The government shutdown is affecting tens of thousands of federal employees. | Photo credit: Emw / WIkimedia Commons (CC BY-SA 3.0)

The Longest-Ever Government Shutdown is Affecting Public Health

<p><i>Editor’s Note: This article was</i> <a href="http://app.nationalproduction.wgbh.org/e/es.aspx?s=2531&amp;e=1177937&amp;elqTrackId=87bceb0e8d45455b8e6ff9d7c932edc8&amp;elq=e281387721134c699f5c69e1f1f96e6c&amp;elqaid=5641&amp;elqat=1"><i>originally published</i></a> <i>in an edition of NOVA’s email newsletter, NOVA Lens, and has now been repurposed for NOVA Next. Sign up for NOVA Lens</i> <a href="http://www.pbs.org/wgbh/nova/newsletters.html"><i>here</i></a> <i>(select “NOVA Newsletters”).</i></p><p>The current partial government shutdown—the longest ever—has obvious effects on employment. Departments that partially ceased operations on or after December 22 employ about <a href="http://app.nationalproduction.wgbh.org/e/er?s=2531&amp;lid=7837&amp;elqTrackId=2C57D362942D1D693F9CE511D84C6308&amp;elq=e281387721134c699f5c69e1f1f96e6c&amp;elqaid=5641&amp;elqat=1">800,000 workers</a>; of those, 380,000 federal employees have been furloughed and 420,000 are working without pay.</p><p>But one of the results brewing out of the public eye is a public health stalemate, particularly for women and underrepresented groups.</p><p>Janelle Pocowatchit, program manager for Native American LifeLines of Boston, says that the shutdown is crippling the organization’s ability to provide its constituents with essential health services. Native American LifeLines is contracted by the Indian Health Service, which reimburses it for money spent at both the Boston site and its sister site in Baltimore. But as money runs dry and reimbursement funds from the federal government remain on hold, Pocowatchit is looking at having to lay off staff. And for some Native people in the Boston area, that might mean reduced access to medical information or canceled rides to and from appointments.</p>
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<p>“We don’t know what’s going to happen,” Pocowatchit says. “We don’t know if they’re going to become homeless [<a href="http://app.nationalproduction.wgbh.org/e/er?s=2531&amp;lid=7838&amp;elqTrackId=9D963C72769F07F5EA21FA18D15D4B90&amp;elq=e281387721134c699f5c69e1f1f96e6c&amp;elqaid=5641&amp;elqat=1">if affordable housing contracts expire</a>] or lose their health insurance. What’s going to happen to the people we serve?”</p><p>Native American LifeLines of Boston doesn’t provide direct medical services (except for dental and behavioral health care). Instead, it connects Native people to services. During a government shutdown, this system of care simply isn’t there.</p><p>“Living in an urban area, we have many different tribes represented, and a lot of [these people] are not living near their tribal communities,” says Ella Blackowl, a program assistant with Native American Lifelines of Boston. “They’re not able to get services from their tribes like in other parts of the United States.”</p><p>From a research perspective, the shutdown may indirectly affect the health of women and newborns, as well. Dr. Tracey Woodruff, a professor of obstetrics, gynecology, and reproductive services at the University of California San Francisco, says that certain grants aren’t getting approved because of the shutdown, which is causing research interruptions. Woodruff studies environmental contributors to disease. In particular, her work investigates how prenatal exposure to pollutants and other chemicals can adversely affect prenatal development.</p>
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<p>“If you have a disruption in the data collection,” she says, “that can leave a hole in your overall analysis.” And there are certain periods of time during pregnancy that are more sensitive than others. “You could miss a critical window of information,” she says, if the science doesn’t happen according to schedule.</p><p>And Woodruff notes that for certain substances, consistent and broad monitoring of chemicals is important—and lags in regulation can cause deaths.</p><p>Here’s an example: At least 64 people have died from acute exposure to methylene chloride, a chemical that can be used for paint stripping, since 1980. But the federal government only <a href="http://app.nationalproduction.wgbh.org/e/er?s=2531&amp;lid=7839&amp;elqTrackId=E2B2C57DF42D29A73762F9969E1C7103&amp;elq=e281387721134c699f5c69e1f1f96e6c&amp;elqaid=5641&amp;elqat=1">recently</a> announced restrictions on this dangerous substance—actions to limit its availability had been on hold for <a href="http://app.nationalproduction.wgbh.org/e/er?s=2531&amp;lid=7840&amp;elqTrackId=164C35967C6D3B1FB6F6E5E5383CE4CB&amp;elq=e281387721134c699f5c69e1f1f96e6c&amp;elqaid=5641&amp;elqat=1">a while</a>, the Environmental Protection Agency having originally proposed a ban in January 2017. For Woodruff, this is a cautionary tale: Detection of harmful environmental and manmade agents requires vigilance and swift, urgent decision-making—both of which take the backseat when the government isn’t operating fully.</p><p>“A cascade of effects can happen as we wait to make decisions about chemicals that can be influencing people’s health,” Woodruff says.</p>
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<p>For employees who’ve been furloughed during the shutdown, day-to-day life could be a struggle.</p><p>“I think there’s a mental health cost, too, of not knowing if you’re going to work tomorrow,” says Maryam Zaringhalam, a leadership member of <a href="http://app.nationalproduction.wgbh.org/e/er?s=2531&amp;lid=7850&amp;elqTrackId=47CBFAD5DBE2756F12E67B2D647CD204&amp;elq=e281387721134c699f5c69e1f1f96e6c&amp;elqaid=5641&amp;elqat=1">500 Women Scientists</a>. “Even more than the research, it’s about individual researchers’ lives.”</p>

<p>One of the results brewing out of the public eye is a public health stalemate, particularly for women and minorities.</p>

Dsuvia is a form of sufentanil, an opioid. Photo credit: Craig Sherod/AcelRx Pharmaceuticals, via Associated Press

Is the F.D.A.-Approved Dsuvia As Dangerous As It Seems?

<p><i>Editor’s Note: This article was </i><a href="http://app.nationalproduction.wgbh.org/e/es.aspx?s=2531&amp;e=1126289&amp;elqTrackId=87bceb0e8d45455b8e6ff9d7c932edc8&amp;elq=d6468db945df4844a6c4939468498fac&amp;elqaid=5499&amp;elqat=1"><i>originally published</i></a><i> in an edition of NOVA’s email newsletter, NOVA Lens, and has now been repurposed for NOVA Next. Sign up for NOVA Lens</i> <a href="http://www.pbs.org/wgbh/nova/newsletters.html"><i>here</i> </a><i>(select “NOVA Newsletters”).</i></p><p>On Friday, November 2, the F.D.A. approved a new tablet form of <a href="https://www.ncbi.nlm.nih.gov/pubmed/2903821">sufentanil</a>, an extremely potent synthetic opioid. The drug is called Dsuvia, and the decision to approve it has <a href="https://www.npr.org/sections/health-shots/2018/11/02/663395669/despite-warnings-fda-approves-potent-new-opioid-painkiller">proven controversial</a>.</p><p>Dsuvia is 10 times stronger than fentanyl, the parent drug that the F.D.A. approved for medical use in 1968—but which also has illegal correlates that have been linked to recreational drug use and deaths due to <a href="https://www.pbs.org/video/addiction-afsxne/">overdose</a>.</p>
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<p>The F.D.A. advisory committee responsible for evaluating the drug voted to recommend its approval in the absence of the committee’s chair, Dr. Raeford Brown. Dr. Brown later wrote <a href="https://www.citizen.org/sites/default/files/2451.pdf">a letter</a> to top F.D.A. officials voicing his concerns. He and other critics of the F.D.A.’s assessment say that a drug this powerful risks abuse—especially given the escalation in illicit opioid overdoses in recent years (in 2017, <a href="https://www.drugabuse.gov/related-topics/trends-statistics/overdose-death-rates">it’s estimated</a> that more than 72,000 Americans died from drug overdoses). After the final approval, F.D.A. commissioner Dr. Scott Gottlieb released <a href="https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm624968.htm">a statement</a> defending the decision, stating that Dsuvia is only delivered through a “pre-filled, single-dose applicator” and will only be admissible in medically-supervised environments.</p><p>There’s a particular type of person that might benefit from Dsuvia, experts say: soldiers wounded in the battlefield.</p><p>“Somebody in the army realizes that there’s going to be a time when a soldier in the battlefield needs to be given an analgesic [painkiller] in a safe way that’ll work quickly and last up to three hours,” says Dr. John Aldis, an addiction medicine specialist in the Eastern Panhandle of West Virginia. “And [Dsuvia] doesn’t need any syringes or needles; it can just be put under his tongue.” If a person is in the military, Dr. Aldis adds, his or her prescribing history will likely have been documented, giving those administering the drug added assurance as to whether or not the patient can handle the dosage.</p>
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<p>The <a href="https://www.mayoclinic.org/drugs-supplements/fentanyl-transdermal-route/proper-use/drg-20068152">fentanyl skin patch</a>, for example, is safe only if given to a person who has taken oral narcotics for severe pain. And Dsuvia itself, the brand-name form of sufentanil (<a href="https://en.wikipedia.org/wiki/List_of_fentanyl_analogues">a fentanyl analogue</a>), is not prescribed. It is given in the hospital by a healthcare provider. This makes Dsuvia significantly different from OxyContin, which has a history of lax prescription behavior on the part of medical doctors—a practice that has led to its abuse and reputation as a “gateway” to other drugs like heroin and fentanyl, or cocaine-laced compounds.</p><p>And unlike past market-approved opioids, Dsuvia has a Risk Evaluation and Mitigation Strategy (REMS) document attached to it (<a href="https://www.accessdata.fda.gov/drugsatfda_docs/rems/Dsuvia_2018_11_02_REMS_Full.pdf">here’s a PDF</a> of the full REMS document for Dsuvia). This outlines the steps that the pharmaceutical company—in this case, AcelPx Pharmeceuticals—must take to monitor distribution of the drug and ensure that healthcare providers are using it properly.</p><p>“When OxyContin came out, they weren’t using REMS’s,” Dr. Aldis says. “The REMS is pretty important. It’s a way the F.D.A. says, ‘Okay, we’re in a new world now. We’re not in the OxyContin world anymore.’ They’re accepting the fact that narcotics are a big problem.”</p><p>The REMS document and the ease of administration, according to Dr. Aldis, are some of the clear advantages that Dsuvia has over other opioids that might be administered in extreme situations.</p><p>“You have to look at the pharmacodynamics of it,” he says. Dsuvia is absorbed effective and fairly reliably when placed under the tongue. “They know it does work and that is works uniformly pretty well every time it is given.”</p><p>Of course, the new drug isn’t a catch-all solution to instances of catastrophic pain, and it might not work for everyone. A person whose jaw has been blown off in battle might not have a tongue under which to place a Dsuvia tablet.</p><p>But worries about the introduction of a new fentanyl analogue might be moot; illegal derivatives of fentanyl, often originating in China, flood the streets already. “These people who are buying what they think is fentanyl, they may be buying this drug,” Dr. Aldis says. An F.D.A. approval makes it more subject to strict regulation.</p><p>Dr. Aldis adds that all of this is being taken very seriously, as it should be—proceeding with caution and regulation is critical. “This,” he says, “is a different time.”</p>
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<p>The drug, called Dsuvia, is 10 times stronger than fentanyl and will be limited to medical use in hospitals and other supervised sites.</p>

In 2016, an estimated 16.2 million people in the United States had at least one major depressive episode. Of those, 37 percent did not receive treatment. | Photo credit: Pixabay

FDA Approves First Major New Depression Treatment in Decades

<p>The U.S. Food and Drug Administration has approved a drug called esketamine—the first major new depression treatment to hit the market in decades.</p><p>The drug, developed by Janssen Research &amp; Development (a pharmaceutical company of Johnson &amp; Johnson), is administered in the form of a nasal spray as opposed to an oral pill. Designed specifically for people suffering from the most extreme forms of treatment-resistant depression, esketamine could affect millions of people living in the U.S. who are at high risk of suicide due to existing therapies’ inability to manage their disease. The nasal spray will be administered only in approved and certified treatment centers, and will be restricted to people who have tried at least two other antidepressants without success. Patients who receive the drug will also need to be monitored for at least two hours every time they use it.</p><p>“This is the first truly novel mechanism that has been presented in over 50 years,” says Dr. Gerard Sanacora, a professor of psychiatry and director of the Yale Depression Research Program.</p>
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<p>Unlike antidepressants like Prozac, which appeared on the scene in 1987, esketamine is a glutamatergic agent—that is, it targets glutamate, the most abundant neurotransmitter in our brain and central nervous system. “About 60-80 percent of all the cells in the brain use glutamate as their primary chemical messenger,” Sanacora says. Previous treatments have all targeted the <a href="http://www.health.gov.au/internet/publications/publishing.nsf/Content/drugtreat-pubs-modpsy-toc~drugtreat-pubs-modpsy-2~drugtreat-pubs-modpsy-2-3~drugtreat-pubs-modpsy-2-3-intr">monoamine system</a>, which is comprised of a different set of neurotransmitters: dopamine, noradrenaline, and serotonin.</p><p>In the 1990s, researchers began accruing evidence that the glutamate system was disrupted in patients suffering from depression. They also knew that ketamine, known as “Special K” in illicit party drug-speak, targets the glutamate system—so scientists decided to investigate exactly how ketamine works in the brain and whether or not it could alleviate symptoms of depression.</p><p>In 2000, Dr. Dennis Charney, along with Dr. John Krystal, published the <a href="https://www.ncbi.nlm.nih.gov/pubmed/10686270">first study</a> showing that intravenous infusions of ketamine produced rapid (within a few hours) antidepressant effects.</p><p>“I don’t think anybody was anticipating a rapid onset,” Sanacora says. That’s a big deal, since drugs like Prozac and Zoloft often take weeks or months to have any noticeable effect.</p><p>Charney and his colleagues at the National Institutes of Health then <a href="http://bit.ly/2ITFFvW">replicated the study</a> in more treatment-resistant patients. At Icahn School of Medicine at Mount Sinai (ISMMS), where Charney is now dean as well as professor of psychiatry, neuroscience, and pharmacological sciences, he and others conducted the first study of the intra-nasal version of the drug, as well as the first study that showed the neurobiological response could be repeated. Since then, research groups around the world have begun to take heed of the drug’s potential.</p><p>Janssen's derivative product—called esketamine because it is a close cousin of ketamine—blocks a particular glutamate receptor, the NMDA receptor, from absorbing the glutamate it secretes. As a result, connections between neurons are restored and the brain’s neuroplasticity increases through the production of more synapses. (<b>Disclosure:</b> Charney is named as co-inventor on patents filed by ISMMS relating to the treatment of treatment-resistant depression. ISMMS has a licensing agreement with Janssen related to these patents, and it receives payments from Janssen under that agreement. Charney, by extension, is entitled to a portion of those payments.)</p><p>“When we undergo chronic stress, neurons actually shrink,” says Dr. Scott Russo, a professor of neuroscience and director of the Center for Affective Neuroscience at the Icahn School of Medicine at Mount Sinai. “It’s thought that they underperform. Ketamine rejuvenates those cells” particularly in the prefrontal cortex, a region of the brain responsible for higher cognitive functions like judgment and decision-making.</p><p>But Russo notes that the blocking of the glutamate receptor is not indisputably responsible for the antidepressant effects. While that mechanism is certainly a catalyst, a series of “downstream effects” occur after the receptor is blocked; a single wave or ripple within that cascade of events could actually be what’s giving patients relief. “I’d want to see [additional] animal studies to prove that [the blocking of NMDA receptors] is the sole mechanism of action,” he says. For example, <a href="https://www.ncbi.nlm.nih.gov/pubmed/30153752">one study</a> showed that the brain's system of opioid receptors might be involved.</p><p>In addition, Russo says that there is evidence to suggest that ketamine can reduce inflammation—<a href="https://www.pbs.org/wgbh/nova/article/brain-inflammation/">a burgeoning topic</a> in neuropsychiatric research—but again, it’s likely not a primary functioning of the drug.</p><p>Despite these nuances, Russo is enthusiastic about the drug's approval. "I think it's a game changer," he says. "I haven’t seen that type of discovery in my lifetime—I was probably five years old when the last drug came on the market. I hope this starts a chain reaction of new drugs in psychiatric medicine."</p>
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<p>Not everyone is waxing poetic about esketamine's promise. Dr. Erick Turner, a psychiatrist at Oregon Health and Science University, served on the FDA advisory committee that evaluated the drug—but he wasn’t present at the review panel earlier this month. He says that Johnson &amp; Johnson <a href="https://www.statnews.com/2019/02/20/psychiatry-awaits-esketamine-with-excitement-hesitation/">fell short</a> of the required number of adequate and well-controlled trials (two) that indicate a drug’s efficacy (see the second paragraph of page 9 in <a href="https://www.fda.gov/downloads/AdvisoryCommittees/CommitteesMeetingMaterials/Drugs/PsychopharmacologicDrugsAdvisoryCommittee/UCM630970.pdf">this FDA briefing document</a> for an acknowledgement of the exception the FDA made to this rule).</p><p>“As a former regulator, I worry that this has been overly-hyped and that it’s not going to live up to expectation,” Turner says. He also has concerns about monitoring, distribution, and insurance coverage. Still, Turner concedes that the new mechanism is exciting. “I would like to see it explored further.”</p><p>Turner notes that a combinatory drug called <a href="https://www.accessdata.fda.gov/drugsatfda_docs/label/2003/21520_symbyax_lbl.pdf">Symbyax</a>, released in 2009, appeared to have an effect of similar magnitude. “I guess I haven’t seen any evidence that this [esketamine] is better than what we already have,” he says, pointing to studies in elderly patients that show ketamine’s effect sometimes <i>doesn’t</i> take hold in as quickly as a few hours—that it could instead take up to weeks.</p><p>Nevertheless, that speed of onset is, according to proponents of esketamine, one of its fundamental advantages.</p><p>“As a clinician, it’s really hard to tell a patient, ‘I know you’re feeling terrible, but I’d like you to start taking this medicine. You may feel worse for a week or two or three before you start to feel better, but just keep taking it,’” Sanacora says. “When somebody’s suffering from depression, every day feels like an eternity—and now you’re telling them to wait weeks and possibly months before I can you tell if it’s even going to work. So this is a huge advance.”</p><p>In 2016, <a href="https://www.nimh.nih.gov/health/statistics/major-depression.shtml">an estimated 16.2 million adults</a> in the United States had at least one major depressive episode. Of those, 37 percent did not receive treatment. A drug like esketamine—which is at <a href="https://theconversation.com/promising-new-drug-for-treatment-resistant-depression-esketamine-111966">low risk for abuse</a> (though the drug's label will list possible side effects and warn that there is a risk for misuse) and has only moderate side effects—could be an option for those people who might really need it.</p><p>“This shouldn’t be something everybody jumps to,” he says. “But there are clearly situations where you need a rapid onset.”</p><p>“The approval opens up a whole new vista of potential treatments,” Sanacora says. He praises his colleagues—Charney, Krystal, and others—for experimenting with ketamine so many years ago.</p><p>“Serendipity favors the prepared mind,” he says. “They were playing in the right sandbox.”</p>
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<p>Experts&#x27; opinions on the new drug, designed for people suffering from the most extreme forms of treatment-resistant depression and administered in the form of a nasal spray, are split.</p>

Google Balloons Send Internet Soaring Through the Clouds

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  Jon Brodkin, writing for ArsTechnica:
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   Google this week launched 30 balloons into the stratosphere in the first step toward creating what it calls a “network in the sky” that could eventually bring “balloon-powered Internet [to] everyone.”
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<p>
   Dubbed “Project Loon,” Google’s balloon-based wireless networks aim to bring 3G-like speed to what Google says are the “2 out of every 3 people on Earth” who lack a fast, affordable Internet connection. Google’s plan has been rumored for weeks. As we
   <a href="http://arstechnica.com/information-technology/2013/06/googles-balloon-based-wireless-networks-may-not-be-a-crazy-idea/">
    wrote earlier this month
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   , balloon-based communications are well established for military communications and have been proposed for public safety use in disaster areas. Google could be the first to make balloon-based networks widely used for commercial Internet access.
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<p>
  One of the key hurdles Google had to surmount was how to maintain coverage with a fleet of balloons that is, at least partially, at the mercy of the winds. They solved it like they have many other problems—by throwing massive amounts of computing power at it. That way each balloon can piggyback on air currents, and when the winds aren’t in its favor, nudge the craft onto a favorable course.
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<img alt="Project Loon" class="richtext-image full-width" src="https://www.pbs.org/wgbh/nova/media/images/google-balloons.width-990_MOc45IA.jpg"/>
<figcaption>Google is not the first to pursue balloons as vehicles for commercial Internet access, but its use of wind and solar power to direct their paths is innovative.
        
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  Discover how Google dreamt up this way to access the cloud through technology held aloft
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   in
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  the clouds:
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 Photo credit:
 <a href="http://www.flickr.com/photos/ilitephoto/9052643301/sizes/l/in/photolist-eMXasV-8367w1-8369Jd-81JAH3-81JzpW-81JA6w-81FrFK-81FtLe-81JCL1-81JzLb-81EsMc-83zxqq/">
  iLighter/Flickr
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Why Naked Mole Rats Don't Get Cancer

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  When a group of researchers at the University of Rochester in New York tried growing skin cells from naked mole rats in lab flasks, they noticed that the fluid the cells were growing in became thick and syrupy. After some investigation, they discovered that the cells, like other cells of mammalian connective tissue, were secreting a sugar called hyaluronan, except the naked mole version was five times bigger. Andrei Seluanov, who led the study, believes that larger hyaluronan can trap potential cancer cells and prevent them from growing into tumors. Writes Ed Yong for Not Exactly Rocket Science:
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<blockquote>
<p>
   But it also allows cells to stop each other from growing if they become too crowded. This is called ‘
   <a href="http://www.ncbi.nlm.nih.gov/pubmed/19858485">
    contact inhibition
   </a>
   ’—it’s why healthy cells form a flat layer if they’re grown in a dish but cancerous ones pile on top of each other.
  </p>
<p>
<a href="http://www.nature.com/news/blind-mole-rats-may-hold-key-to-cancer-1.11741">
    Based on an earlier study
   </a>
   , Seluanov’s team suspected that naked mole rat cells are protected against cancer because they’re especially sensitive to contact inhibition. Now, they’ve shown that large hyaluronan is responsible. The rodents’ cells are very receptive to the sugar; as they get close, hyaluronan sticks to their surface and triggers a genetic programme that stops them from growing.
  </p>
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<p>
  The team switched on cancer genes in naked mole rat cells and transplanted them into mice. No cancer. But when they reduced the amount of hyaluronan created by the naked mole rat cells in the mice, tumors formed.
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How to Make a False Memory

<p></p><p><i>“Remembrance of things past is not necessarily the remembrance of things as they were.”</i> —Marcel Proust</p><p>Proust was on to something. As powerful as our memories may be, they’re certainly not infallible. Our minds lead us astray all the time, but experts hadn’t gotten to the root of the brain’s deceptiveness—until now.</p><p>Scientists at the Massachusetts Institute of Technology say they have successfully implanted a false memory in a mouse, giving insight into how memories—true and false—may form in the human brain. Led by Susumu Tonegawa (a Nobel laureate for his work in immunology), the team <a href="http://www.sciencemag.org/">reported Thursday in the journal Science</a> that they caused genetically modified mice to remember being shocked in a particular place when, in reality, that electric shock was delivered when the mouse was somewhere else entirely. Here’s <a href="http://www.technologyreview.com/news/517226/scientists-make-mice-remember-things-that-didnt-happen/">Susan Young, writing</a> for Technology Review:</p><p>Previously, the MIT-based team had <a href="http://www.ncbi.nlm.nih.gov/pubmed/22441246">shown</a> that it could pinpoint the location and assemblage of cells that carry a memory, and that activating those cells stimulated memory recall in mice. To create the new, false memory, Tonegawa’s team reactivated a mouse’s memory of a safe place while the animal received shocks in its feet, thus transforming the original memory.</p><p>First, the team used genetic tricks to label the brain cells involved in the memory of a chamber that was safe and neutral. The next day, they put the animal in a second chamber, a completely different setting. There, the animal got foot shocks while the researchers simultaneously shone light to reactivate the memory of the harmless first chamber. When the animal was put back in the first chamber, it fearfully froze—a clear indication that it remembered getting shocked in that chamber, even though that never happened.</p><p><a href="http://www.nytimes.com/2013/07/26/science/false-memory-planted-in-a-mouse-brain-study-shows.html">James Gorman wrote in The New York Times</a> that although mice and people are evolutionarily distant, the processes that govern memory formation in mammals are ancient. In both mice and men, memories form in an area of the hippocampus called the dentate gyrus—so conclusions drawn from this study are likely to apply to humans as well. Moreover, the scientists’ ability to locate and edit a memory is a significant achievement. Gorman quotes <a href="http://www.nytimes.com/2013/04/30/science/may-britt-and-edvard-moser-explore-the-brains-gps.html?pagewanted=all">Edvard I. Moser</a> , a neuroscientist at the Norwegian University of Science and Technology:</p><p>“What I find fascinating about this,” Dr. Moser said, “is that you actually can point to a physical substrate to memory,” what the researchers call an engram. Neuroscientists have long talked about engrams, but Dr. Moser said the recent research is the closest they have gotten to pointing to a spot in the brain and saying, “That is the memory.”</p><p>Of course, researchers have long known that memory blurs fact and fiction. But this new discovery is an important step toward figuring out how that actually works. <a href="http://www.guardian.co.uk/science/2013/jul/25/false-memory-implanted-mouse-brain">Writes Alok Jha</a> for <i>The Guardian</i> :</p><p>The mouse models created by the MIT team will help scientists ask ever more complex questions about memories in people. “Now that we can reactivate and change the contents of memories in the brain, we can begin asking questions that were once the realm of philosophy,” said Steve Ramirez, a colleague of Tonagawa’s at MIT.</p>

Nearing Certainty About Heisenberg's Uncertainty... Or Not

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  One of the basic tenets of quantum mechanics is Heisenberg’s uncertainty principle, which states that the more precisely one measures a particle’s momentum, the more uncertain its position becomes. The reverse is also true, which means that in theory, it’s impossible to know the exact position and momentum of a subatomic particle at the same time.
 </p>
<p>
  Heisenberg originally used the principle to show that there is a limit to the accuracy of particle detectors, but he never offered direct evidence to support his ideas. Now, UK physicist Paul Busch and his colleagues believe they have a proof. Here’s Ron Cowen, writing for Nature:
 </p>
<blockquote>
<p>
   In their theoretical work, Busch and his colleagues imagined making simultaneous measurements of a particle’s position and momentum in an arbitrary quantum state. They compared the errors in such measurements to two special cases — in which either the position or the momentum of the particle is well known. They found that the combined errors in measurements of the position or momentum in these two cases obeyed Heisenberg’s principle and was always smaller than for cases in which the two properties were measured simultaneously. This step allowed them to prove Heisenberg’s original conjecture.
  </p>
</blockquote>
<p>
  Scientists remain skeptical, though. Read the
  <a href="http://www.nature.com/news/proof-mooted-for-quantum-uncertainty-1.13270" title="full article">
   full article
  </a>
  to learn more about one physicist’s objection to Busch’s proof, as well as what those doubts mean for quantum computing. For some background on quantum computing, hear from
  <a href="http://www.pbs.org/wgbh/nova/tech/quantum-computing.html" title="MIT's Seth Lloyd">
   MIT’s Seth Lloyd
  </a>
  . And for some comic relief, watch this video:
 </p>
<div class="cove-box flex-video" data-cove-id="18121247" data-cove-params="&amp;topbar=false">
</div>
<div class="inline-caption">
  Quantum mechanics is nothing to laugh at. Well, sometimes it is.
 </div>
</section>

Allison Eck

Articles