Katherine J. Wu is a Digital Editor at NOVA and Story Collider producer. She holds a Ph.D. in Microbiology and Immunobiology from Harvard University. Previously, she served as a AAAS Mass Media Fellow at Smithsonian magazine.

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As the planet’s thermostat <a href="https://www.smithsonianmag.com/smart-news/world-was-just-issued-12-year-ultimatum-climate-change-180970489/?no-cache">ticks steadily upwards</a>, life forms around the world may be in grave danger—and plants like rice are no exception. Already, global rice yields have <a href="http://www.pnas.org/content/114/35/9326">taken a hit</a> from rising temperatures. If the upward creep in heat continues, declines in this starchy staple could imperil the 3.5 billion people around the world who rely on rice for over 20% of their daily caloric intake.Today, in the journal PNAS, researchers <a href="http://www.pnas.org/lookup/doi/10.1073/pnas.1807988115">report</a> that rice plants are sensitive to the damaging effects of high heat even in the short term. Brief exposures to sweltering temperatures unraveled plant cells’ messenger RNA—a critical molecular envoy that ferries the instructions contained within DNA to the cell’s protein-producing factories—cuing the messages up for destruction. Though the rice eventually recovered, the new finding underscores just how sensitive plants may be to the hazards of a fast-warming world.
 

 
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 With each degree-Celsius increase in average global temperature, rice crop yields fall by <a href="http://www.pnas.org/content/114/35/9326">about 3%</a>. And as the planet warms and <a href="http://www.un.org/en/development/desa/news/population/2015-report.html">the human population expands</a>, the gap between supply and demand for this staple crop continues to widen. But while these trends are clear at a macroscopic level, the inner workings of plant cells coping with toasty temperatures remain far less clear.To better understand heat tolerance in crops, a team of scientists led by <a href="http://www.personal.psu.edu/sma3/people.html">Zhao Su</a>, a plant biologist at Pennsylvania State University, heated cuttings of young rice shoots (Oryza sativa) to a temperature of 42º Celsius (nearly 108º Fahrenheit) for 10 minutes. Though temporary, the mini heat wave constituted a rapid 20º-Celsius shift upwards from room temperature—an escalation that’s “more than a human could ever withstand,” explains study author <a href="http://chem.psu.edu/directory/pcb5">Philip Bevilacqua</a>, an RNA chemist also at Pennsylvania State University.When the researchers analyzed the shoots’ cellular contents, they found that the temporary trauma had compromised the rice’s ability to relay genetic information through their messenger RNA, or mRNA.
 <figure class="richtext-image full-width"><img alt="PIXNIO-15202-2700x1767.jpeg" class="richtext-image full-width" height="523" width="800"
 src="https://www.pbs.org/wgbh/nova/media/images/PIXNIO-15202-2700x1767.width-800.jpg"/><figcaption>With every degree-Celsius increase in temperature, rice crop yields drop by over 3%. Photo Credit: Pixnio<div class="credit"></div></figcaption>
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 Plants, like humans, store their genetic information in the form of DNA. Contained within this molecular manuscript are all the necessary instructions for growth and survival—including all the cell’s contingency plans for emergencies or unanticipated changes in the surrounding environments. The DNA manual is extremely comprehensive, so cells access excerpts from it on an as-needed basis, making short-lived photocopies of the original text in the form of mRNA. Without mRNA, cells can’t receive the intel necessary to manufacture the building blocks necessary for life.But for such a critical piece of the cellular puzzle, mRNA is frustratingly fickle. Unlike DNA, which is stored in two strands that lock into each other like the halves of a zipper, the synthesis of mRNA creates an unwieldy single-stranded molecule. These open-faced strands can loop around and bind to themselves in a semblance of secure structure, but this makeshift jumble is inherently far less durable than that of double-stranded DNA.Because of mRNA’s infamous instability, the scientists reasoned it might be particularly susceptible to suffering at high temperatures. When they dosed the rice cells with a chemical marker that tags single-stranded mRNA molecules, Su and his colleagues discovered that heated plants contained higher proportions of unfurled mRNA compared to shoots lounging at room temperature. The head and tail ends of many mRNA strands appeared particularly fragile, accruing more of the incriminating chemical tags. In the heat of the moment, it seemed, these cellular messengers were melting.
 

 
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 When the researchers probed the plants further, they discovered that several of the mRNAs slumping into single strands were being chewed up by a destructive machine called the exosome. The looser the mRNA, the more likely it was to be ghosted out of existence—implying that mRNA unfolding made the messages <a href="http://rstb.royalsocietypublishing.org/content/373/1762/20180160">more prone to annihilation</a>. As the rice shoots attempted to weather the warmth, their exosomes were disposing of cells’ hottest messes, along with the genetic information they carried.Luckily, the short spikes in temperature didn’t appear to put any of the rice plants permanently out of commission. Because the cells’ DNA remained intact, new mRNAs were eventually copied and redistributed as the rice recovered from the sizzling onslaught. But it took about 10 hours for the shoots’ mRNAs to fully reset—quite the price to pay for a 10-minute hot flash.Over a thousand mRNA transcripts, all carrying instructions from different genes, became more or less abundant after the rise in temperature. Some of them even appeared to code for proteins that control how certain stretches of DNA are photocopied into mRNA—which means the effects of heat stress could be even more widespread than they already appear.
 <figure class="richtext-image full-width"><img alt="rice-1736909.jpg" class="richtext-image full-width" height="607" width="800"
 src="https://www.pbs.org/wgbh/nova/media/images/rice-1736909.width-800.jpg"/><figcaption>When subjected to just 10 minutes at a high temperature, messenger RNA in rice plants becomes unstable and is degraded by a molecular cleanup crew. Photo Credit: einszweifrei, Pixabay<div class="credit"></div></figcaption>
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 Until the researchers learn more, it’s unclear what exactly these molecular fluxes signify, explains <a href="https://www.danforthcenter.org/scientists-research/principal-investigators/ru-zhang">Ru Zhang</a>, a plant biologist at the Donald Danforth Plant Science Center who was not involved in the study. They could be adaptive, allowing the rice to acclimate to the warmth. Or they could be indicative of just how vulnerable plants’ internal infrastructure is to temperature changes of this magnitude. Either way, resources were likely being diverted away from normal growth.“The paper is an elegant piece of science,” says <a href="https://agronomy.unl.edu/cassman">Kenneth Cassman</a>, an expert in food security and agriculture at the University of Nebraska, Lincoln who did not participate in the new research. “It’s a significant advance in helping us understand how short term exposure to heat affects rice… and how a plant grows and yields.”However, 10 minutes under high heat in a laboratory environment isn’t the same as chronic exposure to, say, the gradual onset of global warming. According to Cassman, there may not be a ton of overlap in the processes that govern plants’ responses to long-term changes in temperature and to short exposures like the one in this study—but there are still several key instances in which the new findings may translate directly.
 

 
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 For one, the changes associated with climate change affect <a href="http://science.sciencemag.org/content/305/5686/994">both averages and extremes</a> in temperature, so daily spikes in heat could involve a 108º-Fahrenheit stint in the sun. Additionally, crops like rice and maize that are grown in high densities often experience temporary spikes in sun exposure when winds disrupt the foliage, says study author <a href="http://bio.psu.edu/directory/sma3">Sarah Assmann</a>, a plant biologist at Pennsylvania State University. Given the vast changes that occurred in the rice plants after just a few minutes of heat, even the ephemeral passing of a cloud overhead could disrupt some of these cells’ internal functions.Additionally, the researchers’ findings will likely translate over to other vital crops, Cassman says. Ironically, he points out, because most (<a href="http://ricepedia.org/rice-as-a-crop/where-is-rice-grown">but not all</a>) rice is grown in standing water, it’s actually one of the few crops that are a bit buffered against rising temperatures. But much of the plant, including its shoots, is warmed by direct sunlight, and rice yields have still been <a href="http://www.pnas.org/content/114/35/9326">curbed</a> by <a href="http://www.pnas.org/content/101/27/9971">global warming</a>. This could prove even more ominous for the vast majority of cultivated plants that don&#x27;t enjoy such liquid luxury, and remain especially vulnerable to surges of heat on dry land.Moving forward, Su, Bevilacqua, and Assmann hope to repeat their work in other strains of rice—including cultivars that have proven <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4052674/">hardy</a> in climes that tend to pack the heat. Comparing the responses of these different varieties to changes in temperature, along with the current findings, may help researchers target certain regions of plant genomes for manipulation in the future, Assmann explains, informing the production of more heat- and drought-resistant crops.
 <figure class="richtext-image full-width"><img alt="Corncobs.jpg" class="richtext-image full-width" height="533" width="800"
 src="https://www.pbs.org/wgbh/nova/media/images/Corncobs.width-800.jpg"/><figcaption>Maize is another staple crop that will continue to suffer from rising temperatures. The molecular changes that occur in rice plants are likely to translate over to other plants. Photo Credit: Sam Fentress, Wikimedia Commons<div class="credit"></div></figcaption>
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 One possible intervention may already be apparent. It’s the sloppiest mRNAs (that is, those with particularly frayed heads and tails) that are especially susceptible to destruction, Bevilacqua explains. So genetic modifications that secure these ends—the molecular equivalent of clipping an aglet onto the end of a frazzled shoelace—might just increase their longevity.Even with exquisite knowledge of the coping mechanisms of plants in peril, however, there’s no guarantee a magic bullet will unveil itself, Cassman says. Plants have spent millennia adapting to heat, and researchers may not get much bang for their buck by trying to optimize their resilience further. If that’s the case, the ceiling on genetically engineering heat-resistant plants could be far lower than expected.But tinkering with the genes of crops is far from the only option, Bevilacqua says. “You can only go so far [with genetic engineering],” he adds. “Yes, it’s possible for us to intervene and help with plant production and response to these stresses as they increase. The bigger answer is to have policies to address and try to reverse climate change.”

India_-_Sights_&_Culture_-_Planting_Rice_Paddy_5_(3245008474).jpg

Women planting in a rice paddy in the Kancheepuram district of Tamil Nadu, India. Photo Credit: McKay Savage, Wikimedia Commons

Brief exposures to high temperatures compromise rice plants’ ability to relay genetic information.

The Planet’s Getting Warmer. Can Plants Take the Heat?

Somewhere along our evolutionary trajectory, we humans lost our regenerative powers. Sure, we can manage <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2701258/">a hunk of liver here</a>, <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5454966/">the tip of a finger there</a>—but in contrast to the <a href="https://www.pbs.org/wgbh/nova/article/saving-axolotls/">salamanders</a>, flatworms, and <a href="https://www.popularmechanics.com/science/animals/a27571/starfish-disease-science/">sea stars</a> of the world, the spontaneous remaking of entire organs and limbs eludes humankind.For biologist <a href="http://ase.tufts.edu/biology/labs/levin/">Michael Levin</a> of Tufts University, however, “lost” isn’t the same as “nonexistent.”Only a few million years separate humans from our closest regenerating relatives. If our animal ancestors built bone and tissue from scratch throughout adulthood, these superpowers may still lie buried within our own tissues, waiting to be reawakened. All it would take, says Levin, is the right signal.Now, Levin and his colleagues may have taken the next steps in pinpointing that very trigger by reviving these clandestine capabilities in African clawed frogs. Their work, <a href="https://www.cell.com/cell-reports/fulltext/S2211-1247(18)31573-0">published today</a> in the journal Cell Reports, kick-started the growth of partial but high-functioning hind legs in amphibian amputees after 24 hours of hormonal treatment. Though the work is still preliminary, such findings may someday inform researchers on the path to finding—and flipping—a similar switch in humans.
 

 
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 Cut the tail off a tadpole, and <a href="https://www.nationalgeographic.com/science/phenomena/2013/01/13/tadpole-heal-thyself-vilified-chemicals-spur-regeneration/">another will take its place</a>. But even in the amphibian world, there are sobering consequences to growing up: If a mature frog loses a leg, the best it can hope for is a frail cartilaginous spike to take its place. This ability is technically regenerative—certainly far more than what any human could accomplish—but the resulting appendage does little for a creature that relies heavily on its hind limbs to navigate its aquatic environment.As the frog ages, its regenerative skills seem to go into hibernation—making it “a good stepping stone between animals that [fully] regenerate, like salamanders, and animals that don’t, like mammals,” Levin explains.To rouse regeneration from its slumber, the researchers first needed to identify the right molecular alarm. The ideal candidate, they reasoned, would be a powerful chemical cue that is both naturally produced by animal bodies and capable of directing a vast array of cellular functions—a winning combination that, for the researchers, pointed to progesterone.<div>
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Every month, as a natural part of the female menstrual cycle, progesterone regenerates the entire endometrium, or lining of the uterus. “We thought, ‘It’s impossible that progesterone is only acting at this level,’” explains lead author <a href="http://sites.tufts.edu/celiaherrerarincon/">Celia Herrera-Rincon</a>, a neuroscientist at Tufts University.Progesterone wields far more power than simply preparing the uterus for pregnancy. Receptors for this hormone exist all over the bodies of both male and female mammals, and in the past several decades, researchers have shown it to be a potent catalyst for wound healing, promoting <a href="https://docplayer.net/74761056-Role-of-progesterone-in-peripheral-nerve-repair.html">nerve repair</a>, <a href="https://www.cell.com/developmental-cell/fulltext/S1534-5807(01)00064-8?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1534580701000648%3Fshowall%3Dtrue">bone remodeling</a>, and <a href="https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1524-475X.2008.00440.x">blood vessel formation</a>. If applied in the right place at the right time, progesterone could very well coax an injured limb onto a regenerative cascade.“Progesterone is very useful and safe,” explains <a href="https://www.popcouncil.org/research/expert/regine-sitruk-ware">Régine Sitruk-Ware</a>, a reproductive endocrinologist at the Population Council’s Center for Biomedical Research who did not participate in the new research. “It’s helpful for the uterus, but in many other layers of the body—in vessels, in bone, in the brain, and in the [nervous system] in general—progesterone has a positive, regenerative aspect.”
 

 
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 To harness the power of progesterone, the researchers designed a silicon apparatus filled with a hydrating gel and stitched it onto <a href="https://www.sciencedaily.com/releases/2016/10/161019155533.htm">African clawed frogs</a> (Xenopus laevis) whose right hind legs had been amputated three hours prior. Some of the devices also contained a dose of progesterone, which was steadily fed to the wound site for 24 hours. When the day was up, the team carefully detached the device—and waited.Within a matter of weeks, the progesterone-treated frogs had a serious leg up on their peers. In the absence of the hormone, frog amputees produced the typical featureless rods, regardless of whether or not they’d been fitted with the apparatus. But the frogs hit with progesterone began to sprout bigger, more structured appendages. And nearly ten months out from the initial spark of progesterone, partial, paddle-like limbs had pushed their way out of the wound site.When the researchers inspected the burgeoning limbs more closely, they found that, unlike the simple, cartilaginous spikes of typical amputees, they seemed to have the form and patterning of true legs. The limbs were thick and full of new blood vessels, nerves, and bone, and were forming what looked like tentative knees: the beginnings of actual joints. These frogs’ legs weren’t just regenerating more than their untreated counterparts—they were regenerating better. It’s a phenomenon that regenerative biologist <a href="http://firm.uni-frankfurt.de/john-barker">John Barker</a> of the Frankfurt Initiative for Regenerative Medicine praises as “smart proliferation”: the ability to form order out of the chaos of growing, dividing cells.
 <figure class="richtext-image full-width"><img alt="Herrera-Rincon Figures for Katie Wu.jpg" class="richtext-image full-width" height="247" width="800"
 src="https://www.pbs.org/wgbh/nova/media/images/Herrera-Rincon_Figures_for_Katie_Wu_F8vWy65.width-800.jpg"/><figcaption>Amputation of adult frogs&#x27; hind limbs usually results in the formation of a cartilaginous &quot;spike&quot; (left). But attaching a device that feeds progesterone to the amputation site for just 24 hours stimulates the growth of a paddle-like structure (right). The dashed line indicates the plane of amputation. Photo Credit: Celia Herrera-Rincon, Tufts University<div class="credit"></div></figcaption>
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 “It was amazing that we were creating structures with only 24 hours of treatment,” Herrera-Rincon says. “I remember showing Mike [Levin] and being fascinated.”When the frogs got the chance to stretch their legs, the untreated, spike-toting regenerates proved to be feeble swimmers and spent more time loitering in place. Meanwhile, the animals that had worn the progesterone-dosing device glided merrily by, almost indistinguishable from their unamputated kin.Though the legs could function, the regeneration was far from complete. While the limb that appeared had clear features, the growth stopped abruptly before the frog’s hind digits would otherwise appear. And, importantly, not all the treated frogs responded to the same extent, indicating that the approach is unlikely to be a one-size-fits-all treatment. But for a first pass, Levin says, the amount of regeneration achieved was “really striking.”“If the person grew a limb like the frogs did, no one would say it was perfect,” says <a href="https://www.whitedlab.com/">Jessica Whited</a>, a regenerative biologist at Harvard University’s Brigham Regenerative Medicine Center who frequently collaborates with Levin’s lab, but was not involved in the newest finding. “But it’s important to demonstrate something that would be better than what grows naturally.”
 

 
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 Levin and his team are currently tinkering with their cocktail of apparatus-administered drugs, as well as with the duration for which the device is worn after amputation. With just a few additions and adjustments, he says, the preliminary results are already looking good.“To rebuild any structure, you need to give the cells some signal about what they’re rebuilding,” Levin explains. “And progesterone [alone] gives an incomplete message.”The rest of this message, Whited adds, will involve a lot of fine-tuning. When limbs grow (and regrow) naturally, they rely on a suite of complex anatomical signals that both drive the production of new tissue and bone and tell it when and where to stop. But the domino effect likely still applies: The key will be finding the right recipe of chemicals to jumpstart the process, then sit back and let nature take its course.
 <figure class="richtext-image full-width"><img alt="4819444864_4a99e4cc5b_o.jpg" class="richtext-image full-width" height="545" width="800"
 src="https://www.pbs.org/wgbh/nova/media/images/4819444864_4a99e4cc5b_o.width-800.jpg"/><figcaption>Deer antlers are mammalian appendages capable of repeated rounds of regeneration. Male deer (and female reindeer) shed and sprout their antlers anew each year. Credit: USFWS Mountain-Prairie, flickr<div class="credit"></div></figcaption>
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 “This isn’t ready for human trials… but it’s also not science fiction,” Levin says of the device. “I don’t think humans are barred from regeneration in any fundamental way.”We’re not exactly a hop, skip, and a jump away from regenerating limbs in people—even partial ones. Though frogs and humans share quite a few genes and basic anatomical structures, Barker explains, we’re still fundamentally very different creatures. But, even if the packaging varies from species to species, the basic toolkit of regeneration might translate across even fairly far-flung species. There are even <a href="/pages/videopages/extreme-animal-weapons/">mammals that naturally regenerate</a>: Deer regularly <a href="https://www.sciencedirect.com/science/article/pii/S135727251400226X">regrow their antlers</a> well into adulthood—a process that, not-so-coincidentally, is also driven by sex hormones.Even as technology advances, it’s unclear if humans will ever regenerate as slickly as salamanders. But maybe these able-bodied amphibians are inching us just a bit closer: One small leap for a frog may someday mean one giant step for humankind.

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Adult African clawed frogs (Xenopus laevis) usually develop spike-like structures at sites of limb amputation. But researchers can now equip these frogs with bioreactors that help them partially regenerate their hind legs. Photo Credit: TimVickers, Wikimedia Commons

Twenty-four hours of the hormone progesterone can kickstart over nine months of limb regeneration in amphibian amputees.

A Progesterone-Pumping Device Helps Frogs Regenerate Lost Limbs

As autumn gives way to winter in the northern hemisphere, it’s sometimes easy to forget that the planet is getting hotter. Air conditioners and electric fans account for <a href="https://www.iea.org/newsroom/news/2018/may/air-conditioning-use-emerges-as-one-of-the-key-drivers-of-global-electricity-dema.html">about 10 percent of global electricity consumption today</a>—and as average global temperatures continue to rise, the world’s reliance on air conditioners will likely more than triple by 2050.This has created a bit of a vicious cycle. Homes in the United States alone expel <a href="https://www.energy.gov/energysaver/home-cooling-systems/air-conditioning">over 100 million tons of carbon dioxide</a> into the atmosphere each year from AC alone, nudging temps further upwards—and prompting people around the world to seek even more solace in temperature-controlled buildings.But researchers are now developing tools that allow us to boot unwanted heat into outer space without using any of the power air conditioning requires. Today, in the journal Joule, a team from Stanford University takes the innovation <a href="https://www.cell.com/joule/fulltext/S2542-4351(18)30471-9">one step further</a> with a device that could not only keep us cool in the absence of air conditioning, but also simultaneously harness <a href="https://www.pbs.org/wgbh/nova/tech/how-solar-cell-works.html">solar power</a> to meet energy demands elsewhere in the grid.
 

 
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 The cooling half of this new technology, pioneered by electrical engineer <a href="https://web.stanford.edu/group/fan/">Shanhui Fan</a> of Stanford University, takes advantage of the natural ability of all objects and organisms to emanate heat through radiation. Unlike conduction and convection—the other methods through which <a href="https://mass.pbslearningmedia.org/resource/lsps07-sci-phys-thermalenergy/thermal-energy-transfer/">thermal energy is transferred</a>—radiation doesn’t require direct contact or the movement of fluids to move heat from place to place: It simply emanates from all matter that’s at a temperature above absolute zero (or -459.67 degrees Fahrenheit… so, for all intents and purposes, let’s call it “all matter”). For example, radiation is responsible for the heat you feel wafting out from a toasty oven even when its door is shut.Through radiation, heat can be jettisoned spaceward—and if it clears the hurdle of the atmosphere, then it’s past the point of no return: Outer space is pretty much a vast, insatiable heat sink. Unfortunately, though, outbound radiation of most wavelengths doesn’t always make it that far. Some of it ricochets off water molecules in the atmosphere and boomerangs right back to Earth; another portion in the is absorbed and retained in the atmosphere by carbon dioxide and other greenhouse gases.But not all materials emit radiation at the same wavelength. If a surface emits radiation with a wavelength between eight and 13 micrometers, it hits a sweet spot that bypasses many of these atmospheric hurdles. By slipping through this mid-infrared “window,” heat can finally enter cold, cold space—allowing the radiating object to dip below the temperature of the surrounding air. Voilà: cooling achievement unlocked.<div>
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Fan and his colleagues first exploited this window and its associated chill factor in 2014, with the design of a so-called radiative cooler. Because the device was engineered with silicon compounds and other materials that emit in the mid-infrared range, it was able to remain <a href="https://www.nature.com/articles/nature13883?foxtrotcallback=true">around 5 degrees Celsius (or 9 degrees Fahrenheit) below</a> ambient air temperatures while atop the roof of a building in sunny California. Two years later, Fan’s lab published a follow-up that used a similar setup to <a href="https://www.nature.com/articles/nenergy2017143">cool flowing water</a>—a breakthrough that, if scaled up appropriately, could reduce the reliance of air conditioning and refrigeration on electricity.For Fan, outer space is the ultimate untapped well of renewable energy. One of the most exciting potential applications of this technology involves speckling the world’s rooftops with radiative coolers. Unfortunately, this move could ruffle the feathers of those attempting to do the same with solar absorbers and solar cells, which typically colonize that same space to harvest energy from the Sun.At first glance, the two strategies seem incompatible: one hungers for heat, while the other is keen on keeping cool: Placing conventional radiative coolers and solar panels side-by-side could even reduce the efficiency of both processes. But as humankind struggles to curb carbon emissions, it’s pretty clear we need all the help we can get. Together with lead author <a href="https://sites.google.com/site/zchen0203/">Zhen Chen</a>, a mechanical engineer at the Southeast University of China, Fan assembled a team of researchers to engineer a peaceful coexistence between the two technologies.
 

 
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 “The solar energy that’s coming into Earth must eventually come out of Earth,” Fan explains. “So these technologies are complementary: Solar energy harvesting is trying to benefit from the incoming flux of energy, while radiative cooling is trying to benefit from outgoing flux.”In fact, the spectrum of the Sun’s energy most relevant for a solar panel doesn’t actually overlap with the mid-infrared window—meaning that even if the two devices were stacked atop one another, they wouldn’t have to cancel each other out. To put this idea to the test, Chen, Fan, and their colleagues slid a silicon-based radiative cooler beneath a germanium solar absorber, which soaks in sunlight for the purposes of energy-efficient heating (not to be confused with a solar cell, which adds in the extra step of converting this energy into electricity). Unlike conventional solar absorbers, however, this particular panel is transparent to radiation in that mid-infrared range of eight to 13 micrometers. This allows the cooler to pass infrared heat through the solar absorber and eject it into space unimpeded.Importantly, the two layers of this device operate completely independently of each other. The solar absorber hoards heat—but none of this energy needs to be funneled to the radiative cooler below, which, by definition, works power-free. This means that the solar payload collected above can, theoretically, be routed elsewhere.
 <figure class="richtext-image full-width"><img alt="184921.jpg" class="richtext-image full-width" height="533" width="800"
 src="https://www.pbs.org/wgbh/nova/media/images/184921.width-800.jpg"/><figcaption>The researchers&#x27; double-layered rooftop panel. On the bottom is a radiative cooler that emits heat in the mid-infrared range into outer space. On top is a solar absorber that is transparent in the aforementioned infrared range. Photo Credit: Linda Cicero, Stanford News<div class="credit"></div></figcaption>
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 While the two halves of this device aren’t interdependent, they can still benefit from each other’s company. Many conventional radiative coolers function best at night, out of the heat of the Sun; for efficient use in the daytime, the devices need <a href="https://www.nature.com/articles/nature13883?foxtrotcallback=true">highly reflective surfaces</a> capable of deflecting light. While this keeps the temperature down, it also wastes what could otherwise be a serious kick of solar power. With the solar panel on top sponging up sunlight, though, the cooler doesn’t need this reflective boost.Shielded by the solar panel, the temperature of the team’s radiative cooler plunged as low as 29 degrees Celsius (52 degrees Fahrenheit) below ambient temperature, while the absorber roasted at a pleasant 24 degrees Celsius (43 degrees Fahrenheit) above the surrounding air—an enormous differential. One immediate application, Chen says, has already revealed itself: The temperature gradient created by these two extremes could eventually be harnessed to power <a href="https://www.youtube.com/watch?v=p1woKh2mdVQ">a thermal engine</a>.Even more exciting to Chen and Fan is the idea of replacing the solar absorber half of their device with an electricity-generating solar cell. If this switch pans out, the dual-action technology could serve as a supplement to our conventional, electricity-sapping cooling methods while simultaneously supplying a source of renewable energy.“We’re trying to change how people view rooftops to harvest renewable energy,” Chen explains. “On hot summer days, you could continuously harvest electricity, and at the same time, you could use the device to cool down your house.”
 

 
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 However, Chen doesn’t think radiative cooling will ever progress to the point of completely replacing air conditioning or refrigeration. Even the <a href="http://science.sciencemag.org/content/early/2017/02/08/science.aai7899">highest-efficiency coolers</a> would probably need to be scaled up to cover entire rooftops or more—probably an untenable engineering ask, especially given the costs of the materials the team used in their prototype. The mid-infrared window also bangs shut on cloudy or rainy days, making this technology the most literal of fair-weather friends. But, Chen explains, radiative cooling could still have its day in the Sun (on a small scale, at least) in arid climes or regions with inconsistent access to power. The researchers are also looking into rebuilding their apparatus with more cost-effective materials.In the meantime, there are still many technological roadblocks to clear. While the theory behind the methods is elegant, explains <a href="https://daedalus.caltech.edu/team-member/dr-emily-warmann/">Emily Warmann</a>, a mechanical engineer studying solar cells at the California Institute of Technology who did not participate in the study, “any practical implications are very, very far away.” Simple though they sound, the necessary tweaks to boost the device’s efficiency, or make the swap from solar absorber to solar cell, could very well compromise the panel’s critical infrared transparency.Furthermore, the prototype’s radiative cooler is sealed up in a vacuum chamber to minimize unwanted heat loss through conduction and convection. To function as an air conditioning or refrigeration alternative, as in their previous work, it would need access to water—but the exposure to the surrounding air would slash its cooling capabilities <a href="https://www.nature.com/articles/nenergy2017143">back down to about 5 degrees Celsius (9 degrees Fahrenheit) below ambient temperature</a>, as opposed to the 29 degrees Celsius (52 degrees Fahrenheit) achieved within the vacuum.<div>
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Despite these obstacles, Chen, Fan, and their colleagues have demonstrated something new and important, says <a href="https://www.researchgate.net/scientific-contributions/2030818528_Mark_A_Nurge">Mark Nurge</a>, a physicist at NASA’s Applied Physics Lab who did not contribute to the new finding. For the first time, it’s clear from the one-two punch of this device that these two sources of renewable energy don’t have to jostle for space—and with radiative cooling on our side, even the sky is no longer the limit.“This is a creative idea,” says <a href="http://www.schlaucohenlab.com/">Gabriela Schlau-Cohen</a>, a chemist studying light harvesting at the Massachusetts Institute of Technology who was not involved in the study. “If we want to actually address our growing energy needs, we need to do it in a way that’s paradigm shifting. And that means ideas that are different than incremental improvements on our current structure.”

Engineers Shanhui Fan (left) and Zhen Chen (right) with their dual-action device, which simultaneously harvests solar energy and cools surfaces without the need for electricity. Photo Credit: Linda Cicero, Stanford News

Scientists are pioneering technology that may someday cool buildings without electricity, while harvesting solar energy at the same time.

The Forecast on Energy-Efficient Cooling Just Got a Bit Sunnier

The viruses that cause <a href="https://mass.pbslearningmedia.org/resource/den08.sci.life.stru.dengue/dengue-virus-invades-a-cell/">dengue</a> fever and <a href="https://www.pbs.org/wgbh/nova/video/zika-the-untold-story">Zika</a> fever have established themselves as formidable forces of devastation. About <a href="http://www.who.int/news-room/fact-sheets/detail/dengue-and-severe-dengue">390 million</a> dengue infections occur globally each year, and 3.9 billion people worldwide—over half the human population—are at risk of infection. Zika is newer to the scene, but infections have already been reported in <a href="http://www.who.int/news-room/fact-sheets/detail/zika-virus">at least 86 countries</a>.Though neither disease carries a particularly high fatality rate, it appears that these stealthy viruses are capable of leaving their mark on a person long after they’ve vacated the body—in a way that could affect the health of generations to come.Today, in the journal Cell Host &amp; Microbe, two new studies report that dengue and Zika viruses may be exploiting a loophole in the human immune system that enhances the severity of both diseases. In the <a href="https://www.cell.com/cell-host-microbe/fulltext/S1931-3128(18)30499-2">first article</a>, a group at the La Jolla Institute for Immunology shows that having a mother who survived Zika may inadvertently worsen the symptoms of dengue in young offspring; in the <a href="https://www.cell.com/cell-host-microbe/fulltext/S1931-3128(18)30546-8">second</a>, researchers from Emory University indicate that fetuses with mothers previously infected with dengue virus may be at a higher risk of acquiring Zika through the placenta.
 

 
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 The viruses that cause dengue and Zika are closely related, making it easy for the human body to confuse one for the other. This results in a bait-and-switch: When one of these viruses is misidentified, it’s able to conscript the body’s own immune molecules into ushering the pathogen into a susceptible cell. Because dengue and Zika viruses often run rampant in the same geographic regions, especially in the Americas, the new findings underscore the lasting effects of outbreaks, but could also inform the development of future <a href="https://www.pbs.org/wgbh/nova/video/vaccinescalling-the-shots/">vaccines</a>.“These are both really great studies,” says <a href="http://labs.icahn.mssm.edu/lim-lab/dr-lim/">Jean Lim</a>, an immunologist at the Icahn School of Medicine at Mount Sinai who was not involved in the research. “They’re really adding important clues about Zika and dengue, and how preexisting immunity impacts another virus.”Normally, when a virus infects a human, the <a href="https://www.pbs.org/wgbh/nova/video/immunity-and-vaccines-explained">immune system</a> dispatches a cavalry of neutralizing antibodies—Y-shaped molecules that recognize a specific feature of the pathogen, latch onto its surface, and block it from infecting cells. The virus, now coated with a cluster of antibodies, is then swallowed whole and destroyed by white blood cells. If the same virus ever tries to set up shop in the body again, the immune system will recall previous infections and rouse the same set of antibodies to nullify the threat before it can do any significant damage.
 <figure class="richtext-image full-width"><img alt="Jenna Hambrick La Jolla Institute for Immunology.jpg" class="richtext-image full-width" height="483" width="800"
 src="https://www.pbs.org/wgbh/nova/media/images/Jenna_Hambrick_La_Jolla_Institute_for_Immunolo.width-800.jpg"/><figcaption>Many of the world&#x27;s tropical regions are home to the viruses that cause dengue and Zika, increasing the likelihood that individuals may be infected with both pathogens in a single lifetime, or pass compromising antibodies from mother to child. Photo Credit: Jenna Hambrick, La Jolla Institute for Immunology<div class="credit"></div></figcaption>
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 But dengue has a bad reputation for refusing to play by the rules. Many different subtypes of this virus exist, and surviving infection with one subtype doesn’t guarantee protection from another. In fact, these subsequent viral encounters can often be far worse than the first. When neutralizing antibodies that have been trained on one dengue subtype run up against another many years later, two issues may arise. First, the virus is just different enough that antibodies will bind poorly to its surface. Second, antibody levels eventually wane in the body, and there are fewer around to put the virus out of commission.As a result of these dips in quality or quantity, the antibodies that confront the new virus fail to disarm it—and when white blood cells arrive on scene to clean up the mess, dengue is gobbled up in a still-active form. From here, the virus will replicate and destroy the immune cell, perpetuating the cycle of infection. This phenomenon, in which antibodies become a composite Trojan horse that unwittingly chauffeurs viruses into these vulnerable cells, is called <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3185591/">antibody-dependent enhancement</a>.To make matters worse, antibody-dependent enhancement doesn’t just cause problems for <a href="http://science.sciencemag.org/content/358/6365/929">individuals infected with multiple strains of dengue</a>. As they develop, fetuses inherit antibodies from their mothers through the placenta. These antibodies stick around throughout the first year or so of life as the offspring develop their own immune systems. But if their mothers happened to have even a glancing blow with dengue, <a href="https://academic.oup.com/femspd/article/59/2/119/647508">babies can be at high risk</a> for <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4340501/">developing severe dengue</a> if they’re infected with a different subtype in the months after birth, while their bodies still contain maternal antibodies.
 

 
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 So when a very similar-looking virus called Zika began causing serious outbreaks a few years ago, researchers like <a href="https://www.lji.org/faculty-research/labs/shresta/">Sujan Shresta</a>, an immunologist at the La Jolla Institute for Immunology and senior author of the <a href="https://www.cell.com/cell-host-microbe/fulltext/S1931-3128(18)30499-2">first study</a>, began to worry. Zika belongs to the same group of viruses as dengue—flaviviruses—which also include the nasty pathogens that cause West Nile fever, yellow fever, and Japanese encephalitis. If Zika was popping up in the same areas as its infectious cousin, Shresta reasoned, the same-same-but-different concept of antibody-dependent enhancement could spell trouble for the countless individuals and their children exposed to both viruses.Shresta and her colleagues, led by immunologist <a href="https://www.lji.org/careers/postdoctoral-association/#executive-committee">Angela Fowler</a>, decided to test if a mouse mother’s previous Zika infection could worsen dengue symptoms in her offspring. The researchers infected two groups of mouse pups with Zika: one set born to mothers who had been previously infected with Zika virus, and the other born to mothers who hadn’t. They found that the first group of pups had acquired Zika antibodies from their mothers, and were consequently protected from Zika infection, showing that the antibodies were active against their intended target. But when the team repeated their experiment, this time exposing the pups to dengue, the antibodies were instead weaponized by the new virus: The pups who had inherited Zika antibodies suffered more severe dengue symptoms and were more likely to die from the infection.When the researchers next assessed the ability of these maternal Zika antibodies to subdue dengue, unsurprisingly, they weren’t up to snuff. While the antibodies were able to attach to dengue, they did nothing to neutralize it. Instead, they seemed to do the opposite, ferrying the virus into the arms of unsuspecting cells.
 <figure class="richtext-image full-width"><img alt="placental macrophages with Zika Mehul Suthar Matt Zimmerman Emory University.jpg" class="richtext-image full-width" height="471" width="800"
 src="https://www.pbs.org/wgbh/nova/media/images/placental_macrophages_with_Zika_Mehul_Suthar_M.width-800.jpg"/><figcaption>Placental immune cells infected with Zika virus. Zika may more easily infect placental cells by hitching a ride on maternal antibodies to dengue virus. Photo Credit: Mehul Suthar &amp; Matt Zimmerman, Emory University<div class="credit"></div></figcaption>
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 “The antibody responses to these viruses are highly complex,” Shresta explains. “One infection can affect subsequent ones, and in this case, the antibody response to Zika has an enhancing effect on dengue.”And the problem of mistaken identity between dengue and Zika could be a two way street. In the <a href="https://www.cell.com/cell-host-microbe/fulltext/S1931-3128(18)30546-8">second study</a>, <a href="http://vaccines.emory.edu/faculty-evc/primary-faculty/suthar_mehul.html">Mehul Suthar</a> and <a href="https://med.emory.edu/MDPHD/trainees/current_students/zimmerman_matthew.html">Matthew Zimmerman</a>, immunologists at Emory University, led a team of researchers in testing this possibility.One of the most dangerous aspects of a Zika infection is the virus’ ability to cross a mother’s placenta into her fetus, often leading to severe birth <a href="https://www.pbs.org/wgbh/nova/article/birth-defects-20-times-higher-for-women-infected-with-zika/">defects</a> like microcephaly. If dengue antibodies have a nasty tendency to guide similar-looking viruses into cells, it’s possible a placental Zika infection could be exacerbated by this inappropriate immune response, endangering a child before it’s even born.
 

 
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 Unlike the previous study, which used mice, Suthar and his team conducted their experiments on human placental immune cells. When the researchers introduced only Zika to the cells, very few viruses took hold—but if they added dengue antibodies to the mix, the antibodies stuck to the viruses and shepherded them into the cells, where Zika quickly multiplied. This could be a clear-cut way for Zika to pass easily from mother to child, explains Zimmerman, “as if the virus is hitching a ride on a normal, physiological system.”A preexisting dengue infection is by no means necessary for Zika to have devastating effects on a developing fetus, Suthar says, and antibody-dependent enhancement is unlikely to be the only way Zika traverses the placental barrier. However, the researchers’ experiments highlight a subtle way Zika can hijack the body to some potentially devastating ends. Millions of women worldwide harbor low levels of dengue antibodies in their blood from prior exposures—and because infections are often asymptomatic, many of those interested in having children may be unaware of just how vulnerable their fetuses could be to Zika.Of course, neither mice nor donated placental tissue is a perfect stand-in for a human. For instance, mice often have to be genetically manipulated to become susceptible to dengue virus, explains <a href="http://facultypages.vetmed.lsu.edu/faculty/rcarri1">Rebecca Christofferson</a>, an infectious disease expert at Louisiana State University who did not contribute to the new findings. Additionally, antibody-dependent enhancement is often easier to show in cells growing in a dish than in the body of a living animal. But simply raising the possibility of one virus feeding off the dregs of the response to another could make a huge difference in preventing future outbreaks.
 <figure class="richtext-image full-width"><img alt="Sanofi Pasteur : Gabriel Lehto : Novas Imagens Cine Video.jpg" class="richtext-image full-width" height="533" width="800"
 src="https://www.pbs.org/wgbh/nova/media/images/Sanofi_Pasteur__Gabriel_Lehto__Novas_Imagens_C.width-800.jpg"/><figcaption>Future dengue and Zika vaccines may need to be designed carefully to avoid antibody-dependent enhancement of other flaviviruses. Photo Credit: Sanofi Pasteur, Gabriel Lehto, Novas Imagens Cine Video<div class="credit"></div></figcaption>
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 The new findings may also affect how researchers counteract these diseases in the future. Infections aren’t the only ways a body can generate antibodies—vaccines for either dengue or Zika would induce their production as well. Vaccine safety may need to be re-evaluated in areas where both viruses are prevalent, explains <a href="https://pediatrics.duke.edu/faculty/sallie-robey-permar-md-phd">Sallie Permar</a>, an immunologist at the Duke University School of Medicine who did not participate in the research, so that protection against one disease doesn’t accidentally exacerbate another. Still, this doesn’t invalidate vaccination in the fight against these pathogens: Rather, with the issue of antibody-dependent enhancement in mind, some of the most effective vaccines of the future might be carefully concocted mixtures of strong, neutralizing antibodies active against multiple flaviviruses.And far more than the potential synergy between dengue and Zika may be at play, Christofferson points out. There’s limited evidence that other flaviviruses like <a href="https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0001311">Japanese encephalitis virus</a> might also augment the severity of future dengue infections, but it’s still unclear how widespread antibody-dependent enhancement really is outside the lab. More research is needed—and now that more and more countries harbor multiple flaviviruses, Shresta explains, the urgency of understanding these threats is greater than ever.The critical next experiments will be epidemiological studies in humans, says <a href="https://www2.fgcu.edu/CAS/879.asp">Sharon Isern</a>, a virologist at Florida Gulf Coast University who was not involved in the studies. Such future work will be challenging, requiring large numbers of people and extensive clinical history, but reports like these underscore the importance of human-centric follow-up.“Animal models provide good information,” Isern adds, “but the answers are in large human populations.”

James Gathany, courtesy of Centers for Disease Control aedes aegypti.jpg

Aedes aegypti mosquitoes thrive in the world's tropics and can carry the viruses that cause dengue fever and Zika fever, among others. Photo Credit: James Gathany, Centers for Disease Control

Due to the similarities between these closely-related viruses, mothers who have experienced Zika infections may have babies with a higher risk of suffering severe dengue, and vice versa.

How Zika and Dengue Exploit the Mother-Child Relationship

Can you suffer the symptoms of jet lag without even stepping foot outside your current time zone? Much to the chagrin of the reluctant traveler, the answer is apparently yes.And, if you’re reading this, you probably already have. A hefty chunk of the human population—especially those living in particularly plugged-in parts of the world—maintains a different sleep schedule on weekdays than on weekends, staying up later and sleeping in on their days off from work.This phenomenon of so-called <a href="https://www.cell.com/current-biology/fulltext/S0960-9822(12)00325-9?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0960982212003259%3Fshowall%3Dtrue">social jet lag</a> is so ingrained in us that, according to <a href="https://www.cell.com/current-biology/fulltext/S0960-9822(18)31345-9">a new study</a>, it’s even reflected in how we tweet—and the offset could be taking a serious toll on our health.“This study is indicative of the amazing amount of data that’s out there,” says <a href="https://www.imp.med.uni-muenchen.de/research/molecular_chronobiology-merrow/index.html">Martha Merrow</a>, who studies the biology of sleep at the Ludwig Maximilian University of Munich’s Institute of Medical Physiology, but did not participate in the research. “It shows the power of social media in revealing aspects of human behavior to us.”
 

 
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 When left to their own devices, our bodies’ internal clocks naturally respond to sunlight, the evolutionarily-ancient cue of the day’s beginning and end. But in the last few centuries, humans have retreated indoors for both business and pleasure, diminishing our exposure to the outside environment and gradually uncoupling our physiologies from the Sun. Now, rather than being governed by available daylight, our schedules are shackled to the constantly changing demands of society. And as a result, there’s a serious mismatch between the times we’re asleep on weekdays versus weekends.“There’s this persistent idea that light, because it’s not tangible, doesn’t have an effect on your body,” says study author <a href="http://oliviawalch.com/">Olivia Walch</a>, a mathematician and sleep researcher at the University of Michigan. “And that’s not true. Light is this huge factor in sleep that doesn’t get the credit it deserves.”
 <figure class="richtext-image full-width"><img alt="StockSnap pixabay.jpg" class="richtext-image full-width" height="532" width="800"
 src="https://www.pbs.org/wgbh/nova/media/images/StockSnap_pixabay.width-800.jpg"/><figcaption>For most of human existence, natural sunlight has driven our sleep-wake cycles. But now, most people&#x27;s schedules are severely uncoupled from the Sun. Photo Credit: StockSnap, Pixabay<div class="credit"></div></figcaption>
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 Social jet lag tends to go hand-in-hand with chronic sleep-deprivation, which itself is a public health issue that costs the United States <a href="https://www.rand.org/pubs/research_reports/RR1791.html">up to $411 billion</a>—over 2 percent of our gross domestic product—each year. But for most individuals, social jet lag also entails being active when one should be asleep and vice versa, putting people in all-too-frequent states of physiological disorientation. The effects of social jet lag spill over to many other aspects of health and wellbeing: Toiling through this weekly flux has been tied to <a href="https://www.cell.com/current-biology/fulltext/S0960-9822(16)30333-5">heavier drinking</a> and <a href="https://www.dovepress.com/social-jetlag-in-health-and-behavioral-research-a-systematic-review-peer-reviewed-fulltext-article-CPT">smoking</a>, as well as <a href="https://linkinghub.elsevier.com/retrieve/pii/S0960-9822(12)00325-9">obesity</a>, <a href="https://www.dovepress.com/social-jetlag-in-health-and-behavioral-research-a-systematic-review-peer-reviewed-fulltext-article-CPT">depression</a>, and even <a href="https://www.nature.com/articles/s41598-018-23044-8">decreased academic performance</a>.Not everyone experiences social jet lag in the same way. On the one hand, each person’s internal clock is unique. Some people are early risers, while others are night owls, for example—and it’s often the latter group that struggles the most transitioning between the slog of early weekday mornings and their more natural nocturnal pattern on weekends. Even the duration of someone’s morning commute or the latitude of one’s hometown can affect the ways in which an individual experiences, and thus suffers from, sleep schedule variations.Gathering this kind of data can be tough through traditional mail-and-return surveys, especially considering the staggering diversity of culture, climate, and careers in the United States alone. So a team of researchers, led by biophysicist <a href="https://biophysics.uchicago.edu/the-students/eugene_leypunskiy/">Eugene Leypunskiy</a> and biologist <a href="http://rustlab.uchicago.edu/people.html">Michael Rust</a> of the University of Chicago, looked to the modern era’s best proxy for human behavior: the Internet—more specifically, the social media juggernaut of Twitter.
 

 
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 The new report, <a href="https://www.cell.com/current-biology/fulltext/S0960-9822(18)31345-9">published today</a> in the journal Current Biology, tracks every publicly available, geographically-tagged tweet from the beginning of 2012 to the end of 2013—two years of data from about 246,000 Twitter users in 1,521 counties across the entire United States. “We weren’t interested in looking at what people were tweeting, but when they were tweeting,” Rust explains.The researchers found that, across the country, tweets—like many Americans—rose slowly in the morning, increased steadily to a peak in the afternoon or evening, then dipped back down at typical bedtimes. Lengthy lulls in Twitter activity indicated when people were probably asleep. And, as expected, these tweeting troughs shifted to later intervals on weekends relative to weekdays. Across counties, the average amount of “Twitter social jet lag”—or the amount of time people were shifting their sleep schedules between work and free days—clocked in at about 75 minutes.When the researchers mapped tweeting patterns across time zones, they discovered striking differences based on geography. For one, latitude and longitude both had an effect on social media habits. In general, tweeters in the American Southwest took longer breaks at bedtime than their Central U.S. and Northeastern counterparts and had less social jet lag overall. The westernmost counties within time zones, however, experienced more pronounced social jetlag—which may have to do with the fact that the Sun rises later in local time in these regions.
 <figure class="richtext-image full-width"><img alt="kansas city traffic Thomanication flickr.jpg" class="richtext-image full-width" height="530" width="800"
 src="https://www.pbs.org/wgbh/nova/media/images/kansas_city_traffic_Thomanication_flickr.width-800.jpg"/><figcaption>Something as subtle as the length of a person’s morning commute can affect the severity of social jet lag. Individuals with long, early commutes may not be sleeping for as long as they need to, or be waking up much earlier than they naturally would. Photo Credit: Thomanication, flickr<div class="credit"></div></figcaption>
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 Across counties, certain lifestyle habits also seemed to predict a higher degree of social jet lag, including earlier average start times for commutes and the proportion of the population involved in shift work—both of which may indicate less flexibility in weekday schedules. Pronounced Twitter social jet lag also coincided with higher obesity rates, mirroring <a href="https://linkinghub.elsevier.com/retrieve/pii/S0960-9822(12)00325-9">previous findings</a>.Additionally, Twitter social jet lag ebbed and flowed with the seasons. The sleep schedule mismatch was most severe in early autumn and late winter, but mellowed out during the summer. When the researchers examined the relationship closer, they found that a common contributor to this pattern was the occurrence of summer breaks from school, during which some families seemed shift their weekday sleep cycles later to more closely match their (likely more biologically natural) weekend schedules. The same rules appeared to apply to school holidays spiked intermittently throughout the rest of the year.“The amount of social jet lag can be thought of as a proxy for how on vacation these places are,” Walch explains.Not all counties experienced reprieve from social jet lag in the summer, however. Certain locales felt the same amount of mismatch year-round—and these counties also tended to be more urban, and host residents that attended college, commuted late in the day, and were less likely to smoke or be obese.
 

 
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 Because counties vary in not only their physical location, but also countless cultural characteristics, Rust says, it’s still difficult to disentangle exactly what factors contribute the most to social jet lag place by place. “We were looking at 1500 counties in the US,” Leypunskiy adds, “and every single one tells its own story.”But Merrow suggests it’s likely that culture plays a role. For instance, the tweeters of Orange County, California appear to have longer nighttime lulls in Twitter activity and milder social jet lag than Lafayette County, Louisiana—but the two counties lie at similar latitudes, indicating that the drivers behind behavior may be more complicated than sunlight exposure.Fortunately, there may still be a silver lining to the plight of social jet lag. <a href="https://www.mcn.uni-muenchen.de/members/regular/roenneberg/index.html">Till Roenneberg</a>, a sleep biologist at the Ludwig Maximilian University of Munich’s Institute of Medical Physiology, advises trying to tailor our schedules to our natural rhythms—which inevitably differ from person to person. Night owls, for instance, may benefit from nudging their work schedules later—a strategy that could help close the gap between weekday and weekend sleep habits without compromising total rest. But of course, not everyone has this flexibility. According to Roenneberg, society has yet to wake up to the idea of respecting sleep.An easier fix? Simply being a little more aware of our exposure to light at both appropriate and inappropriate times, Walch says. If your goal is to fall asleep earlier at night, you might try <a href="https://www.scientificamerican.com/article/q-a-why-is-blue-light-before-bedtime-bad-for-sleep/">minimizing evening phone time</a> (or, at the very least, use an app that will filter out the stuff most likely to mess with our internal clocks: <a href="https://www.health.harvard.edu/staying-healthy/blue-light-has-a-dark-side">short wavelength blue light</a>). Or take it a step further and avoid bright electronics entirely in the hours before bedtime—even if it means forsaking that final midnight tweet.
 <figure class="richtext-image full-width"><img alt="Tookapic Pexels.jpg" class="richtext-image full-width" height="531" width="800"
 src="https://www.pbs.org/wgbh/nova/media/images/Tookapic_Pexels.width-800.jpg"/><figcaption>Exposure to artificial light late at night can negatively affect sleep-wake cycles by tricking the body&#x27;s internal clock. As a result, many of us may be active when we should be asleep, and asleep when we should be active. Photo Credit: Tookapic, Pexels<div class="credit"></div></figcaption>
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 “Social jet lag is something people experience all the time and don’t even realize it,” Leypunskiy says. “And I think if people want to change it, they have the means to do it… but it’s probably not a one-size-fits-all thing.”In the future, Rust hopes to zoom in on the biology of sleep at an individual level. Aggregations of tweets can only tell us about the average activity of a whole county, he explains. But gathering information from something like a Fitbit or other personal health monitor—with appropriate consent—could shed light on each person’s behaviors, patterns, and preferences.Even a future analysis of the content of tweets could be informative about the culture of social jet lag, says <a href="http://cs.iit.edu/~culotta/">Aron Culotta</a>, a computer scientist who conducts social media analysis at the Illinois Institute of Technology. “That’s one huge advantage of social media,” he explains. “You get to explore the ‘why’ behind a behavior.”However, Culotta cautions that, as with any work that draws from social media, findings from a subset of the population may not always capture the entire picture. Not everyone’s on Twitter—and there could be bias in the way people tweet on weekdays versus weekends. Nonetheless, he praised the current study for its “rigorous approach” to social jet lag research.For Rust, this study has already showcased the astounding diversity of humankind. “Many of us live in bubbles and see people who live similar lives to us,” he says. “But the way people live their lives and structure their time is very different—it isn’t like there’s a generic American.”

Many people maintain a different sleep schedule on weekdays than on weekends, with potentially serious health consequences—but scientists can now track this form of “jet lag” using Twitter. Photo Credit: pxhere

A two-year analysis of nearly a quarter of a million Twitter users reveals how Americans’ social lives are taking a toll on their sleep schedules.

Scientists Track “Social Jet Lag” Sleeping Habits With Twitter Data

A new treatment for <a href="https://www.pbs.org/wgbh/nova/video/can-alzheimers-be-stopped">Alzheimer’s disease</a> might now be in the works—and it targets a microbe found in your mouth.A <a href="http://advances.sciencemag.org/content/5/1/eaau3333">study</a> published today in the journal Science Advances pinpoints an unlikely villain in neurodegenerative disease: Porphyromonas gingivalis, a bacterium known to cause gum disease, might be capable of traversing the path from mouth to brain, where it can trigger chemical changes that damage cognitive function. These findings suggest that some cases of Alzheimer’s might have an infectious cause—and a new drug that blocks this process is now in clinical trials.“This is very exciting in many ways,” says <a href="https://www.uclan.ac.uk/staff_profiles/dr_sim_k_singhrao.php">Sim Singhrao</a>, who studies neurodegenerative disease at the University of Central Lancashire in the United Kingdom, but was not involved in the new study. “This work not only highlights the problem of poor oral hygiene as a risk factor for Alzheimer’s, but it might also offer a futuristic solution.”
 

 
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 P. gingivalis is best known for causing periodontitis, an inflammatory disease that steadily eats away at gums and bone that support teeth, due in part to this microbe’s production of gingipains, powerful enzymes that chew through other proteins. But in recent years, scientists <a href="https://www.pbs.org/wgbh/nova/article/alzheimers-disease-may-be-caused-by-brain-infections/">have begun</a> to tentatively link Alzheimer’s disease to <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4430664/">P. gingivalis infection</a>—pointing to the possibility that these mouth-loving microbes might have the capacity to set up shop in the brain.In the new study, a team led by Stephen Dominy and Casey Lynch of Cortexyme, a San Francisco-based company developing Alzheimer’s therapeutics, found bacterial gingipains in the brains of over 90 percent of a group of more than 50 deceased Alzheimer’s patients. And the more gingipains an individual had, the more that brain showed chemical signs of deterioration, including the accumulation of a protein called tau. Under normal circumstances, tau helps neurons maintain structural integrity. But in brains progressing toward Alzheimer’s, this protein can undergo abnormal chemical changes and tangle into knots inside brain cells, compromising their ability to send each other signals.
 <figure class="richtext-image full-width"><img alt="150210-F-LM669-064.JPG" class="richtext-image full-width" height="534" width="800"
 src="https://www.pbs.org/wgbh/nova/media/images/150210-F-LM669-064.width-800.jpg"/><figcaption>Porphyromonas gingivalis, a bacterial species that&#x27;s known to cause gum disease, might be capable of infiltrating the brain. Once there, its presence could trigger an immune response that ultimately compromises the function of brain cells. Image Credit: Airman 1st Class Dillian Bamman, U.S. Air Force<div class="credit"></div></figcaption>
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 When the researchers introduced P. gingivalis into the mouths of eight mice, they found that the bacteria migrated into all of their brains within a few weeks. In response to the infection, the mice also seemed to be boosting production of a protein called amyloid beta. Like tau, amyloid beta occurs in the brain naturally but behaves abnormally in Alzheimer’s patients, forming sticky aggregates outside of cells.What amyloid beta does under normal circumstances isn’t well understood. But some researchers, including Dominy and Lynch, believe that it plays a role in the immune system, and is manufactured when the body senses an unwanted microbe. “It’s kind of like the body sending out a little net, saying, ‘I’m going to trap these bacteria,’” Singhrao says.While that might sound like a good thing, amyloid beta’s protective powers might ultimately cause harm. When P. gingivalis infiltrates the brain, amyloid beta could be cued into overdrive—and if these microbe-trapping nets aren’t cleared out of the way, they might glom together, clogging up lines of communication between brain cells. As with the case with tau, these cellular roadblocks could ultimately nudge the brain in the direction of dementia.But Dominy believes there’s more to the issue than an overactive immune system. “We think the gingipains are really the culprit here,” he says. “They’re damaging the brain directly.”
 

 
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 In keeping with this, when the researchers exposed mice to a strain of P. gingivalis that lacked its destructive gingipains, the rodents suffered fewer Alzheimer’s-like changes in their brains. And when P. gingivalis-infected mice were treated with Cortexyme’s new anti-gingipain drug, fewer bacteria invaded the brain and there was less accumulation of amyloid beta.Cortexyme’s drug is already in human clinical trials, and Lynch says the early results are encouraging. Regardless of the outcome for this particular drug, however, the case on Alzheimer’s is far from closed. Stronger links between oral infections and Alzheimer’s still need to be established in humans, says <a href="https://www.nyuwinthrop.org/reiss-allison">Allison Reiss</a>, an Alzheimer’s researcher at New York University’s Winthrop Hospital who was not involved in the new study. After all, she says, while the study’s findings in mice are encouraging, what happens in rodents isn’t always recapitulated in humans.Even if these results pan out in human populations, not all Alzheimer’s patients are the same, says <a href="http://www.bri.ucla.edu/people/ming-guo-md-phd">Ming Guo</a>, a neurologist and Alzheimer’s expert at the University of California, Los Angeles’ Brain Research Institute who was not involved in the new study. It could turn out that bacterial infections are just one possible avenue for dementia and mental decline to progress in what is a notoriously complex disease.“Alzheimer’s is a complex disorder, not a one stop shop,” Reiss says.
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 Plaques that build up between neurons are a hallmark of Alzheimer's.
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 Many other questions remain. It’s still not entirely clear how P. gingivalis breaches the brain’s barriers in mice or humans—or how risky it is to have these bacteria living inside you in the first place. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC105308/">Numbers</a> <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6092461/">vary</a>, but P. gingivalis might live in the mouths of up to <a href="http://www.jicdro.org/article.asp?issn=2231-0754;year=2016;volume=8;issue=2;spage=106;epage=110;aulast=Joshi">40</a> percent of healthy individuals, and many of these individuals will not suffer adverse effects.In other words, a P. gingivalis infection doesn’t guarantee Alzheimer’s, and there’s no conclusive evidence that all Alzheimer’s cases stem from P. gingivalis. Regardless, Singhrao says, it doesn’t hurt to practice good oral hygiene—if not for your mind, then at least for your mouth.
 

 
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As Alzheimer's disease progresses, communication between brain cells breaks down. New research suggests that one possible cause for this deterioration may be a brain infection by Porphyromonas gingivalis, a bacterium known for causing gum disease. Image Credit: National Institute on Aging/NIH, flickr

New research indicates that some cases of Alzheimer’s disease may involve infection by Porphyromonas gingivalis, a bacterial species that’s best known for causing gum disease in the mouth.

Could Alzheimer’s Begin With Bacteria That Cause Gum Disease?

On this particular morning, as he checked the contents of his live traps in the Sand Hills of Nebraska, <a href="https://barrettlab.ca/">Rowan Barrett</a> found himself three for 800. It wasn’t a great start to the day.Not all the traps he’d set out were empty; far from it. But the cache of sunflower seeds within had mostly drawn unwelcome guests: pocket mice, grasshopper mice, and, bizarrely, rattlesnakes. Only a handful contained the deer mice Barrett, now an evolutionary ecologist at McGill University, was after.For weeks on end, Barrett and his team had been rising before the sun, scouring the dusty landscape for traps jiggling with a catch. Their mission was simple: collect about 500 wild deer mice in a variety of colors, and monitor their survival in the Sand Hills—a cascading series of grass-speckled dunes where the shades of soil range from brown to beige.
 <figure class="richtext-image full-width"><img alt="light4.jpg" class="richtext-image full-width" height="397" width="800"
 src="https://www.pbs.org/wgbh/nova/media/images/light4.width-800.jpg"/><figcaption>The Sand Hills of Nebraska, where a team of researchers led by biologists Rowan Barrett and Hopi Hoekstra conducted a large-scale experiment to monitor the survival of a population of deer mice. Image Credit: Rowan Barrett, McGill University<div class="credit"></div></figcaption>
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 Common sense would predict that rodents with coats that blend into their surroundings should be better camouflaged from hungry birds of prey, while mismatched mice, like brunettes on pale sands, would stick out and be quickly gobbled up (spoiler alert: that is, in fact, <a href="http://science.sciencemag.org/cgi/doi/10.1126/science.aav3824">exactly what they found</a>).It sounds simple; even obvious. “You might think, ‘Well, duh, the camouflaged mice survive better,’” Barrett says. “But actually demonstrating that? It’s different than having an intuition about something.”
 

 
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 In fact, the discovery Barrett truly sought was much bigger than mice, an elusive goal biologists have chased for centuries: Capturing a snapshot of <a href="https://www.pbs.org/wgbh/nova/labs/lab/evolution/">evolution</a> happening in real time.It was a daunting task, requiring a tricky trifecta of variables: genes, traits, and survival. Plenty of studies have shown how genetics affect outward characteristics, like <a href="https://www.cancer.gov/about-cancer/causes-prevention/genetics/brca-fact-sheet">BRCA mutations</a> increasing the risk of breast cancer; others clearly demonstrate that observable, physical features can make the difference between life and death, as with black moths that blend into a backdrop of <a href="https://theconversation.com/natural-selection-in-black-and-white-how-industrial-pollution-changed-moths-43061">soot-covered trees</a>. But few have brought all three elements together in a single experiment, pinpointing how genes can dictate survival—especially in mammals.The work of Barrett and his team, <a href="http://science.sciencemag.org/cgi/doi/10.1126/science.aav3824">published today</a> in the journal Science, highlights how the stresses of the natural environment can directly alter the fate of one gene—all within the span of a single generation. In light of our rapidly-changing world, these findings underscore the idea that, even against the complex backdrop of nature, one small shift can permanently tip the scales for an entire population.“This is a beautiful study,” says <a href="https://nature.berkeley.edu/rosenblum/people.html">Obed Hernández-Gómez</a>, an evolutionary biologist and geneticist at the University of California, Berkeley who was not involved in the study. “Recently we’ve looked at genes and understood that evolutionary processes act very quickly. To see that confirmed in this study, and not in a human-mediated environment... This could end up being one of those prominent examples we use to teach biology students in the future.”
 <figure class="richtext-image full-width"><img alt="IMG_1802.JPG" class="richtext-image full-width" height="533" width="800"
 src="https://www.pbs.org/wgbh/nova/media/images/IMG_1802.width-800.jpg"/><figcaption>A young, dark-colored deer mouse on dark soil studded with bright green grass. This rodent might be better camouflaged from birds of prey because it carries a functioning copy of the Agouti gene, which contributes to fur pigmentation. Image Credit: Rowan Barrett, McGill University<div class="credit"></div></figcaption>
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 It’s been over a century and a half since Darwin first put forth his theories on evolution. Scientists have understood the basics of the process for decades. But putting this knowledge to work to forecast the fates of the species that populate the planet, including our own, is still mostly an exercise in futility.“Even after decades of evolutionary research, we’re only beginning to integrate the different types of approaches we need to truly understand the action of evolution,” says <a href="https://lucyaptran.weebly.com/">Lucy Tran</a>, an evolutionary biologist at Arizona State University. Tran is now a postdoctoral researcher in the lab of study author Susanne Pfeifer, but was not directly involved in the study.One thing, though, is certain: Evolution isn’t exclusively the slow, plodding process that Darwin originally envisioned. <a href="https://www.orlandosentinel.com/news/os-evolution-green-brown-lizards-20141101-story.html">Time</a> and <a href="https://www.the-scientist.com/multimedia/infographic-watching-evolution-in-real-time-31599">time</a> again, researchers have shown that it can be <a href="https://www.pbs.org/wgbh/nova/article/darwins-finches-mating-parents/">witnessed</a> in just a matter of years—or even within the span of a single <a href="https://news.harvard.edu/gazette/story/2014/02/evolution-in-real-time/">experiment</a>.“We took our motivation from microbes in lab environments,” Barrett says. One particularly well-known experiment has been monitoring bacteria <a href="http://myxo.css.msu.edu/">for decades</a>. “The crazy idea was, can we do this with a mammal in nature?”
 

 
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 For their test subjects, the team chose deer mice (Peromyscus maniculatus). In these rodents, the two halves of the equation were already there: The general importance of stealth for survival, and a gene, Agouti, known to control the color of fur. “I wanted to put the two bits of this puzzle together,” Barrett says. “No one had done that before.”In retrospect, Barrett says, there was probably a reason for that. The setup was far from trivial.To test mouse survival, the team needed a way to simulate the natural environment. That meant building eight 80-foot-by-80-foot enclosures, four each on dark and light soil. Six enclosures would house between 75 and 100 microchipped mice each; two others would remain empty. This required finding a lot of flat, rodent-friendly land—in a place named for its hills—and corralling herds of mice onto distinctly colored patches of dirt.Easier said than done. “Deer mice are like little ninjas,” Barrett says. “They burrow, they climb. People told me, ‘You’ll never hold them.’”
 <figure class="richtext-image full-width"><img alt="IMG_9116.jpg" class="richtext-image full-width" height="469" width="800"
 src="https://www.pbs.org/wgbh/nova/media/images/IMG_9116.width-800.jpg"/><figcaption>Evolutionary biologist Rowan Barrett basks in the triumph of the research team&#x27;s manmade mouse enclosures in Nebraska&#x27;s Sand Hills. Image Credit: Naomi Man in’t Veld<div class="credit"></div></figcaption>
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 But with steel plate walls buried two-and-a-half feet into the ground, the barriers held. And while each enclosure started off with a mix of light- and dark-colored mice, by the end of three months, their compositions had changed drastically. First off, the populations had been decimated: Hundreds of mice had died, likely picked off by keen-eyed owls. And the surviving mice were only a very particular subset of the original population. Mice with fur to match the soil—like light mice on cream-colored soil—had been the ones to emerge victorious. Their standout brethren, on the other hand, had not.“I didn’t really think that we would see much change over such a short-term experiment,” Barrett says. “This was kind of a Hail Mary.”And when the researchers sequenced the mice’s DNA, they found they had the genes to match. Surviving mice on the dark side tended to carry a normal version of the Agouti gene, which aided the production of pigment in their coats, while the remaining mice in the light enclosures were more likely to carry a broken copy of Agouti that kept them blonde.
 

 
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 Too many mice died in those early months for the experiment to look past the initial cohort of 500 mice, Barrett says. But one look at the Agouti genes of the remaining mice in each enclosure told him that it would be essentially impossible for their offspring to be very diverse, in terms of coat color. For the most part, lighter mice carrying broken Agouti had been left on light soil, and vice versa; future generations would likely reflect this as well. And for Barrett, this probably represented a sped-up version of what had happened naturally on the Sand Hills over the course of many years, ultimately partitioning the rodents by color.“Typically, we would say, for this to be evolution, you need to see if it’s reflected in the next generation,” he says. “But we know [the traits are] going to be transmitted, because we showed changes at the genetic level.”Others, like Tran, are slightly more hesitant to make this conclusion, however. “Multiple generations would provide stronger evidence [of evolution],” she says. “What’s missing in the study is whether these changes are definitely heritable.”Regardless, the study’s ability to link natural selection in the field to a specific gene makes it a “rare gem,” says <a href="http://blog.uvm.edu/mpespeni/">Melissa Pespeni</a>, an evolutionary biologist at the University of Vermont who was not involved in the research.In the future, Barrett and his colleagues hope to extend the study into a multi-generational approach. “This is just the first step in a long-term project,” says study author <a href="https://hoekstra.oeb.harvard.edu/">Hopi Hoekstra</a>, an evolutionary geneticist at Harvard University. But the staggering rates of change the researchers found might still have a lot to say in other contexts—including species conservation.
 <figure class="richtext-image full-width"><img alt="5907607580_da47cdab55_o.jpg" class="richtext-image full-width" height="533" width="800"
 src="https://www.pbs.org/wgbh/nova/media/images/5907607580_da47cdab55_o.width-800.jpg"/><figcaption>“This study is sure to be a classic example of how natural selection works on both an animal’s [physical characteristics] and the genetics associated with them out in the wild,” says <a href="https://www.colorado.edu/ebio/rebecca-safran">Rebecca Safran</a>, an evolutionary ecologist at the University of Colorado Boulder who was not involved in the study. Image Credit: Rowan Barrett, McGill University<div class="credit"></div></figcaption>
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 “The more we can learn about how organisms adapt, the more we’ll know about how organisms might adapt to, for instance, a changing climate,” Hoekstra says.Already, it’s clear that shifts in global temperatures and other human-motivated changes have done some <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5769427/">serious damage</a> to Earth’s inhabitants. <a href="https://www.nature.com/articles/ncomms1213">Owls</a> are molting out of paler shades in response to warming winters; <a href="https://www.pbs.org/wgbh/nova/article/feminized-turtle-populations-in-trouble/">sea turtle</a> populations with temperature-dependent sex determination systems are skewing heavily female.“A major lesson here is to preserve genetic diversity,” Hernández-Gómez says. “We might lose genes that might be beneficial in the future if we don’t.”Some species may be flexible in the face of harsh environmental change. With others, though, one variable could be all it takes to transform an entire population in just a handful of weeks.As for passing these changes down through the generations? Well—that’s a mouse of a different color.

A light-colored deer mouse (Peromyscus maniculatus) on dark soil in the Sand Hills of Nebraska. This poorly camouflaged rodent might not survive much longer, as it's easily spotted by hungry owls scouring the landscape for prey. Image Credit: Rowan Barrett, McGill University

By watching a population of deer mice shift in the span of a single generation, scientists have captured evolution in action, connecting genes to survival in the wild.

Katherine J. Wu

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