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.

Koch Foundation

Draper





  
      <div class="rich-text"><p>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.</p><p>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.</p><p>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 <i>Joule,</i> 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.</p></div>
  

  
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      <div class="rich-text"><p>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.</p><p>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.</p><p>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 <i>below</i> the temperature of the surrounding air. Voilà: cooling achievement unlocked.</p><div style="padding-bottom: 56.25%;" class="responsive-object">
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<p>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.</p><p>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.</p><p>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.</p></div>
  

  
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      <div class="rich-text"><p>“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.”</p><p>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 <i>cell,</i> 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.</p><p>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.</p>
            <figure class="richtext-image full-width"><img alt="184921.jpg" class="richtext-image full-width" height="533" width="800"
            src="/wgbh/nova/media/images/184921.width-800.jpg"/><figcaption><p>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</p><div class="credit"><p></p></div></figcaption>
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            <p>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.</p><p>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>.</p><p>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.</p><p>“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.”</p></div>
  

  
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      <div class="rich-text"><p>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.</p><p>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.</p><p>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.</p><div style="padding-bottom: 56.25%;" class="responsive-object">
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<p>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.</p><p>“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.”</p></div>
  



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

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





  
      <div class="rich-text"><p>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>.</p><p>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.</p><p>Today, in the journal <i>Cell Host &amp; Microbe,</i> 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.</p></div>
  

  
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      <div class="rich-text"><p>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>.</p><p>“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.”</p><p>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.</p>
            <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="/wgbh/nova/media/images/Jenna_Hambrick_La_Jolla_Institute_for_Immunolo.width-800.jpg"/><figcaption><p>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</p><div class="credit"><p></p></div></figcaption>
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            <p>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 <i>worse</i> 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.</p><p>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>.</p><p>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.</p></div>
  

  
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      <div class="rich-text"><p>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.</p><p>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.</p><p>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.</p>
            <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="/wgbh/nova/media/images/placental_macrophages_with_Zika_Mehul_Suthar_M.width-800.jpg"/><figcaption><p>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</p><div class="credit"><p></p></div></figcaption>
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            <p>“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.”</p><p>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.</p><p>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.</p></div>
  

  
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      <div class="rich-text"><p>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.”</p><p>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.</p><p>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.</p>
            <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="/wgbh/nova/media/images/Sanofi_Pasteur__Gabriel_Lehto__Novas_Imagens_C.width-800.jpg"/><figcaption><p>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</p><div class="credit"><p></p></div></figcaption>
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            <p>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.</p><p>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.</p><p>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.</p><p>“Animal models provide good information,” Isern adds, “but the answers are in large human populations.”</p></div>
  



<p>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.</p>

How Zika and Dengue Exploit the Mother-Child Relationship





  
      <div class="rich-text"><p>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.</p><p>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.</p><p>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.</p><p>“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.”</p></div>
  

  
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      <div class="rich-text"><p>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.</p><p>“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.”</p>
            <figure class="richtext-image full-width"><img alt="StockSnap pixabay.jpg" class="richtext-image full-width" height="532" width="800"
            src="/wgbh/nova/media/images/StockSnap_pixabay.width-800.jpg"/><figcaption><p>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</p><div class="credit"><p></p></div></figcaption>
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            <p>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>.</p><p>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.</p><p>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.</p></div>
  

  
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      <div class="rich-text"><p>The new report, <a href="https://www.cell.com/current-biology/fulltext/S0960-9822(18)31345-9">published today</a> in the journal <i>Current Biology,</i> 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 <i>what</i> people were tweeting, but <i>when</i> they were tweeting,” Rust explains.</p><p>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.</p><p>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 <i>within</i> 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.</p>
            <figure class="richtext-image full-width"><img alt="kansas city traffic Thomanication flickr.jpg" class="richtext-image full-width" height="530" width="800"
            src="/wgbh/nova/media/images/kansas_city_traffic_Thomanication_flickr.width-800.jpg"/><figcaption><p>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</p><div class="credit"><p></p></div></figcaption>
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            <p>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>.</p><p>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 <i>later</i> 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.</p><p>“The amount of social jet lag can be thought of as a proxy for how on vacation these places are,” Walch explains.</p><p>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.</p></div>
  

  
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      <div class="rich-text"><p>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.”</p><p>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.</p><p>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.</p><p>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.</p>
            <figure class="richtext-image full-width"><img alt="Tookapic Pexels.jpg" class="richtext-image full-width" height="531" width="800"
            src="/wgbh/nova/media/images/Tookapic_Pexels.width-800.jpg"/><figcaption><p>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</p><div class="credit"><p></p></div></figcaption>
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            <p>“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.”</p><p>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.</p><p>Even a future analysis of the <i>content</i> 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.”</p><p>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.</p><p>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.”</p></div>
  



<p>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.</p>

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





  
      <div class="rich-text"><p>For single-celled organisms, <a href="https://www.pbs.org/video/nova-wonders-whats-living-in-you-fnbfuy/">bacteria</a> are surprisingly chatty.</p><p>Though they’re often thought of as solitary, bacteria spend a decent bit of time engaging in conversation. But they don’t use words; instead, these microscopic creatures shoot chemical cues into their environment. When many bacteria are in close proximity, these signals can reach a high enough density to prompt complex, cooperative group behavior.</p><p>Banding together, bacteria can raise collective defenses, enhance access to resources, and even cause serious infections. This collaborative decision-making process is called <a href="https://www.ncbi.nlm.nih.gov/pubmed/11544353">quorum sensing</a>, and it comes in different flavors: Some bacteria collude only with their own kind, while others will speak with other species. But outside the bacterial kingdom, these bugs keep mum. Their chemical code is one that no living creature—<a href="https://www.pbs.org/wgbh/nova/article/bassler-bacteria/">aside from a human researcher</a>—has ever been able to crack.</p><p>The key word here, however, is “living.” Today, in the journal <i>Cell,</i> a team of researchers unmasks <a href="https://doi.org/10.1016/j.cell.2018.10.059">an unexpected decrypter</a> of the dialect of quorum sensing: A bacteria-hunting virus called a <a href="https://www.pbs.org/wgbh/nova/article/phage-alzheimers-cure/">bacteriophage</a>, or phage for short.</p></div>
  

  
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      <div class="rich-text"><p>By learning the lexicon of bacteria in the <i>Vibrio</i> genus—including those that cause <a href="https://www.pbs.org/wgbh/nova/bioterror/agen_cholera.html">cholera</a>—a polyglot phage called VP882 effectively wiretaps the conversations of its microbial prey, which might allow the virus to attack when its target population is at its densest. Genetically manipulating the building blocks of this system could someday equip researchers and clinicians with tools to treat bacterial disease—all inspired by the covert ops of these viral eavesdroppers.</p><p>“This is really beautiful phage biology,” says <a href="https://www.metx.ucsc.edu/research/yildiz.html">Fitnat Yildiz</a>, a microbiologist who studies <i>Vibrio</i> bacteria at the University of California, Santa Cruz but did not participate in the new research. “This is an elegant example of how phage can take a [bacterial] regulatory network and use it to their own advantage.”</p><p>But phages aren’t the only ones listening in. Study author <a href="https://scholar.princeton.edu/basslerlab/home">Bonnie Bassler</a>, a microbiologist at Princeton University, may be humanity’s most fluent ambassador to the world of <a href="https://www.pbs.org/wgbh/nova/article/bassler-bacteria/">quorum sensing</a>. Years of research from her team have deciphered some of the most important facets of this bacterial vernacular. Just last year, a team from Bassler&#x27;s lab, including graduate student <a href="https://scholar.princeton.edu/basslerlab/people/justin-silpe">Justin Silpe</a>, discovered that bacteria in the <i>Vibrio</i> group are <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5391282/">capable of detecting</a> a molecular signal called DPO. In the world of quorum sensing, when it’s loud, there’s a crowd—and blasting DPO allows microbes to announce themselves to others. A single blip means virtually nothing, but a whole slew of DPO messages indicates the presence of a mob. A swarm of microbes can then take this cue to act in concert.</p>
            <figure class="richtext-image full-width"><img alt="Phage.jpg" class="richtext-image full-width" height="936" width="800"
            src="/wgbh/nova/media/images/Phage.width-800.jpg"/><figcaption><p>In this image, multiple bacteriophages are attached to the surface of a bacterial cell. Bacteriophage translates to &quot;bacteria eater.&quot; Photo Credit: Graham Beards, Wikimedia Commons</p><div class="credit"><p></p></div></figcaption>
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            <p>Through chemicals like DPO, bacteria are constantly chattering in the world around us—but we humans never hear a thing. The system functions like a radio station, in that effective communication requires a signal and a receiver. A tower can ping out all the waves it wants, but only those with the right technology can tune in to the message.</p><p>That’s no issue for bacteria: All <i>Vibrio</i> species make DPO’s “receiver”—a protein called VqmA. But Silpe was eager to find who else might be privy to the discourse. While searching for versions of VqmA across the kingdoms of life, Silpe noticed an anomaly on his list that wasn’t alive at all: A <i>Vibrio-</i>infecting virus.</p><p>Both Silpe and Bassler were initially skeptical. “There’s never been a quorum sensing gene on a phage before,” Bassler explains. “Quorum sensing is supposed to be about <i>bacteria</i> communicating.”</p></div>
  

  
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      <div class="rich-text"><p>And when it comes to code breakers, viruses are especially far outside the line of usual suspects. Technically, they’re <a href="https://www.pbs.org/video/where-did-viruses-come-from-rc0f7r/">not even alive</a>. Viral particles are <a href="https://www.pbs.org/wgbh/nova/labs/lab/rna/3/1/">entirely dependent on living cells</a>, like those of humans or bacteria, to replicate and persist. But the viral <i>modus operandi</i> is undoubtedly a successful one. Bacteriophages alone are the <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3109452/">most ubiquitous entities</a> in nature, found wherever their host of choice—bacteria—thrive.</p><p>When a phage encounters a bacterial cell, it will inject its own genome into its host. Then, the virus co-opts the bacterium’s molecular machinery to manufacture more of itself. The process destroys the host, releasing a fresh batch of phage to begin the infectious cycle anew.</p><p>But the timing of this exit can vary. After infecting a cell, some phages will nestle their genes in next to their host’s, genetically immortalizing the virus. When the bacterium copies its own genome during reproduction, the phage’s gets taken along for the ride. In these cases, only specific cues from the environment, like damage to the host, can awaken the phage from dormancy.</p><div style="padding-bottom: 56.25%;" class="responsive-object">
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<p>For the phage, coming out of hiding is irreversible, as the process destroys the original host. But if there’s a new crop of susceptible bacteria nearby, the benefits far outweigh the risk. So for VP882, monitoring the availability of prey—say, by encoding its own quorum sensing cipher—might be an incredibly effective strategy.</p><p>At first, the possibility seemed ludicrous to the researchers. But Silpe followed his hunch, and was amazed to find that the phage gene didn’t just <i>look</i> like VqmA—it listened like it, too. When <i>Vibrios</i> in its vicinity sent out DPO dispatches, VP882 took notice. And if the messages amassed, the phage jolted awake and broke loose from the cell.</p><p>Because more DPO means more bacteria—and, thus, more potential hosts—adding VqmA to its repertoire might be a way for a phage to time a mass exodus, Bassler explains. Though this idea awaits confirmation, Bassler thinks the virus might be using <i>Vibrio’s</i> own secret language against itself. It’s an “insidious and fantastic” tactic, she says.</p></div>
  

  
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      <div class="rich-text"><p>“This is remarkable,” says <a href="https://bsc.ua.edu/profiles/asma-hatoum-aslan/">Asma Hatoum-Aslan</a>, a microbiologist studying bacteria-phage interactions at the University of Alabama who did not contribute to the study. “This shows that this kind of phage, even in the host cell, is clearly not dormant. It’s listening. It’s still interacting with the environment on some level.”</p><p>The surprising crosstalk between such different entities also illuminates the widespread nature of communication—in even its simplest forms. “Viruses don’t carry much genetics around with them, but they actually have a lot of autonomy,” says <a href="https://turnerlab.yale.edu/">Paul Turner</a>, a phage biologist at Yale University who did not contribute to the study. Phages are dependent on cellular life to propagate, but by turning an ear to their hosts, he says, “they’re still encoded to decide their own fate.”</p><p>For Silpe and Bassler, this is only the beginning. This may be the first phage that’s officially recognized for learning the quorum sensing lingo, but the researchers think VP882 is unlikely to be alone.</p>
            <figure class="richtext-image full-width"><img alt="187435.jpg" class="richtext-image full-width" height="449" width="800"
            src="/wgbh/nova/media/images/187435.width-800.jpg"/><figcaption><p>Princeton University microbiologists Justin Silpe and Bonnie Bassler, who discovered a bacteriophage who can eavesdrop on bacterial conversations. Photo Credit: Denise Applewhite, Office of Communications, Princeton University</p><div class="credit"><p></p></div></figcaption>
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            <p>“Phages were discovered over a century ago,” says <a href="https://www.weizmann.ac.il/molgen/Sorek/">Rotem Sorek</a>, a microbiologist who studies bacteriophages at the Weizmann Institute of Science in Israel but did not contribute to the study. “The foundations of microbiology came from phages. And still, after all these years, we are still finding very surprising and new features of phage biology.”</p><p>The researchers have already begun to brainstorm therapeutic applications of this unusual system. One potential avenue might be a riff on <a href="https://www.pbs.org/wgbh/nova/article/phages-for-food-safety/">phage therapy</a>, wherein bacteriophages can be deployed to <a href="https://www.pbs.org/wgbh/nova/article/hacking-a-bacteriophages-genome-may-lead-to-a-cystic-fibrosis-treatment/">selectively kill</a> disease-causing bacteria. VP882 naturally targets bacteria of the <i>Vibrio</i> genus, including cholera-causing <i>Vibrio cholerae.</i> This phage could be engineered to function as something of a Trojan horse, Silpe says, delivering a molecular self-destruct button to dense populations of <i>Vibrio</i> without damaging, say, the <a href="https://www.pbs.org/wgbh/nova/video/nova-wonders-whats-living-in-you/">important gut microbes</a> that live within a human host. Turner compares the technique to “taking a scalpel and cutting something unwanted out of a complex community.”</p><p>Such a system would involve harnessing the power of a natural system derived from phage-microbe interactions—not unlike <a href="https://www.pbs.org/wgbh/nova/video/how-does-crispr-work/">CRISPR</a>, Turner says. “We’re figuring out what’s evolved in the microbial world and appreciating its elegance,” he explains. “But now we can also think about using these tools to solve human problems.”</p><p></p><p><i>Editor&#x27;s Note, December 25, 2018: This article has been updated to clarify the role of Justin Silpe in the discovery of the quorum sensing molecule, DPO.</i></p></div>
  



<p>In a first, scientists have found that viruses that prey on microbes can understand the lingo of bacterial conversations—and may use the intel to time their attacks.</p>

Chatty bacteria may be most vulnerable to viruses





  
      <div class="rich-text"><p>Humans have a knack for <a href="https://www.pbs.org/wgbh/nova/article/the-limits-of-facial-recognition/">remembering</a> <a href="https://www.pbs.org/wgbh/nova/video/where-your-face-comes-from">faces</a>. And when someone forgets yours, it tends to sting.</p><p>The same is true, it turns out, for the Northern paper wasp (<i>Polistes fuscatus</i>). Though often maligned as painful pests, wasps have more in common with humans than some of us might like to believe—including a particular <a href="http://science.sciencemag.org/content/334/6060/1272">aptitude</a> for recognizing individuals <a href="https://www.pbs.org/wgbh/nova/article/facial-recognition-brain/">by their facial features</a>.</p><p>While scientists have been aware of this phenomenon for years, what’s less clear is <i>how</i> these wasps accomplish this feat: The ability to distinguish faces could be inherited, or something learned through experience. Now, in <a href="https://www.sciencedirect.com/science/article/pii/S0003347218303178">a new study</a> published in the journal <i>Animal Behaviour,</i> researchers report that part of the process is built into the wasp brain—and species lacking this innate ability may never entirely make up for the difference.</p></div>
  

  
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      <div class="rich-text"><p>“This work is absolutely groundbreaking,” says <a href="https://www.rmit.edu.au/contact/staff-contacts/academic-staff/d/dyer-associate-professor-adrian">Adrian Dyer</a>, who studies the science of vision at RMIT University in Australia but was not involved in the research. “It shows a bridge between expertise… and a more hardwired system.”</p><p>Even among paper wasps, <i>P. fuscatus</i> is exceptional: This species seems uniquely equipped to home in on <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1691056/">facial features</a>—and it might have something to do with their social structure. Many <i>P. fuscatus</i> wasp colonies are founded by multiple females who tussle for dominance. Once a pecking order is established, each queen can take on a unique social role, which goes on to dictate how workers integrate into the nest hierarchy. As such, the ability to recognize individuals is essential for these wasps to maintain stable relationships within the colony, affecting everything from displays of <a href="https://onlinelibrary.wiley.com/doi/full/10.1111/j.1558-5646.2009.00833.x">aggression</a> to division of labor and food allocation. Accordingly, the facial features of <i>P. fuscatus</i> wasps are highly variable.</p><p>In a closely related species, <i>Polistes metricus</i>, or the metricus paper wasp, nests more commonly support single-queen monarchies—a simplified hierarchy that eliminates the need for detailed distinctions between wasps. Unsurprisingly, metricus faces are mostly indistinguishable, <a href="https://onlinelibrary.wiley.com/doi/full/10.1111/j.1420-9101.2009.01923.x">even to their own kind</a>.</p>
            <figure class="richtext-image full-width"><img alt="sankax flickr.jpg" class="richtext-image full-width" height="600" width="800"
            src="/wgbh/nova/media/images/sankax_flickr.width-800.jpg"/><figcaption><p>The Northern paper wasp (<i>Polistes fuscatus</i>) is capable of distinguishing the facial features of individuals. This comes in handy in their nests, where there a complex hierarchy with multiple queens necessitates that members of different castes keep careful track of each other. Photo Credit: sankax, flickr</p><div class="credit"><p></p></div></figcaption>
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            <p>Study author <a href="https://lsa.umich.edu/eeb/people/faculty/tibbetts.html">Elizabeth Tibbetts</a>, an evolutionary biologist at the University of Michigan, realized these <i>P. metricus’</i> shortcomings might just be the key to unraveling the cognitive basis of facial recognition. Face-savvy <i>P. fuscatus</i> individuals are reared in the presence of facial diversity—which means they’re acquainted with an assortment of colors, shapes, and sizes right from the get-go, whereas metricus wasps don’t enjoy the same privilege. It’s a classic nature versus nurture question: Are <i>P. metricus</i> wasps are inherently ill-suited to the task, or are they simply deprived of the necessary education?</p><p>To test the influence of experience on face learning, Tibbetts and her colleagues set up a series of hybrid hives. In some, <i>P. fuscatus</i> and <i>P. metricus</i> wasps were reared with their own kind; in others, they were mixed with each other. The researchers also added a third, more distantly-related species, <i>Polistes dominula,</i> or the European paper wasp, to the mix. <i>P. dominula</i> individuals take note of features that indicate physical prowess—the faces of stronger wasps have a more splotchy pattern of black spots—but these motifs are too broad to identify individuals. Tibbetts compares the system to belt colors in a karate studio. “To tell how tough someone is, you can look at their belt color,” she explains. “But you don’t need to memorize individual faces.”</p></div>
  

  
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      <div class="rich-text"><p>After five days of co-mingling, the researchers enrolled the wasps in a face-learning boot camp. The wasps were trained to make their way through a convoluted portrait gallery of different <i>P. fuscatus</i> faces—a perfectly pleasant setup, save for the fact that the floors of the museum-like maze were electrified. Some of the images, however, were placed in safe, no-shock zones. The researchers tracked whether the wasps were able to use these images to navigate themselves to safety, even when the photos switched locations—a sign that they recognized and remembered these faces’ distinctive features.</p><p>As expected, <i>P. fuscatus</i> that had pow-wowed with their own species came out ahead in this face-off, quickly learning to discriminate between safe and unsafe images. The same wasn’t true, however, for <i>P. metricus</i> and <i>P. dominula</i> housed with their own kind. This made sense: Only the <i>fuscatus</i> wasps were gleaning instructive information from their peers, and putting it to good use. But Tibbetts and her colleagues found that <i>P. fuscatus</i> also seemed to hold its own when it bunked with <i>P. metricus</i> wasps. Even without direct exposure, <i>P. fuscatus</i> showed a flair for faces—indicating that the <i>P. fuscatus</i> brain might have some unique, face-discriminating hardwiring.</p>
            <figure class="richtext-image full-width"><img alt="P fuscatus individual recognition.jpg" class="richtext-image full-width" height="800" width="800"
            src="/wgbh/nova/media/images/P_fuscatus_individual_recognition.width-800.jpg"/><figcaption><p>The many faces of <i>Polistes fuscatus.</i> Faces vary in many ways, including coloration, patterning, and the size of individual features. Photo Credit: Elizabeth Tibbetts, University of Michigan</p><div class="credit"><p></p></div></figcaption>
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            <p>But this wasn’t the entire story. Tibbetts was next shocked to see that <i>P. metricus</i> wasps—which normally can’t tell faces apart—were also able to successfully maneuver their way through the face maze if they had first fraternized with <i>P. fuscatus</i> wasps. The metricus wasps never did as well as true <i>P. fuscatus</i> wasps, but they outperformed their unexposed peers. Though the metricus wasps had spent only five days with <i>P. fuscatus</i>, this brief stint had apparently been enough for them to learn some of the tricks of the trade. “I thought experience would matter,” Tibbetts explains, “but I didn’t think they would really get <i>better.”</i></p><p>When the researchers repeated the experiment with photos of <i>P. fuscatus</i> lacking antennae—a modification that jumbles the ability of these wasps to recognize a face as a face—neither wasp species did as well. This reinforced the idea that face specialization wasn’t just about recognizing general patterns, like karate belt colors; rather, there was something special about the face itself.</p><p>“This contributes to a growing literature on the idea that things aren’t black and white: It’s not just nature or nurture,” says <a href="https://www.ent.iastate.edu/people/amy-toth">Amy Toth</a>, an entomologist at Iowa State University who did not contribute to the new finding. “It’s the <i>interaction</i> that leads to the development of this complex behavior.”</p></div>
  

  
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      <div class="rich-text"><p>Sadly, <i>P. dominula</i> was not so lucky. Regardless of the company it kept, these wasps didn’t show any particular proficiency for distinguishing faces. For them, experience alone wasn’t enough, indicating that inheritance still plays a big role in face specialization.</p><p>It’s still not entirely clear what underlies these differences between species, but Tibbetts theorizes that there may be an ancestral influence. <i>P. fuscatus</i> and <i>P. metricus</i> are much more closely related than either species is to <i>P. dominula</i>—and <i>P. metricus’</i> latent abilities may be a holdover from its past. But until far more wasp species are studied, no conclusions can be definitively drawn, says <a href="http://www.sumnerlab.co.uk/the-group/seirian-sumner/">Seirian Sumner</a>, who studies wasps and other social insects at University College London in the United Kingdom but did not contribute to the new research.</p>
            <figure class="richtext-image full-width"><img alt="Larah McElroy flickr.jpg" class="richtext-image full-width" height="533" width="800"
            src="/wgbh/nova/media/images/Larah_McElroy_flickr.width-800.jpg"/><figcaption><p>The metricus paper wasp (<i>Polistes metricus</i>) isn&#x27;t capable of distinguishing individual faces. Because each metricus nest tend to be ruled by a single queen, there&#x27;s no need for this level of social intricacy. Photo Credit: Larah McElroy, flickr</p><div class="credit"><p></p></div></figcaption>
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            <p>Even more far-flung is the evolutionary distance between humans and wasps. But the fact that the two species have managed to converge on a similar skill fascinates Tibbetts. “Often, when I’m studying wasps, I can’t believe how smart they are,” she says. “They can do so many complicated things. But at the same time, maybe if wasps can do it, maybe you don’t have to be that smart to do these things.”</p><p>That’s not to knock on wasps, which certainly suffer from an image problem in the eyes of humans, <a href="https://www.smithsonianmag.com/science-nature/why-you-should-let-wasp-be-your-hero-today-180969521/">perhaps unjustly so</a>. Dyer, the vision scientist, thinks studies like these are deeply informative—not just for our understanding of evolution, but also for unexpected applications like <a href="https://www.pbs.org/wgbh/nova/video/can-machines-think-like-us">machine learning</a>. Insect brains have far less computational power than the <a href="https://www.pbs.org/wgbh/nova/video/nova-wonders-can-we-build-a-brain/">human mind</a>, but can still perform exceptionally complex tasks, Dyer explains. “There must be some efficient ways in which miniature brains can do this,” he says. “We can derive real tricks from simple biological systems.”</p>
            <figure class="richtext-image full-width"><img alt="Dann Thombs flickr.jpg" class="richtext-image full-width" height="533" width="800"
            src="/wgbh/nova/media/images/Dann_Thombs_flickr.width-800.jpg"/><figcaption><p>The European paper wasp (<i>Polistes dominula</i>) recognizes only broad patterns in faces that help wasps size up their competition. More splotchy black spots indicate that an individual is stronger than one with a more uniformly patterned face. Photo Credit: Dann Thombs, flickr</p><div class="credit"><p></p></div></figcaption>
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            <p>Tibbetts is also intrigued by this line of questioning. Next, she hopes to uncover what’s actually happening inside the wasp brain during these complicated learning tasks—and if there are further parallels between humans and these ingenious insects.</p><p>“This work really demonstrates why we should love wasps,” Toth says. “They’re fascinating creatures with complex social behavior. They may be the closest thing you can find to a human in an insect.”</p></div>
  



<p>Some types of paper wasps can tell individuals apart by facial features alone. Is the ability built in, or can it be learned?</p>

This Wasp Can Recognize Faces. Others Aren’t So Lucky.





  
      <div class="rich-text"><p>From a young age, marine ecologist <a href="http://gatech.academia.edu/CodyClements">Cody Clements</a> knew he wanted to dedicate his life to studying <a href="https://www.pbs.org/wgbh/nova/video/lethal-seas/">coral reefs</a>. But he never imagined his graduate career would require so many soda bottles.</p><p>Between December 2014 and April 2016, Clements, then a student researcher working with <a href="http://biosci.gatech.edu/people/mark-hay">Mark Hay</a> at the Georgia Institute of Technology, spent hours tracking the wellbeing of three coral species in a lagoon off the coast of Fiji . Clements wanted to know if communities containing three species fared better than those with only one—a task that involved repeatedly weighing nearly 900 individual corals to determine their rate of growth.</p><div style="padding-bottom: 56.25%;" class="responsive-object">
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<p>That’s where the soda bottles came in. For Clements to maintain the colonies for his 16-month experiment, he needed to detach and reattach the corals without damaging them. So he seeded each coral into the epoxy-filled neck of a sawed-off soda bottle, then anchored the bottle tops, caps down, into slabs of concrete in the lagoon—some of which hosted three species, while others supported only one. This setup allowed the corals to be efficiently unscrewed, weighed, and safely returned to base.</p></div>
  

  
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      <div class="rich-text"><p>Still, the sheer number of specimens made the task harrowing. During each weigh-in, Clements was buffeted by the region’s dramatic tides and choked by the saltwater clogging his snorkel. He remembers it as the most work-intensive experiment he’s ever conducted. “At the end of the day, I would have headaches because I’d been holding my breath,” he says. “And my hands were raw from screwing corals into the plots—the skin on my fingers was just gone.”</p><p>But in the end, the effort paid off. The outcome of Clements and Hay’s work, <a href="https://www.nature.com/articles/s41559-018-0752-7">published today</a> in the journal <i>Nature Ecology &amp; Evolution</i>, shows that corals, too, may prosper in the presence of diverse companions. Though they often seek the same resources, would-be competitor corals can actually enhance each other’s growth and survival. As coral reefs <a href="https://www.pbs.org/wgbh/nova/article/mass-coral-bleaching-devastates-great-barrier-reef-for-second-consecutive-year/">around the world</a> <a href="https://www.pbs.org/wgbh/nova/article/first-reefs-to-fall/">continue to decline</a> <a href="https://news.nationalgeographic.com/2017/06/coral-reef-bleaching-global-warming-unesco-sites/">at an unprecedented rate</a>, understanding these interspecies interactions may underscore the factors that most help—or hinder—conservation efforts in faltering marine ecosystems.</p><p>“[The benefits of diversity are] something the research community has sort of taken for granted, but has never tested,” says <a href="https://www.carlosprada.org/">Carlos Prada</a>, a marine ecologist who studies corals at the University of Rhode Island but was not involved in the study. “It’s a simple question, but a very good one.”</p>
            <figure class="richtext-image full-width"><img alt="IMG_6758.jpg" class="richtext-image full-width" height="600" width="800"
            src="/wgbh/nova/media/images/IMG_6758.width-800.jpg"/><figcaption><p>The researchers&#x27; coral setup. Three coral species were grown together or separately to test the effects of diversity on growth and wellbeing. In the end, the corals that had been grown in mixed company fared better. Image Credit: Cody Clements, Georgia Institute of Technology</p><div class="credit"><p></p></div></figcaption>
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            <p>Single corals aren’t always ready to mingle. When different species <a href="https://scripps.ucsd.edu/labs/coralreefecology/battle-zones/">crowd too closely</a> onto reefy real estate, they’ll often duke it out for space, explains <a href="https://profiles.ucsd.edu/elizabeth.drenkard">Liz Drenkard</a>, a climatologist and ecologist at the Scripps Institute of Oceanography who was not involved in the study. Some corals will resort to a simple sting from an outstretched tentacle; others will go as far as to belch digestive juices onto hapless intruders. But Clements’ work shows that not all coral communities are this contentious.</p><p>Four months after Clements had seeded the coral cultures, the mixed-species plots weighed over 60 percent more than single-species communities. When placed amongst only their own kind, corals were often taken over by seaweed—a common coral adversary—and died off at a higher frequency. Corals neighbored by other species, however, seemed to not just tolerate their presence, but flourish <i>en masse</i>, Hay says, turning potential turf wars into temporary truces.</p></div>
  

  
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      <div class="rich-text"><p>More work is necessary to figure out <i>how</i> diversity makes such a difference. It’s possible that a smorgasbord of coral species is less likely to get cleaned out by predators like fish. It may also be that more diverse assortments of corals are better equipped to ward off disease. Both of these factors may be especially critical when coral communities are trying to take root in a new locale, when the stakes are especially high. “In some cases, there may be something facilitative about thinking, ‘The enemy of my enemy is my friend,’” Clements explains.</p><p>Alternatively, these bursts in growth may not be reflective of coral chumminess at all, Drenkard points out. Sensing the presence of foreigners could be sparking rivalry in the community, cuing corals to claim their share of space before someone else gets the upper hand.</p><p>But this study is just the first pass at uncovering the benefits of diversity on coral health, Hay says. In the future, Hay and his team hope to find the answers to these questions, as well as bring a wider variety of coral species into the picture.</p><p>Whatever the reason, though, it seems that sidling up to strangers can bolster coral survival—especially when these critters are working to repopulate a degraded reef like the one in this study. And that could have big implications for coral restoration, says <a href="http://sites.bu.edu/davieslab/members/">Hanny Rivera</a>, a coral researcher at Boston University who was not involved in the study. Several groups have focused their efforts on reintroducing only specific species that have been wiped out by disease or are particularly susceptible to bleaching, she explains. But in light of these new findings, partnering vulnerable species with other corals might just foster reef rehabilitation.</p><p>It’s unclear, however, how the dynamics might play out in the long term. After about a year and a half of growth, the diverse plots still came out ahead as a whole—but individual species had begun to show some differences. A few months into the experiment, one species, <a href="https://www.iucnredlist.org/species/133666/54304631"><i>Acropora millepora</i></a>, had flourished when grown in the presence of diversity. But a year later, these corals no longer seemed to mind going it alone: Whether <i>Acropora</i> was stationed solo or intermingled, it weighed about the same.</p>
            <figure class="richtext-image full-width"><img alt="Acropora_millepora,_GBR.jpg" class="richtext-image full-width" height="550" width="800"
            src="/wgbh/nova/media/images/Acropora_millepora_GBR.width-800.jpg"/><figcaption><p><i>Acropora millepora </i>corals grow fast, but are also particularly sensitive to environmental changes like storms or disease. As such, though they can overrun over species, they&#x27;re often quickly beaten back from the frontlines. Image Credit: Petra Lundgren, Wikimedia Commons</p><div class="credit"><p></p></div></figcaption>
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            <p>Clements stopped measuring the corals after 16 months. Past this point, the <i>Acropora</i> corals may have even gone on to overrun their comrades. But while <i>Acropora</i> is known for its rapid growth rate, it’s also a bit more fragile than other species, and tends to get decimated when storms or diseases ravage reefs, Hay says. As such, it may be beneficial for these corals to adopt something of a live fast, die young strategy.</p><p>Still, this doesn’t negate the fact that <i>Acropora</i> seemed to thrive in mixed company during the early days of settlement. “It’s possible that <i>Acropora</i> doesn’t really need other species once it’s dominant,” Hay says. “But it may need them to get that way in the first place.”</p></div>
  

  
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      <div class="rich-text"><p>And if diversity is important for setting up shop, it’s also possible <i>losing</i> diversity could speed up the deterioration of damaged reefs. There’s a reason richer communities are often better buffered against adversity: If one species that fills a particular role gets taken out of the equation, another may be there to take its place. But as diversity declines, any single loss could be irreversibly devastating. Clements compares the process to stripping parts from an engine. “If you have a complex engine, you can maybe remove some parts and it still works,” he says. “But if it’s simple, then removing a part makes it more likely the whole thing will break down.”</p><p>Faced with increasing temperatures, <a href="https://www.pbs.org/wgbh/nova/video/lethal-seas">ocean acidification</a>, and the catastrophic effects of overfishing, corals are more vulnerable than ever. As reefs die off around the world, it may serve us well to keep in mind that survival isn’t just about quantity, Drenkard says. “It’s not enough to just have a reef,” she adds. “It really matters who’s there.”</p></div>
  



<p>Birds of a feather may flock together, but when it comes to corals, sometimes it helps to mix things up.</p>

It's Not Just Us: Corals Also Thrive Best in Diverse Company





  
      <div class="rich-text"><p>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.</p><p>A <a href="http://advances.sciencemag.org/content/5/1/eaau3333">study</a> published today in the journal <i>Science Advances</i> pinpoints an unlikely villain in neurodegenerative disease: <i>Porphyromonas gingivalis,</i> 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.</p><p>“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.”</p></div>
  

  
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      <div class="rich-text"><p><i>P. gingivalis</i> 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/"><i>P. gingivalis</i> infection</a>—pointing to the possibility that these mouth-loving microbes might have the capacity to set up shop in the brain.</p><p>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.</p>
            <figure class="richtext-image full-width"><img alt="150210-F-LM669-064.JPG" class="richtext-image full-width" height="534" width="800"
            src="/wgbh/nova/media/images/150210-F-LM669-064.width-800.jpg"/><figcaption><p><i>Porphyromonas gingivalis, </i>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</p><div class="credit"><p></p></div></figcaption>
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            <p>When the researchers introduced <i>P. gingivalis</i> 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.</p><p>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.</p><p>While that might sound like a good thing, amyloid beta’s protective powers might ultimately cause harm. When <i>P. gingivalis</i> 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.</p><p>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.”</p></div>
  

  
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      <div class="rich-text"><p>In keeping with this, when the researchers exposed mice to a strain of <i>P. gingivalis</i> that lacked its destructive gingipains, the rodents suffered fewer Alzheimer’s-like changes in their brains. And when <i>P. gingivalis-</i>infected mice were treated with Cortexyme’s new anti-gingipain drug, fewer bacteria invaded the brain and there was less accumulation of amyloid beta.</p><p>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.</p><p>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.</p><p>“Alzheimer’s is a complex disorder, not a one stop shop,” Reiss says.</p>
            <figure class="richtext-image full-width"><img alt="plaque-neuron-connection-loss-cropped" class="richtext-image full-width" height="450" width="800"
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  Plaques that build up between neurons are a hallmark of Alzheimer's.
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            <p>Many other questions remain. It’s still not entirely clear how <i>P. gingivalis</i> breaches the brain’s barriers in mice <i>or</i> 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 <i>P. gingivalis</i> 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.</p><p>In other words, a <i>P. gingivalis</i> infection doesn’t guarantee Alzheimer’s, and there’s no conclusive evidence that all Alzheimer’s cases stem from <i>P. gingivalis.</i> Regardless, Singhrao says, it doesn’t hurt to practice good oral hygiene—if not for your mind, then at least for your mouth.</p></div>
  

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

Katherine J. Wu