s different about people who got COVID-19.
So far, more than 7,000 people have signed up, and the group plans to recruit around 10,000 more. It’s a lot of data, but early results may soon start coming in.
“We’ll probably try to do an interim peek at those data this fall,” Horwitz says. “It’s tricky because we deliberately wanted to enroll 18,000 people so we would have enough power to really look at the things we care about. I don’t want to cheat and look too early, but we also know that there’s a lot of interest.”
Striking similarities Some long COVID symptoms — brain fog, fatigue and trouble sleeping — mirror another illness: myalgic encephalomyelitis/chronic fatigue syndrome, or ME/CFS. Other long COVID symptoms, such as rapid heartbeat and dizziness, fall in the category of nervous system disorders called dysautonomia. Similar symptoms could belie similar risk factors.
Yet potential risk factors for those conditions are largely missing from long COVID research, says Davis, who has had long COVID since March 2020. Among the possibilities that scientists are considering are things like Epstein-Barr virus, migraines and some autoimmune diseases.
Epstein-Barr virus could be a big one, Davis says. Infections last a lifetime because the virus can go into hiding in the body and possibly reemerge. That virus has been linked to ME/CFS for decades, though its role in the disease remains unclear, Davis says. Some early hints of a link between Epstein-Barr virus and long COVID already exist. Multiple studies have found evidence in blood samples from some long COVID patients that the immune system recently battled with Epstein-Barr virus, which can cause infectious mononucleosis, a disease characterized by extreme fatigue. Other studies have found signs of the virus itself. And in 2021, Davis and colleagues found that 40 out of 580 people with symptoms of long COVID who responded to an online survey reported having a current or recent Epstein-Barr virus infection.
With ME/CFS, it’s possible that another illness caused by a different virus triggers the Epstein-Barr virus, which then causes the fatigue syndrome. Given the parallels between that condition and long COVID, some scientists are wondering if the two are actually the same disease, with the coronavirus now known as one trigger.
Examining health conditions that raise the chances of long COVID could provide answers for both diseases, says Nancy Klimas, an immunologist at Nova Southeastern University in Fort Lauderdale, Fla. That’s in part because researchers can more easily identify people who developed lingering symptoms after a bout of COVID-19 compared with unknown infections that may precede ME/CFS.
Also, “there’s a huge difference in these two fields and it’s money,” Klimas says. She now has funding from the CDC to compare long COVID patients with people who have ME/CFS. The team hopes that physical exams and specialized tests will reveal whether the two diseases are indeed the same and be a step toward understanding the mechanisms behind the lingering symptoms.
Still, since long COVID as a whole encompasses such a wide range of symptoms, it will take time to uncover who is at risk of what.
If COVID-19 were just one disease impacting the lungs, heart or brain, the research might be easier, Horwitz says. “But we have to test everything.”
The one-of-a-kind pattern of ridges and valleys in a fingerprint may not only betray who was present at a crime scene. It may also tattle about what outlawed drugs a suspect handled.
With advanced spectroscopy, researchers can detect and measure tiny flecks of cocaine, methamphetamine and heroin — in some cases as little as trillionths of a gram — on a lone fingerprint. The study, led by researchers at the National Institute of Standards and Technology in Gaithersburg, Md., appears May 7 in Analytical Chemistry. Using an ink-jet–printed array of known quantities of drugs, researchers calibrated their spectroscopy techniques to measure specks of the chemicals. Then, using a 3-D printed plastic finger and a synthetic version of finger oil, researchers created drug-tainted fingerprints pressed onto paper or silicon.
On paper, the researchers detected as little as 1 nanogram of cocaine and amounts above 50 nanograms of methamphetamine and heroin. On silicon, the method picked up as little as 8 picograms of cocaine and heroin and around 1 nanogram of methamphetamine.
Researchers could also point to the location of the drugs on the fingerprint— at the peaks or dips of the pattern, for instance. Such information, the authors say, could help investigators finger what chemicals a suspect handled first and help corroborate a timeline of events in a crime.
In the animal world, just like the human one, sometimes it’s not easy being mom. Fellow blogger Laura Sanders will tell you all about the trials and tribulations of being a mother to Homo sapiens. But some moms of the animal kingdom make sacrifices that go far beyond carrying a baby for nine months or paying for college.
Binge-eating sea otters Adult female sea otters spend six months out of every year nursing at least one pup, sometimes two. Feeding herself isn’t easy — she’s got to eat the equivalent of 20 to 25 percent of her body mass every day to survive. But that amount has to increase while she’s nursing. By the time a pup is weaned at six months old, mom has to nearly double her food intake, researchers reported last year in the Journal of Experimental Biology. And to make matters worse, sometimes her kid will steal her food. Single, starving mom About two months before giving birth, a polar bear will enter her maternity den, remaining there for four to eight months. She stays holed up for that entire time, never eating, never drinking. Her cubs, only about half a kilogram at birth, grow quickly feeding on mom’s rich milk. And once they’re big enough to venture out, mama bear leads her babies straight to the sea so she can finally catch herself a meal.
Walled in by poo Various species of Asian hornbills all share a similar nesting strategy: To protect her eggs from predators, mom walls herself up in a tree with a combination of mud, feces and regurgitated fruit. She leaves one tiny hole, through which dad feeds her for up to four months when mother and children are finally ready to emerge.
Endless sleepless nights Human babies are known for their ability to rouse mom with their cries and prevent her from getting much sleep. But orca and dolphin moms don’t sleep at all for a month or more after they give birth. Unlike human babies that need a lot of sleep, tiny orcas and dolphins don’t sleep in the weeks after they’re born. That means no sleep for mom.
It’s mom for dinner There’s a hint in the name of a limbless amphibian called Microcaecilia dermatophaga — young caecilians eat the skin of their mother, researchers reported in 2013 in PLOS ONE. But in a recent issue of Science News, Susan Milius highlighted an even more disgusting case of mom serving herself up for her kids: A female Stegodyphus lineatus spider feeds her young on a regurgitated slurry made up of the last meals she’ll ever eat — and her own guts. Milius writes:
“As liquid wells out on mom’s face, spiderlings jostle for position, swarming over her head like a face mask of caramel-colored beads. This will be her sole brood of hatchlings, and she regurgitates 41 percent of her body mass to feed her spiderlings.”
The next time your mom talks about how much she sacrificed for you, say thanks, but remember, at least you didn’t eat her stomach.
Mother’s Day is on my mind, and I’ve been thinking about the ways I’m connected to my mom and my two little daughters. Every so often I see flickers of my mom in my girls — they share the lines around their smiles and a mutual adoration of wildflowers. Of course, I’m biased. I know that I’m seeing what I’m looking for. But biologically speaking, mothers and their children are connected in a way that may surprise you.
Way back when you and your mom shared a body, your cells mingled. Her cells slipped into your body and your cells circled back into her. This process, called fetal-maternal microchimerism, turns both mother and child into chimeras harboring little pieces of each other.
Cells from my daughters are knitted into my body and bones and brain. I also carry cells from my mom, and quite possibly from my grandma. I may even harbor cells from my older brother, who may have given some cells to my mom, who then gave them to me. It means my younger brother just might have cells from all of us, poor guy. This boundary blurring invites some serious existential wonder, not least of which might involve you wondering if this means your family members really are in your head.
These cellular threads tie families together in ways that scientists are just starting to discover. Here are a few of my favorite instances of how cells from a child have woven themselves into a mother’s body: Fetal cells are probably sprinkled throughout a mother’s brain. A study of women who had died in their 70s found that over half of the women had male DNA (a snippet from the Y chromosome) in their brains, presumably from when their sons were in the womb. Scientists often look for male DNA in women because it’s easier than distinguishing a daughter’s DNA from her mother’s. If DNA from daughters were included, the number of women with children’s cells in their brains would probably be even higher.
When the heart is injured, fetal cells seem to flock to the site of injury and turn into several different types of specialized heart cells. Some of these cells may even start beating, a mouse study found. So technically, those icky-sweet Mother’s Day cards may be right: A mother really does hold her children in her heart.
Fetal cells circulate in a mother’s blood. Male DNA turned up in blood samples from women who were potential stem cell donors. That result may have implications for stem cell transplants. This cell swapping may make parents better donor candidates for their children than strangers, for instance. Other studies have found fetal cells in a mother’s bones, liver, lungs and other organs, suggesting that these cells have made homes for themselves throughout a mother’s body. Maybe this is a way for a child to give back to the mother, in a sense. Growing fetuses slurp nutrients and energy out of a mother’s body during pregnancy (not to mention the morning sickness, heartburn and body aches). In return, fetuses offer up these young, potentially helpful cells. Perhaps these fetal cells, which may possess the ability to turn into lots of different kinds of cells, can help repair a damaged heart, liver or thyroid, as some studies have hinted.
Before I get carried away, a caveat: these cells may also make mischief. They may have a role in autoimmune disorders, for instance.
Microchimerism also has implications here for women who have lost pregnancies, an extremely common situation hidden by the taboo of talking about miscarriages. Fetal cells seem to migrate early in pregnancy, meaning that even brief pregnancies may leave a cellular mark on a woman.
Scientists are just starting to discover how this cellular heritage works, and how it might influence health. The scientist in me can’t wait to see how this story unfolds. But for now, I’m content to marvel at the mother and daughters in me.
A zap to the head can stretch the time between intention and action, a new study finds. The results help illuminate how intentions arise in the brain.
The study, published in the May 6 Journal of Neuroscience, “provides fascinating new clues” about the process of internal decision making, says neuroscientist Gabriel Kreiman of Harvard University. These sorts of studies are bringing scientists closer to “probing some of the fundamental questions about who we are and why we do what we do,” he says. Figuring out how the brain generates a sense of control may also have implications for people who lack those feelings. People with alien hand syndrome, psychogenic movement disorders and schizophrenia can experience a troubling disconnect between intention and action, says study coauthor Biyu Jade He of the National Institutes of Health in Bethesda, Md.
In the study, the researchers manipulated people’s intentions without changing their actions. The researchers told participants to click a mouse whenever the urge struck. Participants estimated when their intention to click first arose by monitoring a dot’s position on a clockface.
Intention to click usually preceded the action by 188 milliseconds on average, the team found. But a session of transcranial direct current stimulation, or tDCS, moved the realization of intention even earlier, stretching time out between awareness of intention and the action. tDCS electrodes delivered a mild electrical zap to participants’ heads, dialing up the activity of carefully targeted nerve cells. After stimulation, intentions arrived about 60 to 70 milliseconds sooner than usual. tDCS seemed to change certain kinds of brain activity that may have influenced the time shift, EEG recordings suggested.
The results highlight how thoughts and intentions can be separated from the action itself, a situation that appears to raise thorny questions about free will. But these tDCS zaps didn’t change the action outcome or participants’ feelings of control, only the reported timing of a person’s conscious intention.
