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    <title>Massive Science</title>
    <description>We&#39;re a community of scientists telling fascinating, true stories about the science that&#39;s happening now.</description>
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<guid isPermaLink="true">https://massivesci.com/articles/the-great-pandemic-stress-test/</guid>
<link>https://massivesci.com/articles/the-great-pandemic-stress-test/</link>
<pubDate>Fri, 17 Dec 2021 05:27:40 EST</pubDate>
<title>The Great Pandemic Stress Test</title>
<description>How emergency forces innovation &amp; one Italian scientist advanced our understanding of COVID variants.</description>

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  <media:description>a visualization of the covid19 virus</media:description>
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  <dc:creator><![CDATA[Peter Weinberg]]></dc:creator>
  <atom:author>
    <atom:name>Peter Weinberg</atom:name>
    <atom:uri>https://massivesci.com/people/peter-weinberg/</atom:uri>
  </atom:author>


  
  <content:encoded><![CDATA[
    <p>In February 2020, people all over the world watched with mounting anxiety as a novel coronavirus, then referred to as 2019-nCoV, began its unyielding spread across the globe. What at first seemed, to western eyes, like a worrying but well-contained viral outbreak on the other side of the world, had suddenly appeared in northern Italy and was crushing the country’s health system with the sheer number of patients needing intensive care. European and North American news cycles began to fill with countless stories of people desperate for treatment in overloaded hospitals, and soon after, Italy imposed a strict lockdown on the movement of its citizens in order to try to slow the exponential growth of coronavirus infections. Videos of Italians singing to each other across balconies and alleyways in an attempt to maintain some sort of interpersonal connection spread widely on social media as containment measures were put into place.</p>
<p>For Dr Gabriele Ibba, a postdoctoral researcher at the University of Sassari in Sardinia, Italy, lockdown was not an option. As a post-doctoral researcher working in a public-health oriented lab, his work was just beginning. In the early days of the pandemic, so little reliable information about the novel coronavirus was available that people simply didn’t know what to expect. This was especially stressful for scientists and physicians working on the front lines of the COVID response. Dr Ibba recalls the distinct anxiety of going to work in his basement testing lab, part of the hospital at the University. While he and his colleagues were working feverishly to develop effective coronavirus testing workflows, COVID patients were filling the wards a few floors above.</p>
<aside class="pullquote"><blockquote>Most scientific discoveries, both big and small, start when a researcher notices something that just doesn’t quite fit.</blockquote></aside>
<p>As if the pervasive sense of dread and personal danger weren’t enough, the scientists at the University of Sassari and other testing centers like it were grappling with even more basic problems: the novelty of the virus itself, coupled with the disruption of global supply chains that it caused, meant that simply getting one’s hands on the COVID testing kits—or even the basic ingredients that go into the kits—was incredibly difficult. Eventually, they were able to establish a steady supply of a particular kit, and were able to start pushing back against the tide of coronavirus infections. As it happens, though, this struggle to find a reliable supply of test kits ended up putting Dr Ibba and his team (led by Prof Sergio Uzzau) on the path to a discovery that could help scientists and clinicians better understand the way that viruses like SARS-CoV-2 spread—an invaluable tool in fighting future pandemics.</p>
<h3 id="the-breakthrough">The Breakthrough</h3>
<p>Most scientific discoveries, both big and small, start when a researcher notices something that just doesn’t quite fit. With a little bit of poking around, that little incongruity can sometimes turn out to be a sign of something much more interesting. For the COVID testing team at the University of Sassari, that first observation came when someone noticed that some of the amplification signals coming out of their testing machines didn’t look right. The tests were coming back positive, but the way they were doing so just seemed...odd. Instead of just filing that datapoint away and moving on, though, Dr. Ibba and his colleagues decided to dig a little deeper.</p>
<p>In order to do so, they would need to go back into their records of previous lab tests, which was key to solving this particular mystery. And because the lab had maintained digital records of all of the tests performed by their PCR machines, they could rapidly check the amplification curves from COVID tests going all the way back to the beginning of the pandemic. When they started looking closely, it turned out that a noticeable proportion of their tests were all showing that same funny amplification signal, but it wasn’t clear why. Only when they sequenced the suspected viral samples to analyze their entire genomes, everything started to make sense. The weird amplification signals they were seeing in their data were being caused by the mutations that have accumulated in the more infectious B.1.1.7 variant (now officially referred to as Alpha) that was originally discovered in Kent, UK. In a previous era, this sort of on-the-fly genetic sleuthing would not have been possible, but thanks to the rise of easy-to-use genetic analysis suites from companies like <a href="https://www.sophiagenetics.com/hospitals/solutions/sars-cov-2/?utm_source=authority_magazine&amp;utm_medium=referral&amp;utm_campaign=211201-sarscov2-global-awareness-webpage" target="_blank">SOPHiA GENETICS</a>, sorting through large collections of genetic data has become significantly easier for the average researcher. If it weren't for modern genetics suites' automated genetic lineaging, this work could have taken several days instead of a few hours of scientific labor allowing the clinicians to save an outstanding amount of time.</p>
<aside class="pullquote"><blockquote>It wouldn’t have been possible to move this fast even 2 decades ago.</blockquote></aside>
<p>Because the standard PCR tests for detecting SARS-CoV-2 are really only able to provide a binary detected / not detected result, they can’t tell you much of anything about what particular variant of the virus a patient might be infected with. On top of that, if a variant has mutated enough, the genetic probes used to detect the virus might not work at all. Luckily, that was not the case here, and luck really did have a big role in this discovery: if the scramble to find a reliable source of SARS-CoV-2 testing kits hadn’t led so many labs in Dr. Ibba’s region to adopt the same test kits, there might not have been a noticeable pattern in the amplification curve data. Other kits might simply have returned no results or false negatives, which means no one would have noticed this little clue to the Alpha variant’s presence.</p>
<p>With the sequencing results in hand, the researchers realized they could take their analysis even further. As a public service, the lab Dr. Ibba works in was required to retain records and samples of all tests, which meant that they essentially had a historical record of B.1.1.7’s spread in southern Italy going back at least 6 months. With this data, they were able to show that the UK variant had actually spread to the area they monitored before January 15th 2021—much earlier than previously believed.</p>
<p>Now, Dr. Ibba and his extended team of epidemiologists, virologists and molecular biologists are trying to use this trove of data to better understand the dynamics of SARS-CoV-2 variant spread, and try to help get ahead of the curve in preparing for the next pandemic. No two pandemics are exactly the same, but the lessons learned in fighting one disease can often be applied to fighting another, so there’s reason to be optimistic about our chances next time around if humanity can maintain the pace of scientific and technological development that it set in responding to the coronavirus pandemic.</p>
<h3 id="a-reason-for-optimism">A Reason for Optimism</h3>
<p>For Dr. Ibba, despite the dread of those early days of the pandemic—and the massive loss of life globally—the speed of the scientific response to the COVID crisis is a story of human technological and scientific triumph. The combined efforts of scientists around the globe, as well as huge improvements in technology and logistics, allowed for the development and testing of a highly effective vaccine within months of the public release of the virus’s genome. It wouldn’t have been possible to move this fast even 2 decades ago—when, notably, we experienced a pandemic of a related coronavirus, the original SARS.</p>
<p>“This pandemic was a stress test for humankind, and I think that we passed the stress test ... All of us fighting against SARS-CoV-2 absolutely passed the test, and I think we are even stronger and better than before the pandemic. We learned a lot about our potential and how to face new challenges and threats. I have a very positive view of how we performed.” What’s one thing that’s made him particularly optimistic for the future? The new technology that’s come his way as the lab has ramped up its testing and sequencing capabilities, from the brand new sequencers at his university’s core facility to genetic analysis software like the <a href="https://www.sophiagenetics.com/hospitals/solutions/sars-cov-2/?utm_source=authority_magazine&amp;utm_medium=referral&amp;utm_campaign=211201-sarscov2-global-awareness-webpage" target="_blank">SOPHiA DDM™ platform</a>.</p>
<p>Scientific research often involves long hours of careful, focused work, and a small mistake or lost data can destroy days or even weeks of effort. That can wear on a person under normal circumstances, but when it happens under the extreme pressure of a state of emergency due to a global pandemic, anything that makes the process of data collection and analysis even a little bit easier is a very welcome development. “I’m used to processing the data myself which is a very laborious and error-prone process—but these new devices make this processing much easier. When my boss told me that this part was going to be done by the <a href="https://www.sophiagenetics.com/hospitals/solutions/sars-cov-2/?utm_source=authority_magazine&amp;utm_medium=referral&amp;utm_campaign=211201-sarscov2-global-awareness-webpage" target="_blank">SOPHiA GENETICS</a> pipeline, I was so grateful.” The relief is palpable. This is one of the few upsides to a novel pandemic like COVID-19: it compels us to innovate, forcing progress that could stave off similar catastrophes in future.</p>
    


<p><em><a href="https://massivesci.com/people/peter-weinberg/">Peter Weinberg</a> studies 

<p class="mb0">

<span class="scientist__field">Biology</span>

</p>

.</p>



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<guid isPermaLink="true">https://massivesci.com/articles/biology-spectrum-genes-species-sex/</guid>
<link>https://massivesci.com/articles/biology-spectrum-genes-species-sex/</link>
<pubDate>Tue, 30 Nov 2021 13:11:25 EST</pubDate>
<title>Biology is a spectrum</title>
<description>Life on Earth is complex and irreducible</description>

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  <media:title></media:title>
  <media:description>A path through a forest</media:description>
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  <dc:creator><![CDATA[Dan Samorodnitsky]]></dc:creator>
  <atom:author>
    <atom:name>Dan Samorodnitsky</atom:name>
    <atom:uri>https://massivesci.com/people/dan-samorodnitsky/</atom:uri>
  </atom:author>


  
  <content:encoded><![CDATA[
    <p>If I placed before you an atom with one proton and one electron, you would be forced to admit it was a hydrogen atom. One proton paired with one electron <em>is </em>hydrogen. It can’t be helium, or lithium, or anything else.</p>
<p>Nothing like this occurs in biology. The way life thrives on Earth is by breaking rules; it must by definition defy definitions. Divisions in biology are drawn by humans, reflect the desires and biases of the person holding the pencil, and inevitably become so unclear as to not exist at all. This has been a guiding instinct for <em>Massive</em>’s editorial team, and if you are ever confused or disoriented by some new discovery in biology, this way of looking at the world might help.</p>
<p>It’s almost passé at this point, like an annoying friend who keeps talking about yesterday’s news, to point out that “species,” as a concept, don’t really exist. There are upwards of <a href="https://blogs.scientificamerican.com/evo-eco-lab/species-concepts/" target="_blank">two dozen</a> different ways to define what any group of organisms constitutes a species. None are any better than the other, &nbsp;especially for biologically fluid organisms like bacteria.</p>
<p>This extends to every level of biology, big and small. Sex, for example, is a spectrum.</p>
<div class="oembed"><div class="iframely-embed"><div class="iframely-responsive" style="height: 140px; padding-bottom: 0;"><a href="https://massivesci.com/articles/sex-gender-intersex-transgender-identity-discrimination-title-ix/" data-iframely-url="https://cdn.iframe.ly/api/iframe?url=https%3A%2F%2Fmassivesci.com%2Farticles%2Fsex-gender-intersex-transgender-identity-discrimination-title-ix%2F&key=a91f6c63822d2172297a7435cae7a9eb"></a></div></div><script async src="https://cdn.iframe.ly/embed.js" charset="utf-8"></script></div>
<p>Other outlets like <em>Quillette </em>have gone out of their way to write articles claiming that biological sex only depends on whether you produce sperm (male) or eggs (female), with anyone intersex or otherwise not fitting into that binary waved away. I asked <a href="https://scholar.harvard.edu/srichard/home"><ins>Sarah Richardson</ins></a>, historian and philosopher of science at Harvard whether this model held water. She said, “The gametic model has very little explanatory power...it doesn’t do much for you in science, where we are trying to understand processes towards various pragmatic aims. It doesn’t seem like they’ve engaged with the relevant literature. I’m not sure what they think it shows or proves.” (Richardson herself <a href="https://scholar.harvard.edu/srichard/publications/sex-contextualism"><ins>advocates</ins></a> for a model similar to race, where biological sex is treated not even so much as a spectrum but altogether a construct.)</p>
<p>I also asked Anne Fausto-Sterling, professor of biology and gender studies at Brown University and author of <a href="http://www.annefaustosterling.com/"><ins><em>Sexing the Body</em></ins></a>, whether there was one good, authoritative definition for what biological sex is. She said, “The simple answer to your question is NO. There is no unified definition for ‘biological sex’ as applied to humans or other animals. What definition you choose depends on context.”</p>
<p>To see how something seemingly cut-and-dry like biological sex can become fuzzy and blurred, it’s helpful to go back to genes. What happens to the product of a gene? Where does it go? How long does it last? What does it do? When does it do it? How is it affected by the environment? What other genes does it interact with? What do those genes do to it? When and where and how and why are <em>those </em>genes turned on? Each step along the path of gene expression branches out in an uncountable number of directions. As genetic information rises from DNA to RNA to protein into the cell, bringing, finally, a phenotype to the surface, each subtle change in expression accumulating in every step, together with the infinite branching paths of the tens of thousands of genes in your body being expressed (or not) can literally <em>only</em> result in a spectrum of outcomes for all traits. It is the only realistic way to see life.</p>
<p>Of course it helps to see that genes themselves are just as much a construct as sex. Genomes are jammed together strings of DNA like a box of knitting supplies, one on top of the other, inseparably intertwined. Where does a gene start and end? If it’s just “the part that’s transcribed,” that doesn’t mean much, especially in eukaryotes where there are no real boundaries on transcription, no fixed starting and stopping points. Depending on how you calculate things, across all cells between 75 percent and 90 percent of the human genome is transcribed into RNA, when the percentage that codes for proteins is only in the single digits. <a href="https://genome.cshlp.org/content/16/1/37.full.pdf"><ins>One report</ins></a> estimated that up to five percent of tandem genes in humans (two coding sequences sitting next to each other) can be mixed-and-matched into chimeric proteins, containing bits from both sequences. There are years-old <a href="https://pubmed.ncbi.nlm.nih.gov/16141064/" target="_blank">reports</a> of multiple parts of a coding sequence residing on <em>completely different chromosomes</em>, only stitched together, through some unknown mechanism, after the fact.</p>
<p>The further you pull back, the fuzzier things get. Whether “species” as a firm and consistent concept is even useful for biologists seems to depend on the person you’re asking. Even <a href="https://www.gutenberg.org/files/1228/1228-h/1228-h.htm"><ins>Darwin</ins></a> was ambivalent about the reality of species:</p>
<blockquote><em>“From these remarks it will be seen that I look at the term species, as one arbitrarily given for the sake of convenience to a set of individuals closely resembling each other, and that it does not essentially differ from the term variety, which is given to less distinct and more fluctuating forms. The term variety, again, in comparison with mere individual differences, is also applied arbitrarily, and for mere convenience sake.”</em></blockquote>
<p>Roping off different species based on whether they can exchange genes is particularly thorny with the recognition that horizontal gene transfer — the movement of genes within organisms in a generation, rather than between parents and offspring — happens <em>all the time</em>. Bacteria swim in an ocean of each other’s genetic material and are constantly picking it up like loose trash on the side of the road. It even happens in humans: the famed adaptation to high altitudes of people living in Tibet came via horizontal gene transfer from <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4134395/"><ins>Denisovans</ins></a>. The barriers humans build between groups of organisms don’t hold back the flow of genes. Every organism on Earth is nothing but a far distant relative of the last universal common ancestor, just branches off the single great trunk of a towering tree.</p>
<p>So of course the borders around things don’t exist. Organisms are not reducible to their individual parts. Asking what defines a species or a gene is akin to art criticism, the ideals of one beholder being complete nonsense in the eyes of another.</p>
<p>This extends backwards and forwards, from the genotype all the way out to physical characteristics and complex phenotypes. Biological sex is not simply a matter of either male or female, but rather a spectrum of different states. What sex chromosomes you possess, how your “genes” are expressed, your physical genitalia, what gametes you produce, and your secondary sex characteristics are all just that, characteristics, but none of them definitively place people into only one of two categories. Genes are where you see them. A species is in the eye of the beholder.</p>
<p>Every time there is a new advancement in biology, there is always push back from people who prefer the old ways. I see it most often in the people who strenuously insist that biological sex must be only two things, even though the existence of a spectrum of sexes would not in any way change much (the only thing it would really do is be a more accurate view of the world and offer dignity to millions of people). But there is no reason to do this — the knowledge that biology is itself a spectrum, not just in one phenotype but in all of them, is liberation from a boxed-in world. Of course fixed definitions for species, genes, or sex don’t exist. What use would there be, evolutionarily, for life to restrict itself that way? The simplest explanation for any new complication is not to insist that there are hard-and-fast rules and everything else is an exception (or mewl something about political correctness). In accepting that biological life is infinitely complex and irreducible, you will quickly become tired of people trying to find single nucleotide changes linked to intelligence, immediately forget retrograde ideas of divisions between men and women, and become nauseated by the search for “gay genes.”</p>
<p>It is extremely clear to me, in my time as a scientist and a journalist, that organic life simply cannot exist with borders placed around it. Others look out over the unlimited variety of biology and see only the parameters of an orthodoxy, where once something is established it can’t be changed.</p>
<p>Truthfully I don’t understand this. It’s a sign of a stunted view of the world to perceive an infinite and boundless space as just large things to be stuffed into small containers. Sex, genes, and species, and all descriptors of phenotypes, are just boxes with limited and crushing dimensions. You cannot succeed by making biology simple. It’s not simple and would not be biology if it were.</p>
    


<p><em><a href="https://massivesci.com/people/dan-samorodnitsky/">Dan Samorodnitsky</a> studies 

<p class="mb0">

<span class="scientist__field">Biochemistry</span>

</p>

 at 

<p class="mb0 o7">

<span class="scientist__institution">SUNY Buffalo</span>

</p>

.</p>



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<guid isPermaLink="true">https://massivesci.com/articles/genetic-lottery-review-paige-harden-kevin-bird/</guid>
<link>https://massivesci.com/articles/genetic-lottery-review-paige-harden-kevin-bird/</link>
<pubDate>Mon, 29 Nov 2021 23:12:02 EST</pubDate>
<title>The Genetic Lottery is a bust for both genetics and policy</title>
<description>Kathryn Paige Harden’s book tries to demonstrate how genetics can ameliorate societal ills. She falls well, well short</description>

<media:content url="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/51193e98-80bd-48e2-8fa5-4afb97792609/genetic_lottery_tripled.png?auto=compress%2Cformat&amp;crop=faces&amp;fit=crop&amp;fm=jpg&amp;h=600&amp;q=75&amp;w=900" type="image/jpeg">
  <media:title></media:title>
  <media:description>The cover of Kathryn Paige Harden&#39;s book &quot;The Genetic Lottery&quot;</media:description>
</media:content>


  
  <dc:creator><![CDATA[Kevin Bird]]></dc:creator>
  <atom:author>
    <atom:name>Kevin Bird</atom:name>
    <atom:uri>https://massivesci.com/people/kevin-bird/</atom:uri>
  </atom:author>


  
  <content:encoded><![CDATA[
    <p>The last decade has seen genetics and evolution grapple with its history; one composed of figures who laid the foundations of their field while also promoting vile racist, sexist, and eugenicist beliefs.</p>
<p>In her new book, <em>The Genetic Lottery</em>, Kathryn Paige Harden, professor of psychology at University of Texas at Austin, attempts the seemingly impossible task of showing that, despite a history of abuse, behavioral genetics is not only scientifically valuable but is an asset to the social justice movement.</p>
<p>In this attempt, she fails twice. For the first half of the book, Harden tries to transform the disappointment of behavioral genetics in the years following the Human Genome Project into a success that proves that genes are a major and important cause of social inequality, like educational attainment or income levels. In the second half, she tries to show that this information is not a justification for inequality, rather it is a tool to use in our efforts to make society more equitable and cannot be ignored if we wish to be successful. To say the least, this section too falls short. Harden refuses to engage with the history and trajectory of her field, and ultimately the science fails to uphold the idea that not considering genetic differences hinders our attempts to create a more equitable world.</p>
<p><br></p>
<hr/>
<p><br></p>
<p>In the book <a href="https://bookshop.org/books/misbehaving-science-controversy-and-the-development-of-behavior-genetics/9780226058450" target="_blank"><ins><em>Misbehaving Science</em></ins></a>, sociologist Aaron Panofsky documents the history and progression of behavioral genetics, from its formal inception in the 1960s. Throughout its history behavioral genetics has responded to criticism in a variety of ways.</p>
<p>In 1969, the educational psychologist Arthur Jensen used behavioral genetics methods to argue that IQ gaps between white and Black Americans had genetic origins and, therefore, could not be remedied by educators or social policy. As criticism from mainstream geneticists and evolutionary biologists tied Jensen and behavioral geneticists to each other, the field attempted to hold a middle ground between Jensen’s racist conclusions and the belief that human behavioral genetics was fundamentally flawed. However, in this attempt to preserve their field from criticism, behavioral geneticists progressively defended the importance of race science research and adopted some core premises about the influence of genetic differences on the racial IQ gap.</p>
<p>In the following decades, Jensen and like-minded researchers like J. Philippe Rushton, Richard Lynn, and Linda Gottfredson received funding from the Pioneer Fund, an organization explicitly <a href="https://www.splcenter.org/fighting-hate/extremist-files/group/pioneer-fund"><ins>dedicated</ins></a> to “race betterment.” All the while, they were integrated into editorial boards of journals that published behavioral genetics work and treated as colleagues. Even mainstream behavioral genetics work like the Minnesota Study of Twins Reared Apart and the Texas Adoption Project would <a href="https://web.archive.org/web/20111106210310/http:/www.pioneerfund.org/Grantees.html"><ins>receive funding</ins></a> from the noxious Fund.</p>
<div class="oembed"><div class="iframely-embed"><div class="iframely-responsive" style="height: 170px; padding-bottom: 0;"><a href="https://bookshop.org/books/misbehaving-science-controversy-and-the-development-of-behavior-genetics/9780226058450" data-iframely-url="https://cdn.iframe.ly/api/iframe?url=https%3A%2F%2Fbookshop.org%2Fbooks%2Fmisbehaving-science-controversy-and-the-development-of-behavior-genetics%2F9780226058450&key=a91f6c63822d2172297a7435cae7a9eb"></a></div></div><script async src="https://cdn.iframe.ly/embed.js" charset="utf-8"></script></div>
<p>In attempts to justify their field against continued criticism, behavioral geneticists themselves used twin study results to argue social interventions would be ineffective. As Panofsky wrote:</p>
<blockquote><em>“Behavior geneticists’ polemical style of valorizing their re­search led them to plant deep stakes that were tightly clustered around a particular, basically genetic determinist, interpretation.”</em></blockquote>
<p>This history, including behavioral genetics' own role in generating, promoting, and defending scientific racism and determinist views of genetics is completely absent from Harden's book. This history matters; it is the source of the isolation of behavioral genetics from mainstream genetics research. This isolation has produced the intellectual and ideologically stagnant lineage that Harden operates in.</p>
<p>These biases are most pronounced in the early chapters walking readers through the science, which often leads to an incomplete, misleading, or mistaken account of genetic research and behavior. Harden presents an argument about the major causal role of genetic differences. These results span decades, including twin studies, and recent developments like genome-wide association studies (GWAS), polygenic scores (a single value combining individual estimated effects of genome-wide variations on a phenotype), and genomic analyses of siblings. Unfortunately, Harden often gives these results in such a misleading way that it obscures how damaging they actually are to her own core thesis.</p>
<div class="oembed"><div class="iframely-embed"><div class="iframely-responsive" style="height: 170px; padding-bottom: 0;"><a href="https://www.ucpress.edu/book/9780520379602/race-monogamy-and-other-lies-they-told-you-second-edition" data-iframely-url="https://cdn.iframe.ly/api/iframe?url=https%3A%2F%2Fwww.ucpress.edu%2Fbook%2F9780520379602%2Frace-monogamy-and-other-lies-they-told-you-second-edition&key=a91f6c63822d2172297a7435cae7a9eb"></a></div></div><script async src="https://cdn.iframe.ly/embed.js" charset="utf-8"></script></div>
<p>For example, Harden extols sibling analyses as unassailable evidence of independent, direct genetic causation free of biases found in other methods. While it’s true that polygenic scores from sibling analyses resolve substantial problems that sometimes create inaccurate associations between DNA and a phenotype, Harden fails to mention several key differences between these sibling-based methods and other genomic or twin-based methods. It is rarely stated clearly that these family methods<a href="https://www.sciencedirect.com/science/article/pii/S0002929721002780"><ins> produce much smaller estimates of genetic effect</ins></a>, often <a href="https://www.cell.com/ajhg/fulltext/S0002-9297(19)30231-9"><ins>nearly half the size</ins></a> as population-based methods, making the 13% variance explained by current education polygenic scores a likely overestimate. Harden also fails to mention that a commonly used method employed <a href="https://elifesciences.org/articles/61548"><ins>does not fully eliminate the problems from population structure</ins></a> or that estimates from siblings can still include confounding effects that create correlations between genes and environment.</p>
<p>Even worse, Harden moves between the less biased, but smaller, results from sibling methods to the more biased but larger estimates from population-based polygenic scores without being clear this is what she is doing. This happens frequently when discussing research claiming that educational polygenic scores substantially explain differences in income. The result is Harden obscures the fact that <em>more reliable</em> techniques result in <em>lower</em> predicted genetic effects. Readers may be wrongfully led to believe genetic effects are both large and reliable when in reality they are more often one or the other.</p>
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<p>Harden’s failure to engage with critics of behavioral genetics, often from the political left, veers between simple omissions and outright misrepresentation. This treatment is in stark contrast to how she treats biological determinists on the political right. The work of Charles Murray, the co-author of <em>The Bell Curve</em>, which claimed that differences in IQ scores between the rich and poor were genetic, and whose research aligns neatly with Harden’s, is described as mostly true and his political implications are lightly challenged. The most prominent critic of behavioral genetics, Richard Lewontin, gets much rougher treatment.</p>
<p>In one of the three cases in which Harden bothers to mention Lewontin’s decades-long engagement with behavioral genetics, she gets it wrong, claiming that Lewontin merely said that heritability is useless because it is specific to a particular population at a particular time. In reality, Lewontin showed why the statistical foundation of heritability analyses means it is unable to truly separate genetic and environmental effects. Contra Harden’s characterization of her opponents, Lewontin recognized genetic factors as a cause of phenotypes; however, he stressed their effects cannot be independent of environmental factors and the dynamics of development.</p>
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<p>Harden implies that giving people access to equal resources <em>increases</em> inequality and genetic influence. Lewontin explained why the outcome of equalizing environments precisely depends on <em>which environment you equalize</em>. As a toy example, a cactus and a rose bush respond differently to varying amounts of water. Giving both plants the same, small, volume of water is good for the cactus’s health and bad for the rose, giving both a larger volume of water is bad for the cactus and good for the rose. Equalized environments regardless of quality can reduce or increase inequality and can reduce or increase the impact of genotypic differences depending on the environment and the norm of reaction for a trait and set of genotypes. Heritability analyses cannot provide insight on this distribution or nature of genotype and environment interactions. These detailed, quantitative, and analytic arguments are entirely ignored by Harden.</p>
<p>In her story, people on the political left are ideologically driven to oppose behavioral genetics because they believe it invalidates their desire to ameliorate inequality. In the powerful book-length criticism of behavioral genetics, <a href="https://www.haymarketbooks.org/books/929-not-in-our-genes"><ins><em>Not in Our Genes</em></ins></a><em>,</em> Lewontin, with neuroscientist Steven Rose and psychologist Leon Kamin, all socialists, defy Harden’s characterization of her critics from the left, writing:</p>
<blockquote><em>“The antithesis often presented as an opposition to biological determinism is that biology stops at birth, and from then on culture supervenes. This antithesis is a type of cultural determinism we would reject… Humanity cannot be cut adrift from its own biology, but neither is it enchained by it.”</em></blockquote>
<p>They further write:</p>
<blockquote><em>“Against this we counterpose a view not of organism and environment insulated from one another or unidirectionally affected, but of a constant and active interpenetration of the organism with its environment. Organisms do not merely receive a given environment but actively seek alternatives or change what they find.”</em></blockquote>
<p><em>Not in Our Genes </em>criticizes biological determinism for oversimplifying the processes that create diversity in the natural world. And the ways that biological determinism is employed for political and ideological reasons by people like Arthur Jensen, Daniel Patrick Moynihan, or Hans Eysenck, to undermine movements for social and economic equality on the basis of biological data. Lewontin, Kamin, and Rose did not oppose biological determinism simply on ideological grounds. They knew there was no true threat to egalitarian beliefs posed by biological data if one properly understands biology in a non-determinist way. Instead, they wanted to move beyond just a scientific critique and provide a social analysis of why the mistakes of biological determinism are made, persist, and gain in popularity. They write:</p>
<blockquote><em>“The errors of the biologi­cal determinists’ explanation of the world can be explicated and under­stood without reference to the political uses to which these errors have been put. A large part of what follows in this book is an explication of these errors. What cannot be understood without reference to politi­cal events, however, is how these errors arise, why they come to characterize both the popular and scientific consciousness in a particular era, and why we should care about them in the first place.”</em></blockquote>
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<p>This lack of meaningful engagement with critics is not just poor scholarship, it weakens Harden’s case. Problems arise with Harden’s discussion of heritability, for example, which would be remedied with a genuine engagement with critics from mainstream genetics and evolutionary biology. Harden takes a hardline position that heritability is a measure of genetic causation within a sampled population; however, despite her attempt over two chapters to build this case, she is still fundamentally mistaken about the concept.</p>
<p>Early work in plant breeding and genetics can help shed light on the source of this confusion. The pre-eminent statistical geneticist, Oscar Kempthorne, in a <a href="https://doi.org/10.2307/2529584"><ins>1978 critique</ins></a> of behavioral genetics, wrote that the methods employed by the field can tell us nothing about causation because all they really represent is simply a linear association between genetics and phenotypes, without any further ability to connect the two to each other.</p>
<p>The extent to which correlations can be interpreted as causation depends on properly controlling for confounding variables. In the context of heritability, this means that genetics and environment need to be independent of each other, but this cannot be the case without direct experimental manipulation. In fields like plant breeding, it is possible to experimentally randomize which environments a plant genotype experiences, and genetically identical plants can be put in different environments for extra control, so these inferences are safer to make. In human genetics, however, this is not possible even with the sibling and twin methods Harden focuses on. These processes that <a href="https://link.springer.com/article/10.1007/s10519-018-9939-6"><ins>complicate causal interpretation of heritability </ins></a>estimates have been discussed <em>ad nauseum </em>by other behavioral geneticists, which is why Harden is one of the few who comes to her conclusions.</p>
<p>One final glaring omission worth noting occurs in Harden’s chapter on race and findings of behavioral genetics. Here, Harden does an admirable job trying to prevent the misapplication of behavioral genetics to questions of racial differences. Surprisingly absent though is the fact that across a variety of studies, genetic variation is much larger <em>within</em> races compared to between races. This finding undermines core perceptions about the biological nature and significance of race. It also has important implications for our assumptions about the role of genetics in phenotypic differences between races, namely that they will be small to nonexistent. One could speculate the omission is because the finding was from none other than Richard Lewontin. This case is particularly problematic because in<a href="https://onlinelibrary.wiley.com/doi/full/10.1002/tea.21670"><ins> randomized control trials,</ins></a> biology classes emphasizing Lewontin’s findings have shown very strong evidence of reducing racial essentialism, prejudice, and stereotyping. Few science education interventions against racism and prejudice have such strong evidence in their favor.</p>
<p>Above all, Harden desperately wants to impart one idea in the first part of the book: genes cause social inequality. Here she argues for causation as “differences makers” in counterfactual scenarios. In other words, X causes Y if the probability of Y occurring is different were X not to happen. As Harden notes, experimental science adopts a similar and in ways stronger, &nbsp;“interventionist theory” of causation, based around experimental interventions. Here X is said to cause Y if there is a regular response of Y to an intervention on X.</p>
<p>Under the interventionist theory, Harden’s account of genetic causation runs into trouble. First, it requires us to be able to isolate a specific property on which we can intervene. This is possible in cases of simple genetic disorders with clear biological mechanisms and short pathways from gene to trait, like sickle cell anemia or Tay-Sachs. However, this doesn’t work for behaviorally- and culturally-mediated traits involving large numbers of genes, with small effects and diffuse associations between genetic and non-genetic factors. There is simply no method to isolate and intervene on the effects of specific genetic variants that holds environmental factors constant in a way we would normally recognize as an experimental intervention. This applies still to the sibling analyses that Harden tries to portray as randomization experiments. Contrary to one of Harden’s more bizarre claims, meiosis does not approximate a randomized experiment. All it does is randomize genotypes with respect to siblings, it does not randomize environments experienced by genotypes. Our broad array of social and cultural institutions still acts in a confounding way. Instead, we just have a polygenic score, which is more a statistical construct than a tangible property in the world.</p>
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<p>Second, for Harden’s causal claims to hold weight, genetic and environmental factors must be distinct components that are independently disruptable. This reflects what the philosopher John Stuart Mill called the <a href="http://www.isnature.org/Files/Mill1859-Composition_of_Causes.htm"><ins>principle of the composition of causes</ins></a>, which states that “the joint effect of several causes is identical with the sum of their separate effects.” At the core, Harden assumes that genetic and environmental influences on human behavior are independent and separable. To say the absolute least, this is a highly dubious assumption. Based on the arguments from critics like Lewontin and the work from research programs like developmental systems theory, there is very good reason to think that biological systems are not modular, especially in the case of educational attainment. Genetic and environmental influences interact throughout development, the interactions are dynamic, reciprocal, and highly contingent. It simply isn’t plausible to estimate the independent effect of one or the other <em>because they directly influence each other</em>.</p>
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<p>A further weakness of Harden’s book is that just because genes make a difference in phenotype, it does not mean that genes are even relevant to the analysis of these phenotypes. In reality, Lewis’s account of causation, that X is a cause if a different outcome would have occurred in the absence of X, can be a pretty low bar, and the causes it identified may not be very relevant. An obviously absurd example is that the argument could be made that the sun caused me to wake up this morning since it is the origin of the trophic cascade that nourished my body enough to continue necessary biological functions. Under Lewis’ account, the sun is a cause of my waking up, but it’s hardly a relevant or informative cause compared to my alarm clock or to the bus I need to catch at 8:35am.</p>
<p>In <em>Biology as Ideology</em>, Lewontin discusses the causes of the disease tuberculosis. He notes that in medical textbooks the tubercle bacillus, which gives people the disease when infected, is <em>the</em> cause of tuberculosis. Lewontin writes that this biological explanation is focused on the individual level and treats the biological sphere as independent from external causes related to the environment or social structure. While we can surely talk about the role of the tubercle bacillus in causing the disease we can also talk about the social conditions of unregulated industrial capitalism and its role in causing outbreaks and deaths by tuberculosis and can gain far more insight by analyzing the causes of tuberculosis in that way.</p>
<blockquote><em>“...there have been complex social changes, resulting in increases in the real earnings of the great mass of people, reflected in part in their far better nutrition, that really lie at the basis of our increased longevity and our decreased death rate from infectious disease. Although one may say that the tubercle bacillus causes tuberculosis, we are much closer to the truth when we say that it was the conditions of unregulated nineteenth-century competitive capitalism, unmodulated by the demands of labor unions and the state, that was the cause of tuberculosis.”</em></blockquote>
<p>This distinction of whether a cause is relevant for particular social and scientific issues becomes a problem for Harden in the climax of her book where she tries to convince the reader that genetic information is a crucial tool for addressing social inequality.</p>
<p>One example given by Harden is that children who perform well but are in poor schools are able to “achieve” less, and that poor people with higher education end up making less money than rich people in the same fields. These findings are neither novel nor do they require the use of potentially misleading genetic data. While Harden tries to defuse right-wing arguments about shortcomings of social science research, this isn’t a given. As research Harden herself presents shows, results from behavioral genetics<a href="https://onlinelibrary.wiley.com/doi/full/10.1002/ajpa.24150"><ins> bolster the far right</ins></a> and they regularly <a href="https://doi.org/10.1371/journal.pbio.3000860"><ins>share this research</ins></a> to promote their beliefs and challenge egalitarian policies. Instead of engaging with this bad-faith criticism from the right, we can simply disregard them, just as Harden disregards their co-option of her field of research.</p>
<p>Finally, Harden expresses a general concern that social science and psychological studies are plagued by “genetic confounding,” that is the correlations they observe are actually due to unconsidered genetic forces that relate an individual to their outcome (i.e. low income doesn’t cause poor health, genes cause both low income and poor health). For this example, Harden is hard on these complaints, equating research that does not include genetic information as tantamount to robbing taxpayers, but light on evidence that this genetic confounding is a widespread problem, or that it can only be addressed with behavioral genetic research.</p>
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<p>Surprisingly, all these examples abandon the earlier bluster about genes being crucial causal factors in our life and instead opt for genetic data as one of many methods for causal inference of environmental interventions. We no longer care about heritability estimates; instead, we use twins as an experimental design. In some cases this is fine, however using individuals who have similar genotype, environmental characteristics, and phenotype does not mean that genes are significant causes, it’s just a good experimental design. Here, some of Harden’s arguments about social science research are accurate. Observational and correlation-based studies are weak for a number of reasons, not simply because they ignore genetic differences. The goal should be strengthening <a href="https://mixtape.scunning.com/introduction.html"><ins>causal inference</ins></a> in the social sciences, and we have some <a href="https://mixtape.scunning.com/introduction.html"><ins>idea</ins></a> of how to do that from other fields. To strengthen the ability to identify causes, epidemiologists employ direct experiments, like randomized control trials, exploit “natural experiments” that can approximate experimental randomization, such as studies that observe changes in outcome shortly after changes in government policy are enacted, or designs that use statistical methods to match people based on background demographic information like income, neighborhood quality, family education, etc.</p>
<p>In fact, there are principled reasons to think genetic data has little to no benefit above and beyond the kinds of data we can collect from non-genetic social science experiments. Eric Turkheimer, Harden’s doctoral advisor, has articulated the <a href="https://doi.org/10.1146/annurev-psych-113011-143752"><ins>“phenotypic null hypothesis”</ins></a> which states that for many behavioral traits the genetic variance identified from behavioral genetics studies is not an “independent mechanism of individual differences” and instead reflects deeply intertwined developmental processes that are best understood and studied at the level of the phenotype. This certainly appears to hold for the traits Harden talks about. Even with GWAS and polygenic scores, we are given no coherent biological mechanism beyond...something to do with the brain, they interact with and are correlated with the environment, and they are contextual and modifiable. Harden laments focus on mechanisms, but identifying specific causal mechanisms would be precisely how education polygenic scores could be actually helpful. For example, in medicine, GWAS have helped identify potential drug targets by identifying biological mechanisms of disease, and can <a href="https://doi.org/10.1371/journal.pgen.1008489"><ins>double the likelihood</ins></a> of a drug making it through clinical trials.</p>
<p>However, this situation doesn’t exist for things like education. Instead, we can understand the role of correlated traits like ADHD, or the effect of interventions purely at the phenotypic level by seeing how educational performance and attainment itself change upon interventions from well-designed experiments. In fact, several polygenic scores, from <a href="https://elifesciences.org/articles/49962"><ins>educational attainment</ins></a> to <a href="https://www.nature.com/articles/s41591-021-01475-7"><ins>schizophrenia</ins></a>, and <a href="https://www.nature.com/articles/s41436-018-0418-5"><ins>even diseases like cardiovascular disease</ins></a> have been shown to have virtually no predictive power beyond common clinical or phenotypic measures, meaning we do not more accurately predict the outcome of those particular phenotypes even with robust polygenic scores. So why not focus our efforts on phenotypes instead of genotypes in cases like education, income, and health where we have some ability to do randomized experiments and a wealth of quasi-natural experiments?</p>
<p>There are existing studies that attempt some kind of true experimental manipulation related to education. Despite what Harden or the charter-school supporting billionaire John Arnold says, we do have some idea on what can improve schools. Research indicates that de-tracking education, that is ending the separation of students by academic ability and having all students engage in challenging curriculum, regularly improves student performance for those with lower ability and does not hinder students with higher ability.</p>
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<p>Experiments have shown large benefits to those passing classes and the grades they receive when courses are structured around a more pedagogically informed curriculum that actively engages students. Detracking and active learning have the added advantage of greatly affecting racial gaps in educational performance. To achieve these goals it is likely that teachers will need to be better trained and compensated, and student-pupil ratios would need to change. These changes would likely be related to school funding, teacher salary and quality, and school resources even if those factors are not sufficient to improve educational outcomes in every situation.</p>
<p>Simply identifying that other methods can improve social sciences doesn’t mean we shouldn’t use every tool in our toolbox, as Harden says. However, there are convincing reasons we ought not to rely on genetic data for this kind of research. One reason is that polygenic scores are not very good as controls for experiments testing the effect of environmental intervention. <a href="https://t.co/sWy7YfPd6j?amp=1" target="_blank">Research has found</a> that the pervasive interplay of genes and environment weakens their ability to control for genetic confounding or identify the efficacy of environmental interventions. Since polygenic scores can reflect contingent social biases without us knowing, it is possible, and likely, that by relying on them to identify effective interventions we are in fact reifying ingrained social and economic biases further in our systems.</p>
<p>One final concern is how this research is interpreted by people, were it to be widely adopted. <a href="https://link.springer.com/article/10.1007/s11218-021-09632-z"><ins>Researchers found</ins></a> in online experiments that the very act of classifying someone based on their educational polygenic score led to stigmas and self-fulfilling prophecies. Those with high scores were perceived to have more potential and competence while those with low scores were perceived in the opposite way. Not only does this research suggest genetic data leads to essentialist beliefs that can re-entrench existing inequalities, but this kind of dependency can also create even more confounding influences that complicate the application of genetic data for social science questions.</p>
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<p>Finally, we reach the last issue with <em>The Genetic Lottery</em>: we don’t need the concept of genetic luck to pursue egalitarian policies. Harden regularly remarks that the alternative is to perceive people’s outcomes as their individual responsibility. Either something is the result of genes they have no control over, or it is their fault for not working hard enough. However, progressive politics revolves around structural and systemic factors that are outside of people’s control and contribute to their outcomes. There is already a recognition of moral luck, or that people’s outcomes are not their fault, but due to the situations they find themselves in. This engagement with progressive motivations and philosophy is absent in Harden’s analysis.</p>
<p>In Harden’s penultimate chapter she contrasts “eugenic,” “genome-blind,” and “anti-eugenic” approaches to policy. What ultimately occurs is a strawman of “genome-blind” policy approaches and often anti-eugenic policies that are hard to distinguish from eugenic policies. For example, what is the difference between Harden’s description of the eugenic policy <em>“Classify people into social roles or positions based on their genetics”</em> and the anti-eugenic policy <em>“Use genetic data to maximize the real capabilities of people to achieve social roles and positions</em>”? &nbsp;While the genome-blind position is described as<em> “Pretend that all people have an equal likelihood of achieving all social roles or positions after taking into account their environment.“, </em>all we really need to do to achieve our progressive goals is ensure that people’s ability to succeed and thrive in life is not conditioned upon their origin, preferences, or abilities. There’s simply no need to use genetic data on people at all.</p>
<p>In another case involving healthcare Harden suggests the genome-blind approach is to keep our system the same while prohibiting the use of genetic information, while the anti-eugenic approach is creating “systems where <em>everyone</em> is included, regardless of the outcome of the genetic lottery”. However, the system Harden describes is not universal social programs that ensure healthcare, housing, or education regardless of economic situations. Rather it is a system that resembles means-testing social welfare with genetic data. Of course, universal social programs do achieve exactly the anti-eugenic goal while still being genome-blind! Harden’s complete disregard for actual rationale and form of progressive policies when crafting the genome-blind caricatures is inexcusable from someone who claims to be progressive.</p>
<p>For a progressive that supports universal healthcare, a living wage for all, housing as a human right, or free education, it does not matter that people are different and it does not matter the cause for that difference. The fact that some people need healthcare to survive is the reason why it should be available for free, whether the need is from an inherited or acquired disease. It is acknowledged that people have different preferences and strengths, which ultimately results in them living different lives. The fact that for some people this means the difference between a living wage and poverty is what progressives take issue with, and it doesn’t matter what the cause of these differences are, simply that we address them.</p>
<p>Ultimately, Harden tries to sell us on research that we don’t need, based on faulty premises, and that is incapable of delivering on what she promises. Her failure to engage with the history of her own field, her scientific critics, or the actual content of progressive political goals leaves this book in a very poor place. In a way, <em>The Genetic Lottery</em> represents the fact that behavioral genetics no longer has a place to go after the tenets of genetic determinism and biological reductionism were shown to be untenable. If one wants to gain an understanding of modern genetics, or to learn how we may strengthen progressive causes, they should look elsewhere.</p>
    


<p><em><a href="https://massivesci.com/people/kevin-bird/">Kevin Bird</a> studies 

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<span class="scientist__field">Evolutionary Biology</span>

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<span class="scientist__institution">Michigan State University</span>

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<guid isPermaLink="true">https://massivesci.com/articles/urbanization-rural-agriculture-knee-osteoarthritis/</guid>
<link>https://massivesci.com/articles/urbanization-rural-agriculture-knee-osteoarthritis/</link>
<pubDate>Mon, 29 Nov 2021 11:13:00 EST</pubDate>
<title>Urbanization increases risk for knee osteoarthritis, even in young children</title>
<description>A study shows that rural children tend towards a healthier future for their joints compared to kids in cities</description>

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  <media:description>Three children walk through a city marketplace</media:description>
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  <dc:creator><![CDATA[Matthew Bomkamp]]></dc:creator>
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    <atom:name>Matthew Bomkamp</atom:name>
    <atom:uri>https://massivesci.com/people/matthew-bomkamp/</atom:uri>
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    <p>Many countries with agricultural-based economies are experiencing rapid urbanization as they transition to market-based economies. On top of the the broad societal changes experienced in these countries, research is studying the significant health consequences that this rapid urbanization can cause.</p>
<p>Many of the health changes associated with urbanization are thought to be a direct result from reductions in physical activity levels. As physical activity is well documented to be protective against <a href="https://onlinelibrary.wiley.com/doi/full/10.1111/j.1467-3010.2007.00668.x" rel="noopener noreferrer" target="_blank">many ailments</a>, such as cardiovascular disease, type 2 diabetes, and some types of cancer, urbanization has the potential to negatively impact human health. &nbsp;A recent study has indicated that the urbanization additionally may have widespread effects on the joints of its citizens.</p>
<p>In a <a href="https://onlinelibrary.wiley.com/doi/pdf/10.1002/acr2.11323" rel="noopener noreferrer" target="_blank">study</a> from Nicholas Holowka and Ian Wallace, Harvard University, the University of Buffalo, and the University of New Mexico, knee cartilage thickness was examined via ultrasonography in children living in both urban and rural Kenya. Western Kenya is an ideal location to study the effects of urbanization as many small communities still practice small-scale farming while being closely located to the more populated city of Eldoret. Children from ages 8 to 17 were recruited in order to see how knee cartilage thickness changed throughout childhood.</p>
<figure class="right medium"><img alt="A diagram showing osteoarthiritis in the knee, with cartilage degrading and the joint narrowing in width " src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/c2ca70e6-963b-44d8-bedf-46e188ff910d/Osteoarthritis.jpeg"/><figcaption><span class="caption"><p>A diagram showing osteoarthiritis in the knee, with cartilage degrading and the joint narrowing in width in the knee on the right, compared to a healthy knee on the left</p></span> <span class="credit"><p>Via <a href="https://commons.wikimedia.org/wiki/File:Osteoarthritis.jpg" target="_blank">Wikimedia</a></p></span></figcaption></figure>
<p>As loss of knee cartilage thickness is a <a href="https://www.nature.com/articles/s41584-018-0073-x" rel="noopener noreferrer" target="_blank">risk factor</a> for the development of osteoarthritis, this study aimed to uncover any differences in risk for developing knee osteoarthritis later in life due to urbanization. Interestingly, despite the study focusing only on osteoarthritis, a disease often associated with old age, the rate of reduction in knee cartilage thickness was still significantly less in the rural children compared to the children living in an urban environment. For the urban participants, knee cartilage thickness declined an average of .11mm per year during childhood. However, the rural children only saw knee cartilage thickness reduced an average of .047 mm per year. These results suggest that urbanization results in a greater risk for knee osteoarthritis, which can be seen even within childhood. So what is causing this increased risk in urbanized children?</p>
<p>One hypothesis that has been suggested is that the increased risk of knee osteoarthritis for those living in urban environments is due to dietary changes and increased fat accumulation. This <a href="https://ard.bmj.com/content/78/12/1693.full#ref-20" rel="noopener noreferrer" target="_blank">theory</a> holds that the dietary changes of urbanization promotes low-grade inflammation from the release of adipokines from excess adipose tissue. Adipokines, such as leptin, are cell signaling proteins that are secreted from fat tissue and can promote inflammation throughout the body. However, as mentioned previously, there were no differences between rural and urban children in terms of BMI in the current experiment and yet, knee cartilage thickness was still reduced in children living in urban areas. This would be unlikely if obesity-derived low-grade inflammation was the main culprit for loss of knee cartilage.</p>
<div class="oembed"><div class="iframely-embed"><div class="iframely-responsive" style="height: 140px; padding-bottom: 0;"><a href="https://massivesci.com/articles/cities-microbes-bacteria-urban/" data-iframely-url="https://cdn.iframe.ly/api/iframe?url=https%3A%2F%2Fmassivesci.com%2Farticles%2Fcities-microbes-bacteria-urban%2F&key=a91f6c63822d2172297a7435cae7a9eb"></a></div></div><script async src="https://cdn.iframe.ly/embed.js" charset="utf-8"></script></div>
<p>A <a href="https://www.nature.com/articles/pr2003389" rel="noopener noreferrer" target="_blank">similar study</a> as the current investigation conducted within an urbanized country may help provide more insight. This study revealed that there was an association with low levels of physical activity and decrements in knee cartilage thickness within children. &nbsp;<a href="https://www.sciencedirect.com/science/article/pii/S1063458416304241?via%3Dihub#bib42" rel="noopener noreferrer" target="_blank">Animal studies</a> &nbsp;also confirm that &nbsp;decreased physical activity through unloading promotes &nbsp;a loss of cartilage, potentially due to &nbsp;metabolic changes in chondrocytes. In the current study, children who were overweight did not show a correlation in a reduction in knee cartilage thickness. Taken together, these results suggest that physical activity levels, but not obesity, are likely responsible for the decrements in knee cartilage thickness seen within urbanized environments.</p>
<p>For those living in an urbanized country with a market-based economy, these results are potentially troubling. The health consequences of urbanization likely extends far beyond just obesity, as seen by the current study. And these changes and risk factors are already present within children living in urbanized environments. Additionally, this study challenges one of the commonly held paradigms of what constitutes healthy living. So often the numbers on the scale are considered the gold standard measurement that reflect overall health and wellness. However, physical activity levels, regardless of fitness levels and BMI, may play an important role as well.</p>
<p>Indeed, osteoarthritis rates are very prevalent within the United States, especially within the aging population. As many as <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2920533/#R2" rel="noopener noreferrer" target="_blank">10-13%</a> of Americans over 60 will be diagnosed with osteoarthritis. As living within an urbanized environment has been shown to be correlated with <a href="https://d1wqtxts1xzle7.cloudfront.net/54614930/Effect_of_urbanization_on_objectively_me20171003-2819-i4lwz6.pdf?1507071341=&amp;response-content-disposition=inline%3B+filename%3DEffect_of_urbanization_on_objectively_me.pdf&amp;Expires=1633568106&amp;Signature=VOOaI572Cfj8k9pZgTeOhONPxZt~oA5qJrUqYZbwcPuDaYndNE68GloCwg2eH5RXR2U4XcxUU-aHFei-0~Y5mCbtI3dSWrNRSP8iNS4E8cRX9O2GV1~VDMj4CmNprocDB7OJRBk6aLCNM2vtgPYyVjO1ac8K14shz9Mu7wxlDLcA4Ka9qZAaihdx7xz1MG96YPygA4QcHrSUd--RvvXq5gnZUyMuuil6k1MO10R376t8yeJUlTwkRZMZUHnDjFqq~ZHwmjaRRShqXgijBw9LM~eTlqkVh7a03kNPlBiZlYOxdstcPYx-rB5al7HKrHTeSmrP4~Oq1seYBp0MGZH2zw__&amp;Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA" rel="noopener noreferrer" target="_blank">reductions in physical activity levels</a>, this may not come as a big surprise. However, research such as the current study is vital in providing a clear understanding of the health issues deriving from urbanization. As the topic is increasingly investigated and the wide-spread effects of urbanization on human health is understood more thoroughly, hopefully these challenges can be met with better preventative health measures.</p>
    


<p><em><a href="https://massivesci.com/people/matthew-bomkamp/">Matthew Bomkamp</a> studies 

<p class="mb0">

<span class="scientist__field">Physiology</span>

and <span class="scientist__field">Applied Physiology and Kinesiology</span>

</p>

 at 

<p class="mb0 o7">

<span class="scientist__institution">University of Florida</span>

</p>

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<pubDate>Mon, 29 Nov 2021 08:20:36 EST</pubDate>
<title>A newly discovered cryosphere-dwelling yeast stays alive by making ethanol</title>
<description>Rhodotorula frigidialcoholis was isolated from 150,000-year-old permafrost in the McMurdo Dry Valleys of Antarctica</description>


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  <media:description>a close up of ice marked with dark blue swirls</media:description>
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  <dc:creator><![CDATA[Mitra Kashani]]></dc:creator>
  <atom:author>
    <atom:name>Mitra Kashani</atom:name>
    <atom:uri>https://massivesci.com/people/mitra-kashani/</atom:uri>
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    <p>Most of the Earth’s biosphere is <a href="https://link.springer.com/chapter/10.1007/978-3-662-06285-2_1">permanently cold</a> and contains environments below 0° C, &nbsp;known as the cryosphere. Microorganisms like bacteria and fungi call the cryosphere home, despite the seemingly inhospitable conditions. Some can even stick around in the ice for <a href="https://sfamjournals.onlinelibrary.wiley.com/doi/abs/10.1046/j.1462-2920.2003.00422.x">thousands of years</a>.</p>
<p>To make this happen, microorganisms have evolved adaptations that help them survive their forever winter – whether it’s because they prefer cold environments (known as psychrophiles) or they can tolerate them (psychrotolerants) until more favorable conditions arise.</p>
<p>One example of cryosphere adapted fungi are a genus of single celled, pink pigmented yeast called <a href="https://link.springer.com/chapter/10.1007/978-3-319-62683-3_11"><em>Rhodotorula</em></a>, which have been isolated and characterized from a range of cold ecosystems. In order to survive the coldest and driest parts of the Earth, they’ve evolved unique strategies to handle the elements. In a <a href="https://www.nature.com/articles/s41396-021-01030-9" target="_blank">recent study</a> by scientists at McGill University, a novel species of <em>Rhodotorula </em>yeast is changing our understanding of fungal cold adaptations in new and unexpected ways.</p>
<div class="oembed"><div class="iframely-embed"><div class="iframely-responsive" style="height: 140px; padding-bottom: 0;"><a href="https://massivesci.com/articles/antarctica-dry-valley-melting-ozone-water-climate-change-science-friday/" data-iframely-url="https://cdn.iframe.ly/api/iframe?url=https%3A%2F%2Fmassivesci.com%2Farticles%2Fantarctica-dry-valley-melting-ozone-water-climate-change-science-friday%2F&key=a91f6c63822d2172297a7435cae7a9eb"></a></div></div><script async src="https://cdn.iframe.ly/embed.js" charset="utf-8"></script></div>
<p>The newly identified psychrotolerant yeast, <em>Rhodotorula frigidialcoholis,</em> was isolated from 150,000-year-old ice cemented permafrost in the McMurdo Dry Valleys of Antarctica. The researchers found it has two novel responses to extreme cold temperatures: it can switch its metabolism from respiration to ethanol fermentation as its main pathway, and can overexpress molecules called small non-coding RNAs (sRNAs) that help regulate which genes are expressed after transcription. <em>R. frigidialcoholis</em> now also holds the record for the lowest temperature reported for ethanol production by any microorganism.</p>
<p>Scientists are still working to understand the precise role of sRNA expression in cold adaptation, but the metabolic switch from respiration to ethanol fermentation by <em>R. frigidialcoholis</em> may help the novel yeast – and potentially others like it – save energy, slowing down the freezing point in their cells as a long-term survival strategy.</p>
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<pubDate>Mon, 29 Nov 2021 08:06:28 EST</pubDate>
<title>El sur de Inglaterra alberga a una pequeña, pero prospera población de walabíes de cuello rojo</title>
<description>Los walabíes fueron introducidos al país al principio del siglo XX</description>


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  <media:description>a close-up image of a small kangaroo-looking gray creature that is a wallaby</media:description>
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  <dc:creator><![CDATA[Maria Gatta]]></dc:creator>
  <atom:author>
    <atom:name>Maria Gatta</atom:name>
    <atom:uri>https://massivesci.com/people/maria-gatta/</atom:uri>
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    <p>Walabíes: son muy monos, relativamente pequeños, y para los europeos, tienen una apariencia inédita. Esto es lo que llevó a la introducción del walabí de cuello rojo, una especie australiana, a principios del siglo XX a países como Inglaterra, Irlanda, y Francia. En aquellos tiempos, los walabíes se mantenían <a href="https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2907.1990.tb00105.x" target="_blank">en zoos</a> y colecciones privadas. <a href="https://zslpublications.onlinelibrary.wiley.com/doi/10.1111/j.1469-7998.1971.tb02203.x" target="_blank">Algunos escaparon</a>, sobre todo durante la segunda guerra mundial, cuando la gente tenía cosas más importantes por las que preocuparse por mantener vallas.</p>
<p>Hoy en día, hay muy poca información disponible sobre que les pasó a aquellos walabíes introducidos. Dos científicos, <a href="https://twitter.com/Lycaonpictus93" target="_blank">Holly English</a> y <a href="https://twitter.com/thonoir" target="_blank">Anthony Caravaggi</a>, decidieron investigar qué pasó con aquellos animales. Recogieron información sobre avistamientos de walabíes en los registros oficiales, las redes sociales, y los periódicos. Gracias a lo monos e inusuales que son, los avistamientos suelen ser mencionados en los periódicos locales.</p>
<p><a href="https://onlinelibrary.wiley.com/doi/full/10.1002/ece3.6877" target="_blank">En su artículo reciente</a> publicado en la revista científica <em>Ecologia y Evolución</em>, los investigadores encontraron pequeñas poblaciones de walabíes viviendo a lo largo del sur de Inglaterra. Aunque alguno de estos animales es probablemente un fugitivo moderno de una colección privada o un zoo, es improbable que tales escapadas sean el origen de todos los avistamientos de la región. Por ello, los investigadores creen que las poblaciones del sur de Inglaterra se están reproduciendo en libertad.</p>
<p>Así que, si alguna vez estas en el sur de Inglaterra y crees que has visto a un walabí, ¡no te sorprendas demasiado!</p>
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<guid isPermaLink="true">https://massivesci.com/articles/arctic-elegy-bering-sea-melting/</guid>
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<pubDate>Sun, 28 Nov 2021 23:58:20 EST</pubDate>
<title>An Arctic Elegy</title>
<description>What happens when the Bering Sea loses its ice?</description>

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  <media:description>A view of the Bering Sea from St. Lawrence Island</media:description>
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  <dc:creator><![CDATA[Lois Parshley]]></dc:creator>
  <atom:author>
    <atom:name>Lois Parshley</atom:name>
    <atom:uri>https://massivesci.com/people/lois-parshley/</atom:uri>
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    <p>When the Bering Sea freezes over, it sings. As wind and current shift, the ice crackles and moans, piping through the polar night.</p>
<p>Among these moving giants rises St. Lawrence Island. Closer to Russia than the United States, its granite cliffs uplift rock as old as the <a href="https://www.livescience.com/37584-paleozoic-era.html"><ins>Palezoic era</ins></a>, when an explosion of life spilled over the Earth. Waves have since cut away lake-dotted plains, and its headlands, once hugged by ice for much of the year, are rugged, with spare, bouldered beaches.</p>
<p>When Delbert Pungowiyi was born in 1959, the island had no electricity or cars. People were just beginning to use heaters. His family and their Yupik community relied on dog teams to travel, and ate what the land and sea gave them. When he was six, Pungowiyi’s father passed away in a hunting accident. “We had to grow up real fast to contribute,” he says. The winters were long and hard, and Pungowiyi’s family worried about running out of food. But the light always crept back. The sea would unlock, fast ice clinging to the shore. Then one day, the birds would come.</p>
<p>“It was a spectacle,” Pungowiyi says. “They would literally blacken the skies, swarms and swarms, circling.” A critical nesting ground, St. Lawrence Island draws millions of seabirds — puffins and auklets and murres — in migratory flocks, traveling vast distances to arrive precisely with the last of the ice. Pungowiyi could hear their calls from his bed, and ventured out to the cliffs with a homemade slingshot to harvest what his family needed. He was a good shot, but “a lot of times, I’d just lay there and look up at the sky, and watch the birds go around and around.” He marveled how, despite their careening speeds, the birds never seemed to collide. The air would still to the whoosh and thump of wings.</p>
<p>But the Bering Sea, the only marine gateway between the icy Arctic and the Pacific Ocean, is warming. More and more of its multi-year ice has melted. Normally, more than 193,000 square miles of ice would form across the Bering Strait each winter. In 2018, there was almost none, a development that <a href="http://www.washingtonpost.com/wp-dyn/content/article/2007/09/06/AR2007090602499.html"><ins>scientists originally didn’t forecast</ins></a> until the end of the century. “That’s about two Texas’s worth of ice that is missing,” <a href="https://climate.nasa.gov/news/2726/historic-low-sea-ice-in-the-bering-sea/"><ins>wrote</ins></a> Walter Meier, a scientist at the National Snow and Ice Data Center. The sea’s winter ice extent in 2018 and 2019 was the lowest it has been for <a href="https://www.science.org/doi/10.1126/sciadv.aaz9588"><ins>5,500 years</ins></a>.</p>
<p>Ice is the keystone of this ecosystem: When it melts, it releases fresh water and nutrients, sustaining algae and phytoplankton blooms, which in turn support some of the biggest fisheries on the planet. When floes form, they shed briny, cold water, forming a frigid ocean curtain that supported Arctic species and kept southern ones, like pollock and cod, out of the Arctic Ocean. This cold pool has been shrinking. In 2018, researchers were shocked when it <a href="https://agupubs.onlinelibrary.wiley.com/doi/full/10.1029/2019GL083816"><ins>vanished</ins></a> almost entirely.</p>
<figure class="center large"><img alt="A map showing St. Lawrence Island, between the Russian far east and Alaska in the Bering Sea" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/a302fed3-2354-4536-9f86-1a21739622db/st_lawrence_island.jpg"/><figcaption><span class="caption"><p>St. Lawrence Island, between the Russian far east and Alaska in the Bering Sea</p></span> </figcaption></figure>
<p>The Bering Sea is now trapped in a feedback loop: Open water absorbs more heat from the sun, warming the dark waters, and making it harder for ice to form the next year. Summer sea-bottom temperatures have increased by more than <a href="https://uaf-iarc.org/wp-content/uploads/2020/06/Bering-Science_June-4-2020_HMcfarland-WEB-2.pdf"><ins>12 degrees</ins></a> in less than a decade, impacting everything from the patterns of currents to nutrient availability to what fish thrive where. Even the <a href="https://link.springer.com/article/10.1007/s10872-017-0453-x"><ins>salinity</ins></a> of the water itself is changing as older ice melts. Before, Pungowiyi says, “Young ice — we call it <em>sikuliaq </em>— was almost like a water bed, every step bends.” Hunters trusted it when they ventured out to fish or crab. But thinner, newer ice, he says, “is brittle, and breaks up.”</p>
<p>This loss is echoing up the food chain. The Alaska snow crab population <a href="https://www.adn.com/alaska-news/2021/10/09/alaska-snow-crab-harvest-slashed-by-nearly-90-after-population-crash-in-a-warming-bering-sea/"><ins>has crashed</ins></a>. Ice seal carcasses have increased <a href="https://www.arctictoday.com/ice-seal-die-offs-in-alaska-have-spurred-a-government-investigation/"><ins>five-fold</ins></a>. Emaciated gray whales are <a href="https://www.fisheries.noaa.gov/national/marine-life-distress/2019-2021-gray-whale-unusual-mortality-event-along-west-coast-and#gray-whale-strandings-(as-of-october-1,-2021)"><ins>stranding themselves</ins></a>. And in 2021, for the <a href="https://www.nps.gov/subjects/aknatureandscience/2021-seabird-die-off.htm"><ins>fifth consecutive summer</ins></a>, communities all over western Alaska reported dead seabirds washing ashore. Residents from small towns along the Bering Sea have been mailing corpses to biologists in boxes, hoping the scientists can figure out what’s killing them.</p>
<p>At times on St. Lawrence Island, Pungowiyi says, “The beaches have been literally littered with carcasses.” He mourns over the bodies of crested auklets, slick, black diving birds with a splash of feathers like bangs. When they wash up, their keels curve out of gaunt chests. “Since the cold curtain lifted, the impact has been accelerating,” Pungowiyi says. “It literally sends chills down my spine to see this in my lifetime.” These changes are altering peoples’ relationship with the food they depend on. In town, the constant murmur and chatter from the cliffs is eerily quiet.</p>
<p>“As a young man growing up, I thought this will always be. And now I see that what I thought is really not…” he trails off. “It’s heart-wrenching.”</p>
<hr/>
<p>A crested auklet colony can be smelled before it's seen: The chunky, raucous birds give off the smell of tangerines from a hundred yards. In the thrill of spring, males will puff up their distinctive crest. If a potential partner is interested, she’ll bury her beak in his neck feathers, where the citrus scent is strongest. Then the pair twist their necks together and rub, cackling. Onlookers egg them on in a scrum, pressed close as if on a crowded dance floor.</p>
<p>Although seabirds of many species gravitate to St. Lawrence, Alexis Will, a biologist at the Institute of Arctic Biology, says the extent of the island’s crested and least auklet colonies make it unique. They are so large that she needs an ATV to survey them. “You’re driving along and it’s just these clouds of birds,” she says. Bumping over the tundra, the nesting cliffs dropping off to the ocean look like the edge of the world. The island is one of only about 100 known crested auklet nesting sites. “You just see these swirls of birds for kilometers. They go on forever.” Her voice breaks. “It’s hard to see how amazing it is — and then to see that start to fall apart.”</p>
<figure class="right medium"><img alt="A crested auklet" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/d9930b44-ddee-438d-bc0e-3e3fe346ff7d/AWill%20Crested%20Auklet.JPG"/><figcaption><span class="caption"><p>A crested auklet</p></span> <span class="credit"><p>Alexis Will</p></span></figcaption></figure>
<p>The lives of seabirds are perilous, and occasional die-offs are normal. But recent events are different: They’re <a href="https://www.nps.gov/articles/keeping-a-finger-on-the-pulse-of-coastal-birds.htm"><ins>happening</ins></a> more frequently, lasting longer, impacting more species, and covering larger geographic areas.</p>
<p>In 2015, as many as <a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0226087"><ins>a million common murres</ins></a><ins> </ins>— a highly adaptive species — died in the Gulf of Alaska after an unusual <a href="https://earthdata.nasa.gov/learn/sensing-our-planet/blob#:~:text=By%20summer%20of%202014%2C%20the,triggered%20extended%20harmful%20algae%20blooms."><ins>marine heat wave</ins></a>. That catastrophic event was soon followed <a href="https://www.usgs.gov/centers/asc/science/seabird-die-offs-alaska?qt-science_center_objects=0#qt-science_center_objects"><ins>by many others</ins></a>, with die offs happening year after year around the Bering Sea. This September alone, <a href="https://www.nps.gov/subjects/aknatureandscience/2021-seabird-die-off.htm"><ins>650 dead birds</ins></a><ins> </ins>— shearwaters and common murres and horned puffins — were reported around St. Lawrence Island; Will says that since most birds die unobserved at sea, that’s likely a large underestimate of the true mortality.</p>
<p>There isn’t a single, easily explainable cause. Rather, the likely culprit, climate change, is impacting each location and species differently. “There are lots of ways to die off,” Will says.</p>
<p>Seabirds like the crested auklet eat small zooplankton called <a href="https://www.fisheries.noaa.gov/feature-story/copepods-cows-sea"><ins>copepods</ins></a>, tiny shrimp-like creatures. Kathy Kuletz, a seabird biologist with the U.S. Fish &amp; Wildlife Service, explains that as the Bering Sea warms, large, lipid-rich copepods <a href="https://academic.oup.com/plankt/article/39/2/257/3052904"><ins>have declined</ins></a>. While smaller copepods are proving more resilient, they provide less energy for the fish and birds who rely on them. The collapse of the Bering Sea’s cold pool may have also increased competition for prey, as predatory fish like pollock <a href="https://www.fisheries.noaa.gov/feature-story/study-shows-pollock-stocks-are-mixing-more-due-changing-ocean-conditions-and-weather"><ins>move north</ins></a>. “To feed a chick, a bird might have to catch three pollock, instead of one arctic cod, which is richer in lipids,” Kuletz says, causing chicks to mature slower, or fledge late, with fewer surviving to breed. “Things are changing, probably faster than some species of birds can respond.”</p>
<p>Starting in 2017, Will found that copepods nearly disappeared from both auklet species’ diets. This summer, when a friend of Pungowiyi’s went to harvest birds, he was devastated by their condition: The stomachs of the emaciated birds weren’t the usual color — they clearly weren’t eating their normal prey. Punguk Shoogukwruk, a St. Lawrence resident, has been collaborating with Will for the last three years, catching and measuring birds. He has noticed chicks dying of hunger, as well as starving fledglings abandoning their nests prematurely. “To be going around checking nests and seeing one dead chick after another is pretty much the worst thing,” Will says. Neither auklet species produced any surviving chicks in 2018 or 2019; the pandemic has limited her field research since.</p>
<p>Scientists have found that shifting <a href="https://research.noaa.gov/article/ArtMID/587/ArticleID/1435/Arctic-summer-wind-shift-could-affect-sea-ice-loss-and-USEuropean-weather"><ins>wind patterns</ins></a> have broken down the normal transport of sea ice and currents, impacting how nutrients are dispersed through the ocean, and possibly changing where auklets can find their staple prey. Strong, warm southerly winds have been forcing the remaining ice north, redistributing zooplankton — and everything that depends on them.</p>
<p>It’s difficult to track the rapid changes occurring in this critical habitat, much less predict their consequences. The thick-billed murre, for example, which also nests on St. Lawrence Island, mostly eats small fish that live near the sea bottom. These fish populations appear stable, for now. But even though the murres seem to have enough food, they died in droves around St. Lawrence in 2018. The number of returning thick-billed murres fell the following summer by <a href="https://uaf-iarc.org/wp-content/uploads/2020/06/Bering-Science_June-4-2020_HMcfarland-WEB-2.pdf"><ins>25 percent</ins></a>. Scientists wonder whether their prey moved to unusual or harder to access locations. Worsening <a href="https://www.nsf.gov/discoveries/disc_summ.jsp?cntn_id=303666&amp;org=NSF&amp;from=news"><ins>toxic algae blooms</ins></a> and avian disease could also be contributing factors, but so far, research has been inconclusive. “The Bering Sea is in such a state of flux right now that there’s not necessarily any established pattern,” Will says. “It’s all broken down — the system is in a state of freefall.”</p>
<figure class="right medium"><img alt="A least auklet" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/8290b0a4-d44e-46bf-acb0-3ed7d23f66a5/AWill%20Least%20Auklet.JPG"/><figcaption><span class="caption"><p>A least auklet</p></span> <span class="credit"><p>Alexis Will</p></span></figcaption></figure>
<p>Will has been studying seabirds that nest on St. Lawrence since 2016. By measuring a stress hormone called corticosterone, she recently found that all five of the species she examined on the island are <a href="https://www.dropbox.com/s/9atdtwk5d9j383i/Alexis%20Will's%202020%20Seabird%20Die-Off_Final.pdf?dl=0"><ins>experiencing high nutritional stress</ins></a>. Each dives to a different depth, and targets different prey, but starvation is their common <a href="https://www.nps.gov/subjects/aknatureandscience/2021-seabird-die-off.htm"><ins>suspected</ins></a> enemy. “The seabirds we’ve been tracking encompass pretty much the range of how you can make a living in a marine environment,” Will says. “Basically, none of the birds are winning.”</p>
<p>Some seabirds live for a long time. Kittiwakes, for example, can live to 30 years old. But crested auklets have flash-in-the-pan lives; they sport their tangerine smiles for less than a decade, intensifying pressure on the efforts to understand what is going wrong. Least auklets live for even shorter periods. After two years with a complete failure to breed, their population may already be slipping away. On St. Lawrence Island, if this trend continues “we have about a decade for least auklets, maybe less,” Will says. “And there’s really nothing we can do — it’s climate change.”</p>
<hr/>
<p>In 1983, Pungowiyi was sitting in his grandfather’s house, the home he inherited and lives in today. “Things were pretty normal back then,” he says. They were on the couch watching TV when his grandfather turned to him. “Remember what I tell you,” he said in Yupik. “I will not be here, but you will witness the loss of ice.” Although Pungowiyi’s grandfather didn’t use scientific terms like “climate change” or “unusual mortality events,” he knew through close observation that the weather had begun to shift.</p>
<p>By the <a href="https://eric.ed.gov/?id=ED475289"><ins>1990s</ins></a>, Indigenous reports that the Arctic was changing made it into a few academic studies. It took another decade for the wider scientific community to pay attention. “Our ancestors believed all oceans were connected,” Pungowiyi says. The Bering Sea plays a crucial role in the marine conveyor belt that regulates the world’s oceans. Changes here can possibly interfere <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6800673/"><ins>with the jet stream</ins></a>, weakening the polar vortex and affecting everything from drought in the American West to record-breaking rainfall in Europe. “I fear if the Bering Sea ecosystem collapses, it will have a domino effect,” he says.</p>
<p>When Pungowiyi learned to hunt from his grandfather, the island saw nine months of solid winter, with freeze up starting in October and break up extending into June. He learned to predict the weather by ocean ripples, and the formation of drifting snow. The long cold thickened the ice, making it possible to hunt and travel. Village monitors on St. Lawrence Island began recording the daily ice extent in 2000, when gleaming, multi-year bergs still blued the islands’ beaches. Now, winter lasts for three months, Pungowiyi says, four “if we’re lucky.” When it snows, he hears kids saying that it’s winter, and explains to them that the season, <em>uksuq,</em> only begins when “the whole of the sea is locked up, and there’s no more open water. That’s winter.” Some years now, <em>uksuq</em> doesn’t come at all.</p>
<figure class="right medium"><img alt="Punguk Shoogukwruk, a St. Lawrence Island resident, performing field research" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/ed366328-c338-425f-b53e-40e8106dd498/AWill_Punguk%20Picking.JPG"/><figcaption><span class="caption"><p>Punguk Shoogukwruk performing field research</p></span> <span class="credit"><p>Alexis Will</p></span></figcaption></figure>
<p>In the old patterns of life, animal behavior was once so habitual that the Yupik word for July is <em>alpaarusvik</em>, literally “time when the murres leave.” But in 2007, for the first time in the elders’ memory, flying cormorants arrived in mid-winter. The seals come early, and the whales late. “We’re seeing big shifts in availability and abundance of species,” says Lisa Sheffield Guy, a biologist and the project manager at the Arctic Research Consortium of the U.S. Hunting requires an intricate understanding of the weather, but travel on thin ice is perilous, and recently, warm, dangerous winds rise out of nowhere, sweeping ice and anyone on it offshore. “One thing we do still rely on is clouds,” Pungowiyi says. “They always tell the truth.” For everything else, the changes are so fast, and so fundamental, they are outstripping traditional knowledge.</p>
<p>These shifts are driving food insecurity on the island. “People depend on the yearly harvest of eggs, and lately there have been less and less,” Shoogukwruk says. In addition to hunting birds, residents collect eggs during the brief nesting window, and then freeze them. But as access to these kinds of food sources change, many are having to increasingly rely on imported food. The cost of shipping goods out to St. Lawrence is high, and grocery prices are steep; a half-gallon of milk costs over $10 and a box of cereal can cost $8. Pungowiyi is among the many residents who visit the food bank in town, but it struggles to keep up with demand.</p>
<p>Pungowiyi has spent the last few years trying everything he can think of to get people to pay attention, including inviting Senator Lisa Murkowski out to the island. Yet scientific and governmental responses have been slow. As the former tribal president, Pungowiyi recently traveled to an Arctic Council meeting, where he was excited to speak to some of the world’s top scientists. He <a href="https://www.youtube.com/watch?v=lLOZOIk6N5s"><ins>planned a talk</ins></a>, hoping to describe the die-offs he’d witnessed, but “they had us in a tiny little room on the second floor,” during the lunch hour. He decided he was going to find a way to speak to the full gathering, in the big room. In a break for questions, he walked up to one of the microphones, wearing a hat his mother had embroidered with two polar bear heads. “I had made up my mind to speak as quick as I can, until they cut me off,” he says. And then he told the room about his grandfather’s warning, and the island’s birds dying.</p>
<p>Pungowiyi hoped sharing what he’d seen would wake people up, get them to do something. Instead, it became clear no one was grasping the urgency of the crisis. “I feel at the end of my rope,” he says. He was distressed by the recent international climate talks in Glasgow, which he felt failed to recognize either Indigenous voices or the major impact he’s seen on the oceans. “The table they are talking at was our table,” he says. “But they have just pushed us aside.”</p>
<p>Igor Krupnik, an anthropologist and Arctic ethnology curator at the Smithsonian’s National Museum of Natural History, has known Pungowiyi for years, and watched him grow more and more desperate. Drama is antithetical to a culture where people had to tolerate each other through long winters, Krupnik says, so Pungowiyi’s outward-facing advocacy is particularly striking. “Delbert is a very strong person, who is now in a moment of hopelessness,” Krupnik says. He, too, seems troubled. “Is this what our life is going to be, without birds, and without ice?”</p>
<figure class="center medium"><img src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/5218f389-ee4d-44d5-96ff-52bb9aa7d0f4/AWill%20Kitnik.JPG"/><figcaption><span class="caption"><p>Kitnik, a beach outside Savoonga</p></span> <span class="credit"><p>Alexis Will</p></span></figcaption></figure>
<p>As I continued reporting, I kept hearing the same story. “Yeah, Delbert called me too,” says Jon Rosales, a climate scientist at St. Lawrence University in New York who has been <a href="http://www.aksik.org/"><ins>documenting</ins></a> the impacts of global warming on Native peoples in the Arctic, and whose mother-in-law is from St. Lawrence Island. “You feel helpless, that’s where the despair comes in,” he says. “You hear these stories from the frontlines, and yet the solutions are really global.”</p>
<p>Even if every country meets its current climate targets, there will still be <a href="https://www.unep.org/resources/emissions-gap-report-2021"><ins>catastrophic amounts</ins></a> of warming. Scientists recently found that if the world continues business-as-usual, likely temperature increases will cause biological and chemical conditions in <a href="https://www.cell.com/one-earth/fulltext/S2590-3322(21)00602-3"><ins>more than half the ocean</ins></a> to become “new and significantly different.” Not everything will suffer: Without ice, a different kind of plankton will bloom, supporting fish that swim near the ocean surface, and the animals that eat them. But the balance has shifted. Far short of extinction, the island’s old ecology is unraveling. “The biggest realization for me is it’s not done,” says Will. “We’re in this wobbly state, where the system probably won’t ever go back to how it functioned before, but it also hasn’t settled into a new steady state of being.”</p>
<p>Everyone is handling these changes differently. Shoogukwruk says he knows the island’s residents can adapt, because they have before: when the Russians came, when their land was sold to the United States, and when they were forced into living in villages. “We’re still here. And the animals are fighting the same way. It might be hard,” he says, “but if we can’t adapt, then what are we going to be?”</p>
<p>One weekday morning, I reach Pungowiyi while he’s making pancakes for his grandson. He’s tired. “It won’t get any better for our children. Those are the ones I hurt for the most.” In the background, his grandson calls to him. “I wish I could tell those giant [fossil fuel] companies, all the wealth they accumulated will become useless, and their children and grandchildren will suffer. For god’s sake — what are you going to leave behind for them?”</p>
<p>We sit for a moment, and then he says he was “thinking about the environmental lady who wrote about the birds that sang, and are no longer there.” I tell him she also <a href="https://www.newyorker.com/magazine/2018/03/26/the-right-way-to-remember-rachel-carson"><ins>loved the sea</ins></a>. “It’s really on the verge of collapsing. We can’t stop it,” he says. “But it needs to be documented. The world needs to know it is unfolding.”</p>
<p>Anyone who has stood on a shore and watched a bird dive to where they can’t follow knows its dip and disappearance, like a trick of the eye. Seabirds live in the in-between, plunging from the sky into the deep, slipping back and forth between laws of motion. Their future might be liminal, too. “If you cannot save the physical birds, you probably can save a memory of the birds in culture,” Krupnik says. Small salvage, knowing that even as the island’s colonies dwindle, our very longing might preserve a time when the sky here drummed to life with wings.</p>
    




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<guid isPermaLink="true">https://massivesci.com/articles/extraterrestrial-aliens-seti-telescope-array/</guid>
<link>https://massivesci.com/articles/extraterrestrial-aliens-seti-telescope-array/</link>
<pubDate>Sun, 28 Nov 2021 23:58:17 EST</pubDate>
<title>To find extraterrestrials, we have to think like extraterrestrials</title>
<description>Researchers must ponder what extraterrestrials might know and how they might behave</description>

<media:content url="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/52071ae9-0a13-4417-8aad-e8aae556f795/night-1.jpg?auto=compress%2Cformat&amp;crop=faces&amp;fit=crop&amp;fm=jpg&amp;h=600&amp;q=75&amp;w=900" type="image/jpeg">
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  <media:description>The Allen Telescope Array seen at night</media:description>
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  <dc:creator><![CDATA[Charlie Wood]]></dc:creator>
  <atom:author>
    <atom:name>Charlie Wood</atom:name>
    <atom:uri>https://massivesci.com/people/charlie-wood/</atom:uri>
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    <p>Over lunch one day in 1950, the Nobel Prize winning nuclear physicist Enrico Fermi posed a question that would reverberate through parts of astronomy for decades.</p>
<p>“Where is everybody?” he mused.</p>
<p>He and a few other physicists had been discussing technological extraterrestrials, and Fermi appeared to be making the innocuous argument that since no aliens had landed on Earth, interstellar travel must be a tall order.</p>
<p>Seventy years later, his question has morphed into something else — a case against the very existence of extraterrestrial civilizations and an implication that astronomers are wasting their time looking — the infamous “Fermi Paradox.” Its continued occupation of the popular consciousness tends to make the researchers doing this work salty.</p>
<p>“There is no Fermi Paradox,” says <a href="https://sites.psu.edu/szs714/"><ins>Sofia Sheikh</ins></a>, a postdoctoral researcher at the Berkeley SETI Research Center . “You can’t say something about why there isn’t something there if you haven’t searched for it.” (Others point out that the academic argument <a href="https://www.liebertpub.com/doi/epub/10.1089/ast.2014.1247"><ins>does not actually belong to Fermi</ins></a><ins>,</ins> and is not a paradox.)</p>
<p>Despite decades of talk, the Search for Extraterrestrial Intelligence (SETI) has been a field of comparatively little action — largely starved of federal funding due in part to Fermi Paradox-influenced thinking. SETI pioneer Frank Drake spent four months in 1960 <a href="https://www.seti.org/project-ozma"><ins>scanning two stars</ins></a> for radio signals. More than a half century later, SETI researchers have made only modest progress. The privately funded Breakthrough Listen project is currently conducting one of the most exhaustive searches to date, listening to nearby stars for roughly fifteen minutes each. Preliminary results suggest that of our closest couple hundred neighbors, no star system harbors a civilization that broadcasts a powerful radio signal in our direction all the time. That leaves a couple hundred billion stars in the galaxy yet to be searched.</p>
<p>In 2012, Jill Tartar, a foundational SETI astronomer and inspiration for Carl Sagan’s novel <em>Contact</em>, likened the search for signals that could arrive from any direction at any time to hunting for marine creatures in a volume as vast as the Earth’s oceans. She estimated that SETI efforts had, collectively, sampled roughly <a href="https://www.npr.org/2012/07/23/156366055/jill-tarter-a-scientist-searching-for-alien-life"><ins>one glass of water</ins></a>. An academic calculation suggested that, as of last year, SETI astronomers were up to perhaps “<a href="https://arxiv.org/abs/1809.07252"><ins>a large hot tub</ins></a>” of water.</p>
<p>To speed the cosmic trawl, researchers are increasingly leaning on a concept first articulated in — of all places — economics. Due to the current limits of technology, the modern SETI enterprise is mainly a search for potential civilizations that <em>want</em> to be found. Extraterrestrial intelligences would, by definition, be rational agents, and might intentionally beam out signals indicating their presence, shouting “We are here!” into the void. If so, astronomers could turn our common intelligence to their advantage, working out how to cooperate even without communicating. All they need to do is think like aliens.</p>
<p>“This is clearly the way we should think about how to design things,” says <ins>James Davenport</ins>, an astronomer at the University of Washington. “It’s a natural framework to think about how you might communicate with an unknown actor.”</p>
<p><strong>A galactic game of seek and don’t hide</strong></p>
<p>Stripped of its science-fiction trappings, the challenge of making contact looks like a special kind of game in economic theory: two players share one goal, but they can’t communicate as they attempt to achieve it.</p>
<p>While such an exercise might initially seem futile, Thomas Schelling, an iconoclastic and Nobel prize winning economist who popularized the Cold War concept of Mutual Assured Destruction, realized that games where players can’t communicate are still games. They may lack sure-fire paths to victory, but some strategies beat others. In Schelling’s 1960 book <em>The Strategy of Conflict</em>, he described how to identify such “focal” or “Schelling” points; focus on what you suppose your counterpart might know and what your counterpart supposes you might know.</p>
<p>A classic example is two strangers tasked with finding each other in Manhattan. An organized, but rather hopeless plan might be to walk the streets in a grid from Battery Park to Inwood, from the Hudson to the East River. Rather, Schelling reasoned, canny players might consider unique places and times that jump out to both parties as special, such as Grand Central Terminal at noon. Schelling’s theory has been born out in real demonstrations. In 2006, ABC staged just such a game, dropping off six pairs of people at random spots in the city. <a href="https://abcnews.go.com/Primetime/story?id=1730849&amp;page=1"><ins>Within hours</ins></a>, the teams converged on two spots: Time Square and the observation deck of the Empire State Building. All six groups independently choose noon as their meeting time.</p>
<p>As technology improves and bigger astronomical data sets become available, SETI astronomers are rolling out a wide variety of novel searches based on the same principle. But it’s &nbsp;easier said than done. What, if anything, can SETI researchers hope to have in common with alien civilizations? What do we know extraterrestrials know, and what do they know we know?</p>
<p>“We’ve got to pick some signal strategy or signal reception strategy that will match with what someone else comes up with,” Sheikh says. “Otherwise, the task is hopeless.”</p>
<p><strong>Special frequencies</strong></p>
<p>Human astronomy remains, for the time being, firmly attached to Earth. Presumably, other civilizations have a home base from which they broadcast too. In SETI, the question of “where to meet” often becomes a question of “what frequency to chat on.” After all, even just here on Earth humans reach each other on a dizzying array of radio channels, microwaves, and with beams of visible and infrared light.</p>
<p>In a foundational SETI publication appearing in <em>Nature</em> in 1959, physicists Giuseppe Cocconi and Philip Morrison proposed that <a href="http://www.coseti.org/morris_0.htm"><ins>1420 MHz or thereabouts</ins></a> would be a good place to start the conversation. Hydrogen gas buzzes at precisely this radio frequency, and since hydrogen is the most common element in the galaxy (and the universe), this channel might be of particular interest. Schelling himself called out the frequency as an example of a Schelling point the next year in <em>The Strategy of Conflict</em>, <a href="https://books.google.com/books?id=5AcPEAAAQBAJ&amp;pg=PT105&amp;lpg=PT105&amp;dq=just+in+the+most+favored+radio+region+there+lies+a+unique,+objective+standard+of+frequency,+which+must+be+known+to+every+observer+in+the+universe:&amp;source=bl&amp;ots=_2SYIE29B6&amp;sig=ACfU3U18Zfta8ixx0cY29NHtbVhwJMgGfw&amp;hl=en&amp;sa=X&amp;ved=2ahUKEwi0_buQm9nzAhVdQzABHfPZCBkQ6AF6BAgCEAM#v=onepage&amp;q=just%20in%20the%20most%20favored%20radio%20region%20there%20lies%20a%20unique%2C%20objective%20standard%20of%20frequency%2C%20which%20must%20be%20known%20to%20every%20observer%20in%20the%20universe&amp;f=false"><ins>writing in a footnote</ins></a>, “In the most favored radio region there lies a unique, objective standard of frequency, which must be known to every observer in the universe.”</p>
<p>The “hydrogen line” has since fallen out of favor in SETI, partially because all that hydrogen makes the channel rather noisy, and partially because astronomers no longer need to spend months turning the radio dial by hand as Drake did. “In the first SETI searches you’d look at a channel at a time,” Sheikh says. “Now we're doing billions of times that with a single observation with a single instrument.”</p>
<p>Yet researchers continue to think about special frequencies. When analyzing a billion signals at once, there are a billion chances for the algorithm to mistakenly flag one channel as artificial. Identifying the most promising candidates ahead of time could lend confidence to future detections.</p>
<p><a href="https://sites.psu.edu/astrowright/jason-t-wright-assistant-professor-of-astronomy-and-astrophysics/"><ins>Jason Wright</ins></a>, a Penn State astrophysicist, described a novel set of <a href="https://www.cambridge.org/core/journals/international-journal-of-astrobiology/article/abs/planck-frequencies-as-schelling-points-in-seti/4FD25BC6BD6D557D5F6E48AACD928426"><ins>Schelling point frequencies</ins></a> last year in the <em>International Journal of Astrobiology</em>. Using base ten numbers and the units of Hertz to measure radio frequencies are merely conventions of human culture, so Wright sought culture-independent frequencies in fundamental physics. He found inspiration in research from the pioneer quantum physicist, Max Planck, who in 1900 wrote about physical quantities that “remain meaningful for all times, and also for extraterrestrial and non-human cultures, and therefore can be understood as ‘natural units.’”</p>
<p>These fundamental constants of nature describe the speed of light, the strength of gravity, and the relationship between a photon’s energy and its frequency. Any civilization capable of building a radio beacon would likely be able to measure these numbers as humans have, and by mixing them together could find a particular frequency — a universal frequency specified by fundamental physics. “If you know those three things, you say huh, something funny happens at that frequency,” Wright says.</p>
<figure class="center medium"><img alt="Planck’s constant, the gravitational constant, and the speed of light define a unique duration of time — the Planck time — which Wright used to build up a set of universal frequencies. " src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/97bd8535-8a5c-4120-b5a7-70454cfab01c/planck_time_equation.png"/><figcaption><span class="caption"><p>Planck’s constant, the gravitational constant, and the speed of light define a unique duration of time — the Planck time — which Wright used to build up a set of universal frequencies.</p></span> </figcaption></figure>
<p>Electromagnetic radiation with the fundamental frequency would be impossible to detect, so Wright added the fundamental charge of atomic particles to the mix and used the four constants to construct a base — like we use the number 10 as a base — to formulate a list of more reasonable frequencies in both radio waves and visible light, a frequency “comb,” that SETI researchers could use to sift through the haystack of radio channels.</p>
<p><strong>Special times</strong></p>
<p>As some SETI researchers ponder <em>how</em> aliens might reach out, others wonder <em>when</em>. Transmitting beacons take energy, and civilizations may not transmit all the time. (We certainly don’t. Our highest profile message lasted for <a href="https://news.cornell.edu/stories/1999/11/25th-anniversary-first-attempt-phone-et-0"><ins>three minutes in 1974</ins></a>, a powerful blast from the recently ruined Arecibo radio dish in Puerto Rico.)</p>
<p>To get picked up during Breakthrough Listen’s 15-minute scans, for instance, our nearest neighbors would need to be beaming out an all-directional signal using around a trillion watts of power, according to Wright, or about <a href="https://www.theworldcounts.com/stories/current_world_energy_consumption"><ins>five percent of humanity’s total energy consumption</ins></a>. That’s an expensive porch light to leave on all the time. To hear from cultures on a budget, researchers may need to work out the cosmic equivalent of noon — a universal hailing time.</p>
<p>Sheikh reasons that any civilizations engaged in sending interstellar messages are likely to be at least as good at astronomy as we are. In recent decades, astronomers have spotted thousands of exoplanets, often by looking for stars that regularly dim as planets pass in front of them. Any aliens doing the same could already know Earth is here.</p>
<p>That knowledge could focus their efforts to make contact by specifying a unique time to say hello — the moment when Earth eclipses the sun, dimming our star and revealing our presence. Sheikh is moving to the SETI Institute in California in January, and for her first project there she plans to use the institute’s Allen Telescope Array to sweep the night sky directly overhead when the sun is positioned “behind” the Earth from the perspective of any inhabitants of star systems in view.</p>
<figure class="center large"><img alt="The Arecibo Radiotelescope in Puerto Rico, before its destruction" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/683c0aa0-cfa9-4e74-b470-885458a07ed2/2048px-Arecibo_Radiotelescopio_SJU_06_2019_7472.jpeg"/><figcaption><span class="caption"><p>The Arecibo Radiotelescope in Puerto Rico, before its destruction</p></span> <span class="credit"><p>Via <a href="https://commons.wikimedia.org/wiki/File:Arecibo_Radiotelescopio_SJU_06_2019_7472.jpg" target="_blank">Wikimedia</a></p></span></figcaption></figure>
<p>She estimates that the survey will be sensitive to radio broadcasts from an extraterrestrial dish analogous to Arecibo transmitting within about 220 light years. Weaker signals, or signals coming from deeper in the galaxy — which spans 100,000 light years — would go unnoticed.</p>
<p>Sheikh admits that her plan might seem like a long shot, but argues that it beats scanning the sky from one side to the other — the celestial equivalent of wandering Manhattan south to north. “You have to start somewhere,” she says. “Why not start somewhere you think is more likely?”</p>
<p>Another Schelling-inspired lesson is to test out as many Schelling points as possible. If your counterpart doesn’t show up at Grand Central at noon, try Times Square at midnight. In that spirit, Sheikh is collaborating with Davenport, at the &nbsp;University of Washington to study another temporal landmark.</p>
<p>Nearly 35 years ago, astronomers witnessed a star just outside the Milky Way explode like a bomb. “SN 1987a” quickly became the subject of more academic papers than any other supernova. &nbsp;“It’s the only supernova that’s gone off in our neighborhood in the last 100 years,” Davenport says. “It’s kind of a big event. It’s rare, visible, and outshone the entire galaxy.</p>
<p>If any civilizations were poised, waiting for a special galactic moment to announce their presence, SN 1987a would have been a great opportunity, suggested Argentinian astrophysicist Guillermo Lemarchand <a href="https://ui.adsabs.harvard.edu/abs/1994Ap%26SS.214..209L/abstract"><ins>in 1994</ins></a>. Now Sheikh and Davenport, together with undergraduate physics and astronomy student Bárbara Cabrales at Smith College, are working out the math to look for signals that would just be reaching Earth now, had they been sent in response to SN 1987a.</p>
<p>As light from the supernova reaches new stars, and potential signals from those stars ripple out through space, the zone of the sky to search changes. Using data from NASA’s Transiting Exoplanet Survey Satellite (TESS), which watches for stars being eclipsed by exoplanets, the group is developing an algorithm to look for stars that dim or flash at precisely the right moment. They don’t expect to find a smoking gun with TESS, which keeps tabs on hundreds of thousands of stars. Their main goal is to get the software tools ready for the upcoming Vera Rubin Telescope, which will monitor 10 to 20 <em>billion</em> stars on a weekly basis.</p>
<p>Further down the line, other SETI researchers could tweak the software to search for radio signals, rather than looking only for civilizations with the technology to make their star flicker. “We’re looking at signals now in [visible light] because that’s where the data is,” Davenport says. “We’re scavengers. We’re taking what is already available to us. Astronomers have to be crafty.”</p>
<p><strong>Shy Civilizations</strong></p>
<p>The central conceit of seeking Schelling points in modern SETI is the assumption that both sides are playing the same game. But with more powerful instruments, researchers might be able to start looking for more bashful &nbsp;civilizations. In that case too, crafty astronomers are already thinking about what common behaviors might give an inhabited planet away, even if it’s not actively broadcasting.</p>
<p>Humanity, for instance, has benefited from putting television, radio, and weather satellites in high enough orbits that they continuously face the same part of the Earth. These spacecraft in “geosynchronous” orbits form an artificial ring around our planet roughly 22,000 miles above the ground. If another planet sported a thick enough artificial ring, it might block the light from its star in a peculiar way that astronomers could spot.</p>
<p>Our ring is sparse today but gets slightly denser every year. In 200 years, the satellite belt would become notable enough to be seen by extraterrestrial astronomers at a distance of ten light years using current telescopes, astrophysicist Hector Socas-Navarro <a href="https://iopscience.iop.org/article/10.3847/1538-4357/aaae66"><ins>calculated in 2018</ins></a><ins>.</ins></p>
<p>Another proposal assumes that civilizations have a vested interest in their long-term survival and may develop the technology to watch out for catastrophic asteroid collisions. As Carl Sagan <a href="https://www.space.com/15994-carl-sagan.html"><ins>reportedly quipped</ins></a>, “If the dinosaurs had had a space program, they would not be extinct."</p>
<p>Some of the loudest radio pulses humanity has sent out into space have been for exactly this purpose, with much of the responsibility of monitoring the trajectories of asteroids falling to Arecibo’s 2.5-million-watt radar beam, before its destruction. Most of that radio signal bounced back to Earth carrying vital information about its target, but some would spill past the asteroid into the galaxy. Similar signals from another world would come sporadically. But since the orbits of asteroids and planets form a flat disk, any radar signals originating from a planet and directed toward an asteroid would always spill outward from the plane of the disk. Future eavesdropping attempts could use this fact to prioritize systems that are oriented “edge on” to Earth, rather than “top down.”</p>
<p>Some researchers recoil from efforts to get into the heads of extraterrestrial beings, considering them too outlandish, and Sheikh understands the instinct to avoid assumptions. Nevertheless, since coming to view SETI through a Schelling-tinted lens, she has realized that every project assumes some shared attributes between humanity and whomever else could be out there. Even the fact that many SETI searches target stars betrays a presumption that other lifeforms, like us, are more likely to live on planets than in deep space.</p>
<p>“Everything is a Schelling point, Sheikh says. “You can't get away from it.”</p>
<p><strong>Seeking universality</strong></p>
<p>The more Schelling-inclined researchers can intuit commonalities between terrestrials and hypothetical extraterrestrials, the better their odds of success. And the only commonalities likely to span light years are going to be potential universalities, like knowing how fast sunbeams travel, or not wanting to be taken out by an asteroid. In the interest of ferreting out such universalities, some researchers point out that Earth might hold more than just one example to learn from.</p>
<p>Human cultures have risen and fallen for millennia,and have a long history of misinterpreting each others’ legacies. Spanish conquistadors, for instance, <a href="https://www.academia.edu/36288634/How_Humans_Matter_Now_The_Relevances_of_Anthropology_and_Archaeology_for_the_New_SETI_White_paper_for_SETI_Institute_call_2017_"><ins>mistook the Great Pyramid of Cholula</ins></a> (the world’s largest pyramid by volume) for a hill and built a church on it. “Looking at the full sweep of human behaviors, anthropology-style, is useful for shaking us out of our own cultural biases,” &nbsp;<a href="https://www.yorku.ca/kdenning/"><ins>Kathryn Denning</ins></a>, an anthropologist at York University in Toronto.</p>
<p>She goes even farther, suggesting that observing how dolphins, whales, birds, and other social animals interact while sharing or dividing up territory would be a “good way to broaden our thinking beyond the human.”</p>
<p>Penn State’s Wright conceives of Schelling points in a similar way. The goal isn’t to get into an alien’s head per se, but rather to decipher the essential behaviors of all intelligent beings, starting with animals here on Earth. “They have to use energy. They have to move around. At some point they have to interact with each other. They have to eat. And so, we hope that there are similar fundamental things the alien species out there might be doing,” he says.</p>
<p>Perhaps in another 70 years, equipped with more sensitive instruments and smarter searching algorithms, SETI astronomers will have checked enough galactic Schelling points to start to answer Fermi’s question. If we show up at enough interesting landmarks at enough unique times and fail to connect, we’ll have to conclude that no one else is trying to meet up. Or, if they are, they’re going about it in a way that’s truly alien.</p>
    




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<guid isPermaLink="true">https://massivesci.com/articles/single-nucleotide-variants-polymorphisms-mutations-cancer/</guid>
<link>https://massivesci.com/articles/single-nucleotide-variants-polymorphisms-mutations-cancer/</link>
<pubDate>Fri, 26 Nov 2021 10:57:00 EST</pubDate>
<title>Researchers can trace the family tree of individual mutations inside our cells </title>
<description>The task is like looking through a book with six billion letters for individual typos</description>

<media:content url="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/a07af20b-9649-4a75-9c07-be961c09a764/Flower-Mutant-1145.jpeg?auto=compress%2Cformat&amp;crop=faces&amp;fit=crop&amp;fm=jpg&amp;h=600&amp;q=75&amp;w=900" type="image/jpeg">
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  <media:description>A red and yellow flower head with a mutated floret cluster</media:description>
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  <dc:creator><![CDATA[Malosree Maitra]]></dc:creator>
  <atom:author>
    <atom:name>Malosree Maitra</atom:name>
    <atom:uri>https://massivesci.com/people/malosree-maitra/</atom:uri>
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    <p>We all start out as a <a href="https://www.britannica.com/science/zygote">single cell</a>. That cell <a href="https://askabiologist.asu.edu/cell-division">divides</a> many, many times to form the <a href="https://www.smithsonianmag.com/smart-news/there-are-372-trillion-cells-in-your-body-4941473/">trillions of cells</a> in an adult human body. Each of these cells has two copies of all the <a href="https://www.genome.gov/genetics-glossary/Gene">genes</a> in the <a href="https://www.britannica.com/science/human-genome">human genome</a>, inherited from our biological parents. While copying the genome trillions of times, unsurprisingly, some mistakes are made. Slight genetic variations, called <a href="https://www.genome.gov/genetics-glossary/Mutation">mutations</a>, accumulate in our cells as we grow from a single cell to an adult.</p>
<p>We usually think of mutations as harmful, but they often have no consequence and don’t change the meaning of our genetic code. There are two main categories of mutations — germline mutations and somatic mutations. Germline mutations found in our sperm or egg cells, can be passed on to our children. Somatic mutations in other cells of our body — such as in the brain, liver, or lungs, are never passed on to our children. Although somatic mutations cannot be inherited, they can still be important for human health. For example, somatic mutations in a subset of brain cells can cause seizures within a brain region either <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5752134/">with</a> or <a href="https://pubmed.ncbi.nlm.nih.gov/29679388/">without</a> visible changes to brain structure.</p>
<div class="oembed"><div class="iframely-embed"><div class="iframely-responsive" style="height: 140px; padding-bottom: 0;"><a href="https://massivesci.com/articles/dawkins-selfish-gene-mothers-curse-louis-xiv/" data-iframely-url="https://cdn.iframe.ly/api/iframe?url=https%3A%2F%2Fmassivesci.com%2Farticles%2Fdawkins-selfish-gene-mothers-curse-louis-xiv%2F&key=a91f6c63822d2172297a7435cae7a9eb"></a></div></div><script async src="https://cdn.iframe.ly/embed.js" charset="utf-8"></script></div>
<p>Over many years, the <a href="http://www.walshlab.org/">Walsh lab</a> at Harvard University has contributed to our understanding of somatic mutations in the human brain. The group has studied how somatic mutations in brain cells may contribute to seizures, developmental disorders, or psychiatric and neurological conditions including <a href="https://www.nimh.nih.gov/health/topics/autism-spectrum-disorders-asd/">autism spectrum disorders</a>. They, and others, have investigated how often changes in a single letter of the DNA genetic code — called “<a href="https://www.cancer.gov/publications/dictionaries/genetics-dictionary/def/single-nucleotide-variant">single-nucleotide variants</a> (SNVs)”— can be detected in typical and atypical brain cells.</p>
<p>Interestingly, by finding which somatic mutations are present in which cells, we can build a “family tree” of cells in the body and trace back the path of cell divisions that produced our trillions of cells from the single original cell. This “family tree” would be a treasure trove for understanding how our bodies develop. The <a href="https://science.sciencemag.org/content/356/6336/eaal1641">Brain Somatic Mosaic Network</a> is a group of researchers who study this problem specifically in the area of human brain development. Since we cannot watch the cells dividing inside a human embryo and cannot “see” the mutations within cells in tissue samples, these types of studies are quite technically challenging.</p>
<div class="oembed"><div class="iframely-embed"><div class="iframely-responsive" style="height: 140px; padding-bottom: 0;"><a href="https://massivesci.com/notes/prime-editing-cystic-fibrosis-organoids/" data-iframely-url="https://cdn.iframe.ly/api/iframe?url=https%3A%2F%2Fmassivesci.com%2Fnotes%2Fprime-editing-cystic-fibrosis-organoids%2F&key=a91f6c63822d2172297a7435cae7a9eb"></a></div></div><script async src="https://cdn.iframe.ly/embed.js" charset="utf-8"></script></div>
<p>The Walsh group recently applied several ingenious methods to trace the developmental path of single cells in the human brain. How complex would this task be? The genome is like a book with six billion letters. Our cells are like trillions of copies of this book in a gigantic library – our body. Trying to find somatic SNVs is like trying to find single letter typos present in some of the copies of the book but not all of them. It is a mammoth task. So how would you find these typos? You could read the entire book multiple times or focus on a section you suspect has a typo and read that section multiple times. The first approach would be akin to “<a href="https://medlineplus.gov/genetics/understanding/testing/sequencing/">whole genome sequencing</a>” while the second would be equivalent to “<a href="https://www.illumina.com/techniques/sequencing/dna-sequencing/targeted-resequencing/amplicon-sequencing.html">targeted amplicon sequencing</a>”, and the researchers used both approaches in their study.</p>
<p>They also compared somatic SNVs in different organs, including the brain, liver, spleen, and heart, among others. Different body organs grow from different parts of the embryo and start out as distinct groups of cells. The authors were able to see these patterns of “branches” in the cell family tree. The fraction of cells in each organ with a specific somatic SNV varied depending on the organ’s origin within the embryo. Even within the brain, a single organ, the fraction of cells with specific sSNVs varied from the forebrain to the hindbrain, showing that they develop from different groups of cells in the embryo.</p>
<p>Measuring the frequency of specific somatic SNVs, the authors also estimated that around 50-100 cells within the embryo probably contributed to forming the brain. The estimate is not exact, because there are many unknowns. The methods used cannot detect all the somatic SNVs in the samples. Even with very deep genome sequencing (“reading the book” many times) somatic mutations present only in a small number of cells can still be missed. Moreover, the estimate was based on measurements mostly in one individual donor, highlighting another limitation of these approaches. Such studies are technically challenging and expensive, so they mostly include only a few individuals and a few organs from those individuals.</p>
<p>Nevertheless, the study brings us closer to understanding the complex, awe-inspiring process of human development from a single cell. It demonstrates that we can track how individual cells in a human embryo give rise to the organs of an adult human, and how even within the same organ, groups of cells have unique “barcodes” made of somatic SNVs recording the history of their “ancestor” embryo cells.</p>
    


<p><em><a href="https://massivesci.com/people/malosree-maitra/">Malosree Maitra</a> studies 

<p class="mb0">

<span class="scientist__field">Neuroscience</span>

</p>

 at 

<p class="mb0 o7">

<span class="scientist__institution">McGill University</span>

</p>

.</p>



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<guid isPermaLink="true">https://massivesci.com/articles/blue-morpho-butterfly-neural-growth-hearing/</guid>
<link>https://massivesci.com/articles/blue-morpho-butterfly-neural-growth-hearing/</link>
<pubDate>Fri, 26 Nov 2021 10:56:00 EST</pubDate>
<title>A butterfly&#39;s wings are the perfect mold to grow neurons on</title>
<description>Butterfly wings provide the right topography for nerve cells to grow, with an aim towards ameliorating hearing loss </description>

<media:content url="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/3096f7b4-15a8-4732-a1ff-41c5a4d8dd7f/Blue_Morpho.jpeg?auto=compress%2Cformat&amp;crop=faces&amp;fit=crop&amp;fm=jpg&amp;h=600&amp;q=75&amp;w=900" type="image/jpeg">
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  <media:description>A blue morpho butterfly with its wings spread open</media:description>
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  <dc:creator><![CDATA[Reinack Hansen]]></dc:creator>
  <atom:author>
    <atom:name>Reinack Hansen</atom:name>
    <atom:uri>https://massivesci.com/people/reinack-hansen/</atom:uri>
  </atom:author>


  
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    <p>Around <a href="https://www.nidcd.nih.gov/health/statistics/quick-statistics-hearing#5">15% of American adults</a> report some trouble hearing. That is about 37.5 million people who may need hearing aids for the majority of their lives. A common cause of hearing loss stems from special cells called spinal ganglion neurons (SGN) that transmit signals from hair cells in the ear to the brain. In these cases, regenerating SGN in the inner ear is our best bet to restore hearing. However, controlling how and where nerve cells grow is notoriously difficult. Fortunately, our dependence on hearing aids may soon wind down thanks to the beautiful blue morpho butterfly.</p>
<p>When nerve cells grow on a surface, they respond to physical features such as bumps and grooves. They also communicate with neighboring nerve cells through electrical signals. So, a good growth surface for nerve cells must provide topological cues and be electrically conductive.</p>
<p>The blue morpho butterfly wing has an intricate structure consisting of parallel ridges. Turns out these ridges are perfect templates for cell growth. Engineering an equivalent surface with ridges that is flexible yet light is impossible with today's technology. Rendering a butterfly wing biocompatible on the other hand, is possible. This is what inspired scientists to consider growing cells directly on butterfly wings. In 2019, <a href="https://onlinelibrary.wiley.com/doi/abs/10.1002/adma.201805431">cardiac tissue assembled on blue morpho – carbon nanotube composites</a> was shown to recover its beating ability. In that case, the elastic composite wing mimicked the cyclic contractions of cardiac cells and shifted colors. By simply observing color changes, they could assess if the cells were behaving as expected.</p>
<p>For nerve cells, which are long, could the parallel ridges on the wing also align neurons end-to-end and make them grow in one direction? This is what Renjie Chai and team at Nanjing University sought to find out, as directionally controlled regeneration of auditory nerve cells is critical to restore hearing. Through a collaborative effort involving university researchers and surgeons, <a href="https://onlinelibrary.wiley.com/doi/epdf/10.1002/smll.202102062" rel="noopener noreferrer" target="_blank">they transferred a thin layer of super aligned carbon nanotubes onto the wing of a blue morpho butterfly to make it conductive</a>. Not only was the conducting composite wing excellent at orienting nerve cells as they grew, it facilitated maturation of neuronal junctions, which is the site where nerve cells transmit electrical signals.</p>
<figure><img alt="A close-up view of the veins and details of a blue morpho butterfly&#39;s wings" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/bbd0afa5-8ac1-492c-b4be-2492263ba775/15313318454_886a6d7654_k.jpg"/><figcaption><span class="caption"><p>A close-up view of the veins and details of a blue morpho butterfly's wings</p></span> <span class="credit"><p>Tambako the Jaguar via <a href="https://www.flickr.com/photos/tambako/15313318454/in/photolist-pkbL4Y-X8tPN1-ctUDpC-Ss9Wzu-2mxbLZR-5dFosp-2dF2LTJ-M6VbVz-kZRKhJ-aynBPM-dPZYDp-8ZnNbz-bjKPjX-8ZnMw2-8ZnMMe-Vkhn6T-HB2Ugf-4DQF3z-29FoVJP-bmfjyQ-nWK75z-odtHw6-nhaPqX-UUPvBj-fuzz5b-bPjCEB-YqTZv2-ctUDkQ-YqTYwt-dBsFje-am2Z7C-YqU1d4-YqTZkT-3ZraZv-YqU1mv-YdrVQ6-YdrWVx-XPQHL7-XPQHYw-67kNC6-YdrX8g-6WgKtd-dK7MXc-YqTZJD-ipAErn-VU5PmQ-9hcijr-9hfrFu-9hfrBo-2i5zy9b" target="_blank">Flickr</a></p></span></figcaption></figure>
<p>Interestingly, nerve cells grow on both plain butterfly wing and aligned carbon nanotubes. However, only when the two are combined do the cells grow in a specific direction and the neuronal junctions mature. Super aligned carbon nanotubes are special in that they are simply individual nanotubes connected end-to-end. This makes a sheet of this material extremely conductive along one direction – the direction in which the nanotubes are aligned. When these aligned nanotubes are transferred onto butterfly wings, the composite retains the parallel ridges of the wing below while acquiring high conductivity along the ridges thanks to the nanotubes. &nbsp;Further, being extremely thin and lightweight, they hardly add any heft to the wing structure.</p>
<p>Nerve cells have what's called a "growth cone," which is a protein supported structure that explores the environment, determines the direction of growth, and guides the nerve fiber to extend in that direction. Turns out that in the case of nerve cells grown on the composite wing, growth cones aligned along the grooves. Considering the fact that nerve cells grew on butterfly wings as is, this goes to show that these grooves are features that nerve cells readily sense and respond to as they grow. Even with aligned carbon nanotubes, the composite surface retained the ridged butterfly wing structure. &nbsp;Nerve cells could sense the grooves on the composite wing surface and orient within them, just like they would on the unmodified butterfly wing.</p>
<div class="oembed"><div class="iframely-embed"><div class="iframely-responsive" style="height: 140px; padding-bottom: 0;"><a href="https://massivesci.com/notes/hearing-loss-fatigue-sounds/" data-iframely-url="https://cdn.iframe.ly/api/iframe?url=https%3A%2F%2Fmassivesci.com%2Fnotes%2Fhearing-loss-fatigue-sounds%2F&key=a91f6c63822d2172297a7435cae7a9eb"></a></div></div><script async src="https://cdn.iframe.ly/embed.js" charset="utf-8"></script></div>
<p>More importantly, the growth cone filopodia, which are antennas for nerve cells to probe the environment, was much longer for nerve cells that grew on the composite wing. This is important as longer filopodia is a sign of improved communication between nerve cells. Moreover, the density of neuronal junctions, also called synapses, was much higher. The orientation within ridges, long filopodia, and high density of synapses clearly show that nerve cells can be controllably cultured on conductive butterfly wings. As promising as these results are, the SGN used in this study was sourced from mice. So any hearing restorative treatment for humans based on this approach is still years away.</p>
<p>From a materials perspective, the structure of the blue morpho butterfly wing is decades ahead of any microfabrication process available today. As such, this study is a classic example of how borrowing ideas from seemingly unlikely sources in nature can yield incredible results. So the next time you see a butterfly, remember those pretty wings could be our gateway to perfect hearing.</p>
    


<p><em><a href="https://massivesci.com/people/reinack-hansen/">Reinack Hansen</a> studies 

<p class="mb0">

<span class="scientist__field">Materials Science</span>

</p>

.</p>



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<guid isPermaLink="true">https://massivesci.com/articles/cities-microbes-bacteria-urban/</guid>
<link>https://massivesci.com/articles/cities-microbes-bacteria-urban/</link>
<pubDate>Thu, 25 Nov 2021 21:26:00 EST</pubDate>
<title>Even cities have their own unique microbiomes</title>
<description>A study of microorganisms collected from public transportation systems shows even cities have microbial signatures</description>

<media:content url="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/8c05ea6b-2f5c-43af-8857-cfe0784b92e4/euan-cameron-3Es_ZsAxj_Q-unsplash.jpg?auto=compress%2Cformat&amp;crop=faces&amp;fit=crop&amp;fm=jpg&amp;h=600&amp;q=75&amp;w=900" type="image/jpeg">
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  <media:description>a photo from inside singapore&#39;s subway system, with people sitting on benches in a clean white car</media:description>
</media:content>


  
  <dc:creator><![CDATA[Rita Ponce]]></dc:creator>
  <atom:author>
    <atom:name>Rita Ponce</atom:name>
    <atom:uri>https://massivesci.com/people/rita-ponce/</atom:uri>
  </atom:author>


  
  <content:encoded><![CDATA[
    <p>Every city has its unique charms: its weather, its views, its events, its landmarks — and even<strong> </strong>its microbes. <a href="https://www.cell.com/cell/fulltext/S0092-8674(21)00585-7">A study</a> published earlier this year in the journal <em>Cell </em>analyzed the microbes present in 60 cities from six continents, and found that each city has its own unique set of microorganisms —<strong> </strong>its very own microbial signature, if you will.</p>
<p>“If you give me your shoe, I could tell you with about 90 percent accuracy the city in the world from which you came,” said Christopher Mason, senior author of this work and professor at Weill Cornell Medicine in New York in a <a href="https://www.eurekalert.org/news-releases/734958" rel="noopener noreferrer" target="_blank">press release</a>.</p>
<p>Microorganisms are present everywhere on the planet, even within our own bodies. Microbes — from yeast to bacteria to viruses — are extremely diverse. This recent study is part of a <a href="http://metasub.org/" rel="noopener noreferrer" target="_blank">worldwide urban microbe mapping project</a> that aims to make sense of the microbial world around us, with potential benefits to health and forensics.</p>
<p>In this movement, researchers from around the world collected microbes in public transport, mostly in subway stations and trains. “Many people travel in public transportation systems," said study co-author Manuela Oliveira, a researcher at the University of Porto, in Portugal. "By sampling there, we would have a significant sample of the microorganisms transported by the general population.” The microbial composition, or the microbiome, of transportation systems would provide insights into the unseen dwellers of the city.</p>
<aside class="pullquote"><blockquote>“If you give me your shoe, I could tell you with about 90 percent accuracy the city in the world from which you came”</blockquote></aside>
<p>This worldwide project started as Mason's personal curiosity in 2013. Intrigued by the microbial world, he first collected samples in the New York City subway system by rubbing cotton swabs on surfaces — turnstiles, railings, ticket kiosks, and benches — in stations and on trains. His results attracted the interest of other researchers, which<strong> </strong>led to the <a href="https://microbiomejournal.biomedcentral.com/articles/10.1186/s40168-016-0168-z" rel="noopener noreferrer" target="_blank">formation</a> of an<strong> </strong>international <a href="http://metasub.org/">consortium</a> of experts that analyzes urban microbial communities so the knowledge can be applied towards urban planning policies.</p>
<p>Nearly ten years later, teams of researchers and volunteers now collect samples in cities all over the world. Every year <a href="http://metasub.org/projects/gcsd/" rel="noopener noreferrer" target="_blank">on June 21st</a>, the teams swab-collect their microbial samples following the same protocol, an effort they have dubbed "Global City Sampling Day."</p>
<p>The collection process tends to attract a lot of attention from bystanders. “Most of the time, people just stopped, looked, and commented among themselves. However, sometimes the most curious ones approached us and started to question us,” recalls Oliveira, who sampled on the public transport in Porto, Portugal.</p>
<p>“Every year there is a funny story to tell," she says. "In the first year we collected samples, I was asked if I was working with the crime lab from Polícia Judiciária," referring to the criminal investigational police agency in Portugal.</p>
<p>The published work is a culmination of 4,728 samples collected in 60 cities over three years. The gargantuan effort involved 99 individual researchers, including Mason and Oliveira. The researchers identified 10,928 viruses, 1,302 bacteria, two archaea (microorganisms that are distantly related to “true” bacteria), and thousands of sequences that had never been described before. Over 4,000 were known species of “urban microbes” — bacteria and viruses that are characteristic of cities and that are not known to be found on or in the human body. Thirty-one species<strong> </strong>were present in over 97 percent of the samples. The researchers also discovered that each city had its own unique combination of microbes.</p>
<figure class="center large"><img alt="a photo from the streets of london featuring a red double decker bus" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/d0589892-3b96-49f1-b7ff-18e2c98be190/london-gb4e451aae_1920.jpg"/><figcaption> <span class="credit"><p>Image by <a href="https://pixabay.com/users/marlonrondal-4633059/?utm_source=link-attribution&amp;utm_medium=referral&amp;utm_campaign=image&amp;utm_content=3445169">marlon rondal</a> from <a href="https://pixabay.com/?utm_source=link-attribution&amp;utm_medium=referral&amp;utm_campaign=image&amp;utm_content=3445169">Pixabay</a></p></span></figcaption></figure>
<p>“At first it was difficult to make sense of all the data, the latitude [of the cities] by itself did not explain the variations we had,” says Oliveira. For instance, the city of Porto had similarities to the city of Santiago, Chile in the southern hemisphere, which was puzzling at first. Then the reason dawned on the researchers: Just like any animal or plant species, the distribution of microbes in the world depends on the whole ecosystem, including the other species present, geology, and climate.</p>
<p>Some of the microbes the researchers found were pathogenic, but this does not mean they will be able to cause disease. “We have immune defenses that allow us to fight pathogens," says Oliveira. "On the other hand, we also can find<strong> </strong>many good bacteria.”</p>
<p>The researchers also looked at indications of antibiotic resistance, <a href="https://www.cdc.gov/drugresistance/index.html">a serious public health problem</a>. Overall, just a small number of the species collected had signs of resistance. There was also regional variation; the resistances found in some geographic areas were different from those in other areas. The authors suggest that their approach could be used as a way to monitor these defensive adaptations worldwide.</p>
<div class="oembed"><div class="iframely-embed"><div class="iframely-responsive" style="height: 140px; padding-bottom: 0;"><a href="https://massivesci.com/articles/outdoor-green-space-microbiome-benefits-soil-air/" data-iframely-url="https://cdn.iframe.ly/api/iframe?url=https%3A%2F%2Fmassivesci.com%2Farticles%2Foutdoor-green-space-microbiome-benefits-soil-air%2F&key=a91f6c63822d2172297a7435cae7a9eb"></a></div></div><script async src="https://cdn.iframe.ly/embed.js" charset="utf-8"></script></div>
<p>This ongoing project may also potentially detect disease outbreaks. “If regular sampling of surfaces is conducted, it would be possible to identify and quantify the infectious microorganisms circulating among us, helping to pinpoint and anticipate disease outbreaks,” says Oliveira. This would require frequent sampling, ideally every day, but there are limitations because these are expensive procedures.</p>
<p>Currently, the consortium has expanded to sampling other environments, such as <a href="https://www.eurekalert.org/news-releases/734958" rel="noopener noreferrer" target="_blank">sewage systems</a>. Also in the works are plans to study seasonal patterns by performing field collections in urban public transportation on the winter solstice.</p>
<p>In the meantime, the consortium has built the<a href="http://metasub.org/map/"> first worldwide catalog of urban microbes</a> that is available for anyone to access. There are clear benefits to making the raw data available to the general scientific community, says Raul Tito, a microbial metagenomics researcher at the Katholieke Universiteit Leuven in Belgium. For example, publicly accessible data could stimulate more research among other scientists. But he also raises<strong> </strong>ethical concerns on privacy and profiling. "While [the researchers] target microorganisms, [these swabs] may also provide information from humans," said Tito, who was not involved in this study. The data "could be used to profile local populations without explicit consent from the human donors,” he adds.</p>
<p>Aware of these privacy issues and ethical implications of metagenomic studies, the researchers <a href="https://microbiomejournal.biomedcentral.com/articles/10.1186/s40168-017-0349-4#Sec13" rel="noopener noreferrer" target="_blank">advocate</a> for transparency among consortium members in their research and public engagement. On top of that, frequent reviewing of privacy, safety and legal measures<strong> </strong>is necessary when it comes to the collection and storage of microbiome data. The path forward to address these concerns is still unclear, but it starts with honest communication between all parties and constantly revisiting the raised concerns.</p>
    


<p><em><a href="https://massivesci.com/people/rita-ponce/">Rita Ponce</a> studies 

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<span class="scientist__field">Evolutionary Biology</span>

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<span class="scientist__institution">Polytechnic Institute of Setúbal</span>

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<guid isPermaLink="true">https://massivesci.com/articles/planetary-spin-oxygen-producing-aliens/</guid>
<link>https://massivesci.com/articles/planetary-spin-oxygen-producing-aliens/</link>
<pubDate>Tue, 23 Nov 2021 23:50:35 EST</pubDate>
<title>On faster spinning planets, life could be hiding out under the atmosphere</title>
<description>Astrobiologists search for molecular oxygen as an indicator of life on other planets, but finding them isn&#39;t that straightforward</description>

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  <media:description>Mats of purple cyanobacteria carpet the floor of the Middle Island Sinkhole off the coast of Alpena, Michigan. When gas accumulates underneath the bacteria filaments, it can lift up the mat forming the “finger” structures shown here</media:description>
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  <dc:creator><![CDATA[Derek Smith]]></dc:creator>
  <atom:author>
    <atom:name>Derek Smith</atom:name>
    <atom:uri>https://massivesci.com/people/derek-smith/</atom:uri>
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    <p>To find life on other planets, astronomers are on the hunt for biological signatures. They point their telescopes to exoplanets, planets that orbit around stars different than our Sun, and look for gases on those planets' atmospheres that are only produced by life. One important biosignature is molecular oxygen (O2). Organisms are the primary source of oxygen on Earth. Oxygen is also important for habitability, as the <a href="https://pubs.acs.org/doi/abs/10.1021/acsomega.9b03352" rel="noopener noreferrer" target="_blank">large amount of energy</a> locked up in oxygen <a href="https://bmcecolevol.biomedcentral.com/articles/10.1186/1471-2148-4-2" rel="noopener noreferrer" target="_blank">enabled</a> the evolution of complex, multicellular life on Earth.</p>
<p>However, finding oxygen on an exoplanet is not a smoking gun for extraterrestrial life. <a href="https://agupubs.onlinelibrary.wiley.com/doi/full/10.1029/2020AV000294" rel="noopener noreferrer" target="_blank">Computer simulations</a> have suggested that lifeless planets can also have oxygen-rich atmospheres, so an oxygen-rich atmosphere can be a false-positive for extraterrestrial life. Earth's natural history also cautions that the absence of oxygen may not necessarily indicate that an exoplanet is a lifeless rock. <a href="https://onlinelibrary.wiley.com/doi/full/10.1111/pala.12178" rel="noopener noreferrer" target="_blank">Cyanobacteria</a>, the first oxygen producers on Earth, and <a href="https://www.nature.com/articles/s41559-020-01386-9?utm_source=natecolevol_etoc&amp;utm_medium=email&amp;utm_campaign=toc_41559_5_4&amp;utm_content=20210407&amp;WT.ec_id=NATECOLEVOL-202104&amp;sap-outbound-id=EB65CBB69F008F42D9EB8FC2C43623E3EFBACE00" rel="noopener noreferrer" target="_blank">oxygen consuming metabolisms</a> in other bacteria evolved before oxygen accumulated in Earth's atmosphere. In fact, oxygen was only present in high enough concentrations to be <a href="https://www.liebertpub.com/doi/10.1089/ast.2016.1598" rel="noopener noreferrer" target="_blank">detectable</a> with telescopes for the last 10 percent of Earth's history.</p>
<p>Scientists often use observations about Earth systems to predict how life and exoplanet atmospheres may interact and co-evolve. They try to understand why and how oxygen levels go up or down and, by looking back at the history of Earth's atmospheric oxygen content, learn about about the processes that might allow oxygen to accumulate on other planets. It is still not completely clear why Earth's atmosphere is rich in oxygen, but a<a href="https://www.nature.com/articles/s41561-021-00784-3"> new study</a> involving some of the modern Earth's most unique environments suggests that our present day oxygen-rich environment is the result of increasing daylength on Earth over geologic time.</p>
<p>The study, conducted by a team led by Gregory J. Dick at the University of Michigan and Judith M. Klatt at the Max Planck Institute for Marine Microbiology, suggests that atmospheric oxygen concentrations on Earth have increased because Earth's days have been getting longer. The longer days are what allowed oxygen produced during photosynthesis to finally accumulate in the atmosphere. Therefore, photosynthetic life may be present on quickly rotating exoplanets without detectable levels of oxygen in their atmospheres.</p>
<p>In fact, oxygen-producing life may be hidden by oxygen-free atmospheres more often than scientists had previously recognized.</p>
<p>Atmospheric oxygen concentrations on Earth <a href="https://www.nature.com/articles/nature13068" rel="noopener noreferrer" target="_blank">have changed</a> incrementally over Earth's natural history. Initially, Earth's atmosphere was essentially devoid of oxygen. Then, oxygen concentrations suddenly (at least on geologic timescales) increased to about 0.1 percent of present-day levels around 2.4 to 2.1 billion years ago during an event referred to as "the Great Oxidation Event," or the GOE. Atmospheric oxygen later reached modern levels after <a href="https://www.nature.com/articles/s41467-018-06383-y" rel="noopener noreferrer" target="_blank">two additional oxidation events</a> around 800 and 400 million years ago.</p>
<figure class="center large"><img alt="The Gatineau stromatolites along the Ottawa River in Canada are the fossilized remains of ancient oxygen-producing microbial mats" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/4861a4b1-de17-4a75-83ee-3802786046c1/Gatineau_stromatolites3.jpg"/><figcaption><span class="caption"><p>The <a href="https://www.cbc.ca/news/canada/ottawa/ancient-life-resurfaces-along-ottawa-river-1.5274772" rel="noopener noreferrer" target="_blank">Gatineau stromatolites</a> along the Ottawa River in Canada are the fossilized remains of ancient oxygen-producing microbial mats</p></span> <span class="credit"><p>Via Wikimedia</p></span></figcaption></figure>
<p>Scientists still do not agree about what caused the incremental increase in the amount of oxygen in Earth's atmosphere over geologic time. One thing is certain: The evolution of oxygen-producing photosynthesis predates the Great Oxidation Event, so other planetary controls were likely driving the changes in Earth's oxygen content. There are several ideas as to what these processes might be, such as <a href="https://www.nature.com/articles/nature06058" rel="noopener noreferrer" target="_blank">changes in volcanism</a> or <a href="https://www.nature.com/articles/s41467-021-23286-7" rel="noopener noreferrer" target="_blank">increased competitive success</a> of cyanobacteria. Until now, nobody had considered how Earth's day length could have influenced atmospheric oxygen levels.</p>
<p>Thanks to tides caused by the Moon, Earth's days are have been getting longer. The gravitational pull of the Moon causes the Earth to <a href="https://scijinks.gov/tides/" rel="noopener noreferrer" target="_blank">bulge</a> out on the sides closest and furthest away from the Moon. Scientists refer to this stretching of the Earth as the tidal bulge. The location of the Earth that experiences the tidal bulge changes as the Earth spins on its axis, which causes the periodic change in water level with high and low tide that beach visitors are familiar with.</p>
<figure class="center large"><img alt="The gravitational force exerted on Earth by the Moon is strongest on the side closest to the Moon (depicted with arrow lengths). This stretches the Earth’s surface, creating a tidal bulge at the sides of the Earth closest and furthest from the Moon" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/ad1f7898-1440-4416-a01a-5ccb194aa372/Tidal_Friction_Diagram1.jpg"/><figcaption><span class="caption"><p>The gravitational force exerted on Earth by the Moon is strongest on the side closest to the Moon (depicted with arrow lengths). This stretches the Earth’s surface, creating a tidal bulge at the sides of the Earth closest and furthest from the Moon</p></span> <span class="credit"><p>Derek Smith</p></span></figcaption></figure>
<p>However, <a href="https://link.springer.com/referenceworkentry/10.1007%2F1-4020-4520-4_407" rel="noopener noreferrer" target="_blank">friction delays</a> the tidal bulge, and since the Earth rotates faster than the Moon revolves around the Earth, the tidal bulge occurs ahead of the Moon. (This corresponds to the viewpoint of an observer on Earth, as the tide occurs after the Moon passes overhead). However, the Moon's gravity is simultaneously trying to align the tidal bulge with the Moon. This force exerts a torque that slows down the rotation rate of Earth, thereby lengthening a day. The effect of tidal friction is small, but additive; a day on Earth may have only been between <a href="https://www.science.org/doi/abs/10.1126/science.1225542" rel="noopener noreferrer" target="_blank">five to seven hours long</a> over four billion years ago.</p>
<p>The authors of the study hypothesized that the shorter illumination periods for photosynthesis caused by the shorter days on the early Earth would have effected oxygen export from ancient cyanobacteria, which likely grew in microbial mats, or tangled masses of microbes that carpeted <a href="https://www.science.org/doi/abs/10.1126/science.11536492" rel="noopener noreferrer" target="_blank">lake beds</a> and <a href="https://nph.onlinelibrary.wiley.com/doi/epdf/10.1111/nph.14338" rel="noopener noreferrer" target="_blank">perhaps land</a>. To test this hypothesis, the scientists built a computer model that simulates net oxygen export — the difference between oxygen produced by photosynthesis and consumed by respiration — assuming different lengths of days.</p>
<figure class="center large"><img alt="Because the tidal bulge is delayed by friction, and a day is shorter than a month, the tidal bulge is positioned ahead of the Moon. This creates a torque that increases the Moon’s momentum and decreases the rate of Earth’s rotation, thus making days increasingly longer" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/be98a421-a168-419b-8031-5d6ec5bf6974/Tidal_Friction_Diagram2.jpg"/><figcaption><span class="caption"><p>Because the tidal bulge is delayed by friction, and a day is shorter than a month, the tidal bulge is positioned ahead of the Moon. This creates a torque that increases the Moon’s momentum and decreases the rate of Earth’s rotation, thus making days increasingly longer</p></span> <span class="credit"><p>Derek Smith</p></span></figcaption></figure>
<p>The model revealed that when days are longer, oxygen-producing microbial mats export more oxygen to the atmosphere. Diffusion, the natural tendency of molecules to move from areas of high concentration to low concentration, was the key factor. On longer days, cyanobacteria spend more time in the sun, and there is more time for oxygen to accumulate at high concentrations, which increases diffusive export of oxygen from the mat. The increased diffusion allows more oxygen to escape respiration from other microbes, bubble out of the microbial mats, and reach the atmosphere.</p>
<p>When the research team used existing estimates of how Earth's daylength has changed over time in their model, they found that the modeled oxygen concentrations in the atmosphere were similar to the geological record of atmospheric oxygen levels.</p>
<p>While their calculations were promising, the team wanted to prove that their model reflected a real link between between daylength and atmospheric oxygen levels. To test this idea, they needed an environment similar to those that harbored microbial mats on the ancient Earth. They found such conditions off the coast of Michigan, at the bottom of Lake Huron in the<a href="https://www.glerl.noaa.gov/pubs/fulltext/2009/20090012.pdf"> Middle Island Sinkhole</a>.</p>
<p>The carbonate bedrock at the floor of Lake Huron has dissolved overtime, yielding <a href="https://agupubs.onlinelibrary.wiley.com/doi/epdf/10.1029/2009EO080001" rel="noopener noreferrer" target="_blank">numerous sinkholes and caves</a> throughout the basin. There, the groundwater is depleted in oxygen but rich in sulfates and other dissolved salts. This dense, sulfurous groundwater persistently vents onto the surrounding lake bottom and accumulates in sinkholes like the Middle Island Sinkhole. This unique environment supports extensive, otherworldly mats of <a href="https://onlinelibrary.wiley.com/doi/full/10.1111/j.1472-4669.2012.00322.x?casa_token=-JUh0UZJ498AAAAA%3AiEOlkzRoCAZiw3zj835SSTyYogyMiGMRp1xEiejU9LbhCYoYWKELU22-zZMGgQJTZlpwmsL-teSeUW14" rel="noopener noreferrer" target="_blank">purple cyanobacteria</a> that are thought to resemble those present on ancient Earth.</p>
<figure class="center large"><img alt="Mats of purple cyanobacteria carpet the floor of the Middle Island Sinkhole off the coast of Alpena, Michigan. When gas accumulates underneath the bacteria filaments, it can lift up the mat forming the “finger” structures shown here" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/b30f10d1-8f2d-440d-9f2e-e8ab21597cef/MIS%20Hartmeyer%206_11_19%20modified_28.jpg"/><figcaption><span class="caption"><p>Mats of purple cyanobacteria carpet the floor of the Middle Island Sinkhole off the coast of Alpena, Michigan. When gas accumulates underneath the bacterial filaments, it can lift up the mat forming the “finger” structures shown here</p></span> <span class="credit"><p>Phil Hartmeyer, NOAA Thunder Bay National Marine Sanctuary</p></span></figcaption></figure>
<p>Klatt, Dick, and their colleagues collected sections of these purple cyanobacteria mats and measured the amount of oxygen that the mats produced when exposed to simulated daylight of varying length. The bacterial mats only released oxygen when the simulated daylengths were 16 hours or more, roughly the <a href="https://agupubs.onlinelibrary.wiley.com/doi/full/10.1002/2016GL068912" rel="noopener noreferrer" target="_blank">daylength on Earth at the time of the GOE</a>. Their result was a sign that daylength may have been an important threshold for the oxygen content of Earth's atmosphere.</p>
<p>Looking beyond our solar system, exoplanet researchers have daylength estimates for just a few of the exoplanets <a href="http://exoplanet.eu/catalog/" rel="noopener noreferrer" target="_blank">cataloged</a> to date. While exoplanet daylength has been <a href="https://iopscience.iop.org/article/10.1088/2041-8205/787/1/L2/meta" rel="noopener noreferrer" target="_blank">previously considered</a> with regard to its impact on climate and habitability, this study now suggests that astrobiologists should not assume that planets without oxygen lack life that makes and uses oxygen.</p>
<p>Prior to this study, Earth scientists thought that oxygen-rich atmospheres were an <a href="https://theconversation.com/breathable-atmospheres-may-be-more-common-in-the-universe-than-we-first-thought-128648" rel="noopener noreferrer" target="_blank">inevitable feature</a> of a planet harboring oxygen-producing organisms. However, this new study provides evidence to the contrary: Oxygen-producing life may only release oxygen to the atmosphere of exoplanets in sufficient amounts to be detectable from Earth on more slowly rotating planets with longer days.</p>
<p>According to geoscientist Lewis Alcott, the author of the previous models, the new research shows "that the length of day increases over time (for an planet similar to the Earth’s conditions with a Moon, etc.), so this increase in length of day is an inevitable feature which would eventually lead to oxygenation." On other planets with different planet-moon interactions, an oxygen-rich atmosphere may be less of a given. Future study is required to further investigate that possibility. However, Alcott noted that the new research suggests that "a planet with a short day length could potentially 'hide' the identification of worlds which have oxygen producing organisms on them." Because of this, exoplanet daylength ought to be considered when interpreting biosignature data on alien worlds in galaxies far, far away.</p>
    




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<guid isPermaLink="true">https://massivesci.com/articles/caffeine-brown-fat-hypothalamus-in-mice/</guid>
<link>https://massivesci.com/articles/caffeine-brown-fat-hypothalamus-in-mice/</link>
<pubDate>Tue, 23 Nov 2021 10:26:16 EST</pubDate>
<title>Caffeine keeps your body fat warm, on top of lighting up your brain</title>
<description>Hot take: caffeine triggers brown fat thermogenesis via the brain</description>

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  <media:description>A woman sitting the trunk of a car drinking coffee, under a blanket</media:description>
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  <dc:creator><![CDATA[Pamela Hirschberg]]></dc:creator>
  <atom:author>
    <atom:name>Pamela Hirschberg</atom:name>
    <atom:uri>https://massivesci.com/people/pamela-hirschberg/</atom:uri>
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    <p>For many people, drinking a cup of<strong> </strong>coffee in the morning is a sacred ritual. It tastes great, and it helps the morning fog to dissipate. Since it's such a big part of our daily lives, it's hard to think of caffeine as a psychoactive drug. We know plenty about the alerting qualities of caffeine on the brain, but less about caffeine's other benefits. According to a<a href="https://www.nature.com/articles/s41598-020-80505-9" rel="noopener noreferrer" target="_blank"> study</a> published earlier this year by a group from La Trobe University in Australia, lead-authored by Lachlan van Schaik, caffeine increases activity in brain regions associated with brown fat thermogenesis, and increases the temperature of brown fat.</p>
<p>You may be asking, "what is brown fat?" Well, it's is an important part of mammalian physiology. &nbsp;It exists in areas called <a href="https://www.cell.com/cell-metabolism/pdfExtended/S1550-4131(17)30714-3" rel="noopener noreferrer" target="_blank">depots</a> near vital organs and produces heat to defend against cold temperatures. Heat production in brown fat is called "<a href="https://journals.physiology.org/doi/full/10.1152/physrev.00015.2003" rel="noopener noreferrer" target="_blank">non-shivering thermogenesis</a>" because it is different from shivering, which produces heat <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5605160/" rel="noopener noreferrer" target="_blank">using the movement of your muscles</a>.</p>
<p>Non-shivering thermogenesis requires a special protein found in brown fat cells. This protein adjusts the normal energy-producing chain in the mitochondria of the brown fat cells.<strong> </strong>This change causes them to produce heat instead of energy for other cellular processes. Because brown fat burns <a href="https://www.frontiersin.org/articles/10.3389/fendo.2020.571659/full" rel="noopener noreferrer" target="_blank">fuel</a> to make heat independently from exercise, this tissue is a hot<em> </em>topic among endocrinologists &nbsp;as a potential therapeutic avenue to treat type 2 diabetes and other diseases associated with obesity.</p>
<p>Although there have been <a href="https://www.jstage.jst.go.jp/article/jnsv1973/36/2/36_2_173/_pdf/-char/ja" rel="noopener noreferrer" target="_blank">studies</a> in the past that measured the effects of caffeine on brown fat, this one did something a little different. The researchers wanted to be completely sure that they could attribute the effects of caffeine on brown fat to its actions on the brain.<strong> </strong>Other studies administered caffeine <a href="https://www.jstage.jst.go.jp/article/jnsv1973/36/2/36_2_173/_pdf/-char/ja" rel="noopener noreferrer" target="_blank">throughout the body,</a> either by injection or ingestion.<strong> </strong>These researchers cut out the middleman and injected the caffeine straight into live male mouse brains.</p>
<div class="oembed"><div class="iframely-embed"><div class="iframely-responsive" style="height: 140px; padding-bottom: 0;"><a href="https://massivesci.com/notes/coffee-consumption-brain-volume-anxiety/" data-iframely-url="https://cdn.iframe.ly/api/iframe?url=https%3A%2F%2Fmassivesci.com%2Fnotes%2Fcoffee-consumption-brain-volume-anxiety%2F&key=a91f6c63822d2172297a7435cae7a9eb"></a></div></div><script async src="https://cdn.iframe.ly/embed.js" charset="utf-8"></script></div>
<p>They facilitated the injection of caffeine into the brain by surgically placing a tiny metal tube that fed into the ventricles of the brain. The caffeine could then be fed directly through this tube into the ventricles. The ventricles are where the fluid that bathes the brain moves freely, so the caffeine could potentially act on any area of the brain.</p>
<p>The mice used in this study were given doses of caffeine proportionate to those consumed by humans in one cup of coffee. After they injected the caffeine into the mice, the researchers measured activity of brain areas associated with brown fat thermogenesis. They did this by staining brain tissue for the presence of a specific marker for neuronal activity, then looking at it under a microscope.</p>
<p>The brain staining experiment revealed that several regions of the brain were activated in response to caffeine injection, including regions of a brain area called the hypothalamus. Some of these <a href="https://www.frontiersin.org/articles/10.3389/fendo.2015.00136/full" rel="noopener noreferrer" target="_blank">regions of the hypothalamus</a> were previously found to play a role in the brain's control of brown fat thermogenesis.</p>
<aside class="pullquote"><blockquote>After just 10 minutes, they found that the brown fat got warmer in response to the caffeine</blockquote></aside>
<p>The researchers performed other experiments to observe the brown fat response to caffeine as well. They chose the most direct measurement of brown fat heat production, which was to simply measure the temperature of the tissue.<strong> </strong>They surgically placed a tiny thermometer in the mice beneath their brown fat deposits to monitor its temperature of their tissue in real time.<strong> </strong>After just 10 minutes, they found that the brown fat got warmer in response to the caffeine. This temperature increase was independent of the overall body temperature of the mice, which is important in order to distinguish caffeine's effect on the temperature of the whole body versus just the heat production in the brown fat.</p>
<p>Although these results seem to indicate that caffeine ingestion helps increase heat production in brown fat, it doesn't mean you should immediately quit your workout routine and celebrate with a piping hot cup of joe. One main reason is because this study completely ignored female mice. This often happens because researchers do not want to deal with the added variable of hormonal fluctuations associated with their<strong> </strong>estrus cycles. Understanding the link between caffeine and thermogenesis in female mice will be an important follow-up to know how caffeine could potentially affect the brown fat of female mice, particularly because<strong> </strong>brown fat thermogenesis is <a href="https://www.cell.com/cell-reports/pdfExtended/S2211-1247(16)30976-7" rel="noopener noreferrer" target="_blank">modulated by estrogens</a>.</p>
<p>Thus, the results of this study are potentially translational and valuable to healthy males of a normal weight, but the study of brown fat is very often impactful because of its therapeutic potential for diabetic or overweight men and women. Future research should focus on the effect of brain caffeine on brown fat of male <em>and</em> female mice, including diabetic and overweight mouse models.</p>
<p>Despite the caveats in these results, they did reveal that caffeine turns on brain regions that are responsible for brown fat thermogenesis, and that it may help some people burn fat. So until the next set of results come in, we can all patiently sip our coffee or tea, awaiting the heat.</p>
    


<p><em><a href="https://massivesci.com/people/pamela-hirschberg/">Pamela Hirschberg</a> studies 

<p class="mb0">

<span class="scientist__field">Cellular Neuroscience</span>

</p>

 at 

<p class="mb0 o7">

<span class="scientist__institution">Rutgers University</span>

</p>

.</p>



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<guid isPermaLink="true">https://massivesci.com/articles/soil-runoff-reef-tree-planting/</guid>
<link>https://massivesci.com/articles/soil-runoff-reef-tree-planting/</link>
<pubDate>Mon, 22 Nov 2021 11:07:19 EST</pubDate>
<title>To save the reefs, save the trees and the soil they grow in</title>
<description>Soil from the surface can smother reefs. A new study creates a map of corals most susceptible to runoff from land </description>

<media:content url="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/587efb07-e778-4444-b7f6-e2d77d763d1c/hiroko-yoshii-9y7y26C-l4Y-unsplash.jpg?auto=compress%2Cformat&amp;crop=faces&amp;fit=crop&amp;fm=jpg&amp;h=600&amp;q=75&amp;w=900" type="image/jpeg">
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  <media:description>Fish swimming through a coral reef</media:description>
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  <dc:creator><![CDATA[Cassie Freund]]></dc:creator>
  <atom:author>
    <atom:name>Cassie Freund</atom:name>
    <atom:uri>https://massivesci.com/people/cassie-freund/</atom:uri>
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  <content:encoded><![CDATA[
    <p>Tropical rainforests and coral reefs are two of the most vibrant and biodiverse ecosystems in the world. Together they bring to mind images of lush, green vegetation spilling into clear turquoise waters teeming with ocean life. You probably don't think about the ground beneath your feet — but, according to research <a href="https://onlinelibrary.wiley.com/doi/full/10.1111/gcb.15811?utm_sq=gt6hw48olk&amp;campaign=wolearlyview" rel="noopener noreferrer" target="_blank">recently published</a> in <em>Global Change Biology</em>, we need to if we want to keep these two ecosystems healthy.</p>
<p>Farming and land development in coastal areas breaks up soil in these areas, increasing run off into the ocean. This dirt (and the pollutants it carries) is dangerous for coral reefs. It can literally smother corals, <a href="https://www.sciencedirect.com/science/article/pii/S0272771499905383?casa_token=lqDhc7SlHOMAAAAA:mDKF0BNls9zoGid2eR_NoHLpdpnYW2OoEBF_0qyozwQc7PMzpCVyezLd9C7O_jA0oZ5vB_dqTw" rel="noopener noreferrer" target="_blank">covering them like a blanket</a>, making them more sensitive to heat and starving the brightly colored photosynthetic algae, called <a href="https://oceanservice.noaa.gov/education/tutorial_corals/coral02_zooxanthellae.html" rel="noopener noreferrer" target="_blank">zooxanthellae</a>, that live inside of them. The new study, by an international team of researchers led by ecologist Andrés Suárez-Castro, set out to create a global map of corals that are most susceptible to these threats.</p>
<p>Using satellite data, soil information, and mathematical models of how water flows across land, the researchers calculated that at least six gigatons of soil (the weight of at least 33 <em>million </em>adult <a href="https://appliedsciences.nasa.gov/our-impact/story/steering-clear-blue-whales" rel="noopener noreferrer" target="_blank">blue whales</a>) are swept into the ocean within 150 miles of coral reefs each year. They also discovered that 41 percent of reefs worldwide are exposed to sediment runoff. They also saw that Southeast Asia is particularly at risk, with two-thirds of reefs there located in runoff zones.</p>
<figure class="right medium"><img alt="Surface runoff from a hillside after soil is saturated with water" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/77fdd9a5-bb4a-4071-8a30-b2ecd57b7d53/Runoffrazorback.jpeg"/><figcaption><span class="caption"><p>Surface runoff from a hillside after soil is saturated with water</p></span> <span class="credit"><p>Via <a href="https://commons.wikimedia.org/wiki/File:Runoffrazorback.jpg" target="_blank">Wikimedia</a></p></span></figcaption></figure>
<p>The researchers also discovered that sediment-<em>producing</em> regions and sediment-<em>affected</em> regions are not necessarily the same. Sediment runoff was highest in Vietnam and China, but only about 2 percent of it reaches coral reefs. On the other hand, Fiji and the Solomon Islands produce very little sediment runoff, but nearly all of their nearby reefs are affected by it.</p>
<p>According to this analysis, coral reefs in Indonesia and the Philippines are — unfortunately — doubly endangered by sediment runoff. These two countries have both the highest area of affected coral reefs, and receive the most sediment, despite the fact that neither is near the top of the list of sediment-producing countries. Sediment runoff is just one of a handful of threats these reefs, part of the wildly productive and biodiverse <a href="https://www.weforum.org/agenda/2018/09/what-is-the-coral-triangle/" rel="noopener noreferrer" target="_blank">Coral Triangle</a>, face. Protecting them from further harm is a priority for conservationists, as they are home to at least 15 species of unique coral that can be found nowhere else, and 76 percent of all coral species worldwide.</p>
<p>Luckily, having the map of reefs affected by runoff also unlocks opportunities for a rescue. One such opportunity Suárez-Castro and his colleagues explored is a tried-and-true conservation method to save the corals: planting trees.</p>
<div class="oembed"><div class="iframely-embed"><div class="iframely-responsive" style="height: 140px; padding-bottom: 0;"><a href="https://massivesci.com/notes/coral-reef-restoration-florida-keys-bleaching/" data-iframely-url="https://cdn.iframe.ly/api/iframe?url=https%3A%2F%2Fmassivesci.com%2Fnotes%2Fcoral-reef-restoration-florida-keys-bleaching%2F&key=a91f6c63822d2172297a7435cae7a9eb"></a></div></div><script async src="https://cdn.iframe.ly/embed.js" charset="utf-8"></script></div>
<p>Their approach of examining how patterns of land use and other terrestrial human activities affect the ocean is an example of <a href="https://coralreef.noaa.gov/aboutcrcp/news/featuredstories/april16/welcome.html" rel="noopener noreferrer" target="_blank">"ridge to reef"</a> conservation. Marine and terrestrial conservation are often siloed, with forests and the ocean treated as separate entities. But this worldview can hold conservation back from identifying environmental problems and coming up with creative solutions to them.</p>
<p>When coastal forests are intact, the researchers reasoned, tree roots prevent soil from running off into the ocean. So, how much soil could targeted reforestation efforts prevent from eroding into the sea? The potential seems vast: research from the Ivory Coast suggests that <a href="https://rainforests.mongabay.com/0903.htm" rel="noopener noreferrer" target="_blank">soil runoff from treeless areas</a> is 4,600 times greater than runoff from forested slopes.</p>
<p>Suárez-Castro's research team calculated that replanting up to 10 square kilometers of forest in each of thousands coral reef-linked coastal watersheds could reduce sediment runoff to 63,000 square kilometers of coral reefs by an average of 8.5 percent. These reefs comprise not only some of the most biodiverse regions of the planet, but are also irreplaceable resources for people who rely on tourism or fishing for their livelihoods.</p>
<p>The researchers also found that the most effective approach to reforestation differs depending on what region of the world they were focused on. In the Coral Triangle erosion tends to affect entire watersheds, and so tree planting efforts must be widespread to meaningfully reduce the amount of soil entering the ocean. The researchers highlight East Java and Sulawesi, both in Indonesia, along with Mindanao Island in the Philippines as examples. But in East Africa, the sources of soil runoff tend to be more aggregated in space, meaning that reforestation efforts can be more focused in a few specific locations — replanting trees in just a few watersheds along the coast of Mozambique could make a big difference for corals.</p>
<div class="oembed"><div class="iframely-embed"><div class="iframely-responsive" style="height: 140px; padding-bottom: 0;"><a href="https://massivesci.com/articles/coral-health-sickness-bacteria-disease/" data-iframely-url="https://cdn.iframe.ly/api/iframe?url=https%3A%2F%2Fmassivesci.com%2Farticles%2Fcoral-health-sickness-bacteria-disease%2F&key=a91f6c63822d2172297a7435cae7a9eb"></a></div></div><script async src="https://cdn.iframe.ly/embed.js" charset="utf-8"></script></div>
<p>These regional assessments of the potential impacts of reforestation on sediment runoff — and coral health — are, of course, generalizations. The study authors were limited by the coarse spatial resolution of the data currently available. Higher-resolution data would enable them to make more complicated models of sediment runoff and to factor in how the shapes and arrangements of corals in reefs might determine how sediment runoff affects them.</p>
<p>There also remain practical challenges to reforestation. For example, sometimes coral reefs in one administrative boundary are affected by sediment runoff from another district. This is a common difficulty in addressing pollution of any kind, and fixing it requires <a href="https://www.oxfordbibliographies.com/view/document/obo-9780199756223/obo-9780199756223-0290.xml" rel="noopener noreferrer" target="_blank">political</a> cooperation. And, in general, large-scale reforestation is <a href="https://www.discovermagazine.com/environment/10-golden-rules-for-reforestation-show-how-to-plant-trees-the-right-way" rel="noopener noreferrer" target="_blank">not as easy</a> as just planting a few trees — successful reforestation takes time, effort, and funding. It also requires knowing exactly where to plant and which tree species are best suited to local environments.</p>
<p>These findings demonstrate the strength of looking at forests and coral reefs as a single, interconnected system. Forest restoration is a hot topic at this moment in time, the first year of the <a href="https://www.decadeonrestoration.org/" rel="noopener noreferrer" target="_blank">United Nations Decade on Ecosystem Restoration</a>. Replanting forests that have been clear-cut or degraded for agriculture and other human use will help us fight climate change. Linking reforestation to coral reef conservation would not only rejuvenate lush tropical forests, but also preserve the countless species that rely on healthy reefs — including us.</p>
    


<p><em><a href="https://massivesci.com/people/cassie-freund/">Cassie Freund</a> studies 

<p class="mb0">

<span class="scientist__field">Ecology</span>

</p>

 at 

<p class="mb0 o7">

<span class="scientist__institution">Wake Forest University</span>

</p>

.</p>



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<guid isPermaLink="true">https://massivesci.com/articles/natural-selection-evolution-needles-venom/</guid>
<link>https://massivesci.com/articles/natural-selection-evolution-needles-venom/</link>
<pubDate>Mon, 22 Nov 2021 09:14:00 EST</pubDate>
<title>Animals, plants, and even some bacteria use hypodermic needles</title>
<description>Needles are everywhere in nature, evolving independently many times in a variety of organisms</description>

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  <media:title></media:title>
  <media:description>close up of a paper wasp&#39;s stinger against a black background</media:description>
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  <dc:creator><![CDATA[Hayden Waller]]></dc:creator>
  <atom:author>
    <atom:name>Hayden Waller</atom:name>
    <atom:uri>https://massivesci.com/people/hayden-waller/</atom:uri>
  </atom:author>


  
  <content:encoded><![CDATA[
    <p>In 1844, Irish physician Francis Rynd <a href="https://www.irishtimes.com/news/the-irish-doctor-who-invented-the-syringe-1.1105651" rel="noopener noreferrer" target="_blank">performed</a> the first known medical injection using a hollow metal needle that ended in a sharpened point. This instrument, known today as a hypodermic needle, has become one of the most important tools used in medicine and research. <a href="https://www.mddionline.com/drug-delivery/hypodermic-syringes-greatest-medical-device-all-time">Some </a>have even claimed that the hypodermic syringe in particular is responsible for saving more lives and alleviating more suffering than any other piece of medical technology.</p>
<p>It was a brilliant invention, to be sure, but Rynd did not create his hypodermic needle out of whole cloth. Like so many of the devices and tools we use in the modern world, he drew inspiration from nature.</p>
<p>A quick swing through the branches of the tree of life reveals an interesting phenomenon: Everywhere you look, you can find naturally occurring hypodermic needles. They exist<strong> </strong>in everything from bacteria, to plants, to a whole host of different animal lineages. With relatively few exceptions, the purpose of such needles is essentially the same as Rynd's – to efficiently deliver a substance below some outer layer via puncturing and injection.</p>
<h3 id="wasps-bees-and-ants">Wasps, bees, and ants</h3>
<p>Most of the stinging insects belong to the order Hymenoptera, a group which contains the bees, wasps, and ants. Their stingers are highly efficient at delivering toxins and are <a href="https://www.ncbi.nlm.nih.gov/books/NBK518972/" rel="noopener noreferrer" target="_blank">modified from</a> structures that originally functioned as their egg laying apparatus. Their needles are used both as a defensive mechanism and a prey capture strategy.</p>
<figure class="center large"><img alt="saddleback caterpillar, a green and brown caterpillar with long stingers sticking up from its body" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/e2d781a4-fb5e-4057-88be-987dd3ec896d/Saddleback_caterpillar_-_Acharia_stimulea%2C_Prince_William_Forest_Park%2C_Triangle%2C_Virginia.jpg"/><figcaption><span class="caption"><p>While this saddleback caterpillar may look beautiful, you certainly don't want to touch it</p></span> <span class="credit"><p>Judy Gallagher on <a href="https://www.flickr.com/photos/52450054@N04/29127638592/" target="_blank">Flickr</a> (CC <a href="https://creativecommons.org/licenses/by/2.0/" target="_blank">BY 2.0</a>)</p></span></figcaption></figure>
<h3 id="caterpillars">Caterpillars</h3>
<p>It may come as a surprise, but certain butterfly and moth larvae are &nbsp;capable of delivering quite the sting. Hollow hairs on their backs, <a href="https://entnemdept.ufl.edu/walker/ufbir/chapters/chapter_23.shtml" rel="noopener noreferrer" target="_blank">called setae</a>, evolved to protect these juicy, slow moving grubs from attacks by would-be predators. Most caterpillar stings are not fatal to humans, but smaller animals ought to beware. The <a href="https://www.sciencedirect.com/science/article/pii/S0041010110000279?via%3Dihub" rel="noopener noreferrer" target="_blank">exception to this</a> is a species of giant silkworm moth (<em>Lonomia obliquia</em>), which can kill people.</p>
<h3 id="true-bugs">True bugs</h3>
<p>These funny looking insects in the order Hemiptera represent perhaps the only example of &nbsp;organisms whose hypodermic needles contain two channels: one for &nbsp;injecting saliva and another for slurping things back up. Unsurprisingly, given they are often used for feeding, the hollow tube &nbsp;is built from modified mouthparts. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4598556/" rel="noopener noreferrer" target="_blank">Most species are herbivorous</a> and use their needles for sucking nutrients from plants, but there are <a href="https://www.scielo.br/j/babt/a/Y56tfFGg94fSdvCrbtmxXjz/?lang=en" rel="noopener noreferrer" target="_blank">predatory species</a> as well who use the structure for more sinister purposes.</p>
<h3 id="centipedes">Centipedes</h3>
<p><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4663536/" rel="noopener noreferrer" target="_blank">Centipedes</a> use venomous fangs to kill their prey, but these fangs are not modified mouthparts. These toxin delivery structures actually evolved through modifications to the first pair of centipedes' walking legs.</p>
<h3 id="spiders">Spiders</h3>
<p><a href="https://animals.howstuffworks.com/arachnids/spider7.htm" rel="noopener noreferrer" target="_blank">Nearly all spiders</a> possess hollow mouthparts called chelicerae through which they inject their toxins, though less than 30 of the over 43,000 species of spider <a href="https://www.britannica.com/list/9-of-the-worlds-deadliest-spiders" rel="noopener noreferrer" target="_blank">are known</a> to have killed humans. These needles range in size from very small to very large, just as spider venoms range from very weak to very strong.&nbsp;As in several other organisms, spiders use their hypodermic needles for both prey capture and defense.</p>
<figure class="center large"><img alt="a dark brown scorpion with a gold tail/stinger against a white background" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/a19e5663-7207-427d-99d8-86628a49d084/scorpion-white-animal-isolated.jpg"/><figcaption><span class="caption"><p>A scorpion's stinger is a hollow needle at the end of its tail</p></span> <span class="credit"><p><a href="https://www.pxfuel.com/en/free-photo-jyxfo" target="_blank">Pxfuel</a></p></span></figcaption></figure>
<h3 id="scorpions">Scorpions</h3>
<p>Scorpions are arachnids, the same overarching group as spiders. Their stingers are a hollow needle that protrudes from a bulb. Like the stinging insects, this structure is used for both defense and prey capture. However in contrast to the stinging insects, scorpion stingers developed from changes to <a href="https://onlinelibrary.wiley.com/doi/full/10.1111/joa.12582" rel="noopener noreferrer" target="_blank">their final body segment, called the telson</a>, rather than the egg laying apparatus.</p>
<h3 id="snakes">Snakes</h3>
<p>Though many species of snakes do not possess venomous fangs, <a href="https://www.nationalgeographic.com/animals/reptiles/facts/snakes-1" rel="noopener noreferrer" target="_blank">about 20 percent</a> do. <a href="https://www.livescience.com/54023-vipers.html" rel="noopener noreferrer" target="_blank">Vipers</a> in particular are the most well-adapted for delivering venom into the bloodstreams of their prey. Their fangs are modified teeth that form a hollow, hypodermic needle structure designed to deliver death.&nbsp;These needles are incredibly strong and are capable of piercing some of the toughest, thickest hides in nature.</p>
<h3 id="cnidarians">Cnidarians</h3>
<p>Members of the phylum Cnidaria (jellyfish, anemones, coral, hydra) are defined by their stinging cells. The <a href="https://www.smithsonianmag.com/science-nature/whats-behind-that-jellyfish-sting-2844876/" rel="noopener noreferrer" target="_blank">stings delivered</a> by these creatures are the result of a specialized needle-like organelle in some of their cells which, upon being disturbed, explode out through the cell wall and embed themselves in the target. It is through these hollow structures that cnidarians deliver toxins which in &nbsp;some cases can be fatal even to humans.</p>
<figure class="center large"><img alt="a tan and brown Gaboon viper showing its fangs" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/73208e73-7524-462a-9e05-ab8632b74b32/800px-Bitis_gabonica_fangs.jpg"/><figcaption><span class="caption"><p>The fangs of a West African Gaboon viper demonstrate why this animal can be so dangerous</p></span> <span class="credit"><p><a href="https://commons.wikimedia.org/wiki/File:Bitis_gabonica_fangs.jpg" target="_blank">Wikimedia Commons</a> (CC <a href="https://creativecommons.org/licenses/by/2.0/deed.en" target="_blank">BY 2.0</a>)</p></span></figcaption></figure>
<h3 id="cone-snails">Cone snails</h3>
<p>By modifying one of their "teeth" into a barbed harpoon and attaching it to the end of an extendible proboscis, natural selection has generated one of the more terrifying hypodermic needles around. Cone snails are not to be trifled with; their toxins are some of the <a href="https://allthatsinteresting.com/cone-snail" rel="noopener noreferrer" target="_blank">most potent in the sea</a>, with several species possessing stings fatal to humans.</p>
<h3 id="fish">Fish</h3>
<p>Perhaps surprisingly, there are <a href="https://academic.oup.com/jhered/article/97/3/206/2188449" rel="noopener noreferrer" target="_blank">more venomous fish</a> than other venomous vertebrates combined. Many of these fish deliver &nbsp;their toxins through hollow, needle-like barbs that are actually &nbsp;modified fin bones, though not all. For example, stingray stingers are &nbsp;actually an <a href="https://www.ncbi.nlm.nih.gov/books/NBK539785/" rel="noopener noreferrer" target="_blank">outgrowth of their spine</a>. Stonefish, lionfish, and scorpionfish are among the <a href="https://oceanconservancy.org/blog/2020/01/22/stonefish/" rel="noopener noreferrer" target="_blank">most venomous fish in the world</a> and their stings can be fatal if left untreated. In Australia, &nbsp;stonefish antivenom is the second most commonly administered antivenom each year.</p>
<h3 id="platypus">Platypus</h3>
<p>The platypus is one of the strangest mammals on the planet. They lay eggs, can <a href="https://www.amnh.org/explore/news-blogs/news-posts/to-hunt-the-platypus-uses-its-electric-sixth-sense" rel="noopener noreferrer" target="_blank">sense electric fields</a>, and the males possess hollow spurs on their feet capable of delivering a &nbsp;venomous sting. By far the bluntest and crudest of the hypodermic needles on this list, the platypus spur is modified from the heel bone and packs quite <a href="https://pubmed.ncbi.nlm.nih.gov/1454022/" rel="noopener noreferrer" target="_blank">a punch</a>.</p>
<figure class="right medium"><img alt="a close up of a plant with long needle like protrusions" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/c855fe72-42dd-43a3-8d7f-8014078e5eca/stinging%20nettle.jpg"/><figcaption><span class="caption"><p>it's not just animals: plants, like stinging nettles, also have hypodermic needles</p></span> <span class="credit"><p>Carl Graph on <a href="https://www.flickr.com/photos/58753832@N05/49774581127" target="_blank">Flickr</a> (CC BY-ND <a href="https://creativecommons.org/licenses/by-nd/2.0/?ref=ccsearch&amp;atype=rich" target="_blank">2.0</a>)</p></span></figcaption></figure>
<h3 id="plants">Plants</h3>
<p>Hypodermic needles aren’t unique to the animal kingdom; some plants have &nbsp;evolved them as well. Stinging nettles, like many plants, possess hair-like structures called trichomes. <a href="https://www.botany.one/2018/08/stinging-plants-share-needle-designs/" rel="noopener noreferrer" target="_blank">Natural selection has modified the trichomes</a> on stinging nettles such that they have become hollow and needle-like. &nbsp;It is through these structures that the plant delivers its irritating toxins.</p>
<h3 id="bacteria">Bacteria</h3>
<p>Even single-celled organisms have needles. Certain species of pathogenic bacteria possess a structure known as a t<a href="https://elifesciences.org/articles/39514" rel="noopener noreferrer" target="_blank">ype III secretion system</a> which presents itself as an extendible, sensory needle. This allows them to detect and more easily infect eukaryotic cells via direct injection.</p>
<aside class="pullquote"><blockquote><em>So why </em>do hypodermic needles keep evolving?</blockquote></aside>
<p>In addition to all of these organisms, there is also a <a href="https://bioone.org/journals/entomologica-americana/volume-126/issue-1-4/1947-5136-126.1.112/THE-VENOMOUS-BEETLE-ONYCHOCERUS-ALBITARSIS-PASCOE-1859-COLEOPTERA--CERAMBYCIDAE/10.1664/1947-5136-126.1.112.full" target="_blank">single beetle species</a>, <em>Onychocerus albitarsis,</em> with a hypodermic needle appendage. The most unique insect stinger belongs to a rare beetle species native to South America. It is the only known arthropod to have evolved <a href="https://pubmed.ncbi.nlm.nih.gov/18004534/" rel="noopener noreferrer" target="_blank">hypodermic needles at the ends of its antennae</a>. &nbsp;Each stinger closely resembles the bulbous stinger found on scorpions, though they evolved on an entirely different body part.</p>
<p>Perhaps the most remarkable thing about the sheer diversity of needle-possessing organisms is they all evolved independently of one another. This process, known as <a href="https://www.livescience.com/convergent-evolution.html" rel="noopener noreferrer" target="_blank">convergent evolution</a>, occurs when unrelated organisms face similar selection pressures.</p>
<p>So, <em>why </em>do hypodermic needles keep evolving?</p>
<p>One reason is that, “injecting a potent toxin to immobilize the prey or to defend oneself from predators would seem to be advantageous compared to simply overpowering it,” says <a href="https://entomology.cals.cornell.edu/people/cole-gilbert/" rel="noopener noreferrer" target="_blank">Cole Gilbert</a>, professor of insect behavior and physiology in the Department of Entomology at Cornell University.</p>
<p>Indeed, it would seem that injecting toxin through a hollow needle is an elegant solution to the near-universal problem of how to get lunch while avoiding becoming someone else’s. If an organism can save energy and resources it would otherwise need to spend on building a larger body or stronger muscles and build a simple needle instead, why wouldn't it?</p>
<div class="oembed"><div class="iframely-embed"><div class="iframely-responsive" style="height: 140px; padding-bottom: 0;"><a href="https://massivesci.com/notes/cassiopea-upside-down-jellyfish-sting-mucus/" data-iframely-url="https://cdn.iframe.ly/api/iframe?url=https%3A%2F%2Fmassivesci.com%2Fnotes%2Fcassiopea-upside-down-jellyfish-sting-mucus%2F&key=a91f6c63822d2172297a7435cae7a9eb"></a></div></div><script async src="https://cdn.iframe.ly/embed.js" charset="utf-8"></script></div>
<p>Another reason seems to be that hypodermic needles are relatively easy to make. Like a budget tinkerer, natural selection keeps finding ways to build them from whatever body parts and materials are available. Gilbert explains, “Many of the injection devices are <a href="https://www.researchgate.net/figure/Insect-body-axes_fig1_340429575" rel="noopener noreferrer" target="_blank">midline</a> structures derived from a <a href="https://en.wikipedia.org/wiki/Symmetry_in_biology#Bilateral_symmetry" rel="noopener noreferrer" target="_blank">bilaterally symmetric</a> precursor [Ed: the needles develop in the central axis of the body's layout, like a human nose]. Thus, most of them evolved by sticking the structures together, either with slidey bits for easier penetration, or, in the case of the scorpion sting, the structure is fused completely.” In other words, it takes far fewer mutations to take two or three existing structures and make them into a hollow tube than to build an entirely new structure from scratch.</p>
<p>Matural hypodermic needles are made of a wide variety of biological materials. For example, arthropod fangs and stingers are made of <a href="https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/chitin" rel="noopener noreferrer" target="_blank">chitin</a>, the same substance from which their exoskeletons are built. The stonefish, platypus, and snakes all have hollow needles made from bone, whereas a nettle's trichome-derived needles are essentially outgrowths of the plant’s “skin”. The stinging cells in the jellyfish and anemones are made from protein combinations found only in that particular group of animals. The <a href="https://elifesciences.org/articles/39514" rel="noopener noreferrer" target="_blank">type 3 secretion systems</a> found in bacteria are similar.</p>
<p>Natural hypodermic needles have inspired humans for many centuries and continue to be an important focus of <a href="https://www.nature.com/articles/s41598-018-33386-y" rel="noopener noreferrer" target="_blank">biomechanics </a>and <a href="https://pubmed.ncbi.nlm.nih.gov/26478411/" rel="noopener noreferrer" target="_blank">materials </a>research. The extraordinary diversity of organisms that possess them speaks to their utility in aiding with predator defense and prey capture as well as their ability to be created from pre-existing structures and materials. Natural selection produces traits that help organisms survive and reproduce, and often times if a trait works for one organism, it will work for many others as well.</p>
    


<p><em><a href="https://massivesci.com/people/hayden-waller/">Hayden Waller</a> studies 

<p class="mb0">

<span class="scientist__field">Evolutionary Biology</span>

</p>

 at 

<p class="mb0 o7">

<span class="scientist__institution">Cornell University</span>

</p>

.</p>



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<guid isPermaLink="true">https://massivesci.com/articles/elephant-hawkmoth-artificial-light-nighttime-pollination/</guid>
<link>https://massivesci.com/articles/elephant-hawkmoth-artificial-light-nighttime-pollination/</link>
<pubDate>Fri, 19 Nov 2021 00:19:00 EST</pubDate>
<title>Artificial light makes it harder for nocturnal pollinators to find flowers and avoid predators</title>
<description>New research demonstrates that artificial light at night interferes with elephant hawkmoths&#39; senses</description>

<media:content url="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/073df2c7-d09c-493e-8bf1-2088f975b84b/Small_Elephant_Hawk-moth.jpg?auto=compress%2Cformat&amp;crop=faces&amp;fit=crop&amp;fm=jpg&amp;h=600&amp;q=75&amp;w=900" type="image/jpeg">
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  <media:description>a large pink and yellow moth perched on a leaf</media:description>
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  <dc:creator><![CDATA[Siddhant Pusdekar]]></dc:creator>
  <atom:author>
    <atom:name>Siddhant Pusdekar</atom:name>
    <atom:uri>https://massivesci.com/people/siddhant-pusdekar/</atom:uri>
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    <p>If you live in the Global North or one of the rapidly urbanizing parts of the Global South, there may be a stark lack of darkness. The thing that has been a defining feature of the night is gone. Unceasing human activity — all those lights — means the night sky now has a slight red glow to it. This <a href="https://www.wikiwand.com/en/Skyglow" rel="noopener noreferrer" target="_blank">skyglow</a> is the result of light pollution, and it has far reaching consequences on <a href="https://cdnsciencepub.com/doi/full/10.1139/er-2014-0041">human health, </a>&nbsp;<a href="https://esajournals.onlinelibrary.wiley.com/doi/10.1890/1540-9295%282004%29002%5B0191%3AELP%5D2.0.CO%3B2">ecosystems</a>, and animal behavior.</p>
<p>One such behavior is nocturnal pollination. The world is currently facing the imminent threat of <a href="https://grist.org/food/mass-extinction-threatens-the-worlds-pollinators-and-its-crops/">loss of pollinators</a>. Lesser known, but equally critical, pollinating animals are<strong> </strong>nocturnal pollinators like <a href="https://www.wildlifetrusts.org/wildlife-explorer/invertebrates/moths/elephant-hawk-moth" rel="noopener noreferrer" target="_blank">elephant hawkmoths</a>.</p>
<p>On top of<strong> </strong>being threatened by loss of habitat and the use of chemical pesticides, insecticides, and herbicides, these striking insects may also be threatened by artificial light at night.&nbsp;Since pollinators are usually part of a network of plants <em>and </em>pollinators, disrupting pollination, which elephant hawkmoths do at night, reduces plants’ <a href="https://www.nature.com/articles/nature23288">overall ability to reproduce</a>. This feeds back onto all the pollinators that depend on the plants.</p>
<p>Jolyon Troscianko is a visual ecologist, which means he studies how the world appears to animals and how animals use their vision to navigate. To understand the potential effects of artificial light on the visual ecology of elephant hawkmoths, his group turned to mathematical modeling. The results of their research <a href="https://www.nature.com/articles/s41467-021-24394-0" rel="noopener noreferrer" target="_blank">were published</a> earlier this year in <em>Nature Communications</em>.</p>
<aside class="pullquote"><blockquote>...elephant hawkmoths have a special place in plant-pollinator networks</blockquote></aside>
<p>There are several different types of artificial light, and Troscianko's group wanted to test the effects of commonly used sources of light on elephant hawkmoths' natural behavior. As the light source changes so does the wavelengths of the light available to be reflected off surfaces&nbsp;such as leaves and flowers. In turn, this shifts the perceived colors of these surfaces from the moth’s point of view.</p>
<p>Not only do elephant hawkmoths have a special place in plant-pollinator networks, they also fascinate scientists for being the only species that has been studied for its ability to<a href="https://journals.biologists.com/jeb/article/209/5/789/16683/Crepuscular-and-nocturnal-illumination-and-its"> see color at night</a>. However, the results of this research are likely applicable to other nighttime pollinators.</p>
<p>We haven’t evolved to see it, but the natural night sky has a color of its own. That color may be essential for the survival of nocturnal animals like the elephant hawkmoth. Even at night, hawkmoths can detect colors of flowers, which enables them to serve as vital agents of pollination. But the moth's sensitive visual system also makes it vulnerable to subtle <a href="https://journals.biologists.com/jeb/article/209/5/789/16683/Crepuscular-and-nocturnal-illumination-and-its">disruptions of its visual ecology</a>. As the sun dips below the horizon, the proportion of red in the sky decreases. Since most artificial sources of light have higher proportions of red, the natural color of the night is skewed.</p>
<p>"The sheer number of scenarios we tested was quite a challenge — we had to limit ourselves because the number of different hypotheses we could test was vast," Troscianko said.</p>
<p>The researchers compared the ability of hawkmoths to perceive the color of various natural objects — flowers, leaves, and so on — under artificial lighting of different intensities with their ability to do so &nbsp;under full moonlight.</p>
<p>Some common types of light sources, like white LEDs, emit a wide range of wavelengths across the visible spectrum, while others, like orange LEDs, emit a narrower range of wavelengths. The latter are more likely to emit longer wavelengths — the ones that look red or oranges — while broad-spectrum light sources appear white.</p>
<figure class="center large"><img alt="overhead view of a city in Turkey lit up at night" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/a60ae0da-e2c9-4613-b27d-aeb2d2f6ad4f/osman-koycu-c6qF_lYvu2I-unsplash.jpg"/><figcaption> <span class="credit"><p>Photo by <a href="https://unsplash.com/@osmank?utm_source=unsplash&amp;utm_medium=referral&amp;utm_content=creditCopyText">Osman Köycü</a> on <a href="https://unsplash.com/s/photos/city-at-night-turkey?utm_source=unsplash&amp;utm_medium=referral&amp;utm_content=creditCopyText">Unsplash</a></p></span></figcaption></figure>
<p>Since the natural night sky contains lower levels of red than an artificially lit night sky, it isn’t surprising the researchers' model predicted that under redder sources of light, hawkmoths will have a harder time detecting flowers than under full moonlight. On the other hand, broad spectrum white lights actually enhance the moths' color perception. But what surprised Troscianko the most was that the effects of phosphor-converted amber LED lights, which have a mix of yellow, orange and red wavelengths, varied with the intensity of the light.</p>
<p>“You can think of it as lighting that has that eerie twilight property, where colors look odd, but you do still have some color vision. Imagine the moth flying around and trying to remember flower colors while moving between intense lights that enhance colors (but change them entirely), and then to an odd twilight world where some colors disappear, while others are still fairly strong. It's a difficult effect to describe, but similar things happen to humans when we move around in low light and colorful lights,” he explained.</p>
<p>They didn’t just test the ability of the moths to detect flowers. As prey of insectivorous birds, moths are known to camouflage themselves. If their ability to perceive color is disrupted, the moths may choose a hiding spot that wouldn’t camouflage them from the bird’s point of view.</p>
<p>To test this, the team also modeled the visual system of the blue tit — a day time hunter that might see the moth against whatever surface it chose to rest at the end of the night. They found that artificial light may hinder this anti-predation behavior, making the moths more likely to be eaten. In the color-polluted night sky, a surface may seem, to the moth, like a good spot against which to camouflage, but under daylight, the blue-tit would be able to detect it.</p>
<p>It sounds bad.<strong> </strong>But more work needs to be done before we can start making changes to our lighting.</p>
<p>For one, these effects need to be tested on actual animals. “I am most interested in seeing whether the disruptive color intensity effects that our model predicts might also interfere with moth flower handling behavior,” Troscianko said.&nbsp;Flower handling is the behavior when the moths get close to the flower and stick their proboscis in to take up nectar.</p>
<div class="oembed"><div class="iframely-embed"><div class="iframely-responsive" style="height: 140px; padding-bottom: 0;"><a href="https://next.massivesci.com/notes/artificial-light-pollution-fish-marine-reef/" data-iframely-url="https://cdn.iframe.ly/api/iframe?url=https%3A%2F%2Fnext.massivesci.com%2Fnotes%2Fartificial-light-pollution-fish-marine-reef%2F&key=a91f6c63822d2172297a7435cae7a9eb"></a></div></div><script async src="https://cdn.iframe.ly/embed.js" charset="utf-8"></script></div>
<p>Anyone who has stared with dismay at the assortment of dead insects under a lamp may be forgiven for thinking that these effects of light on moth pollinating behavior are relatively unimportant. It is indeed hard to tell without further research whether the tendency of insects to be attracted to light could in itself be more damaging than subtle changes to their behavior.</p>
<p>But as Troscianko explains, “The effects we describe in our study might result in small effect sizes in terms of making flower handling slower or more inefficient, but the artificial light intensities involved could conceivably cover the majority of Europe. So [it is a] smaller effect, but over a much larger spatial scale (and therefore incredibly difficult to quantify). Our study also highlights multiple different potential problems, [such as that] some light types interfere with moth flower detection, make it difficult to color-match to substrates for camouflage, and aid the vision of predatory birds. So death by a thousand cuts.”</p>
    


<p><em><a href="https://massivesci.com/people/siddhant-pusdekar/">Siddhant Pusdekar</a> studies 

<p class="mb0">

<span class="scientist__field">Animal Behavior</span>

</p>

 at 

<p class="mb0 o7">

<span class="scientist__institution">University of Minnesota </span>

</p>

.</p>



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<guid isPermaLink="true">https://massivesci.com/articles/the-accident-brown-dwarf-failed-star-nasa-jpl/</guid>
<link>https://massivesci.com/articles/the-accident-brown-dwarf-failed-star-nasa-jpl/</link>
<pubDate>Thu, 18 Nov 2021 14:39:16 EST</pubDate>
<title>A failed star known as &quot;The Accident&quot; is changing the way we look at the galaxy</title>
<description>The newly discovered brown dwarf is the first of its kind</description>

<media:content url="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/6587554f-b23c-4204-bed3-4240451b1dc8/image2browndwarf.jpeg?auto=compress%2Cformat&amp;crop=faces&amp;fit=crop&amp;fm=jpg&amp;h=600&amp;q=75&amp;w=900" type="image/jpeg">
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  <media:description>Artist&#39;s conception of a brown dwarf</media:description>
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  <dc:creator><![CDATA[Briley Lewis]]></dc:creator>
  <atom:author>
    <atom:name>Briley Lewis</atom:name>
    <atom:uri>https://massivesci.com/people/briley-lewis/</atom:uri>
  </atom:author>


  
  <content:encoded><![CDATA[
    <p>There's a newly observed object in the sky called <a href="https://iopscience.iop.org/article/10.3847/2041-8213/ac0437">WISEA J153429.75-104303.3</a> — more affectionately known as "The Accident." The Accident is a <a href="https://astronomy.swin.edu.au/cosmos/B/brown+dwarf">brown dwarf</a>, a ball of gas that never quite grew large enough to start nuclear fusion and become a <a href="https://science.nasa.gov/astrophysics/focus-areas/how-do-stars-form-and-evolve">star</a> — but it’s cold, strange, and unlike any other brown dwarf we’ve seen. This weird brown dwarf is the first of its kind that we’ve detected, and it’s changing the way astronomers search for the smallest stars in our galaxy.</p>
<p>The Accident’s discovery was, well, a happy accident. Its discoverer, citizen scientist Dan Caselden, a participant in <a href="https://science.nasa.gov/citizenscientists/backyard-worlds" rel="noopener noreferrer" target="_blank">Backyard Worlds: Planet 9</a>, was looking for another moving object when he spotted something unusual. Follow up observations with <a href="https://www.keckobservatory.org/" rel="noopener noreferrer" target="_blank">Keck Observatory</a> and the <a href="https://hubblesite.org/" rel="noopener noreferrer" target="_blank">Hubble Space Telescope</a> revealed some strange properties: it’s a different color than other brown dwarfs we know, and it's one of the coldest ones we’ve seen. What could be making this brown dwarf so different?</p>
<p>Brown dwarfs are ubiquitous, with <a href="https://www.space.com/37401-100-billion-brown-dwarfs-milky-way.html">nearly 100 billion</a> of these failed stars lurking in our galaxy. They’re hard for astronomers to detect, though, since they’re faint and far away; we’ve only spotted around 2,000 of them so far. The hotter the brown dwarf, the brighter and easier to spot it is, so astronomers have had a particularly hard time finding Y dwarfs, the coldest brown dwarfs that are less than 350 degrees Fahrenheit (about the temperature of your oven while baking brownies). For comparison, a star like our Sun burns at around 10,000 degrees Fahrenheit — much much hotter and brighter.</p>
<p>Although they’re difficult to spot, brown dwarfs are a key part of the puzzle of star and planet formation. A cold brown dwarf like The Accident helps scientists suss out the link between planets and stars — where does one draw the line between a gas giant planet and a small star? Right now, the line between planets and brown dwarfs is set at 13 times the mass of Jupiter, but scientists hope to learn more about brown dwarfs' atmospheres, compositions, and more to really understand the differences and similarities between these types of objects. Even without its other puzzling properties, The Accident is notable for being one of the coldest, smallest brown dwarfs found so far, one of only ~50 currently known Y dwarfs.</p>
<p>The most intriguing property of The Accident, though, is its color. Despite being so cold, it appears more blue than other brown dwarfs. (Usually, in the universe, cooler things are redder — think of the outside of a flame burning red, versus the yellow or blue hotter center.)</p>
<p>Astronomers think this is a sign of its age. An old brown dwarf like The Accident also would have formed long ago when the galaxy’s chemical makeup was different. In the early days of the Milky Way, heavier elements hadn't yet formed from supernovae and other processes, so the galaxy would have been mostly composed of hydrogen and helium. Future observations of this ancient relic could then provide a window into the chemistry of our Milky Way’s past.</p>
<p>Most importantly, though, finding The Accident showed astronomers that they’ve been looking for old brown dwarfs in all the wrong places. While most searches look for stationary objects, this discovery made astronomers realize that old brown dwarfs are likely moving quite quickly — they’ve been around the galaxy for so long that they would have been accelerated by other stars they encounter, bouncing around like a game of hot potato. New searches can now look for moving objects, hopefully finding more objects like The Accident to figure out more of the story of brown dwarfs in our galaxy.</p>
    


<p><em><a href="https://massivesci.com/people/briley-lewis/">Briley Lewis</a> studies 

<p class="mb0">

<span class="scientist__field">Astronomy</span>

and <span class="scientist__field">Astrophysics</span>

</p>

 at 

<p class="mb0 o7">

<span class="scientist__institution">University of California, Los Angeles</span>

</p>

.</p>



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<guid isPermaLink="true">https://massivesci.com/articles/songbird-good-bad-cholesterol-heart-disease/</guid>
<link>https://massivesci.com/articles/songbird-good-bad-cholesterol-heart-disease/</link>
<pubDate>Wed, 17 Nov 2021 12:59:47 EST</pubDate>
<title>Songbirds might hold the key to managing our cholesterol levels</title>
<description>Songbirds have lost &quot;bad&quot; cholesterol and some of its associated proteins over time. This makes for plaque-free finch arteries and a hale and healthy heart</description>

<media:content url="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/27f84548-6f49-4c5a-93ce-bd756d402248/Zebra_finch_2_(7325891716).jpeg?auto=compress%2Cformat&amp;crop=faces&amp;fit=crop&amp;fm=jpg&amp;h=600&amp;q=75&amp;w=900" type="image/jpeg">
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  <media:description>Four zebra finches sitting on a branch</media:description>
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  <dc:creator><![CDATA[Sahana Sitaraman]]></dc:creator>
  <atom:author>
    <atom:name>Sahana Sitaraman</atom:name>
    <atom:uri>https://massivesci.com/people/sahana-sitaraman/</atom:uri>
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  <content:encoded><![CDATA[
    <p><a href="https://www.cdc.gov/cholesterol/facts.htm">Heart disease and stroke</a> are two of the leading causes of death <a href="https://www.who.int/news-room/fact-sheets/detail/the-top-10-causes-of-death" rel="noopener noreferrer" target="_blank">globally</a> — and high levels of blood cholesterol increases the chances of both of them. While significant progress has been made in developing a slate of medicines that can maintain normal levels and reduce the associated risks, we’re still a long way from understanding all the ways cholesterol acts and affects humans. Now, a <a href="https://www.pnas.org/content/118/18/e2025167118?utm_source=TrendMD&amp;utm_medium=cpc&amp;utm_campaign=Proc_Natl_Acad_Sci_U_S_A_TrendMD_0">new study</a> published in the journal <em>Proceedings of the National Academy of Sciences</em> suggests that the ultimate solution to managing this disease might come from songbirds.</p>
<p><a href="https://www.ncbi.nlm.nih.gov/books/NBK470561/">Cholesterol</a> is a fatty substance that our body produces and acquires through food. Despite its negative image, this molecule is an <a href="https://www.hsph.harvard.edu/nutritionsource/what-should-you-eat/fats-and-cholesterol/cholesterol/">integral part of most animal bodies</a>. It is an essential component of the membranous packaging of our cells. Cholesterol is also needed to synthesize various vitamins and hormones crucial for the smooth functioning of our body and for the bile necessary for digesting fats. The <a href="https://www.news-medical.net/health/LDL-Cholesterol-and-Heart-Disease.aspx">problem</a> arises when too much of it starts floating around in the blood, clumping together to form plaque on vessel walls and blocking the flow of blood to organs.</p>
<p>Just like oil and water don’t mix, cholesterol also remains insoluble in blood due to its waxy, lipid-like properties. Most vertebrate animals have a system wherein <a href="https://www.ncbi.nlm.nih.gov/books/NBK305896/?report=reader">cholesterol is packaged with lipids and proteins</a> called "apolipoproteins" to form small ‘lipoprotein’ droplets that can be easily moved around in blood. Depending on the amount of lipid and the type of protein, these droplets can be ‘low density lipoproteins’ (LDL) or ‘high density lipoproteins’ (HDL). LDL carries cholesterol to the cells which need it, where it attaches with a protein on the cell surface called LDL-receptor (LDLR) and gets engulfed by the cell. Inside, the cholesterol is taken out of the packaging and LDLR is returned to the cell surface. On the other hand, HDL picks up excess cholesterol from all around and takes it to the liver to be excreted out of the body.&nbsp;</p>
<p>Sometimes, cells do not gulp LDL very efficiently. This could either be because they already have enough of it for cellular function, so they stop decorating their surface with LDLRs. This can lead to high levels in the blood, causing<strong> </strong>a<strong> </strong><a href="https://www.ncbi.nlm.nih.gov/books/NBK343489/">build-up of plaque</a> on artery walls. If not checked in time, the plaque can grow and plug up the artery. It’s like a really slow pile up of cars on the highway.</p>
<p>Genetic causes like a mutation in the LDLR gene can also cause the transport and uptake of these lipoproteins to malfunction, resulting in a genetic disorder called "<a href="https://www.cdc.gov/genomics/disease/fh/FH.htm">familial hypercholesterolemia.</a>" Approximately 1 in 250 people suffer from this condition, in which levels of LDL cholesterol in the blood can shoot up to very high values and lead to heart attacks at young ages. Until recently, scientists believed this was true for all vertebrate animals. In a rather serendipitous turn of events, a group of researchers from Brazil and the U.S.<strong> </strong><a href="https://www.pnas.org/content/118/18/e2025167118?utm_source=TrendMD&amp;utm_medium=cpc&amp;utm_campaign=Proc_Natl_Acad_Sci_U_S_A_TrendMD_0">discovered</a> an exception that left them astonished. They found that zebra finches, as well as other songbirds, lacked three major regions of the LDLR gene, which possibly made the receptor non-functional, yet did not develop high levels of LDL cholesterol or have any heart related issues.</p>
<figure class="center large"><img alt="A diagram showing cholesterol packaged into globules, surrounded by proteins and other molecules to form &#39;lipoprotein&#39; droplets" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/328fb42d-2f23-4cab-ba0a-d0c96056d7f4/Chylomicron.svg"/><figcaption><span class="caption"><p>Cholesterol is packaged into globules, surrounded by proteins and other molecules to form 'lipoprotein' droplets</p></span> <span class="credit"><p>Via Wikimedia</p></span></figcaption></figure>
<p>This is not something the team could have hypothesized out of the blue. The story begins somewhere else entirely. Many animal experiments involve introducing foreign genes into embryos to see the effect on things like animal<strong> </strong>growth, development, or behavior. This is regularly done using <a href="https://link.springer.com/article/10.1007/s00216-010-3821-6#Sec3">viruses engineered with the gene one wants to insert</a>. Engineered viruses decorated with a protein called Vesicular Stomatitis Virus G-protein (VSV-G) are a common tool used to manipulate avian embryos. Zebra finch eggs are notoriously resistant to such virus-aided gene expression. The authors were interested in finding out why. “I’ve had to inject probably 6000 eggs, if not more, [in the course of my research]," said Tarciso Velho, a neurobiologist at Federal University of Rio Grande do Norte in Brazil and the lead author of the study. "I've been trying for several years to make transgenic zebra finches, but it has been difficult. We never quite understood why.”</p>
<p>In 2014, <a href="https://ashpublications.org/blood/article/123/9/1422/32909/Mystery-solved-VSV-G-LVs-do-not-allow-efficient">a study</a> described how the VSV-G protein attaches to LDLRs and enters the cells. All cells which did not have any low density lipoprotein receptors showed resistance to the entry of the virus. This was the perfect starting point for understanding the poor infection rates in zebra finch embryos. The authors combed the finch genome to see if the LDLR gene was present. They found it, but saw that it was missing big chunks important for placing the receptor on the surface of the cell an interaction with G-protein. Essentially, they’d hit the jackpot in their quest. To make sure that this divergent receptor was the reason for the poor infection rates, they introduced the full human low-density lipoprotein receptor, or LDLR, into the finch eggs and then tried introducing the virus with the G protein. These engineered eggs showed a remarkable improvement in expression of the virus-aided genes, proving that the variant LDLR was responsible for the resistance.</p>
<p>But what perplexed the authors was how these birds remained alive and healthy without receptors to clear low-density cholesterol from their blood. They examined the lipoprotein levels of the birds and found that they had no low-density lipoproteins at all. All of their cholesterol was bound to high-density lipoproteins.</p>
<p>No LDLR, no LDL, no plaque build-up, no problem, right? Not quite. Zebra finch cells have the same need for cholesterol as other animals, or at least that’s the assumption for now. What transports it for them? “We still have no idea," Tarciso told me. "This is something we're super curious about. The cholesterol must be (transported) to the peripheral tissue somehow via HDL.” So, then what is this variant LDL receptor even doing? “We don't quite know if this receptor is capable of actually taking up cholesterol or not. This is something that we're pursuing, by putting the receptor into a cell and seeing how it behaves and what it's capable of.”</p>
<figure class="right medium"><img alt="A male zebra finch at the Dundee Wildlife Park, Murray Bridge, South Australia" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/92caa84d-919b-4026-972d-5dc87424f4d5/adult_male_zebra_finch.jpeg"/><figcaption><span class="caption"><p>A male zebra finch at the Dundee Wildlife Park</p></span> <span class="credit"><p>Via <a href="https://en.wikipedia.org/wiki/Zebra_finch#/media/File:Taeniopygia_guttata_-_front_view_-_dundee_wildlife_park.jpg" target="_blank">Wikimedia</a></p></span></figcaption></figure>
<p>These surprising findings tell us that even the most conserved and canonical biological processes can be altered, given the right mix of evolutionary pressures. It’s quite possible that songbirds or their common ancestors lost these receptors as a way to develop resistance against VSV infections, and in doing so, developed a unique system of cholesterol transport. This opens up a host of new avenues to pursue in the attempts to treat the genetic causes of high cholesterol in humans. “Now we know there are different ways to transport cholesterol," Tarciso said. "If we could precisely identify the mechanism and a common receptor that is performing this role, [we] could direct cholesterol transport to that, instead of LDLR.” Though controversial, using genetic approaches such as CRISPR to re-route the movement of cholesterol in patients lacking the necessary receptor could make medication for this condition obsolete.</p>
<p>There’s a ton of work to be done before we fully understand the mysteries of songbird cholesterol. But there’s also much to look forward to during the journey. Unexpected changes in direction, like this one, are the basis on which many serendipitous discoveries stand. As Tarciso puts it, “the unexpected things, how science takes you on turns that you're completely unprepared for,” those are what push you to ask questions like, ‘What can I learn about my body from studying this tiny bird?’</p>
    


<p><em><a href="https://massivesci.com/people/sahana-sitaraman/">Sahana Sitaraman</a> studies 

<p class="mb0">

<span class="scientist__field">Neuroscience</span>

and <span class="scientist__field">Behavior</span>

</p>

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<p class="mb0 o7">

<span class="scientist__institution">National Centre for Biological Sciences, India</span>

</p>

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<guid isPermaLink="true">https://massivesci.com/articles/psychosis-dementia-parkinsons-antipsychotics/</guid>
<link>https://massivesci.com/articles/psychosis-dementia-parkinsons-antipsychotics/</link>
<pubDate>Tue, 16 Nov 2021 13:09:33 EST</pubDate>
<title>A new drug reduces risk of psychosis relapse in patients with dementia</title>
<description>Pimavanserin has not received approval from the FDA, but study results are encouraging</description>

<media:content url="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/8ec79ec6-73a7-420e-a4fb-958545498f1c/vlad-sargu-ItphH2lGzuI-unsplash.jpg?auto=compress%2Cformat&amp;crop=faces&amp;fit=crop&amp;fm=jpg&amp;h=600&amp;q=75&amp;w=900" type="image/jpeg">
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  <dc:creator><![CDATA[Soren Emerson]]></dc:creator>
  <atom:author>
    <atom:name>Soren Emerson</atom:name>
    <atom:uri>https://massivesci.com/people/soren-emerson/</atom:uri>
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    <p><a href="https://www.ncbi.nlm.nih.gov/books/NBK557444/" rel="noopener noreferrer" target="_blank">Dementia</a> is a constellation of progressive cognitive problems, such as memory loss and disorientation, which occurs in Alzheimer’s disease, Parkinson’s disease, and other diseases that reduce brain function.</p>
<p>But dementia affects more than cognition.</p>
<p>Hallucinations occur in up to 50% of the <a href="https://www.who.int/news-room/fact-sheets/detail/dementia" rel="noopener noreferrer" target="_blank">50 million</a> cases of dementia worldwide, and delusions occur in up to 75% of cases, together collectively referred to as "dementia-related psychosis." Although not as well known as the hallmark cognitive decline, dementia-related psychosis <a href="https://www.aafp.org/afp/2006/0215/p647.html">takes a heavy toll</a> on people who experience psychosis symptoms and those who care for them.</p>
<p>There are no approved medications for dementia-related psychosis. <a href="https://pubmed.ncbi.nlm.nih.gov/29412841/">Off-label use</a> of antipsychotic medications, developed to treat the psychosis symptoms associated with schizophrenia, is common <a href="https://pubmed.ncbi.nlm.nih.gov/30457077/">in clinical practice</a>. But, the use of traditional antipsychotics for dementia-related psychosis &nbsp;is problematic because these drugs are <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4994396/">often ineffective</a> and come with a litany of dangerous <a href="https://pubmed.ncbi.nlm.nih.gov/20858909/">side-effects</a>, including excessive sedation, cardiovascular problems, and increased cognitive decline. In fact, the FDA issued a <a href="http://psychrights.org/drugs/FDAantipsychotics4elderlywarning.htm">black-box warning</a> against treating dementia-related psychosis with some traditional antipsychotic medications due to safety concerns. With limited treatment options for dementia-related psychosis and the number of cases of dementia increasing by <a href="https://www.who.int/news-room/fact-sheets/detail/dementia">10 million per year</a>, developing safe and effective medications for dementia-related psychosis is a major clinical need.</p>
<p>Now, as the result of <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa2034634" rel="noopener noreferrer" target="_blank">work</a> conducted by researchers at the University of Exeter and Acadia Pharmaceuticals, scientists may have identified a drug that can prevent dementia-related psychosis for a long period of time with few side-effects. The drug, called pimavanserin, affects the brain differently than the antipsychotics developed for schizophrenia by specifically and strongly <a href="https://www.ncbi.nlm.nih.gov/books/NBK557712/" rel="noopener noreferrer" target="_blank">blocking</a> a type of serotonin receptor in the brain called 5-HT2A.</p>
<div class="oembed"><div class="iframely-embed"><div class="iframely-responsive" style="height: 140px; padding-bottom: 0;"><a href="https://massivesci.com/notes/dementia-caregiving-millenials-employee-assistance/" data-iframely-url="https://cdn.iframe.ly/api/iframe?url=https%3A%2F%2Fmassivesci.com%2Fnotes%2Fdementia-caregiving-millenials-employee-assistance%2F&key=a91f6c63822d2172297a7435cae7a9eb"></a></div></div><script async src="https://cdn.iframe.ly/embed.js" charset="utf-8"></script></div>
<p>The <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7048860/">likely explanation</a> for why traditional antipsychotic medications don't work for dementia-related psychosis is that they were never developed to treat episodes of psychosis in elderly people with dementia; they were developed for <em>young people with schizophrenia</em>. Dementia and schizophrenia are different diseases with different neurological causes, so there is no guarantee that their symptoms will respond to the same medications. In addition, levels of neurotransmitters in the brain <a href="https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC3010414/" rel="noopener noreferrer" target="_blank">change</a> as humans age, which could influence the effects of psychoactive drugs.</p>
<p>In <a href="https://pubmed.ncbi.nlm.nih.gov/22750845/" rel="noopener noreferrer" target="_blank">preclinical studies,</a> pimavanserin reduced psychotic behavior in rodents and <a href="https://linkinghub.elsevier.com/retrieve/pii/S1474-4422(18)30039-5">clinical testing</a> sponsored by Acadia Pharmaceuticals showed that pimavanserin improved psychosis symptoms in people with <a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(13)62106-6/fulltext" rel="noopener noreferrer" target="_blank">Parkinson's disease </a>and <a href="https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(18)30039-5/fulltext" rel="noopener noreferrer" target="_blank">Alzheimer's disease</a>. In 2016, pimvanserin <a href="https://www.fda.gov/news-events/press-announcements/fda-approves-first-drug-treat-hallucinations-and-delusions-associated-parkinsons-disease" rel="noopener noreferrer" target="_blank">became</a> the first drug to receive FDA approval as a treatment for Parkinson's-related psychosis and was taken to market by Acadia Pharmaceuticals under the brand name NUPLAZID.</p>
<p>With positive clinical data for psychosis symptoms in Alzheimer's disease and FDA approval for psychosis symptom's in Parkinson's disease, Acadia Pharmaceuticals <a href="https://www.businesswire.com/news/home/20171004006297/en/ACADIA-Pharmaceuticals-Initiates-Phase-III-Study-Pimavanserin" rel="noopener noreferrer" target="_blank">initiated</a> a <a href="https://clinicaltrials.gov/ct2/show/NCT03325556" rel="noopener noreferrer" target="_blank">clinical trial</a> of pimavanserin for additional subtypes of dementia-related psychosis in 2017. A total of 392 people with Alzheimer's disease, Parkinson's disease, Lewy body, frontotemporal, or vascular dementia participated in the study and the results were published in the <a href="https://www.nejm.org/doi/10.1056/NEJMoa2034634"><em>New England Journal of Medicine</em></a><em> </em>in July of 2021.</p>
<p>For the first 12-weeks of the study, all the participants received pimavanserin open-label. After week 12, participants who met a certain threshold of symptomatic improvement were randomly assigned to receive either pimavanserin or a placebo for 26 weeks to determine if the drug could prevent relapse of psychosis symptoms. The drug was found to be so effective at preventing relapse of psychosis symptoms, however, that the trial was stopped before its intended endpoint at 26 weeks because it would have been unethical to continue giving the control group the placebo. When the trial was stopped, relapse occurred in 28.3% of the placebo group compared to just 12.6% in the pimavanserin group, with minimal side-effects.</p>
<div class="oembed"><div class="iframely-embed"><div class="iframely-responsive" style="height: 140px; padding-bottom: 0;"><a href="https://massivesci.com/articles/covid-19-alzheimers-parkinsons-coronavirus/" data-iframely-url="https://cdn.iframe.ly/api/iframe?url=https%3A%2F%2Fmassivesci.com%2Farticles%2Fcovid-19-alzheimers-parkinsons-coronavirus%2F&key=a91f6c63822d2172297a7435cae7a9eb"></a></div></div><script async src="https://cdn.iframe.ly/embed.js" charset="utf-8"></script></div>
<p>The results of the study are encouraging, but it had several limitations due to the participants it included. One of the more glaring issues is that over 98% of study participants included in the trial after week 12 were white. This, despite “white” individuals being at a lower risk of dementia compared to “African American” and “Hispanic” individuals according to the <a href="https://www.cdc.gov/media/releases/2018/p0920-alzheimers-burden-double-2060.html">Centers for Disease Control and Prevention</a>. In addition, 15% of the participants had dementia-related psychosis due to Parkinson’s disease, a condition for which pimavanserin <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7048860/">has already</a> been approved for as a treatment. Therefore, as the researchers admit, the data generated by these participants “may have skewed the results in favor of pimavanserin.”</p>
<p>But the study's most significant limitation, at least as far as FDA approval is concerned, is that the trial had insufficient statistical power to detect whether pimavanserin improved psychosis symptoms in individual subtypes of dementia. In April of 2021, the FDA <a href="https://ir.acadia-pharm.com/news-releases/news-release-details/acadia-pharmaceuticals-receives-complete-response-letter-us-fda" rel="noopener noreferrer" target="_blank">notified</a> Acadia Pharmaceuticals that after reviewing the existing clinical trial data the agency would not approve pimavanserin as a treatment for dementia-related psychosis, citing an insufficient number of participants with less-common dementia subtypes and a lack of statistical significance in some subgroups of dementia.</p>
<p>For the team at Acadia Pharmaceuticals, the FDA's decision came as a surprise. Generating and analyzing clinical data from study populations that include a mix of dementias without necessarily separating them has become an <a href="https://www.nejm.org/doi/full/10.1056/NEJMe2109010" rel="noopener noreferrer" target="_blank">accepted practice</a> when treating the psychosis symptoms associated with dementia.</p>
<p>Although next steps are not certain, Acadia CEO Stephen Davis <a href="https://www.fool.com/earnings/call-transcripts/2021/08/06/acadia-pharmaceuticals-inc-acad-q2-2021-earnings-c/" rel="noopener noreferrer" target="_blank">outlined</a> three possible outcomes. First, as is the company's position, they could proceed by performing additional statistical analyses of the existing data without additional clinical trials and seek FDA approval for pimavanserin as a broad-spectrum medication for multiple dementia subtypes. Second, rather than seeking broad-spectrum approval, the company could seek approval for pimavanserin as a medication for a smaller number of dementia subtypes such as Alzheimer's dementia or dementia with Lewy bodies, the subtypes for which the company believes they have the strongest data. Under this scenario, the company would not conduct additional clinical trials. Third, as is the FDA's position, the company could conduct additional clinical trials of pimavanesin in each dementia subtype.</p>
<p>The company <a href="https://ir.acadia-pharm.com/news-releases/news-release-details/acadia-pharmaceuticals-reports-third-quarter-2021-financial" rel="noopener noreferrer" target="_blank">has scheduled</a> a meeting with the FDA to discuss the path forward for pimavanserin's development and expects to report on the outcome of this meeting before year end.</p>
<p>Despite the set backs regarding FDA approval, the trial results are an important step forward for clinical neuroscience and dementia research. Although the clinical trial results may be insufficient for FDA approval at present, they suggest that a badly needed safe and effective medication for dementia-related psychosis could come in the next few years.</p>
    


<p><em><a href="https://massivesci.com/people/soren-emerson/">Soren Emerson</a> studies 

<p class="mb0">

<span class="scientist__field">Neuroscience</span>

</p>

 at 

<p class="mb0 o7">

<span class="scientist__institution">Vanderbilt University</span>

</p>

.</p>



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<guid isPermaLink="true">https://massivesci.com/notes/auditory-processing-speech-background-noise/</guid>
<link rel="alternate" type="text/html">https://massivesci.com/notes/auditory-processing-speech-background-noise/</link>
<pubDate>Tue, 16 Nov 2021 08:10:00 EST</pubDate>
<title>Research demonstrates speech-in-noise training helps children with auditory processing disorder</title>
<description>Children with APD have difficulty perceiving speech when there is background noise and may have trouble on cognitive tests</description>


<media:content url="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/20e2b043-a068-4dee-8c53-3dcb175c7497/mi-pham-0DPyb8t_KfI-unsplash.jpg?auto=compress%2Cformat&amp;crop=faces&amp;fit=crop&amp;fm=jpg&amp;h=600&amp;q=75&amp;w=900" type="image/jpeg">
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  <media:description>a group of kids playing outside, a happy boy is in the foreground</media:description>
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  <dc:creator><![CDATA[Stephanie Santo]]></dc:creator>
  <atom:author>
    <atom:name>Stephanie Santo</atom:name>
    <atom:uri>https://massivesci.com/people/stephanie-santo/</atom:uri>
  </atom:author>


  
  <content:encoded><![CDATA[
    <p>Central auditory processing disorder (APD), a hearing disability, can impact cognitive functioning and academic performance in those who experience it. It is typically diagnosed in childhood. Children with APD have difficulty perceiving speech when there is background noise, called speech-in-noise perception, and may have trouble on cognitive tests.</p>
<p>Previous studies on the link between cognitive performance, background noise, and auditory processing in children have <a href="https://www.frontiersin.org/articles/10.3389/fneur.2017.00732/full" target="_blank">included participants</a> without confirmed APD diagnoses. Therefore, researchers in a <a href="https://www.sciencedirect.com/science/article/pii/S0165587621001282?via=ihub" target="_blank">recent study</a> examining the potential utility of a technique called speech-in-noise training selected participants with confirmed diagnoses to understand the relationship between APD, speech-in-noise perception, and working memory.</p>
<p>The researchers administered one cognitive and five auditory processing tests to the participants. They gave the children lists of words and asked them to repeat the words back. In one of the tests, the words were audible only in one ear and the participants were asked to repeat the words regardless of which ear they heard it from.&nbsp;</p>
<div class="oembed"><div class="iframely-embed"><div class="iframely-responsive" style="height: 140px; padding-bottom: 0;"><a href="https://massivesci.com/notes/hearing-loss-fatigue-sounds/" data-iframely-url="https://cdn.iframe.ly/api/iframe?url=https%3A%2F%2Fmassivesci.com%2Fnotes%2Fhearing-loss-fatigue-sounds%2F&key=a91f6c63822d2172297a7435cae7a9eb"></a></div></div><script async src="https://cdn.iframe.ly/embed.js" charset="utf-8"></script></div>
<p>Participants in the experimental group were given <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3450924/" target="_blank">speech-in-noise training</a> within a week of the evaluation. <a href="https://canadianaudiologist.ca/three-aspects-of-speech-in-noise-training/" target="_blank">During this type of training</a>, participants are asked to listen for words or speech presented with background noise, which gets progressively louder or more difficult to navigate as the training progresses. The goal is to help people pick out important words while filtering out background sounds.</p>
<p>The study found a link between how participants did on auditory tests and their performance on cognitive tests. Speech-in-noise training generally improved the participants' results on both tests. This study confirms that speech-in-noise training may be a helpful intervention for children with APD diagnoses.</p>
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<guid isPermaLink="true">https://massivesci.com/articles/fasting-diet-blood-pressure-gut-microbiome/</guid>
<link>https://massivesci.com/articles/fasting-diet-blood-pressure-gut-microbiome/</link>
<pubDate>Mon, 15 Nov 2021 13:45:17 EST</pubDate>
<title>There&#39;s a connection between fasting, gut microbiota and blood pressure</title>
<description>Fasting reduces high blood pressure in rats by changing the gut microbiota composition. But fasting still shouldn&#39;t be a go-to yet</description>

<media:content url="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/ea75e4f4-6a67-41cc-862d-9bea00973243/bonnie-kittle-MUcxe_wDurE-unsplash.jpg?auto=compress%2Cformat&amp;crop=faces&amp;fit=crop&amp;fm=jpg&amp;h=600&amp;q=75&amp;w=900" type="image/jpeg">
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  <media:description>Two guinea pigs eating carrot pieces</media:description>
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  <dc:creator><![CDATA[Mihaela Bozukova]]></dc:creator>
  <atom:author>
    <atom:name>Mihaela Bozukova</atom:name>
    <atom:uri>https://massivesci.com/people/mihaela-bozukova/</atom:uri>
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  <content:encoded><![CDATA[
    <p>Cardiovascular diseases are the leading cause of premature death worldwide, causing over <a href="https://www.who.int/health-topics/cardiovascular-diseases/#tab=tab_1">17 million deaths annually</a>. One <a href="https://www.nhs.uk/conditions/high-blood-pressure-hypertension/">major risk factor</a> for these diseases is high blood pressure (hypertension). With hypertension <a href="https://www.nature.com/articles/s41581-019-0244-2">on the rise globally</a>, there is an urgent need to find treatments and prevention strategies for this condition.</p>
<p>Our lifestyle, and especially our diet, can play an important role in managing hypertension. But how do changes to diet actually aid in regulating blood pressure? A research team led by David J. Durgan at Baylor College of Medicine, in Houston, <a href="https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.120.318155?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub%20%200pubmed">recently showed</a> that alternate-day fasting can reduce high blood pressure in an animal model. These beneficial effects of fasting on blood pressure were mediated through changes in the gut microbiota, the trillions of microorganisms that live inside the digestive tract.</p>
<p>This connection between gut microbiota and blood pressure has gained increasing attention in recent years. Individuals with high blood pressure were <a href="https://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.118.12109?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub%20%200pubmed">observed to have gut dysbiosis</a>, a state characterized by a reduced microbial diversity, loss of beneficial microorganisms, and expansion of potentially harmful ones.</p>
<p>“We know that host health correlates with microbial richness, diversity and certain types of microbes that should be there," Dario R. Valenzano, a professor at the Leibniz Institute on Aging in Jena, Germany, told me. “But we still understand very little about it.” Especially when it comes to causal relationships: observing changes in gut microbiota composition does not prove that these changes are causing the disease. For moving from association to causation, animal models are particularly useful, because they allow for mechanistic investigations and controlled interventions.</p>
<div class="oembed"><div class="iframely-embed"><div class="iframely-responsive" style="height: 140px; padding-bottom: 0;"><a href="https://massivesci.com/notes/mice-diet-high-fat-food-neurons/" data-iframely-url="https://cdn.iframe.ly/api/iframe?url=https%3A%2F%2Fmassivesci.com%2Fnotes%2Fmice-diet-high-fat-food-neurons%2F&key=a91f6c63822d2172297a7435cae7a9eb"></a></div></div><script async src="https://cdn.iframe.ly/embed.js" charset="utf-8"></script></div>
<p>One of the most widely used animal models of hypertension are spontaneously hypertensive stroke-prone (SHRSP) rats, a line of rats that develop hypertension at six weeks of age, much earlier than control animals. Like hypertensive humans, <a href="https://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.115.05315?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub%20%200pubmed">these rats show gut dysbiosis</a>. To investigate whether gut dysbiosis contributes to the development of hypertension, the researchers <a href="https://journals.physiology.org/doi/full/10.1152/physiolgenomics.00081.2016?rfr_dat=cr_pub++0pubmed&amp;url_ver=Z39.88-2003&amp;rfr_id=ori%3Arid%3Acrossref.org">transferred gut microbiota</a> from SHRSP rats to rats with normal blood pressure. The previously healthy rats to develop high blood pressure, pointing towards a causal relationship between gut dysbiosis and hypertension.</p>
<p>Building on these findings, the researchers went one step further and asked whether changing the gut microbiota composition could go the other way and <em>reduce</em> blood pressure in the SHRSP model. For changing the gut microbiota composition, the researchers focused on the animal’s diet. “Feeding leads to massive fluctuations in the overall composition of the microbiome," Valenzano explained. Could changing the feeding pattern through fasting reduce the blood pressure of the SHRSP rats? To test this, the researchers split the SHRSP rats into two groups: one group had unlimited access to food, while the other group was fed only every other day. After nine weeks, the rats that had unlimited access to food had developed high blood pressure, as is expected for the SHRSP model. In contrast, rats that were fed only every other day did not develop high blood pressure.</p>
<p>How to prove causality and show that the fasting lowered blood pressure through changes to the gut microbiota? The researchers resorted to a <a href="https://www.frontiersin.org/articles/10.3389/fphys.2018.01534/full">common technique in the field</a>: they transplanted gut microbiota from SHRSP animals that had fasted into rats that were germ-free. These germ-free rats are bred in isolators without exposure to microorganisms and have no microbiota of their own. Any effect observed after the transplant will be caused by the transferred microbiota.</p>
<div class="oembed"><div class="iframely-embed"><div class="iframely-responsive" style="height: 140px; padding-bottom: 0;"><a href="https://massivesci.com/articles/fasting-silicon-valley-weight-loss-drink/" data-iframely-url="https://cdn.iframe.ly/api/iframe?url=https%3A%2F%2Fmassivesci.com%2Farticles%2Ffasting-silicon-valley-weight-loss-drink%2F&key=a91f6c63822d2172297a7435cae7a9eb"></a></div></div><script async src="https://cdn.iframe.ly/embed.js" charset="utf-8"></script></div>
<p>The researchers observed that germ-free rats that had received microbiota from the fasting SHRSP rats had lower blood pressure than germ-free rats that had received microbiota from normal-fed SHRSP rats. With this, the researchers discovered that modulating the gut microbiota through fasting relieves high blood pressure in the SHRSP animal model. Rikeish R. Muralitharan, a graduate student at Monash University in Australia investigating the association between gut microbiota and hypertension, compliments the approach taken by the research team: “That's one important thing going forward: mechanistically linking the gut microbiome to the effect. The researchers definitely moved away from just association.”</p>
<p>While these findings improve our understanding of the connection between diet, gut microbiota and blood pressure, it is a long road before we can start prescribing fasting to hypertensive patients: “What I would like to see before I can say anything about potential applications in humans is whether transplants of gut contents improve blood pressure in non-hypertension animal models,” Valenzano cautions. Since age is a <a href="https://www.who.int/news-room/fact-sheets/detail/hypertension">risk factor</a> for hypertension, both Valenzano and Muralitharan would like to see whether the research findings also apply to naturally aged laboratory animals. “It would be very important to know what the impact of fasting on age-related blood pressure changes is. Otherwise, we may be looking at only potential applications for individuals that have hypertension for very similar causes to these rats,” Valenzano emphasizes. Thinking ahead about potential human interventions, further research in animal models as well as clinical trials are needed.</p>
<p>When it comes to clinical trials and translating the findings to humans, one difficulty is controlling the diet regimen itself: “You can give rats every other day feeding. But in humans, it's quite hard. You can't make someone eat the same thing every single day or make them fast and then see what happens,” Muralitharan remarks. Compliance with dietary guidelines is a major hurdle in human intervention studies.</p>
<p>Another inherent difficulty is demonstrating causality between diet, gut microbiota and blood pressure in humans. “A decrease in body weight also reduces blood pressure. So sometimes it's very hard to really nitpick whether the effect is really because of how the diet actually reduces blood pressure," Muralitharan explains. The effects of fasting on blood pressure might not be solely mediated through changes to the gut microbiota. While the causal relationships might be more complex in humans, gut microbiota certainly play a role.</p>
    


<p><em><a href="https://massivesci.com/people/mihaela-bozukova/">Mihaela Bozukova</a> studies 

<p class="mb0">

<span class="scientist__field">Bioinformatics</span>

and <span class="scientist__field">Molecular Biology</span>

</p>

 at 

<p class="mb0 o7">

<span class="scientist__institution">Max Planck Institute for Biology of Ageing</span>

</p>

.</p>



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<guid isPermaLink="true">https://massivesci.com/articles/cytomegalovirus-cmv-vaccine-childhood-development/</guid>
<link>https://massivesci.com/articles/cytomegalovirus-cmv-vaccine-childhood-development/</link>
<pubDate>Sun, 14 Nov 2021 22:36:49 EST</pubDate>
<title>After decades of work, an effective cytomegalovirus vaccine is on the horizon</title>
<description>Monoclonal antibodies reveal key vaccine structure</description>

<media:content url="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/dc2abb85-a40f-4fea-8a22-3d26b8d2ca47/Cytomegalovirus_infection.jpeg?auto=compress%2Cformat&amp;crop=faces&amp;fit=crop&amp;fm=jpg&amp;h=600&amp;q=75&amp;w=900" type="image/jpeg">
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  <media:description>Basophils that have been infected with cytomegalovirus (CMV)</media:description>
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  <dc:creator><![CDATA[Georgina To&#39;a Salazar]]></dc:creator>
  <atom:author>
    <atom:name>Georgina To&#39;a Salazar</atom:name>
    <atom:uri>https://massivesci.com/people/georgina-toa-salazar/</atom:uri>
  </atom:author>


  
  <content:encoded><![CDATA[
    <p>Cytomegalovirus infection before birth is a leading cause of sickness affecting children's development.</p>
<p>There are no approved vaccines to prevent this infection, which happens when a pregnant person is exposed to cytomegalovirus (CMV) and the virus passes through the placenta to the fetus. To better evaluate vaccine candidates for clinical trials, we need an "immune correlate of protection," a sign that helps us predict whether a vaccine will protect against CMV infection and disease. Such a sign was discovered through a <a href="https://doi.org/10.1016/j.virol.2020.07.009" rel="noopener noreferrer" target="_blank">study</a> conducted under the leadership of Sallie R. Permar, a physician-scientist at the Duke University School of Medicine. <br>
<br>
CMV infection in healthy children and adults is common and usually asymptomatic or has mild, flu or cold-like symptoms. CMV awareness is fairly poor. In 2011, the US Congress even<strong> </strong>passed a resolution naming June National CMV Awareness Month. This recognition aims to increase awareness of CMV exposure risks. Young children are a common source of CMV. So, there may be a greater risk of congenital CMV infection for people who have frequent contact with young children. This awareness helps reduce the spread of CMV and makes early treatment possible for those severely affected.</p>
<p>The primary objective of this study was to define the immune responses elicited by a CMV vaccine tested in two clinical trials, <a href="https://clinicaltrials.gov/ct2/show/NCT00125502" rel="noopener noreferrer" target="_blank">one</a> with postpartum people and <a href="https://clinicaltrials.gov/ct2/show/NCT00133497" rel="noopener noreferrer" target="_blank">another</a> with healthy adolescents. In this vaccine, a subunit of CMV, called glycoprotein B (gB), is combined with a novel adjuvant, MF59, a proprietary oil-in-water emulsion. Vaccinees were given either the gB/MF59 vaccine or placebo, then followed to assess any side effects experienced. Infants born to participants in one study were checked for CMV infection. Researchers sought to identify an association between those immune responses and the risk of CMV infection that could damage a fetal nervous system if the infection occurred during pregnancy. One aspect of the study that makes it unique is that it investigates the response of the most efficacious CMV vaccine tested at that time.</p>
<p>One hypothesis of this research was that antibodies in the blood of vaccinees should be correlated with vaccine efficacy. One challenge was that many antibodies generated in response to the vaccine being tested don't inhibit viral infection of cells, which is usually expected of antibodies that protect against a virus. Evidence has suggested non-neutralizing antibodies contribute to protection in other ways, but studies presenting that evidence lacked real statistical power. A key result of the study was the discovery that an antibody binding CMV gB on the surface of infected cells, but not free gB that's not associated with a cell, is associated with protection against CMV infection. This suggests that antibody binding to cell-associated gB <em>is</em> an immune correlate of vaccine efficacy.</p>
<figure class="center large"><img alt="Pneumocytes (a type of cell in the lungs) infected with CMV. The central cell displays the dramatically enlarged nuclei characteristic of CMV" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/4730929c-8c45-41a3-9990-ee5afcf39794/lossy-page1-1803px-Cytomegalovirus_01.tif.jpg"/><figcaption><span class="caption"><p>Pneumocytes (a type of cell in the lungs) infected with CMV. The central cell displays the dramatically enlarged nuclei characteristic of CMV</p></span> <span class="credit"><p>Via <a href="https://commons.wikimedia.org/wiki/File:Cytomegalovirus_01.tif" target="_blank">Wikimedia</a></p></span></figcaption></figure>
<p>Results of the study are expected to advance the development of a CMV vaccine that could protect developing infants. A CMV vaccine would also spare transplant recipients the need for expensive, limited antiviral treatments, improving patient survival and procedure success rates.</p>
<p>An obvious next step would be further studies to investigate immune responses and immune correlates of other CMV vaccine antigens. Another step would be to investigate correlates of protection against secondary infection and re-activation since this study focused on primary infection. Studies to confirm that the antibody response described in this paper could serve as an endpoint for vaccine development and evaluation is a third obvious next step.</p>
<p>CMV infection is almost universal and generally mild. But it can have devastating effects when infection occurs during pregnancy. CMV vaccines are hard to develop in part because of participants must be followed for years to determine vaccine efficacy. Studies defining immune correlates of protection, such as this one, facilitate the evaluation of vaccine efficacy and thus accelerate vaccine development.</p>
<p>To scientists, this study is important because it includes results of phase 2 clinical trials of a CMV vaccine; work at the forefront of a research effort that has been a focus of researchers across the world for decades. Also, the study results are expected to have a positive impact because they support understanding of human interaction with CMV. The CMV DNA genome of 236 kilobases (kb), encodes dozens of proteins, making it one of the largest and most complex viruses known to infect humans. By contrast, the sizes of the RNA genomes of <a href="https://www.nature.com/articles/nature04239" rel="noopener noreferrer" target="_blank">influenza A</a>, <a href="https://www.nature.com/articles/s41586-020-2739-1" rel="noopener noreferrer" target="_blank">SARS-CoV-2</a>, and <a href="https://doi.org/10.1093/nar/gkv1039" rel="noopener noreferrer" target="_blank">HIV-1</a> are about 14 kb, 30 kb, and 10 kb. The size and complexity of CMV support many functions that allow CMV to sustain its lifelong, mostly-asymptomatic <a href="https://doi.org/10.3389/fcimb.2020.00130" rel="noopener noreferrer" target="_blank">infection</a> of humans. They also contribute to difficulty preventing and treating the infection in those who are vulnerable to serious effects.</p>
<p>This paper builds on previous research that shows the development of CMV vaccines can be helped by the identification of immune correlates of protection, signs in the immune response of vaccinees that show they're protected. It also builds on research describing the structure of the CMV virus and its interaction with the human immune response.</p>
    


<p><em><a href="https://massivesci.com/people/georgina-toa-salazar/">Georgina To&#39;a Salazar</a> studies 

<p class="mb0">

<span class="scientist__field">Chemical Engineering</span>

and <span class="scientist__field">Biomedical Engineering</span>

</p>

 at 

<p class="mb0 o7">

<span class="scientist__institution">University of Texas Health Science Center at Houston</span>

</p>

.</p>



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<guid isPermaLink="true">https://massivesci.com/articles/new-species-discovery-naming-recognize/</guid>
<link>https://massivesci.com/articles/new-species-discovery-naming-recognize/</link>
<pubDate>Fri, 12 Nov 2021 08:13:00 EST</pubDate>
<title>There&#39;s more than one way to discover a new species</title>
<description>Papers published this year demonstrate the different paths to recognition</description>

<media:content url="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/51665a1c-3b51-4c8f-a631-9aa60ce98956/62961B5CBCB2872228529DCF3C44A822AD837C45E7B834071799BE1B8D3A1CEB.jpg?auto=compress%2Cformat&amp;crop=faces&amp;fit=crop&amp;fm=jpg&amp;h=600&amp;q=75&amp;w=900" type="image/jpeg">
  <media:title></media:title>
  <media:description>Close-up pictures of the minute new parasite wasp, Chrysis parabrevitarsis</media:description>
</media:content>


  
  <dc:creator><![CDATA[Maria Gatta]]></dc:creator>
  <atom:author>
    <atom:name>Maria Gatta</atom:name>
    <atom:uri>https://massivesci.com/people/maria-gatta/</atom:uri>
  </atom:author>


  
  <content:encoded><![CDATA[
    <p>Every once in a while, there's news that a new species has been discovered. But how exactly do scientists find new species, previously unknown to science?</p>
<p>A standard way of finding new species is to simply go on a trip to a place suspected to have undescribed species. That's it, just go and look around.</p>
<p>This was exactly what a team of scientists did that led to the discovery of <a href="https://www.cambridge.org/core/journals/lichenologist/article/abs/four-new-micarea-species-from-the-montane-cloud-forests-of-taita-hills-kenya/14AEA1F95B1F69847B3E8FA1B7BB4B18" rel="noopener noreferrer" target="_blank">a lichen that shines when exposed to polarized light</a>. A collaboration between Finnish and Kenyan scientists collected lichens in the <a href="https://africageographic.com/stories/taita-hills-cloud-forest-fragmented-landscape/" rel="noopener noreferrer" target="_blank">Taita Hills</a> in Kenya. The Taita Hills are a biodiversity hot spot, but despite that, the authors realized that there were no records of a very common type of lichens in the area. So they decided to go and investigate what was growing there.</p>
<p>Just by looking, they found four undescribed lichen species. One of them was dotted with tiny crystals. These crystals reflect light, so under the microscope, the new species looked like it had a belt of shining lights — a microscopic Milky Way's arm. The species was aptly named<em> Micarea stellaris</em> ("stellaris" means star in Latin).</p>
<figure class="right medium"><img alt="Micarea stellaris, a newly described lichen species" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/a29f777a-962d-4c81-b355-90b78c763dc1/197541-micarea_stellaris_annina_kantelinen_skaala_1184.jpeg"/><figcaption><span class="caption"><p>Micarea stellaris, a newly described lichen species</p></span> <span class="credit"><p>Courtesy of Annina Kantelinen</p></span></figcaption></figure>
<p>Sometimes researchers don’t just suspect there is a new species hiding somewhere, they know it for sure. The <a href="https://www.mdpi.com/2076-2615/11/3/687" rel="noopener noreferrer" target="_blank">recently described <em>Luciola singapura</em></a><em> </em>is a perfect example of that. An unidentified specimen was collected 12 years ago during a nationwide survey of fireflies in Singapore. Several years later, <a href="https://twitter.com/wanfajusoh?lang=en" rel="noopener noreferrer" target="_blank">Wan F. A. Jusoh</a>, one of the authors of the study, saw that the unknown firefly collected in 2009 matched three other unknown specimens in the collection of the <a href="https://lkcnhm.nus.edu.sg/" rel="noopener noreferrer" target="_blank">Lee Kong Chian Natural History Museum in Singapore</a>.</p>
<p>So, in 2018 and 2019, scientists arranged an expedition to the area where all unknown specimens had been collected. The expedition was successful, and they were able to find this "unknown" firefly. The Singapore firefly, or as it is known in Malay, kunang-kunang Singapura, is a very small firefly (less than 5 millimeters long). It is orange to yellowish-brown and at night emits flashes of yellow light.<em> </em>This species is the first new luminous firefly described in the country since 1909.</p>
<figure class="center large"><img alt="The Singapore firefly" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/01046779-190e-4aa4-89e6-f9701fa735c4/1920_paratypewanfajusoh.jpeg"/><figcaption><span class="caption"><p>The Singapore firefly</p></span> <span class="credit"><p>Wan FA Jusoh et al <a href="https://www.mdpi.com/2076-2615/11/3/687" target="_blank">2021</a></p></span></figcaption></figure>
<p>Similarly, sometimes scientists know that there are potentially several new species under their noses yet to be properly described. This happens in what is known as "<a href="http://museum.dnalc.org/bold/crypticspecies.html" rel="noopener noreferrer" target="_blank">species complexes</a>." In a species complex, a group of organisms are so closely related and similar in appearance that it is tough to separate them into distinct species.</p>
<p>This is the case with a group of Brazilian frogs called pumpkin toadlets. In the last five years, &nbsp;15 different species have been described. <a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0244812&amp;fbclid=IwAR0mJQThZmWSnyTa7BCA4rf3zsJ09l3BCL0GMTovObT47bMtgPUznN_IanY" rel="noopener noreferrer" target="_blank">In 2021, scientists got to add a new species to the list: <em>Brachycephalus rotenbergae</em></a>. In order to make sure the species was distinct and recognizable, researchers used a variety of methods to describe the toadlet. They used physical characteristics, DNA<em> </em>data, and the song the toadlet sings to ensure it is its own species and future researchers can distinguish it from all other pumpkin toadlets. Some of its distinguishing characteristics are its bright orange color and its call, which contains short notes and a fast rhythm.</p>
<p>Sometimes, even though scientists know that a species complex exists, they might not know much more than that. Science is nothing without data. And no data equals no new species descriptions.</p>
<p>That is the case for members of the "<a href="https://www.fisheries.noaa.gov/resource/peer-reviewed-research/genetic-evidence-reveals-unique-lineage-brydes-whales-northern-gulf" rel="noopener noreferrer" target="_blank">Bryde's whale complex</a>." Scientists suspected this group of whales included different species but couldn't say for sure, due to a lack of genetic data and good research on the animals. Because of this lack of data, they took a conservative approach and considered the group of whales as a single species.</p>
<figure class="right medium"><img alt="Rice&#39;s whale coming up to the surface for a breather" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/efe0b115-10d7-4f00-b991-bc11ff660bd4/anim123736416x800x800.jpeg"/><figcaption><span class="caption"><p>Rice's whale coming up to the surface for a breather</p></span> <span class="credit"><p>NOAA/Wayne Hoggard</p></span></figcaption></figure>
<p>But, in January 2019, a 12-meter long adult male whale became stranded and died in the Everglades. A large group of scientists and citizens were able to take measurements and samples. They also preserved the skull and the skeleton, an important step for species descriptions in whales. Thanks to all this data collected, scientists were able to say that this whale is indeed distinct from other Bryde-like whales. Rice's whale, or <a href="https://onlinelibrary.wiley.com/doi/10.1111/mms.12776" rel="noopener noreferrer" target="_blank"><em>Balaenoptera ricei</em></a>, is a medium-sized baleen whale that lives year-round in the Gulf of Mexico. Rice's whale was named after <a href="https://www.dalewricelibrary.org/About" rel="noopener noreferrer" target="_blank">Dale W. Rice</a>, a renowned American scientist and whale expert. The whales are <a href="https://www.mmc.gov/priority-topics/species-of-concern/northern-gulf-of-mexico-brydes-whale/" rel="noopener noreferrer" target="_blank">critically endangered</a>, due to the population’s small size and the many human disturbances that occur in their habitat.</p>
<p>On other occasions, what prevents scientists from disentangling species complexes is not the lack of data, but rather lack of appropriate methods. Even with the advent of DNA sequencing, sometimes the genetic differences are hard to spot. If the physical characteristics of the species in question are also difficult to disentangle, scientists are out of luck until they can find appropriate methods.</p>
<figure class="right medium"><img alt="An orange pumpkin toadlet" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/3b18018e-534e-4906-9ac9-daa96cb39e19/pumpkin_toadlet.jpeg"/><figcaption><span class="caption"><p>The fluorescent and poisonous pumpkin toadlet</p></span> <span class="credit"><p>Nunes et al, 2021, PLoS One</p></span></figcaption></figure>
<p>There is a widespread cuckoo wasp that ranges<strong> </strong>from Western Europe to Mongolia. <a href="https://www.mapress.com/j/zt/article/view/zootaxa.3786.3.4" rel="noopener noreferrer" target="_blank">A DNA analysis in 2014 revealed high variability in the species’ DNA</a>, suggesting the cuckoo wasp may be made up of different species. But without easily distinguishable features in the DNA or in the wasps' physical appearances, there was no way to say definitively. Recently, <a href="https://academic.oup.com/isd/article-abstract/5/1/3/6141177" rel="noopener noreferrer" target="_blank">a group of Scandinavian scientists</a> identified hormones that insects have in their skin, called cuticular hydrocarbons, to help with species identification.</p>
<p>With their analysis in hand, scientists went back and studied a group of wasps that had the same type of hormonal profile. They were able to find small body differences in the females of that group and the rest of the wasps under the species complex of <em>Chrysis pseudobrevitarsis</em>. Without grouping of these wasps by their hormonal profiles, finding those minute differences would have been like finding a needle in a haystack. They called the new species <em>C</em>. <em>parabrevitarsis </em>(pictured at the top of the page).</p>
<p>Another way scientists sometimes find out about new species is by pure coincidence. When a scientist expert in one group of animals finds a species that doesn’t match anything else they have ever seen before, they know they may have found something very special. For example, during a survey to study deep fish ecology and the potential effects of human disturbances there, a group of researchers discovered a very large predatory fish.</p>
<figure class="center large"><img alt="A peakcock spider, with green eyes and black-and-white striped legs" src="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/18fa73dd-3350-4268-855d-e6ac483443e9/nemo1%20Photographer_%20Joseph%20Schubert%20Source_%20Museums%20Victoria.jpg"/><figcaption><span class="caption"><p>A peakcock spider, with green eyes and black-and-white striped legs</p></span> <span class="credit"><p>Joseph Schubert/Museums Victoria</p></span></figcaption></figure>
<p>Usually, <a href="https://www.britannica.com/animal/slickhead" rel="noopener noreferrer" target="_blank">slickhead fishes</a> are small, around 35 centimeters. But <a href="https://www.nature.com/articles/s41598-020-80203-6" rel="noopener noreferrer" target="_blank">the new species of slickhead has an average length of 113 cm.</a></p>
<p>Researchers analyzed the stomach contents of the novel fish and found that they were at the top of the trophic chain. Such a high position is normally found in predatory fishes like sharks; slickheads usually feed on zooplankton and are usually of a lower trophic position than other fishes in their environment. It's no wonder then why the researchers decided to name the species <em>Yokozuna</em>, after the highest sumo wrestling rank in Japan.</p>
<p>And finally: social media. With increased access to portable cameras and scientists, the public has the opportunity to potentially find something novel and unexpected. That was the case with <a href="https://evolsyst.pensoft.net/article/64922/" rel="noopener noreferrer" target="_blank"><em>Maratus nemo</em></a>. Sheryl Holliday found a peacock spider in a South Australian wetland she did not recognize. <a href="https://www.nationalgeographic.com/animals/article/how-scientists-found-nemo-australias-newest-dancing-spider" rel="noopener noreferrer" target="_blank">She posted a picture of the spider on a Facebook peacock appreciation page</a>. <a href="https://twitter.com/arachno_joe" rel="noopener noreferrer" target="_blank">Joseph Schubert</a>, an arachnologist, saw the pictures and got in contact with Sheryl.</p>
<p>Sheryl went back to the place she had seen the spiders and collected some, not a small feat considering the spiders are the size of a grain of rice. She sent them to Joseph Schubert, who was able to study them and determine that this was indeed a new species. He named it <em>Maratus nemo</em> due to the coloration of the males, who have a bright orange face with a white stripe.</p>
    


<p><em><a href="https://massivesci.com/people/maria-gatta/">Maria Gatta</a> studies 

<p class="mb0">

<span class="scientist__field">Ecology</span>

and <span class="scientist__field">Conservation Biology</span>

</p>

 at 

<p class="mb0 o7">

<span class="scientist__institution">University of the Witwatersrand, Johannesburg</span>

</p>

.</p>



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<guid isPermaLink="true">https://massivesci.com/notes/deep-sea-bacteria-bathypelagic-food/</guid>
<link rel="alternate" type="text/html">https://massivesci.com/notes/deep-sea-bacteria-bathypelagic-food/</link>
<pubDate>Wed, 10 Nov 2021 08:22:34 EST</pubDate>
<title>Deep sea bacteria use selfishness to their advantage</title>
<description>Some bathypelagic bacteria have found a way to maximize their energy intake by taking food into their cells before breaking it down</description>


<media:content url="https://images.takeshape.io/fd194db7-7b25-4b5a-8cc7-da7f31fab475/dev/f0da3fdc-31f3-45b3-9c83-6a5649511fd6/cristian-palmer-3leBubkp5hk-unsplash.jpg?auto=compress%2Cformat&amp;crop=faces&amp;fit=crop&amp;fm=jpg&amp;h=600&amp;q=75&amp;w=900" type="image/jpeg">
  <media:title></media:title>
  <media:description>underwater photo of specks in blue water</media:description>
</media:content>


  
  <dc:creator><![CDATA[Sarah Brown]]></dc:creator>
  <atom:author>
    <atom:name>Sarah Brown</atom:name>
    <atom:uri>https://massivesci.com/people/sarah-brown/</atom:uri>
  </atom:author>


  
  <content:encoded><![CDATA[
    <p>The <a href="https://www.weather.gov/jetstream/layers_ocean" target="_blank">bathypelagic zone</a> of the ocean, which spans depths between 1,000 and 4,000 meters (3,300 – 13,100 feet) below the ocean’s surface, is characterized by permanent darkness, low temperatures, and high pressure. In this hostile environment, slow-growing bacteria survive by relying on <a href="https://la-dwh.com/wp-content/uploads/2018/02/9.2.7.18_Ducklow.pdf" target="_blank">sinking organic matter</a>, including proteins and carbohydrates called polysaccharides, from algae in the sun-lit surface waters of the ocean.&nbsp;</p>
<p>Much of this organic matter is heavily degraded by the time it reaches the deep sea, and intact polysaccharides are hard to come by. For bacteria living in the bathypelagic zone, survival means getting the most out of every rare polysaccharide that reaches these depths – and a new study suggests that for some bacteria, selfishness may be key to their survival.</p>
<p>Bacteria typically feed by releasing <a href="https://www.annualreviews.org/doi/full/10.1146/annurev-marine-120709-142731" target="_blank">enzymes</a> into the water to break down their food into small enough pieces to be taken into the cell. However, by releasing these enzymes into the surrounding water, bacteria naturally lose some of the products of this process. While breaking down food externally can be profitable <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4592861/" target="_blank">when resources are in high abundance</a>, it is a much less successful strategy in environments where resource availability is low, such as the deep sea.</p>
<p>In a recent <a href="https://www.biorxiv.org/content/10.1101/2021.07.26.453833v1" target="_blank">pre-print</a> that I am a co-author on, we suggest that some bacteria at these depths may be using a selfish method of polysaccharide uptake. This method allows them to bring large pieces of polysaccharides into their cells without first breaking them down externally, enabling the bacteria to selfishly keep all the food to themselves.</p>
<p>To make this discovery, we incubated bathypelagic bacteria with fluorescently-labeled polysaccharides. By staining the bacteria with a DNA-binding dye and viewing them under microscopes, we were able to see intact pieces of polysaccharides inside the cells, indicating that these bacteria had not used external enzymes to break them down prior to uptake.</p>
<p>These results provide the first example of selfish behavior in deep-sea bacteria, suggesting that selfishness may be more common among bacteria than previously thought.</p>
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<guid isPermaLink="true">https://massivesci.com/notes/lcd-screen-vocs-emission/</guid>
<link rel="alternate" type="text/html">https://massivesci.com/notes/lcd-screen-vocs-emission/</link>
<pubDate>Tue, 09 Nov 2021 07:45:37 EST</pubDate>
<title>The screen you are reading this on is probably emitting volatile organic compounds</title>
<description>A new study demonstrates that, in addition to a variety of other household products, LCD screens also emit these compounds</description>


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  <media:description>four lcd screens arranged on a desk with a bright pink and blue design on the screens</media:description>
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  <dc:creator><![CDATA[Kay McCallum]]></dc:creator>
  <atom:author>
    <atom:name>Kay McCallum</atom:name>
    <atom:uri>https://massivesci.com/people/kay-mccallum/</atom:uri>
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    <p><a href="https://www.epa.gov/report-environment/indoor-air-quality#note1" target="_blank">We spend a lot of time indoors</a> - so it’s important that we know what’s in indoor air. Indoor chemists are especially concerned with volatile organic compounds (VOCs, a class of molecules that includes benzene, formaldehyde, and more), which can be harmful to human health and are highly reactive.</p>
<p>VOCs are released into indoor air from a number of sources –&nbsp;<a href="https://www.sciencedirect.com/science/article/pii/B9780123462404500035" target="_blank">plants</a>, <a href="https://www.sciencedirect.com/science/article/abs/pii/S0360132314004120?via%3Dihub" target="_blank">wall paint</a>, <a href="https://www.bbc.com/future/article/20200909-why-indoor-air-pollution-is-an-overlooked-problem" target="_blank">cooking and cleaning</a> – and, as <a href="https://www.pnas.org/content/118/23/e2105067118" target="_blank">a recent study</a> by a pair of researchers at the University of Toronto shows, from LCS screens like those in your phone, TV, and laptop.</p>
<p>To measure how LCD screens affect air quality, the researchers collected data on what types of compounds were contained in two types of samples: one of regular indoor air, and one collected near the surface of on an LCD screen like a new TV or an old laptop. They identified the chemical signatures of those compounds using a <a href="https://pubs.acs.org/doi/10.1021/cr800364q" target="_blank">technique</a> called proton-transfer reaction mass spectrometry. They then cross-referenced these signatures against lists of known liquid crystal monomers (the “building blocks” of LCD screens) and other compounds used in LCD screen manufacturing.</p>
<p>They found over 30 VOCs and 10 L liquid crystal monomers were heavily emitted into the air exposed to the screen, including extremely reactive species like isoprene and acetic acid. This finding indicates that LCD screens are an important source of VOCs in indoor environments, and that our screen-time may be exposing us to more than just new things on the internet.</p>
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