Professional golfers keep their eyes on the ball, letting the rest of their body run on autopilot.

Focus Makes Perfect: When To Think, And When Not To, When Playing Sports

<div class="related"></div>
<p>
</p>
<p>
 At mile three of the 2012 Charlottesville Marathon, I was winning. Feeling comfortable and ecstatic about my position, I was also honored with a personal escort, biking alongside, to lead my way. But I knew that a lot could happen in the remaining 23 miles, so I kept myself in check, not allowing my excitement to take over. My legs felt eager to blaze a sub-six minute mile, but instead I reined them in to maintain an easier—and more realistic—6:30 pace.
</p>
<p>
 It was my ninth marathon. By that point, strategizing in a race was nothing new. My running career began when I was 14, and since then my feet have pounded asphalt, concrete, grass, gravel, and more as I’ve logged countless miles and hours training. As I have improved as a runner, my mind wanders less, and I think more about how my body is feeling. It turns out that’s exactly what I should be doing. Just as with other athletes, the relationship between my mind and my body is complex—winning races involves far more than just putting one foot in front of another. Psychologists and neuroscientists are diving into the minds of elite and amateur athletes alike, eager to uncover the mental strategies that create champions. They’re discovering that what produces winners in one sport may be disastrous in others.
</p>
<h2>
 Analyzing the Long Run
</h2>
<p>
 In endurance events, like running and cycling races, elite athletes focus intently on the state of their bodies. This internal focus—on arm and leg movements, breathing, sweating, and so on—is called association by sports psychologists. Endurance athletes who learn to associate are exceptionally in tune with their bodies, which has obvious benefits when strategizing a race. “You get better at reading your body the more miles you put in and run,” says Dr. Robert Weinberg, a professor of sport behavior and performance at Miami University. “An elite marathoner can tell the difference between running a 5:01 mile and a 5:02 mile. These people know their bodies.”
</p>
<figure class="richtext-image full-width">
<img alt="" class="richtext-image full-width" src="https://www.pbs.org/wgbh/nova/media/images/constantina.width-990_rCXXuIv.jpg"/>
<figcaption>Professional runners like Constantina Dita—here leading the 2006 Chicago Marathon—focus internally.
        
    </figcaption>
</figure>
<p>
 But when the mind of an elite runner starts to wander—whether that be concentrating on music, conversation, or simply admiring the scenery—their world-class times start to slip. It’s tempting to tune out by blasting music, but if endurance athletes want to improve, they need to stress their systems and experience pain, says Erik Lind, a kinesiologist at State University of New York, Cortland. And while dissociation can be comforting while training, it can be downright dangerous in competitive events like marathons, where a loss of focus can lead to injury or even death. “At some point the mind has to pay attention to what the body is saying or, at a high intensity, yelling,” Lind says. “If you keep going, something catastrophic might happen.”
</p>
<p>
 Death is an extreme case, of course. While it has happened, it’s more common that marathoners hit “the wall”—the point in a race where their body exhausts its last reserve of fuel. Running becomes exceedingly difficult. People hit the wall, Weinberg says, because they “have dissociated and haven’t checked in at all. All of a sudden stuff is going on in the body but they’re not aware of it. At mile 18…it all hits them, and they hit the wall and they just stop.”
</p>
<p>
 The wall is physiological—people simply don’t have enough calories left to burn—but psychology can play a large part in preventing it. Restraining oneself in the early miles, as I did in Charlottesville, slows the body’s consumption of precious resources and delays the onset of the wall. Starting slowly requires patience, doubly so when you’re being passed by competitors. You have to be aware of your breathing, heart rate, and the overall effort your body is expending. You also have to override what your mind may be telling you—that it’s okay to go fast since you feel excited and energized.
</p>
<div class="pullquote">
<p>
 Being able to monitor pain gives athletes an edge over their competition.
</p>
</div>
<p>
 By mile 22 in Charlottesville, my lead was long gone. I had fallen behind around mile six and was now trailing by at least a minute. My body was exhausted. The hilly course had taken its toll, and every muscle in my body ached. I was running beneath a picturesque canopy of trees wrapping along a lazy river—it was a tempting temporary escape from the relentless hills. But instead of letting my mind wander, I took stock of myself. I was feeling okay, actually. I knew I had enough energy to muscle through and maybe—just maybe—the woman ahead of me didn’t. So I relaxed my shoulders, and I focused, calmly, on my pacing and stride.
</p>
<p>
 “On longer events it is important for you to be in touch with your body and maybe make adjustments or corrections,” Weinberg says. “If you feel your calves are tight you might try to do something. If you feel your breathing is too shallow or too fast you, might do something.”
</p>
<figure class="richtext-image full-width">
<img alt="" class="richtext-image full-width" src="https://www.pbs.org/wgbh/nova/media/images/legs.width-990_KlzeJZ4.jpg"/>
<figcaption>Elite runners constantly assess how they are feeling--from their legs and strides to their heartbeat and breathing rates.
        
    </figcaption>
</figure>
<p>
 By developing an intimate relationship with their bodies, endurance athletes can accurately interpret its signals and push their limits. The success of an athlete “comes down to their personality that allows them to push through their pain,” Lind says. “Or at least monitor their pain.” This gives them an edge over their competition.
</p>
<p>
 As I rounded the bend a half-mile from the finish, I knew I had played my cards right. In the miles since the river, I had slowly chipped away at the lead. Soon, I was briefly neck and neck with the leader. I lengthened my stride, pulled ahead, and regained the lead. Everything hurt. But I ordered my muscles to soldier on, literally muttering encouragement under my breath. This was the moment I had trained for all season; I didn’t want to leave anything on the table. As the finish neared, I dug deeper, willing my last morsel of energy into my exhausted legs, literally forcing them to sprint. They listened. I pushed them relentlessly through the chute and over the line, winning by 13 seconds.
</p>
<div class="ad"></div>
<h2>
 Autopilot on the Green
</h2>
<p>
 In 2011, at the age of 21, Rory McIlroy was a rising star in the world of golf. A year prior, he had won his first PGA tour event—the youngest person to do so since Tiger Woods—and set a course record in the process. Toward the end of the 2011 Masters, McIlroy was just one round away from winning it all and donning the famed Green Jacket. Going into the last day, he was leading by a commanding four strokes.
</p>
<p>
 Mentally, golf is unlike endurance sports. For golfers like McIlroy, focusing on what the body is doing means almost certain failure. The same is true of other precision sports like basketball and tennis. Instead, they need to focus on an external goal. Professional golfers often concentrate on the ball, basketball players frequently on the rim of the hoop. Once they zero in, they go on autopilot, trusting the torsion of their torsos or the pump of their arms to do the rest. Years of practice have etched these motions deep into their muscles.
</p>
<p>
 When athletes first learn to hit a golf ball or shoot a basketball, they focus on every part of the process—the location of their hands, the angle of their wrists, the position of their legs. They run down a mental checklist as they swing or shoot. As they do, the part of their brain responsible for planning and conscious awareness, the frontal cortex, comes alive.
</p>
<p>
 As they improve, their movements become more automatic and the role of the frontal lobe wanes. When professional golfers swing, for example, they have less overall activation in their brains and less in the frontal cortex than beginners. During their stroke, their brains are more efficient—they don’t need to think about what they are doing. In fact, if professional golfers do focus on their movements, their frontal cortex interferes and they often make a mistake. Coaches call this “choking,” and it frequently happens when the stakes are high.
</p>
<div class="pullquote">
<p>
 When told not to worry about accuracy, experienced golfers were more accurate than when told to take their time.
</p>
</div>
<p>
 Which is exactly what happened to McIlroy at the 2011 Masters. After nine holes, his lead had been cut to one stroke. The pressure was on. On the 10th hole, his shot off the tee landed far from the fairway, in between two cabins. He had to make a few more shots—first in the rough and then through the trees—one even hitting a tree—before he hit the green. He then missed a 25-foot putt before finally making it in the hole for a triple-bogey. On the next green, he had to take three putts, including one he missed from just 30 inches. On the 12th hole, he missed four putts from less than 20 feet. Having entering the final day with momentum on his side, McIlroy finished the tournament tied for 15th.
</p>
<p>
 “If you start thinking, ‘I better really make sure I do this right,’ and you start consciously thinking about that putting performance,” says Thomas Carr, a psychology professor at Michigan State University, “then you’re more likely to break up automated sensory motor processes that you’ve practiced so hard to achieve.”
</p>
<p>
 Psychology research confirms this. In her book
 <i>
  Choke: What the Secrets of the Brain Reveal About Getting It Right When You Have To
 </i>
 , Sian Beilock, a psychology professor at the University of Chicago, describes a study of college-level soccer players who dribbled a ball through a row of cones. When they were told to think about where their foot makes contact with the ball, they made more mistakes and navigated the slalom more slowly compared to when they were not prompted. In another set of experiments, experienced golfers forced to putt under distracting conditions were more accurate than when they were told to focus on the components of their swing. Further, if they were told to putt quickly and not worry about accuracy, they were more accurate than when told to take their time to get it right. Presumably, these seemingly not ideal conditions—distracting noises and a rushed setup—kept the golfers from overanalyzing and choking.
</p>
<div class="newsletter"></div>
<h2>
 Adjustments for Amateurs
</h2>
<p>
 Years of practice have honed the skills—mental and physical—of professional and elite athletes. Experienced runners pay keen attention to their strides, their breathing, and their aching muscles. Experienced golfers focus on the ball and let their bodies do the rest. But what should the non-professionals do? It turns out, just the opposite.
</p>
<p>
 If you are a runner or cyclist conquering a new distance or simply getting into shape, distractions may be the best prescription. Turn on your treadmill’s TV, bring your iPod to the track, or find friends to chat with along the trail. “Dissociation seems to be better when you’re practicing and need to stay out there longer,” Weinberg says. “It takes away some of the boredom and fatigue.”
</p>
<p>
 If you are a beginner golfer or basketball player, focus on your technique. Unlike professionals, inexperienced golfers perform poorly when distracted and do better when told to focus on their swing. They are also less accurate when rushed, and hit the target more often when allowed to take their time. Beginning athletes in precision sports are more likely to make a mistake by
 <i>
  not
 </i>
 focusing on the task and the specific steps required—hand goes here, wrist held this way, shoulders squared—than when distracted by an external source.
</p>
<p>
 Put in enough practice, though, and some changes will occur naturally. After enough miles, you’ll be more in tune with your aching legs. Or after enough shots at the driving range, you may start forgetting about your stance and focusing on the ball. As Beilock notes in her book, “Practice can actually change the physical wiring of the brain to support exceptional performance.” Practice does makes perfect because it allows you to focus—to turn your brain on or shut it off—at the moment you need it most. In that moment, focus makes perfect.
</p>
<p>
 Images courtesy
 <a href="http://www.flickr.com/photos/mugen76/276795727/in/set-72157594340321271/">
  mugen76/Flickr (CC-BY 2.0)
 </a>
 ,
 <a href="http://www.flickr.com/photos/tabor-roeder/8113284229/">
  tabor-roeder/Flickr (CC-BY 2.0)
 </a>
 , and
 <a href="http://www.flickr.com/photos/digitalcj/2746572579/">
  digitalcj/Flickr (CC-BY-NC)
 </a>
</p>

<p>Scientists are discovering surprising contradictions about the complex relationship between athletes&#x27; minds and bodies.</p>

Dolphins Remember Voices of Childhood Friends. Do You?

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<div class="add-container clearfix" id="add-block-placer">
</div>
<p>
  If someone you haven’t spoken to since grade school called you, would you recognize his or her name?
 </p>
<p>
  A dolphin would. Two bottlenose dolphins, named Bailey and Allie, lived together in Florida when they were young. More than twenty years ago, they went their separate ways: Allie now lives in Chicago, and Bailey in Bermuda. Recently, when Bailey thought she heard her long lost friend, she got excited and tried to strike up a conversation.
 </p>
<p>
  Karen Ravn, writing for Nature News:
 </p>
<blockquote>
<p>
   Bailey’s recollection of Allie’s name — or more precisely, of her ‘signature whistle’, which functions as a name among dolphins — is the most durable social memory ever recorded for a non-human. Yet it is only one of many data points in a study that found that it is the rule, not the exception, for bottlenose dolphins (Tursiops truncatus) to recognize whistles from their distant past.
  </p>
</blockquote>
<figure class="richtext-image full-width">
<img alt="" class="richtext-image full-width" src="https://www.pbs.org/wgbh/nova/media/images/dolphin.width-990_oijmUsS.jpg"/>
<figcaption>Dolphins can recognize old friends, even after twenty years apart.
        
    </figcaption>
</figure>
<p>
  In captivity, dolphins often move from place to place, spending a few years in one aquarium before being relocated to another. Jason Bruck, a biologist at the University of Chicago and author of the study, inferred friendships by determining which dolphins used to live together.
 </p>
<p>
  Dolphins use whistles as names: they identify themselves by their own whistle and call to friends by imitating their friend’s whistle. To see if the dolphins recognized each other, Bruck played whistles of unfamiliar dolphins and whistles from old friends. Unfamiliar whistles didn’t appear to mean much to the dolphins, but after hearing a friend’s whistle, they perked up, moving toward the underwater speaker or whistling back. They seemed to remember the personality of their old roommate, too—dominant males sparked females’ interest but stressed out young males.
 </p>
<p>
  Bruck is pretty sure that a dolphin’s memory beats his own. Think you’re smarter than a dolphin? Watch this episode of NOVA scienceNOW to find out more about the intelligence of these underwater creatures.
 </p>
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</div>
</section>
<p>
 Photo by
 <a href="http://www.flickr.com/photos/-mbender/">
  mbender/Flickr (CC-BY-NC-ND)
 </a>
</p>

Sneaking into the Brain with Nanoparticles

<section class="entry-content instapaper_body clearfix" itemprop="articleBody">
<div class="add-container clearfix" id="add-block-placer">
</div>
<p>
  About a decade ago, Beverly Rzigalinski, a molecular biologist now at Virginia College of Osteopathic Medicine, was asked by a colleague to look into nanoparticles. “Nanoparticles? Yuck,” she thought. She off-handedly told a student to throw them on some neurons growing in the lab and take notes on what happened. She had no hope for the experiment, sure the nanoparticles would kill all the neurons, but at least she could say she tried.
 </p>
<p>
  Rzigalinski was given cerium oxide nanoparticles to work with, ten-nanometer wide particles derived from a rare earth metal. (Human hair, by comparison, is 100,000 nanometers wide.) No one had looked at their biological applications, and Rzigalinski was not particularly impressed with their résumé. Cerium oxide nanoparticles’ listed industrial uses included glass polishing and fuel combustion, nothing that seemed promising for neuroscience.
 </p>
<p>
  A month and a half later, Rzigalinski noticed the dishes still sitting in the lab’s incubator. She marched straight over to the student, launching into a lecture about not wasting expensive resources on cells that were surely long dead. (Neurons in the lab typically stayed alive for only three weeks.) But the student assured her the cells treated with nanoparticles were still alive. Skeptically, she peered into the microscope and was surprised to find living, flourishing neurons. Rzigalinski has been studying nanoparticles ever since.
 </p>
<p>
  Other neuroscientists are joining her, taking advantage of nanoparticles’ unique properties to identify new therapies, shuttle existing therapies into the brain, and examine the brain on a level and depth never before possible.
 </p>
<h2>
  Recyclable Antioxidants
 </h2>
<p>
  When treated with cerium oxide particles, Rzigalinski’s neurons survived for up to six months, nine times longer than usual. Cerium oxide nanoparticles may extend life in this way by neutralizing free radicals, unpaired electrons that are highly reactive and can damage DNA. The body’s defenses against free radicals may wear down with time; aging may be due in part to free radicals slowly accumulating unchecked.
 </p>
<aside class="pulledquote">
  Rzigalinski’s nanoparticle-treated neurons survived nine times longer than usual.
 </aside>
<p>
  Damage induced by free radicals also contributes to a number of neurological diseases. Rzigalinski’s work is revealing how cerium oxide nanoparticles can prevent or reverse this destruction as well. Treating mouse models of Parkinson’s disease with cerium oxide particles rescued the loss of dopaminergic cells, the death of which leads to the disease’s characteristic tremors and slow shuffling gait. Cerium oxide nanoparticles also seemed to halt the free radical-triggered cascade of damage that typically follows traumatic brain injury; after injury, nanoparticle-treated mice had fewer signs of free radical damage and better memories compared to control-treated mice. Finally, when flies were administered nanoparticles following a stroke (in a timeframe analogous to receiving treatment upon arrival to a hospital), the treated flies not only lived longer but also had improved performance on fly-specific tasks, like quickly buzzing to the top of the cage.
 </p>
<p>
  Antioxidants like vitamins C and E also sop up free radicals, but each antioxidant molecule only destroys one free radical. As Rzigalinski points out, the advantage of cerium oxide nanoparticles is that, “These nanoparticles are regenerative, so they’ll scavenge thousands, or hundreds of thousands, of free radicals.” Cerium oxide nanoparticles neutralize free radicals by snatching the electrons, shuffling them around, and eventually depositing them as water, restoring the nanoparticles to their original state, ready to abolish more free radicals. This recycling means the nanoparticles will continue working after a single dose. Rzigalinski found nanoparticles present as long as six months after injection in mice and, crucially, toxicity has not been an issue, since the dosage is so low. Single doses, or even low doses, can both prevent harmful side effects and keep costs down.
 </p>
<p>
  Cerium oxide nanoparticles are effective because, after injection, they immediately get coated with proteins that help carry them into the heart, lungs, and brain—where they need to be to slash disease-causing free radicals. Not all drugs are so lucky.
 </p>
<h2>
  Trojan Horses
 </h2>
<p>
  The trouble with treating brain diseases is the brain exists in a separate world, sealed off from the rest of the body. Cells are tightly packed around the brain’s blood vessels, forming the blood brain barrier, a heavily guarded barricade separating the blood and its contents from the brain and spinal cord. This security system works to keep any bacterial infections and toxins in the blood from getting into the ultrasensitive brain. If small or fat-soluble enough, certain approved entities—like water, gases, alcohol, and some hormones—can leak across the border. Larger molecules require exclusive receptors to allow them through, a unique key that unlocks a particular door and grants them access.
 </p>
<p>
  While creating an extra level of protection from diseases outside the brain, the blood brain barrier causes trouble for trying to solve diseases within the brain. It’s a notorious nemesis of drug development, preventing an estimated 98% of potential treatments from getting in. Tomas Skrinskas of Precision NanoSystems—a biotechnology company specializing in delivering materials to cells—lamented, “The blood-brain barrier is probably the trickiest [challenge] there is.”
 </p>
<figure class="richtext-image full-width">
<img alt="" class="richtext-image full-width" src="https://www.pbs.org/wgbh/nova/media/images/blood-brain-barrier.width-990_r2St1rD.jpg"/>
<figcaption>In this image of the blood-brain barrier, green-stained glial cells surround the blood vessels (seen here in black), providing support for red-stained neurons.
        
    </figcaption>
</figure>
<p>
  To overcome this hurdle, one current solution involves flooding the blood with drugs, hoping a small proportion passes through by sheer force of will or strength in numbers. But ingesting lots of drugs can trigger nasty side effects elsewhere in the body. Another way to crack through the defenses is to hack into systems already in place for transporting small molecules. Enter nanoparticles.
 </p>
<p>
  While some nanoparticles act as treatments, others play the role of Trojan horse: they pretend to be ordinary, recognized molecules, gain access through special receptors, and sneak the drugs with them as they pass through the restricted entry gates. Nate Vinzant, an undergraduate in Gina Forster’s lab at the University of South Dakota, is using iron oxide to smuggle anti-anxiety drugs into the brain.
 </p>
<p>
  When injected directly into the brain, antisauvagine decreases anxiety in rats. However, direct injection into the brain isn’t a feasible treatment option for humans and antisauvagine is incapable of passing from the blood to the brain on its own. To sneak it in, Vinzant attached antisauvagine to iron oxide nanoparticles, which are regularly taken into the brain via specific receptors. When hitched to iron, antisauvagine goes along for the ride because “the brain thinks it’s iron,” Vinzant says. Indeed, typically anxious rats given iron-bound antisauvagine displayed less signs of stress than untreated rats, confirming that the drug made its way from the injection site in the abdomen, through the blood, and across the barrier.
 </p>
<p>
  More than just a boon for anxiety treatment, this research is a proof of principle. Other drugs can be tethered to nanoparticles like iron and use the same uptake mechanism.
 </p>
<h2>
  Remote Controls
 </h2>
<p>
  In addition to improving treatments, nanoparticles can also help researchers understand diseases and the brain in general. President Obama’s BRAIN Initiative, a program aiming to map the neurons and connections within the human brain, is initially focused on the development of novel technologies that may lead to future breakthroughs. This fall, Sarah Stanley, a post-doctoral researcher in Jeffrey Friedman’s lab at Rockefeller University, received one of the initiative’s first grants to develop technology that uses nanoparticles to control neurons.
 </p>
<p>
  Stanley’s goal is to examine a diffuse network of neurons distributed throughout the brain. “We were really looking for a way of remotely modulating cells,” Stanley explains, but existing tools weren’t able to go deep or dispersed enough. For example, one popular new technique known as optogenetics, which uses light to activate neurons, wouldn’t work for Stanley’s project because light can’t penetrate very far into tissue. Another method involving uniquely designed drugs and receptors can’t be quickly turned on and off. So Stanley turned to nanoparticles.
 </p>
<p>
  Ferritin nanoparticles bind and store iron, and Stanley genetically tweaked the nanoparticles to also associate with a temperature-sensitive channel. When the channel is heated, it opens, leading to the activation of certain genes.
 </p>
<p>
  To generate heat, she used radio waves. Unlike light, radio waves freely penetrate tissue. They hit the ferritin nanoparticle, heating the iron core. The hot iron then heats the associated channel, causing it to open. Stanley tested the system by linking it to the production of insulin; when the radio waves heated the iron, the channel opened and the insulin gene was turned on, leading to a measurable increase in insulin. The nanoparticle is “basically acting as a sensor for radio waves,” says Stanley. It’s “transducing what would be entirely innocuous signals into enough energy to open the channel.”
 </p>
<p>
  To optimize the system, Stanley first tested it in liver and stem cells of mice, but she is now moving into mouse neurons, intending to turn them on and off with her nanoparticle remote control. The radio waves’ penetration should allow researchers to use this technique to manipulate cells that are both deep and spread throughout the brain. “This tool will allow us to be able to modulate any cells in any [central nervous system] region at the same time in a freely moving mouse,” Stanley notes.
 </p>
<p>
  For now, remotely controlling neurons in this way will only be used in research to discover more about these deep or dispersed networks. But eventually, it could potentially be combined with gene therapy to fine-tune protein levels. For example, in diseases with a mutated or dysfunctional gene, like Rett Syndrome, a developmental disorder causing movement and communication difficulties, gene therapy aims to replace the defective gene. Adding a functional gene isn’t always enough, however, as it must be adjusted to produce the appropriate amount of protein. Controlling the gene with radio waves and nanoparticles would allow doctors to carefully tweak the protein production.
 </p>
<aside class="pulledquote">
  Eventually, remote-controlled neurons could potentially be combined with gene therapy to fine-tune protein levels.
 </aside>
<p>
  Although that’s a long way off, nanoparticles are claiming their spot in the future of neuroscience. In a press conference on innovative technologies at November’s Society for Neuroscience Conference in Washington, D.C., David Van Essen, a neuroscientist at Washington University in St. Louis, indirectly praised Stanley’s project. “It was really exciting to see earlier this fall that the [National Institutes of Health] has awarded about 50 new grants for some amazing, innovative ideas.” He then went on to introduce Rzigalinski’s research on Parkinson’s disease, mentioning how nanotechnology is a new tool providing hope for reversing devastating diseases.
 </p>
<p>
  Neuroscientists may need to temper their excitement, however. Clinical trials for cancer treatments have stalled as some nanoparticles—including iron—have been found to generate free radicals, which can trigger cell death. But a compromise may be possible: iron nanoparticles are also being studied to enhance magnetic resonance imaging (MRI) signals and toxicity doesn’t seem to be an issue so long as the doses are kept low. If the drugs the nanoparticles carry with them are powerful enough, lower doses can be used and harmful side effects prevented.
 </p>
<p>
  So far, cerium oxide nanoparticles have avoided this issue, but their relentless crusade against free radicals may lead to a different problem: free radicals are crucial to certain cellular processes, including the regulation of blood pressure and function of the immune system. The question of how much free radical scavenging is too much remains to be answered. But, considering the elevated levels of free radicals in disease, perhaps the nanoparticles will have their hands full lowering levels to a healthy range, let alone reducing them enough to cause trouble.
 </p>
<p>
  It’s still too early to know whether nanoparticles will usher in a new wave of clinical treatments, but to many researchers, it’s clear that they show great promise. Rzigalinski, for example, has long since apologized to her student for her disbelieving rant. Small as they may be, nanoparticles have the ability to take on Goliath-sized tasks, bringing researchers deep inside the brain, past its defenses, ready to fight destructive forces in new ways.
 </p>
</section>
<p>
 Image credit: © C.J. Guerin, PhD/Science Photo Library/Corbis
</p>

Nanoparticles' unique properties could dramatically change the way we understand and treat the brain and its diseases.

"BigBrain" a Small Step Toward Mapping Human Mind

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<div class="add-container clearfix" id="add-block-placer">
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<p>
  Imagine taking a map of a city, shredding it into 7,400 pieces, and then putting it back together. You have to align the landmarks, fix any tear or rip you’ve created in the process, and make sense of any shred you might have lost.
 </p>
<p>
  Now imagine doing the same to a preserved human brain. That’s what scientists at the Institute of Neuroscience and Medicine in Jülich, Germany and the Montreal Neurological Institute in Canada did. It was a monumental undertaking, and one that will undoubtedly contribute to President Obama’s recently announced BRAIN Initiative, which stands for Brain Research through Advancing Innovative Neurotechnologies. But when compared with the lofty goals of BRAIN, BigBrain, as this project is called, is just a small step down a very long and uncertain road.
 </p>
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<img alt="" class="richtext-image full-width" src="https://www.pbs.org/wgbh/nova/media/images/unloading-brain-slices.width-990_OaDTvyh.jpg"/>
<figcaption>Researchers slicing the chilled, preserved brain before staining begins.
        
    </figcaption>
</figure>
<p>
  BigBrain isn’t a part of the BRAIN Initiative, but it is precisely the kind of research that is needed to advance the multibillion-dollar, multiyear federal initiative toward its goal of mapping all the neurons in the human brain. The ambitious BRAIN Initiative is often compared with the Human Genome Project, a research program that had similarly lofty goals and a long timeline. It took the Human Genome Project 13 years to sequence our entire genome, and that’s after the project was officially started. The BRAIN Initiative is still in the planning phases, with timelines and specific goals still being formulated.  If anything, the work on BigBrain, detailed in this week’s issue of the journal
  <i>
   Science
  </i>
  , puts into perspective the enormity of the BRAIN Initiative.
 </p>
<p>
  As the name implies, BigBrain wasn’t a small side-project. Before it, most studies of its kind used the mouse brain, which is 7,500 times smaller than the human brain. Completing BigBrain took a team of scientists 10 years. They started by obtaining the brain of a healthy, 65-year-old woman who died of non-neurological reasons. Before they cut into it, they put the brain through an MRI scanner. That provided them with a reference—like the lid of a puzzle box—that they could use later when reassembling the brain. The team then sliced it into 20-micron sections. (By comparison, a human hair is about 70 microns thick, and a piece of paper is about 100 microns.) Alan Evans, one of the study’s authors, likened them to Saran wrap, except they didn’t come in a single roll but over 7,400 individual sections.
 </p>
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</div>
<div class="inline-caption">
  Another historically famous brain belonged to a man called H.M. After he died, scientists sliced and stained his brain to learn about memory. For more about H.M. and memory,
  <a href="http://www.pbs.org/wgbh/nova/body/how-memory-works.html" target="_blank">
   watch the complete program
  </a>
  .
 </div>
<p>
  Next, they dyed each section to distinguish different cells, and then scanned the sections into the computer, a task that took 1,000 hours to complete. Once digitized, researchers repaired rips and distortions that occurred during slicing and scanning. Finally, they put the entire brain back together, slice by slice, using the MRI as a guide.
 </p>
<h2>
  Zooming In: A Map of Houses
 </h2>
<p>
  Prior to this study, MRI provided the most detailed 3D peek into a human brain. If you think of the brain as a map of a country, the resolution of MRI—about 1 millimeter—would make towns visible, but nothing smaller than that would be. BigBrain, on the other hand, “does 50 times better in each dimension than the typical 1-millimeter resolution of MRI,” says Katrin Amunts, a neuroscientist at the Institute of Neuroscience and Medicine in Jülich, Germany, and lead author of the paper. Specifically, BigBrain’s 20-micron resolution is fine enough to pick out individuals of certain types of cells, but not all; the smallest neurons in the brain are only about 10 microns across. Still, if this were a map, the level of detail provided by BigBrain greatly exceeds MRI, allowing us to see not just towns, but the houses within them.
 </p>
<figure class="richtext-image full-width">
<img alt="" class="richtext-image full-width" src="https://www.pbs.org/wgbh/nova/media/images/bigbrain.width-990_uzpTkUX.png"/>
<figcaption>
</figcaption>
</figure>
<p>
  “It’s an extension of the classic work that’s been done literally since the turn of 20
  <sup>
   th
  </sup>
  century to try to provide a more accurate description of the various areas of the brain and the morphology of the brain,” says Donald Stein, a neuroscientist at Emory University who was not involved with the work. Early in the 20
  <sup>
   th
  </sup>
  century, neuroscientists painstakingly surveyed the brain and documented what the cellular populations looked like, the various shapes, sizes, and groupings of different cells in different parts of the brain—a cul-de-sac of small houses here, large farmhouses scattered across a countryside over there. Certain regions of the brain, known as Brodmann’s areas, were later discovered to have specific functions, such as language, vision, or hearing. Today, BigBrain gives us a clearer picture of these areas.
 </p>
<p>
  But it’s still just one person’s brain, says Joshua Sanes, a neuroscientist at Harvard University and a member of the BRAIN Initiative advisory committee. He doubts that we will learn a whole lot by just looking at one sample. But he’s optimistic, explaining that BigBrain can be used as a reference to help ensure consistency across different studies and subjects. For example, a study comparing brains from healthy people with brains from Alzheimer’s patients would need to compare them to a standard reference brain in order to correct for the typical variability between subjects. Sanes hopes BigBrain will fulfill that role.
 </p>
<p>
  It can also serve as a scaffold, supporting data from other studies, just as the frame of a house supports siding and shingles. Currently, functional MRI can tell us which general region is involved in a function, like reading, but it doesn’t give us much more than a hazy outline. Other types of studies may use BigBrain to mark the location of different neurotransmitter receptors or patterns of gene expression. Allan Jones, the CEO of the Allen Brain Institute in Seattle and not an author on the paper, says BigBrain will be able to “anchor all of the great science being done in imaging to a much higher resolution atlas and framework.”
 </p>
<h2>
  Not So Fast: Life Without Streets
 </h2>
<p>
  Most scientists I interviewed agree this is a great start, but some still question whether BigBrain could live up to the hype surrounding its introduction. Stein likens BigBrain to “the high resolution screen on the latest iPhone. Is it really that much better than the last iteration that came out six months ago?”
 </p>
<p>
  Perhaps the biggest pieces missing from BigBrain are the connections between neurons and the different regions of the brain. Right now, BigBrain is like a map of a city with no streets, just buildings. While that sounds like a glaring oversight, Sanes says it’s a sensible approach; if researchers had tried to trace these physical connections by staining them, the brain would have emerged an inscrutable, tangled mess. To make the next step—understanding how neurons communicate and connect with each other—we’ll need additional studies that use different technologies. But even here, BigBrain can help. Michael Eisen, a biologist at the University of California at Berkley, suggests that we can begin to look at traffic patterns in the brain by overlaying other types of imaging onto the BigBrain atlas.
 </p>
<figure class="richtext-image full-width">
<img alt="" class="richtext-image full-width" src="https://www.pbs.org/wgbh/nova/media/images/mgh_hcp_wedeen_lg-th.width-990_EDIkAjD.jpg"/>
<figcaption>Scientists hope to use BigBrain along with other data to help map connections between different regions of the brain.
        
    </figcaption>
</figure>
<p>
  “There are a lot of other equally valid approaches to understanding how the brain might work and [BigBrain] is just another one in the armamentarium that we should all be able to use and pick and choose from.” Stein says. Eisen agrees that BigBrain is one more tool in the chest. “Collectively, all these things are going to be important in moving the field forward, but any individual one of these things [isn’t] going to revolutionize the world.”
 </p>
<h2>
  Zooming Out: The Bigger Picture
 </h2>
<p>
  BigBrain is an early but important contributor to the BRAIN Initiative, Sanes says. This new paper, “reported one step on a very long path toward understanding the brain,” he says. “I think of it largely in terms of long-term goals. For example, this BRAIN Initiative.”
 </p>
<p>
  What the BRAIN Initiative hopes to accomplish is far beyond what neuroscience can do today. Currently, scientists can count the neurons of simple animals like worms and map some detailed circuits in mouse brains. Sanes suggests the early stages of the BRAIN Initiative will be similar to the Human Genome Project. When that research program began in 1990, genomes of smaller organisms like bacteria and worms had been sequenced, but the human genome remained a daunting and expensive task. The early stages of the genome project involved developing new technology that would ultimately make the rest of the undertaking much cheaper and easier, Sanes says.
 </p>
<p>
  Neuroscience is in much the same position today. Many technologies that will be needed to accomplish the BRAIN Initiative’s goals, like those behind BigBrain, are in their infancy. When the BRAIN Initiative begins next year, BigBrain will serve as a reminder of the difficulty of each step toward the ultimate goal.
 </p>
<p>
  Eisen, though, is optimistic. He predicts that we’ll see similar advances in the coming months. “This is very much a field in a dynamic moment in time,” he says. “This is what it looks like when a field is really humming.”
 </p>
</section>
<p>
 Photo credits: Amunts, Zilles, Evans, et al. and the NIH.
</p>

Two of Pluto’s Moons Named After Public Vote

<section class="entry-content instapaper_body clearfix" itemprop="articleBody">
<div class="add-container clearfix" id="add-block-placer">
</div>
<p>
  Nadia Drake, writing for Wired:
 </p>
<blockquote>
<p>
   Formerly known as P4 and P5, Pluto’s tiniest moons now have official names: Kerberos and Styx.
  </p>
<p>
   The names were among the top three selected by voters during a two-week polling period; they have just been approved by the International Astronomical Union’s official nomenclature committee.
  </p>
<p>
   Thus, from this day forward, the two tiniest of rocks orbiting the overgrown-snowball-formerly-known-as-a-planet will conjure the tales of a three-headed dog guarding the gates of the underworld (Kerberos), and the river that doomed souls must cross (Styx).
  </p>
</blockquote>
<p>
  The votes didn’t come without celebrity endorsements. In February, when voting began, William Shatner suggested Vulcan as one of the names. Vulcan won handily, with over 170,000 votes. Second place went to Cerberus with more than 99,000 votes.
 </p>
<figure class="richtext-image full-width">
<img alt="" class="richtext-image full-width" src="https://www.pbs.org/wgbh/nova/media/images/plutos-moons.width-990_FPB6M1K.jpg"/>
<figcaption>The Hubble Space Telescope has discovered five moons orbiting Pluto. The latest, previously known as P4 and P5, were named Kerberos and Styx, respectively.
        
    </figcaption>
</figure>
<p>
  But the process wasn’t entirely democratic. The International Astronomical Union (IAU) has to approve the names and took issue with Vulcan, saying too many other objects had that name. Second place Cerberus, which is also the name of an asteroid, was rejected, too. Mark Showater, who discovered P4 and P5, suggested the Greek spelling of Cerberus, Kerberos, an alternative which the committee found more palatable. Third place, Styx, took the remaining spot.
 </p>
</section>

The lung-on-a-chip, developed by Dr. Donald Ingber, has many promising applications.

Can We Eliminate Animals from Medical Research?

<p>
 Deep in a lab at the Wyss Institute for Biologically Inspired Engineering at Harvard University, Dr. Donald Ingber has reconstructed a human lung. It absorbs oxygen like a normal human lung. It also transmits that oxygen to blood cells flowing beneath. White blood cells flock to foreign bodies that try to infect its tissue, surrounding the invaders and stamping them out. In many ways, it’s indistinguishable from the lungs that rise and fall inside you and me, with one exception. This lung is on a microchip.
</p>
<p>
 On these microchips smaller than your thumb, Ingber, director of the Wyss Institute, has reconstructed the complicated interface between lungs and their capillaries. The core of the device is a tiny tube created by microfabrication—a technique used to make structures on the micrometer scale—which is divided in two by a flexible, porous membrane. Human lung cells line the top of the membrane, and capillary cells coat the underside. Air flows through the upper chamber, and a liquid containing human blood cells runs through the lower chamber. Graduate students apply suction to compartments on the sides, mechanically stretching the membrane and its tissue to simulate the rise and fall of our own chest
</p>
<p>
 Ingber’s lung-on-a-chip isn’t just a breakthrough because it mimics a human organ, but because it does so in more ways than one. The lung cells that line the upper chamber stand in for your lung’s alveoli, the microscopic air sacs where gasses pass in and out of the blood stream. As grad students stretch the chamber, it fills with air, passing oxygen through the capillary cells on the other side of the membrane to the blood cells streaming through the lower chamber.
</p>
<div class="related"></div>
<p>
 Just as with human lungs, these cells are susceptible to infections. When Ingber’s team added bacteria to the airspace of the lung-on-a-chip, white blood cells swarmed to the bacteria. Again, just as they would in a real lung. As Ingber’s team pumped the airspace full of various foreign bodies, they discovered something more—that breathing increases the absorption of airborne particulates, like those found in pollution and smog, ten-fold.
</p>
<p>
 They have also tested the toxicity of a cancer drug known to fill patient’s lungs with fluid, a condition known as pulmonary edema. When they gave the lung-on-a-chip the same relative dose given to humans over the same timeframe, the drug caused fluid to shift from the blood vessel into the airspace, mimicking a pulmonary edema. The degree to which Ingber’s lung-on-a-chip can emulate a real human organ is uncanny. It’s all possible because the lung-on-a-chip wasn’t designed with just one purpose in mind. It is, Ingber says, “a toxicity model, a drug efficacy model, and a human disease model.”
</p>
<p>
 But perhaps their greatest feat will be the replacement of animal models in research studies. Animals such as chimpanzees, mice, and guinea pigs, have been used in medical research for centuries, and they have taught us much about anatomy and physiology. But in recent decades, we’ve realized the limitations of animal models. In some cases, animal organs and systems serve as passable stand-ins for their human equivalents, but in many cases they do not. Ingber’s lung-on-a-chip is one of many new attempts at replacing animal models with more effective analogs.
</p>
<div class="ad"></div>
<h2>
 The Animal Problem
</h2>
<p>
 The pharmaceutical industry has a problem: about 90% of drug trials fail. Treatments often seem promising when tested in animals, encouraging pharmaceutical companies to start clinical trials that test safety and efficacy in human patients. But the majority of the time, the investment doesn’t pay off. Some are pointing their fingers at animal models, saying they don’t accurately represent the human disorder they are designed to mimic. Moreover, their response to treatments doesn’t predict a human’s response and experiments using them often paint an overly optimistic picture.
</p>
<p>
 Ray Greek, president of Americans for Medical Advancement, a group that seeks to restrict the use of animals in medical research, is among those questioning the efficacy of animal models. Often research animals are bred or genetically modified to develop characteristics of a human disease such as diabetes or Alzheimer’s disease. While most drugs used to treat those afflictions don’t act on genes directly, genes do make proteins that drugs bind to, so tiny differences between species could be the difference between a treatment’s success and failure, Greek says. “Really tiny differences can make a gene lethal to you but perfectly fine for a monkey or a chimp or a mouse,” he says. “That’s Evolution 101. Different genes do different things in different species.”
</p>
<figure class="richtext-image full-width">
<img alt="lab mouse" class="richtext-image full-width" src="https://www.pbs.org/wgbh/nova/media/images/lab-mouse.width-990_mGNMqYK.jpg"/>
<figcaption>The success of treatments given to animal models, such as mice, does not always translate to humans.
        
    </figcaption>
</figure>
<p>
 For many diseases, animal models can be challenging to develop. For others, like neurological and neurodegenerative diseases, it’s even more difficult. “The time that a mouse lives—which is about two or three years—is about seventy years less than it requires a human to develop some of these disorders,” says Dr. Christopher Austin, director of the National Center for Advancing Translational Sciences. Austin says researchers try to manipulate mutations to make their effects even more severe, but “because you have to speed it up to make it happen much faster, you think maybe it’s not terribly surprising it would not be predictive.”
</p>
<div class="pullquote">
<p>
 “I don’t know a single scientist who is not trying to reduce, refine, or replace animal use whenever possible.”
</p>
</div>
<p>
 Besides genetic models, there are a number of different ways researchers simulate diseases in animals, including by introducing an infection or administering a drug. These, too, can be problematic. Take traumatic brain injury, for example. In a controlled experiment, the procedure is standardized such that all mice receive the same injury. On the football field, however, no two injuries may be the same. A neurologically complex disease like schizophrenia is hard to model in an animal in the first place—you can’t ask a mouse questions, after all—so testing if a drug reduces symptoms is even more difficult.
</p>
<p>
 Not only are induced diseases and conditions often different in animals, but how we treat them doesn’t always translate well to humans. Livers of different species metabolize drugs differently, for example, so toxicity may vary. And in the laboratory, a stroke can be induced and then treated immediately; in real world situations with humans, the time between stroke and treatment is often longer and much more variable.
</p>
<p>
 Austin notes that scientists appreciate these problems. “For all kinds of reasons, scientists would love to have some other way to study most phenomena than using animals,” Austin says. “I don’t know a single scientist who is not trying to reduce, refine, or replace animal use whenever possible. It’s just that for many indications, for many applications, for many diseases—particularly in the neurosciences—there is no alternative. That’s the problem.”
</p>
<h2>
 Possible Replacements
</h2>
<p>
 To sidestep the problems with animal models, some scientists use cellular models, which are often derived from human tissues. One way to obtain human cells is to use induced pluripotent stem cells, also known as iPS cells, made from adult tissues such as skin or blood which are reprogrammed into stem cells that can then become any type of cell in the body. This method is useful for studying how a particular drug binds to a receptor, for example, and how the cell responds. But it’s not perfect. “What happens to an isolated cell—even a human cell—growing on a dish, on plastic, is likely to be very different from how that cell is going to react in a tissue surrounded by other cells,” Austin cautions.
</p>
<p>
 This is where Ingber’s organs-on-chips are useful. The chips more closely represent real, live tissue, with various cell types, arranged as in a human, along with their three-dimensional interactions. Importantly, cells grown in a single layer on a dish can’t mimic motion, like the simulated breathing of the lung-on-a-chip. Motion is important in other organs, too. Ingber’s group has modeled an intestine, predictably called the gut-on-a-chip. In addition to hosting the various cell types that make up an intestinal wall, the gut-on-a-chip also pulses in waves, just like our gastrointestinal tracts do to move food along.
</p>
<div class="pullquote">
<p>
 Ingber’s group is working on replicating nearly every kind of organ and tissue.
</p>
</div>
<p>
 Not only does that motion create a more realistic simulation, it also helps the cells thrive. That’s because Ingber’s chips don’t just host human cells. The gut-on-a-chip also contains some of the same microbes found in a living human’s gut. When cells are grown in culture, scientists often try to keep them free of microbes. Any whiff of contamination can kill the other cells. However, in the gut-on-a-chip, fluid flowing through the chamber, along with the peristalsis-like motion, helps gut microbes grow in a healthy, symbiotic way. That allows Ingber’s group to study how microbes contribute to health and disease.
</p>
<p>
<br/>
 By incorporating both lung and capillary cells in a manipulatable structure, the lung-on-a-chip enables more realistic simulations.
</p>
<p>
 Currently, Ingber’s group is working on replicating nearly every kind of organ and tissue, including kidneys, livers, and bone marrow. Eventually, he even hopes to connect different organs to make what he calls a human-body-on-a-chip. “Imagine delivering a drug by aerosol to the lung chip, watch it flow over to the liver and see if it’s metabolized into different breakdown products—which is what happens in animals and humans—and then see if that’s peed out by the kidney.” You could test which dose would be optimal to slow the heart, for example, or check if a chemotherapy drug kills bone marrow cells. Ingber notes that is “what we do in animals, effectively, but it would be all human.”
</p>
<p>
 Organs-on-chips also could be used to study how genetic variability between people changes how drugs and treatments work. Greek says future treatments need to be based on a person’s individual genome, a concept known as pharmacogenetics. “Right now, a drug that cures you of a particular kind of cancer may not cure me,” Greek says. “And a drug that I can take for hypertension may work well for me…but you may have a gene that causes a very severe side effect and you won’t know until you take the drug.” Human clinical trials do test safety and efficacy, but Greek is concerned that they don’t capture enough of the variability among people. Because of this, he warns, “everybody who takes a drug is a guinea pig.”
</p>
<p>
 Austin speculates that organs-on-chips could be used with pharmacogenetics to address Greek’s concern. “It’s interesting to think about the potential intersection between organoid tissue chip technology and iPS technology and personalized medicine technology,” he says. Austin imagines taking iPS cells from 100 people and putting them on chips, then assessing the variation in responses to drugs. It would be faster, cheaper, and safer than testing in animals or humans. “You could do it very quickly,” he says. “You could do it in an afternoon.”
</p>
<h2>
 Or Do We Refine?
</h2>
<p>
 Jonathan Kimmelman, a bioethicist at McGill University, doesn’t think we need to do away with animal models entirely, but thinks we can improve them. He believes part of the reason why treatments on animals models don’t always translate well to humans is the way preclinical research—including testing on animal models—is designed. Once a treatment makes it to clinical trials, which test safety and efficacy in human subjects, there are many rules and regulations in place to prevent bias. One is blinding, where researchers don’t know which treatment the subject received, and another is randomization, where treatment groups are randomly assigned. However, these procedures are only used sporadically in preclinical research, which often involves animals. A recent review of 300 animal studies found that only 14% used blinding and just 13% used randomization.
</p>
<p>
 Another issue is publication bias, where studies with positive results touting the success of a new drug are far more likely to be published than studies with negative results. “That means that when results do get published, you only see a slice or a narrow band of the most positive and encouraging findings,” Kimmelman says. “What’s missing is the perhaps the bottom part of the iceberg, which are inconclusive or negative animal findings.”
</p>
<p>
</p>
<figure class="richtext-image full-width">
<img alt="clinical trial 2" class="richtext-image full-width" src="https://www.pbs.org/wgbh/nova/media/images/clinical-trial-2.width-990_CKm4Kxd.jpg"/>
<figcaption>Clinical trials, like the one pictured above, are better regulated these days, but preclinical trials don't have the same scrutiny.
        
    </figcaption>
</figure>
<p>
 As decisions are made about clinical trials, this vital information is often missing. For example, in 1980, researchers suspected that lorcainide, an anti-arrhythmic drug, might be a promising treatment following a heart attack. They hypothesized that, since lorcainide decreased abnormal heart rhythms in non-heart attack patients, it would be helpful in for those who suffered from a heart attack, a population more likely to have abnormal heart rhythms. They tested it on a small group of 100 volunteers. Of the 50 people who were treated with lorcainide, ten died. Only one person from the control group given the placebo died. Lorcainide was abandoned as a post-heart attack treatment, but the trial was never published. So when other companies investigated anti-arrhythmic drugs for heart attack patients, they were unaware of lorcainide’s failure. In later trials, when the drugs were again given to people following heart attacks, even more people died.
</p>
<div class="newsletter"></div>
<p>
 In the years since, safety regulations for clinical trials have increased dramatically. One current requirement is prospective registration, which requires that details of the study—such as the drug to be tested, the expected enrollment, and the definition of success—are recorded in a publicly accessible database before the study starts. Once the study is completed, researchers can search the database and learn the results of the experiment—even if it was not published in a peer-reviewed journal. Kimmelman would like to see the same registration process used in hypothesis-driven animal studies, such as testing the efficacy of a drug, for example.
</p>
<p>
 “There are no registries out there for prospectively stating the design of an experiment,” Kimmelman says. “Prospective registries are crucial for preventing publication bias.”
</p>
<h2>
 The Middle Road
</h2>
<p>
 Ingber also acknowledges that although animal models have their flaws, we cannot get rid of them entirely. His organs-on-a-chip and proposed human-on-a-chip offer promising ways to reduce dependence on animal models, but they are not the same thing as a whole, living organism. “There are certain things in animals you are not going to replace on chips, like behavior for example.”
</p>
<p>
 “Sometimes people don’t realize,” Austin says, that animal models “are absolutely essential for what’s going on in medical research now. If animals stop being used, progress in medical research would slow dramatically and probably screech to a halt in some cases. Many of the advances that we take for granted now have happened through the use of animal models.”
</p>
<p>
 Researchers are increasingly moving away from using animals to model an entire disease, but rather to replicate one aspect that could be treated with a particular drug or intervention. For example, mice bred to be obese and hyperglycemic can be used to study type 2 diabetes. The mice aren’t perfect models of type 2 diabetes—they do not have beta cell dysfunction, for instance, which causes insufficient insulin levels in the human disease—but researchers use them to test drugs that improve insulin resistance specifically. “There are many examples of where those particular aspects of a disease or human physiology may actually be reproduced quite faithfully in a particular animal model,” Austin says.
</p>
<p>
 Computational advances may also help extend the insight gained from animal models. The European Union’s Human Brain Project, which aims to build a brain from supercomputers, is just one example. It’s an ambitious project—one that won’t be completed for at least a decade. But if it meets its goals, it will hopefully give us a better appreciation for the neurological differences between animals and humans. Eventually, that may lead to better treatments.
</p>
<p>
 “Animal models are not going away,” Ingber says. “But we hope, over time, one animal at a time, maybe we can replace—maybe we can show this chip can replace what people were measuring for this particular model. Maybe we can use less animals,” he adds. “Everyone knows it’s a problem that needs to be solved.”
</p>
<p>
 Photos by the Wyss Institute at Harvard,
 <a href="http://www.flickr.com/photos/51868421@N04/7401820390/">
  Novartis AG/Flickr (CC-BY-NC-ND)
 </a>
 and
 <a href="http://www.flickr.com/photos/nestle/7155349215/">
  Nestlé/Flickr (CC-BY-NC-ND)
 </a>
</p>

<p>Promising new technologies may reduce our dependence on animals in medical research. But will they be enough?</p>

Henrietta Lacks’s Family Finally Gets A Say

<section class="entry-content instapaper_body clearfix" itemprop="articleBody">
<div class="add-container clearfix" id="add-block-placer">
</div>
<p>
  Carl Zimmer, writing for the New York Times:
 </p>
<blockquote>
<p>
   Henrietta Lacks was only 31 when she died of cervical cancer in 1951 in a Baltimore hospital. Not long before her death, doctors removed some of her tumor cells. They later discovered that the cells could thrive in a lab, a feat no human cells had achieved before.
  </p>
<p>
   Soon the cells, called HeLa cells, were being shipped from Baltimore around the world. In the 62 years since — twice as long as Ms. Lacks’s own life — her cells have been the subject of more than 74,000 studies, many of which have yielded profound insights into cell biology, vaccines, in vitro fertilization and cancer.
  </p>
<p>
   But Henrietta Lacks, who was poor, black and uneducated, never consented to her cells’ being studied.
  </p>
</blockquote>
<p>
  In 1973, a researcher interested in comparing family members’ genes to Ms. Lacks’s contacted her children. It was the first they heard of the cells. Rebecca Skloot brought attention to the story in her bestselling book The Immortal Life of Henrietta Lacks, published in 2010.
 </p>
<p>
  In March of this year, a study detailing the genetic sequence of HeLa cells was published, providing public access to a downloadable version of the genome. Another similar study was slated to be published soon after. The family—who had previously been unaware of the projects—objected, citing privacy issues. (Information from Ms. Lacks’s genome could be used to make inferences about her children and grandchildren’s genes—medical information generally kept private.) The published study was taken down and the other postponed until a compromise could be made.
 </p>
<p>
  After months of discussion, the Lacks family and the National Institutes of Health recently reached a compromise. It doesn’t give the family any right to earnings from future research—nor have they received any compensation for profits made in the past. However, it does provide more privacy.
 </p>
<figure class="richtext-image full-width">
<img alt="" class="richtext-image full-width" src="https://www.pbs.org/wgbh/nova/media/images/collins.width-990_98bziOn.jpg"/>
<figcaption>Dr. Francis Collins, the director of the National Institutes of Health, and members of the Lacks family celebrate the compromise.
        
    </figcaption>
</figure>
<p>
  The agreement requires that any scientist who wants access to the genomic data will need to justify their research to a committee first. If access is granted, they must submit annual updates of their findings. Sixty-two years after the cells were unknowingly taken, the Lacks finally have a say—two members of the six-person committee will be from the Lacks family.
 </p>
</section>
<p>
 Image courtesy of NIH
</p>

Teal Burrell

Articles