<?xml version="1.0"  encoding="utf-8" ?><rss version="2.0" xmlns:dc="http://purl.org/dc/elements/1.1/">
	<channel>
		<title>MIT World: Science</title>
		<link>http://mitworld.mit.edu/</link>
		<description>MIT World media in category 'Science'.</description>
		<language>en-us</language>
		<pubDate>Tue, 24 Nov 2009 19:20:22 GMT</pubDate>

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			<title><![CDATA[The Power of Basic Science Applied to Medical Progress: Past Examples and Hope for Schizophrenia and Bipolar Illness]]></title>
			<pubDate>Thu, 12 Nov 2009 00:00:00 -0500</pubDate>
			<guid>http://mitworld.mit.edu/video/721</guid>
			<link>http://mitworld.mit.edu/video/721</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill01212schoolofsciscolnickmedicalprogress22oct2009.jpg"  alt="" />An exemplar of the purpose-driven life in medical science, <b>Ed Scolnick</b> details research milestones from a remarkably varied career, revealing how scientific insight and collaborative effort translate into life-saving solutions for millions.<br><br> 

This physician turned biochemist has held distinguished positions at the National Institutes of Health, Merck, and now at MIT, but common themes unite his pursuits:  “I’m always excited by the inherent beauty of molecular and biochemical insights into how biology works. Making scientific discoveries for me is tremendously emotionally satisfying and in fact addicting.” <br><br>

In his talk, Scolnick touches on such research breakthroughs as identifying virus oncogenes, and developing treatments for cardiovascular disease, Hepatitis B, and osteoporosis, among others.  He emphasizes that teasing out the biochemistry of diseases is “the key to success in drug discovery.”  In Marfan syndrome, for example, investigators learned that a mutant gene leads to a malfunctioning aorta. Finding a cure flowed from understanding the underlying pathological processes.  Scolnick proudly describes research on a gene involved with cholesterol buildup and an elevated risk for cardiovascular disease. This led to the development of statins, which has helped dramatically reduce the death rate in people with heart disease. <br><br>

Scolnick offers a dramatic chronology of his pioneering work at Merck starting in 1981 to find an effective AIDS treatment, an effort leading to the protease inhibitor Crixivan.  His timeline covers more than a decade of scientific collaboration to block the mechanism of HIV, and involves false starts, the death of a key scientist in the Lockerbie bombing, pressure from AIDS activists and corporate overseers, a “miracle” AIDS patient, breakthroughs in measuring viral protein, and more than one “twist of fate.”<br><br>

In 2004, Scolnick turned in a new direction:  toward mental illness, a field stalled for decades due to ignorance “about the underlying biochemistry and physiology of the disease.” Today, with the help of genomics and computative technologies, researchers are beginning to reveal the basic genetic architecture of schizophrenia and bipolar illness, says Scolnick.  The “outline of their biochemistry” is starting to come clear for the first time, leading to the real possibility of novel therapeutics.  While the challenges are formidable, he believes, consolidating MIT’s “first rate neuroscience, human genetics, chemistry (creates) a unique opportunity to do something in a field that desperately needs the kind of approach and change we were able to bring to the AIDS field.”<BR><BR>
<b>NOTE:</b> Audio levels for Kastner and Horvitz are very low, but improve when Scolnick begins his talk.  We apologize for the inferior audio capture in the field.
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			<title><![CDATA[The Art of Science Television]]></title>
			<pubDate>Fri, 30 Oct 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/719</guid>
			<link>http://mitworld.mit.edu/video/719</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitw01202physicspappalardolecapsellscitv15oct2009.jpg"  alt="" /><b>Paula Apsell</b>, NOVA&#39;s senior executive producer laments the sad state of science journalism and discusses how NOVA is more essential than ever.  In a world where the public understanding of science is diminishing, she makes a strong case for NOVA&#39;s tradition of depth and substance, tackling the most pressing issues in science, in a thoughtful and visually complex manner.  <BR><BR>

Apsell brings clips from some recent NOVA programs to illustrate the role of television&#39;s most prestigious science documentary series in the vast television and web content landscape.  She provides insights into the editorial processes of topic selection, treatment, and production standards.  In a world of decreasing attention spans, Apsell considers the challenges of providing meaningful science content, keeping it interesting, while not leaving the audience behind.<BR><BR>
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			<title><![CDATA[Newton and the Counterfeiter: The Unknown Detective Career of the World&#39;s Greatest Scientist]]></title>
			<pubDate>Sun, 25 Oct 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/717</guid>
			<link>http://mitworld.mit.edu/video/717</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill01207writingnewtonlevenson06oct2009.jpg"  alt="" />Who knew that one of mankind’s greatest scientists also worked as a gumshoe on London’s mean streets, or that this same absent-minded professor helped England fix its monetary policy from an office in the Tower of London?  <b>Thomas Levenson</b> brings all sorts of surprises to light in his own sleuthing of a little known but significant episode in British history involving Sir Isaac Newton -- subject of his recent book, <i>Newton and the Counterfeiter: The Unknown Detective Career of the World&#39;s Greatest Scientist</i>. <br><br>

Levenson stumbled onto his story while working on a larger history of science: He read a letter in Newton’s files from a “human voice in desperation:” William Chaloner, stuck in Newgate Jail in 1699, facing the gallows for treason (counterfeiting).  Levenson was unable to link together this unlikely pair for a decade, until he struck gold in a stash of 400 documents signed by Newton while he served as a civil servant in the British Mint.<br><br>

The tale Levenson pieced together follows Chaloner from his rural origins to a cunning criminal career in plague-stricken 17th century London, as well as Newton’s passage from world-renowned natural philosopher in isolated Cambridge University, to a promised sinecure in the Royal Mint.  The tale of their intertwined fates illuminates a time when science was beginning to make its mark not just on the intelligentsia, but on all of society.  Levenson describes how the scientific revolution meant “a much broader change in thinking,” new ways of problem-solving that gave even common people a leg up.<br><br>

Newton entered his second career in London to find the English currency in a state of crisis: rampant counterfeiting, as well as the loss of silver from existing currency. One of the geniuses behind this state of affairs was Chaloner, who had come to “coining” by way of such money-making schemes as pornographic watches.  Levenson describes “Newton’s mind at work” as he builds chains of evidence and pursues his prey with elaborate traps, including informants and double agents placed in counterfeiting gangs. <br><br>

Levenson finds “evidence of Newton’s ruthlessness,” as he brings Chaloner to the gibbet with a case that “was rhetorical and persuasive more than precisely accurate.”  In their calculation and drive, both men somehow captured the new scientific spirit of the times. Says Levenson, “When big ideas happen, they don’t just happen in own spheres. There’s an effect that spreads well beyond them. And if they matter to the way people lead their lives, then people will find out about them and do things with them...”
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			<title><![CDATA[America&#39;s Leadership in Clean Energy]]></title>
			<pubDate>Fri, 23 Oct 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/716</guid>
			<link>http://mitworld.mit.edu/video/716</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill01219officeofpresobamacleanenergy23oct2009.jpg"  alt="" />In welcoming President Obama, MIT President<br>  <B>Susan Hockfield</b> summarizes the vast array of energy innovation at MIT, including the MIT Energy Initiative and the student-led 1700 member Energy Club, and declares, "We share President Obama&#39;s view that clean energy is the defining challenge of this era." <BR><BR>

In his introduction of President Obama, Professor <B>Ernest Moniz</b>, Director of the MIT Energy Initiative (MITEI) and member of the President&#39;s Council of Advisors on Science and Technology (PCAST), discusses global issues on clean energy, science and innovation, and credits Obama for expanding the nation&#39;s energy vision. <BR><BR>

<b>Barack Obama</b> came to MIT not just to praise the Institute&#39;s leading edge energy research but to encourage <u>all</u> of America’s “heirs to a legacy of innovation” in their pursuit of discovery.  The nation owes much of its prosperity to risk-takers and entrepreneurs, Obama said, and now, given the linked challenges of energy and climate change, we need such pioneers more than ever.<br><br>

After visiting MIT labs working on more efficient solar cells and lighting, batteries “that aren’t built, but grown,” and offshore wind plants that function even when the air is still, Obama told a large crowd that as the nation inevitably transitions from fossil fuels to renewable energy, we’re counting on the kind of “innovative potential on display at MIT.”  <br><br>

 Obama acknowledges the great challenges facing energy researchers and entrepreneurs. As traditional energy supplies become more precious, and energy demands grow, nations are competing to develop new ways to produce and use energy, said Obama, and the winner will lead the global economy. “I want America to be that nation.  It’s that simple.”<br><br>

His administration’s response has been to make massive investments in both clean energy and basic science. Obama aims these efforts at both the current recession, and the nation’s future economic health.  Clean energy jobs today and research “to produce the technologies of tomorrow” will “lay a new foundation for lasting prosperity.”  He hopes this comprehensive approach will culminate in legislation that will transform America’s entire energy system. <br><br>

But Obama is under no delusion that all will embrace his plan.  “The closer we get,” says Obama, the “more we’ll hear from those whose interest or ideology run counter to that much-needed action we’re engaged in.”  What worries the president more, though, is a dangerous pessimism shared by many, “that our politics are too broken and our people too unwilling to make hard choices for us to actually deal with this energy issue.”  Implicit in this argument, he says, is that America has lost its fighting spirit. <br><br>

Obama rejects this argument “because of what I’ve seen here at MIT … and because of what we know we are capable of achieving when called upon ….”  The nation that harnessed electricity and the atom is one that has always sought out new frontiers, “and this generation is no different.” Obama invokes the achievements of the past as a call to arms “in what is sure to be a difficult fight in the months and years ahead” -- to ensure that “we are the energy leader that we need to be.”

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			<title><![CDATA[Neural Basis of Drug Addiction]]></title>
			<pubDate>Sat, 10 Oct 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/712</guid>
			<link>http://mitworld.mit.edu/video/712</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill01171mcgovernbasaleverittaddiction07may2009.jpg"  alt="" />How does someone move from recreational drug use to addiction?  <b>Barry Everitt’s</b> group at the University of Cambridge has been trying to break down the stages and neural circuitry of addiction with great precision.<br><br> 

Everitt’s research attempts to operationalize a progression in animals from the voluntary taking of drugs, to the acquired habit of drug-taking, to the stage of compulsive drug-seeking and consumption, “where individuals have really lost control.”  This progression seems rooted in the sequential activation of different learning  systems in the brain, which are particularly sensitive to the neurotransmitter dopamine. <br><br>

Research suggests that drug-taking is initially dependent on the nucleus accumbens (part of the ventral striatum), but its establishment involves the dorsal striatum.  Studies show that dopamine in the dorsal striatum is causally involved in establishing drug-seeking behavior in rats. As the animal gets accustomed to taking the cocaine, there’s a “shift in the balance of associative encoding from ventral to dorsal striatum.”  Cocaine craving and self-administration seem to change the functioning of the dorsal striatum in monkeys and humans as well.  <br><br>

While this shift from ventral to dorsal striatum depends to some degree on  “pharmacology” (cocaine’s impact on dopaminergic systems), Everitt has hypothesized that it may also involve “spiraling circuitry” connecting the ventral striatum, the midbrain -- the brain’s motivational and motor mechanisms -- and the dorsal striatum.  Everitt speculates that the compulsive nature of drug seeking may be rooted in part in the prefrontal cortex, home to “top-down executive control mechanisms.”  He describes research that attempted to model this type of compulsion.  Animals with short-term access to cocaine and most animals with long-term access to cocaine suppressed their drug-seeking responses when punished.  But a subgroup of 20% “persisted in seeking cocaine in the face of punishment.”  This result has been replicated many times now, and turns out to have a parallel among humans.  This, says Everitt, “brings up the issue of vulnerability to drug addiction.”<br><br>

Additional research suggests that impulsivity is a “behavioral characteristic that predicts the transition from initial drug intake to loss of control … to compulsive seeking and taking” of drugs. Highly impulsive animals denied cocaine become more impulsive and drug seeking over time, leading to relapses.  Everitt and others  are tracing the neural basis of compulsivity to impairment in the prefrontal cortex, which involves “a loss of control over maladaptive habits” established after long-term drug taking.
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			<title><![CDATA[Imaging the Human Striatum and its Modulation by Dopamine ]]></title>
			<pubDate>Sat, 03 Oct 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/708</guid>
			<link>http://mitworld.mit.edu/video/708</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill01165mcgovernbasalcoolsdopamine07may2009.jpg"  alt="" />Researchers have known for some time that the neurotransmitter dopamine is centrally involved in learning and working memory, <b>Roshan Cools</b> tells us, and that dopamine-responsive circuits connect these parts of the human brain to other structures like the striatum, which also helps orchestrate motor control. Cools has been investigating in detail how dopamine acts within these cortico-striatal circuits to influence different types of cognitive processing.<br><br>

Specifically, Cools examined the effects of dopaminergic drugs (compounds that modulate the quantity of dopamine available to neurons, or the neurons’ responsiveness to dopamine) on human subjects as they performed a variety of performance tasks.  She notes that there’s a “huge variability within and across individuals” to such drugs.  The same chemical within the same subject may improve performance in one task, and impair it in another.  The drug effect depends on an individual’s baseline levels of dopamine: If someone starts with suboptimal levels, a dopamine-enhancing drug can restore someone to baseline, whereas someone starting with optimal levels of dopamine might be overdosed by the same drug.  <br><br>

One of Cools’ studies looked at the impact of dopaminergic drugs in Parkinson’s disease (PD) patients, where “the primary pathology is dopamine depletion in the striatum.”  This depletion is not uniform, though, in the early and late stages of the disease, and impacts different sites in the striatum. Early stage PD patients suffer more from motor deficiencies than from higher level cortical deficiencies.  Through performance tests and fMRI scans,Cools confirmed her hypothesis that in mild PD, dopamine-enhancing medication impaired performance on probabilistic reversal learning (a higher level cognitive task), “presumably by overdosing relatively intact levels of dopamine” in one part of the striatum.  Yet these same drugs improved performance on other tasks associated with a part of the striatum concerned with motor systems.  <br><br>

Cools has recently been testing healthy U.C. Berkeley undergrads with dopaminergic drugs, fMRI and PET scans, to see how levels of dopamine impact their performance on different learning tasks. Says Cools, “Dopaminergic medication improves reward- but impairs punishment-based learning in low-dopamine subjects and PD patients.  Conversely, it improves punishment- but impairs reward-based reversal learning in high-dopamine subjects. This shift in the balance between reward- and punishment-based reversal likely reflects modulation by dopamine of striatal processing.”
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			<title><![CDATA[Monitoring Dopamine Release During Reward Learning ]]></title>
			<pubDate>Sat, 03 Oct 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/709</guid>
			<link>http://mitworld.mit.edu/video/709</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill01170mcgovernbasalphillipsrewardlearning07may2009.jpg"  alt="" />In the process of learning, we “sometimes make more deliberative choices, and sometimes make more visceral ones,” says <b>Paul Phillips.</b>  These are “semantic terms we intuitively know,” and scientists have become well-versed in creating tasks for animals and humans that demonstrate how these different kinds of learning (analytical- reflective vs. impulsive -reflexive) play out.  Phillips has been trying to track dopamine release (a neurotransmitter linked to learning) in such divergent learning processes.<br><br> 

The model-based learning system pairs a stimulus with a reward, and after training, a subject creates a “model representation of the world” that allows it to predict the appearance of the reward after the stimulus. In contrast, the model-free system of learning “uses a one dimensional value that gets updated” as the subject accumulates experience and begins to weigh the difference between expectation and the reward that’s actually delivered. <br><br> 

One of Phillips’ studies involved implanting electrodes for measuring dopamine release in the striatum of rats participating in different types of learning tasks. Phillips work shows time-dependent changes in the release of dopamine during classic conditioning tasks.  At first the dopamine spikes only after the reward, but over time, the animal learns it will receive the reward after the stimulus (a light cue), and soon, the cue alone elicits the dopamine response.  Phillips has also found that two distinct parts of the striatum register increased dopamine at different points in the training. “This is quite interesting in terms of thinking about what these brain regions have been implicated in, and specifically the idea of habits in the dorsal striatum.”<br><br>

The results of some research suggest that during these learning processes, all the dopamine neurons should be firing.  But Phillips says this doesn’t explain why “we’re getting signals in (one) part of the brain but not in the other.”  Phillips speculates that dopamine’s “arch nemesis acetylcholine” might be inhibiting dopamine release in certain parts of the striatum during specific phases of reinforcement learning.<br><br>

Phillips has also been working with selectively bred lines of rats, which seem to exhibit behaviors, and dopamine release patterns, suggestive of two distinct learning strategies.  He concludes that “associations between stimuli and rewards can be learned through multiple strategies with different computational demands,” and he doesn’t believe that animals “are locked into one strategy or another.”  
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			<title><![CDATA[Computational Models of Basal Ganglia Function]]></title>
			<pubDate>Tue, 29 Sep 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/707</guid>
			<link>http://mitworld.mit.edu/video/707</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill01168mcgovernbasaldoyacomputation07may2009.jpg"  alt="" />As a mathematical engineer, <b>Kenji Doya</b> approaches the goal of describing the most intricate brain mechanisms from a computational perspective. He constructs models of reinforcement learning involving the networked structures of the basal ganglia.  His efforts are captured and expressed quantitatively as probabilities, regressions, and algorithms.<br><br>

In this presentation, Doya covers basic concepts of reinforcement learning, then surveys the last decade of inquiry into the components of the basal ganglia circuit governing voluntary motion.  Among the topics: action values, action candidates, and reward prediction involving the neurotransmitter dopamine; model-free versus model-based learning strategies; and the essential role of serotonin as modulator in the complex information loop.<br><br>

Doya’s recent research is carried out via robots he calls “cyber rodents.”  His dream as an undergraduate was to “build a robot that learns the variety of behaviors on its own.”  That is, the computer, <i>not</i> the human engineer, teaches the robot to move.  He accomplished this in designing a machine-creature exhibiting emotion-like attributes characterized as “depression,” “impulsivity,” “greed,” and “patience.”<br><br>

Doya believes the “metaparameters” of reinforcement learning must be “tuned appropriately…Otherwise the performance of your learning is very, very poor.”  The iterative process involves three terms -- the reward itself, the expected reward for a new state based on choice of action, and memory of the reward gained in the previous state.  In the comparison, any differential greater than zero can be exploited for learning. The tradeoff: “No pain, no gain.”<br><br>

As research advanced to increasing levels of structural specificity, Doya posited that “there seems to be spatial segregation in the function” of basal ganglia components.  Specialization in aspects of reinforcement learning is now seen, for instance, in ventral versus dorsal areas of the striatum.<br><br>

Differentiation is also found in the cortico-basal ganglia information network: not a simple closed loop, but parallel electrical pathways conducting distinct neural operations.  Further, the neuromodulators each have their respective missions.  Dopamine encodes the temporal difference error -- the reward learning signal. Acetylcholine affects learning rate through memory updates of actions and rewards. Noradrenaline controls width or randomness of exploration.  Serotonin is implicated in “temporal discounting,” evaluating if a given action is worth the expected reward.  Doya reminds us that clinically “it is well known that the serotonin function is impaired in the depression patient.”<br><br>

The system of basal ganglia components and neuromodulators requires dynamic balancing. A delicate interplay determines outcomes for learning, actions, and affective states.  Doya’s synthetic models are proxies for human behavior, and his computational framework describing the moving parts ultimately has therapeutic implications for psychiatric and neurological disorders.
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			<title><![CDATA[What Harm Does Pathological Synchronization in Parkinson&#39;s Disease Do?]]></title>
			<pubDate>Thu, 24 Sep 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/704</guid>
			<link>http://mitworld.mit.edu/video/704</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill01167mcgovernbasalbrownparkinson07may2009.jpg"  alt="" />Like tuning in a station on the FM band of a radio, neuroscientists can detect the particular frequencies of our brains in action.  And just as on the radio, a little noise and static is to be expected.  In Parkinson’s Disease (PD), as <b>Peter Brown</b> and colleagues are finding, too much of a certain type of frequency is a bad thing.  Neurons in the basal ganglia produce a kind of overly synchronized beta frequency (in the 20 Hz range) that seems deeply implicated in some of the telltale symptoms of Parkinson’s.<br><br>

Brown’s talk outlines efforts to record this “oscillatory synchrony” in PD, to figure out the physiological mechanisms behind it, and to connect beta synchrony directly to such key symptoms in PD patients as rigidity and bradykinesia (slowness in executing movements).  Scientists can detect clusters of neurons in the subthalamic nucleus (a key component of the basal ganglia) “beating” at 20 Hz.  Brown says the “exaggerated synchrony” of these neurons seems to have something to do with a chronic loss of the neurotransmitter dopamine.  Ordinary subjects have a “fair amount of healthy beta activity,” notes Brown, and when these subjects engage in voluntary movements, such as extending a forefinger, the beta activity is suppressed.  But in PD patients, says Brown, uncontrolled beta activity seems to promote postural contraction “at the expense of voluntary movement.” <br><br>

Brown and others have recorded activity in the brains of PD patients undergoing two key treatments, Deep Brain Stimulation (where electrodes implanted in the brain try to break the pattern of normal neuronal firing), and dopaminergic therapy.  Both methods relieve the symptoms of slow movement and rigidity.  Excessive beta oscillations are suppressed during these two treatments.  This is “correlative evidence,” says Brown, that beta activity is behind the symptoms.  Scientists are trying to connect the dots, and find a causal link: After stimulating the neurons of the subthalamic nucleus to beat at 20 Hz, they observe a 20% slowing of movement.  Brown is conducting additional studies that provide evidence in PD of a looping brain pathway involving not just the basal ganglia, but parts of the cortex, which has an “innate tendency for activity at 20 Hz,” causing bradykinesia and rigidity,  and which can be damped by the input of dopamine.  In closing, Brown acknowledges he must bring “the beta story …down to reality,” since it doesn’t seem to connect to other PD symptoms such as tremor, and “I’ve been a beta chauvinist here, and ignored other frequencies.” 
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			<title><![CDATA[Deep Brain Stimulation Therapy for Movement Disorders]]></title>
			<pubDate>Thu, 17 Sep 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/703</guid>
			<link>http://mitworld.mit.edu/video/703</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill01166mcgovernbasallozanodeepbrain07may2009.jpg"  alt="" />New tools are enabling neuroscientists to break therapeutic ground against daunting disorders like Parkinson’s Disease (PD). <b>Andres Lozano</b> is one “of a small group of heroes,” in <b>Ann Graybiel’s</b> estimate, whose work is yielding astonishing advances on a variety of fronts.<br><br>

Treatments for PD, a progressive, degenerative brain disorder, have until recently dealt primarily with the loss of dopamine-releasing neurons, leading to the classic movement disorders associated with PD:  tremor, rigidity, akinesia.  But Lozano says that by the time these physical problems are diagnosed, “the reality is that the disease started 10-15 years earlier,” and has involved other brain areas.  Lozano determined to focus on three such non-motor symptoms of the disease -- gait and posture, depression (in PD and other patients), and cognitive disorders -- and if possible, “reach these circuits, intervene and help patients.”<br><br>

PD patients have serious problems controlling balance and posture, and animal studies helped pinpoint an area in the brainstem responsible for these functions.  Lozano got permission to plant electrodes in humans in this area, and mapped out the sensitivities of neurons to voluntary movements such as flexing an ankle or walking. In six PD patients, Lozano sent a mild electric current into these neurons.  He shows videos demonstrating the remarkable improvement in control (a patient pushed no longer falls) with deep brain stimulation (DBS). A serendipitous offshoot of this therapy is that it improves REM sleep, in which PD patients are deficient.<br><br>

Lozano has been working as well on mapping and targeting areas of the brain involved in depression, which he has found to be hyperactive. He labeled neurons that responded exclusively to sad and disturbing images, and using DBS, he was able to “turn down the hyperactivity,” successfully reversing severe depression in 60% of his 36 subjects.<br><br>

His final accomplishment emerged by accident: While attempting to treat a patient’s morbid obesity through DBS, Lozano was startled to find when stimulating the man’s thalamus the patient experienced a vivid sense of déjà vu. (He recalled being in a field 30 years earlier with a girlfriend.) The stronger the current, the more details emerged.  When the stimulus ended, the memory ceased. Lozano hopes, via DBS, to help patients with memory disorders.  Another intriguing discovery:  stimulation in the hippocampus, deeply involved in memory, seems to lead to a burst of new neuron development.  These DBS studies suggest, says Lozano, that brain circuits for mood, motor control and cognition can be modulated, and we now “need to determine whether they are safe and beneficial to patients.”
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			<title><![CDATA[Representation of Value in the Primate Brain]]></title>
			<pubDate>Sat, 12 Sep 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/702</guid>
			<link>http://mitworld.mit.edu/video/702</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill01164mcgovernbasalglimchervalue07may2009.jpg"  alt="" />Pigeons really like millet seed, monkeys crave juice, and humans get a kick out of winning money.  While all animals don’t enjoy the same rewards, <b>Paul Glimcher</b> has discovered some common features in the way animal brains learn to recognize and pursue something of value.<br><br> 

Glimcher is one of the founding fathers of the young field of neuroeconomics, in which economic theories help inform investigations of brain function.  It’s not surprising then, that his approaches include game theory as well as measuring the firing of single neurons.  Glimcher’s talk details his research from the past 15 years, what he describes as an attempt to “add something” to the classic studies on the basal ganglia circuit conducted by fellow symposium speaker Okihide Hikosaka.  From Hikosaka’s data and other research, Glimcher came to believe that neurons of the substantia nigra (part of the basal ganglia) were coding for something of worth to an animal, but that these neurons were “responding not to reward per se, but to deviations to expectation.” For instance, if a pigeon expected a delivery of millet seed following a conditioned cue, no neurons fired, but if the reward was delayed, then suddenly delivered, the pigeon would find its initial prediction in error, and its neurons burst into action.<br><br>

Various models emerged to capture the ways in which these neurons, energized primarily by the neurotransmitter dopamine, enabled animals to adjust expectations about and predict rewards.  But Glimcher found fault with others scientists’ “conditional parameters.”  He says, “As an economist, this is frustrating.”  So he developed three mathematical axioms for testing the so-called Reward Prediction Error (RPE) models.  His work “suggested a way of unifying the data,” with the notion that the basal ganglia learns “the values of actions in a quantitative way … from the dopamine neurons and the incoming stimulus.”<br><br>

Glimcher hypothesized that dopamine neurons take the value of a reward just received, “and subtract it from a weighted exponential average of previous rewards, and if there’s no mismatch, there should be no firing of…dopamine neurons.”  Human, monkey and pigeon studies -- based on gambling, juice, and seed rewards, respectively -- solidified his notion that dopamine neurons are part of an RPE encoding system where they convey the differences between rewards expected and rewards received.  This has led Glimcher to believe that “one of the principle functions of the basal ganglia is to learn the values of our actions, represent them, and pump out the data to produce choice.”
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			<title><![CDATA[How the Brain Encodes Reward]]></title>
			<pubDate>Tue, 08 Sep 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/701</guid>
			<link>http://mitworld.mit.edu/video/701</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill01163mcgovernbasalhikosakareward07may2009.jpg"  alt="" />As <b>Ann Graybiel</b> puts it, “basal ganglia were dark basement structures” until <b>Okihide Hikosaka</b> began his classic 1980s research demonstrating how these neuronal clusters influenced eye movements.  Hikosaka has deepened and broadened his work in this once neglected area of the brain, and brings a McGovern audience up to date on his latest discoveries.<br><br>

Hikosaka briefly sketches what is known about the basic pathways leading in, around and out of the basal ganglia, circuits that have been associated with stress, pain, mood, memory and arousal.  This specialized cluster of neurons seems especially attuned to the neurotransmitter dopamine, and Hikosaka has been investigating “a number of unsolved questions,” including how dopamine neurons form circuits for movement control, whether such neurons encode “motivational values,” and what other parts of the brain guide them.<br><br>

Hikosaka describes research demonstrating that certain dopamine neurons become excited if a visual cue indicates a future reward, and become inhibited with a visual cue indicating no reward.  Dopamine also increases after an action delivers a reward and decreases when an action produces no reward.  Research began to explore whether dopamine neurons “encode motivational values, including reward and punishment.”  After others’ studies yielded contradictory or uncertain conclusions, Hikosaka designed a set of studies on monkeys involving classical Pavlovian conditioning, with juice rewards and air puffs as aversive stimuli.<br><br>

Among Hikosaka’s findings: some dopamine neurons were excited primarily by positive, reward-predicting stimuli, others inhibited by air puff-predicting stimuli.  But he also found another group of dopamine neurons excited both by positive and negative reward-predicting stimuli (as well as the stimuli themselves). Hikosaka posited two types of neurons that react in very different ways to motivational signals, which he described as value-coding and salience-coding.  He also determined that the lateral habenula, a part of the brain sitting at one end of the thalamus, seems to regulate dopamine pathways involved in some motivational responses. By sending a weak electric pulse through the lateral habenula, Hikosaka saw a very strong inhibition of the dopamine neurons that “encode mostly motivational values.”
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			<title><![CDATA[Computers with Commonsense: Artificial Intelligence at the MIT Round Table]]></title>
			<pubDate>Mon, 03 Aug 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/695</guid>
			<link>http://mitworld.mit.edu/video/695</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill01140alumnitechday2009winstoncommonsense06jun2009.jpg"  alt="" />Visiting the San Diego Zoo’s orangutans and chimpanzees inspires <b>Patrick Henry Winston</b> to ponder what makes humans different from our primate cousins.  His field of artificial intelligence extends that question to thinking about how humans differ from computers.  Winston’s goal is to “develop a computational theory of intelligence.”<br><br>
Bridging the gap from people to machines requires a complex understanding of how we think.  Winston asserts we think with our eyes, our hands, our mouth.  Humans rely upon visual, motor, and linguistic faculties to learn and solve problems. Perceptual powers enable naming, describing, categorizing and recalling.  In the aggregate, these processes are “commonsense,” a hallmark of cognition that Winston aims to vest in computer programs -- to endow transistors with the nuanced capabilities of neurons.<br><br>

Crucially, we also think with our <i>stories</i>.  Throughout childhood and formal education, we are taught via fairy tales, myths, history, literature, religion, and popular entertainment.  Professional disciplines like law, science, medicine, engineering, and business are conveyed through stories too.<br><br>

Recognizing patterns, relationships, and mistakes, as well as abstract concepts like revenge or success, helps us explain, predict, answer questions.  The delicate processes of extracting knowledge and capturing meaning may appear seamless or instinctive in the evolved mind, but must be parsed syntactically to “teach” a computer to achieve the same ends.<br><br>

What might be practical applications “for systems that understood stories”?  Winston suggests that decision-making in business and military strategy would benefit.  And no less, comprehending cultures.  If a computer program could derive clues from context, perhaps it could determine why “what plays in Peoria” doesn’t translate to Baghdad.<br><br>

Early efforts to build a computational theory of intelligence focused on “symbolic integration…We figured out how to make programs do calculus by 1960…but  computers remained as dumb as stones,” Winston says.  When we progressed to building robots -- “things that move” -- language was still lacking. “We forgot that the distinguishing characteristic of human intelligence is that linguistic veneer that stands above our perceptual apparatus,” he remarks.<br><br>

A paradox emerging from Winston’s study of how humans think is that “computers make us stupid.”  For instance, when students are freed from taking notes, absence of “forced engagement” with the material hinders learning.  He cautions that teachers confuse the “presentation of information with the delivery of information.” Too many words on a slide (or talking too fast) “jams the language processor” and impedes digesting content.<br><br>

Winston summarizes with an appealing prescription for becoming smarter. “Take notes…draw pictures…talk and imagine…tell stories!” The very act of explaining to another elucidates a lesson for oneself.
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			<title><![CDATA[Opening the Mind’s Eye- Learning to See]]></title>
			<pubDate>Fri, 31 Jul 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/694</guid>
			<link>http://mitworld.mit.edu/video/694</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill01139alumnitechday2009sinhavision06jun2009.jpg"  alt="" />It’s rare to find research that simultaneously advances basic science and brings good into people’s lives, but <b>Pawan Sinha’s</b> Project Prakash does precisely that.  An investigator of human visual processing, Sinha is interested in how these brain mechanisms develop.  For his work, Sinha realized the ideal subjects would be individuals who developed sight after blindness. Since he could not ethically create such an experimental population, he had to “rely on natural experiments” -- children born blind, but who recovered their vision. <br><br>

Sinha found these subjects in his native India, which has the world’s highest number of blind children -- more than one million.  They are victims of Vitamin A deficiency, congenital cataracts, and absent or atrocious medical care.  But salient to Sinha’s research, many of these blind children could be treated.  He glimpsed a humanitarian and scientific opportunity, and Project Prakash (Sanskrit for light) was born.<br><br>

Starting a few years ago, Sinha and his team began screening blind children in a few villages to identify cases of treatable blindness, and remedy their disorders.  More recently, he’s gained support from hospitals and schools for the blind, reaching many more children.  He began to establish a test population.  Research on this unique group has yielded many original insights into the development of vision, and shaken some major scientific dogmas.  Sinha found that after years without visual stimuli, the brains of these children could process new information flooding in -- challenging the notion of early critical periods in brain development.  He discovered that patients who once learned about objects simply via touch could, once they gained sight, identify the same objects simply by looking at them.<br><br>

Sinha has also delved into the mechanisms of visual integration -- how our brains make sense of visual cues containing diverse colors, illumination, and patterns.  He’s learned that newly sighted patients have difficulty parsing overlapping images (such as triangles, squares, circles), but moving these images around magically sparks recognition.  Research results are consistent across all ages, and show that early stages of sight acquisition involve seeing the world in a fragmented way, compromising recognition, and that motion cues are critical for putting pictures together meaningfully, serving “a critical bootstrapping function for visual learning.”<br><br>

The kinds of integrative difficulties experienced by Project Prakesh children bring to mind similar difficulties in autistic children, for whom motion processing also seems to be deficient, and Sinha is now seeking a possible “causal chain in autism” that leads to the disorder’s devastating social impairments -- a research path that might someday yield new therapies.
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			<title><![CDATA[Opening Remarks/How the Brain Invents the Mind]]></title>
			<pubDate>Tue, 28 Jul 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/693</guid>
			<link>http://mitworld.mit.edu/video/693</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill01138alumnitechday2009hockfieldsaxe06jun2009.jpg"  alt="" />In trying financial times, <b>Susan Hockfield</b> remains optimistic and committed to pursuing MIT’s massive, multi-year initiatives in energy and life sciences. She prefaces her “whirlwind” tour of MIT for an alumni audience by referencing the campus-wide relief at the change in presidential administrations, which promises to make science and engineering more central, and to make “MIT values more mainstream.”  If it indeed becomes “cool to be smart,” Hockfield believes MIT can count on taking a prominent national role in research, policy and education.<br><br>

One key area in which MIT hopes to make a major contribution is sustainable energy. The MIT Energy Initiative, two years old, brings together faculty and students across all disciplines to develop a portfolio of new technologies (although the focus seems increasingly to fall on solar). Campus interest is so intense that the Institute has committed to a minor in energy, and it’s seeking five new professorships in the area. The other major enterprise involves fusing biological sciences with engineering, especially in the study of cancer.  At the new Koch Institute, cancer biologists and engineers have already made “fundamental discoveries underlying new targeted cancer drugs,” and they are hard at work decoding the disease, and devising new methods for diagnosis and treatment.<br><br>

Hockfield also candidly describes the impact of the economic downturn on the Institute, acknowledging that “most revenue streams have been compromised,” except for research.  With the endowment down by 20-25%, departments across the board are making significant but strategic cuts for the next two to three years.  MIT will not compromise on providing financial aid to needy students, a cost that understandably has risen in the past year, nor on hiring faculty. Hockfield hopes that private philanthropy will help MIT “preserve core strengths and values.”  At the end of the recession, she says, “We want to come out with a leaner, stronger Institute.”<br><br>

Fellow neuroscientist <b>Rebecca Saxe</b> outlines her research investigating the neural basis for a Theory of Mind -- how the human mind seems geared to “glean what others are thinking and feeling.”  From her work with children and adults, Saxe has determined that there’s a very specific region of the brain -- the right temporal-parietal junction -- dedicated to thinking about how others think.  This area lights up in the fMRI scanner when people read stories involving another person’s beliefs and moral judgments, but not when they digest other kinds of written material.  The RTPJ develops this special function slowly (young children don’t have it), and Saxe has discovered that she can interfere with this region’s activities, altering her subjects’ sense of what constitutes morally permissible behavior.  She’s exploring whether these distinct neural networks develop differently in children with autism, with the hope of finding therapies that might someday help treat the disorder.
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			<title><![CDATA[New Frontiers in Schizophrenia and Bipolar Disorder Research]]></title>
			<pubDate>Thu, 09 Jul 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/687</guid>
			<link>http://mitworld.mit.edu/video/687</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill01155picowerbrainspt4scolnickpsychiatric04may2009.jpg"  alt="" />In contrast to cardiovascular disease, few breakthrough remedies for psychiatric illness have emerged in the past half century.  <b>Edward Scolnick</b> lays blame for this dismal situation on barriers to understanding the genetic basis behind such illnesses.  But the research drought may be over, as the current revolution in human genetics opens wide a door into the molecular biology and brain physiology behind diseases like schizophrenia and bipolar disorder.<br><br>

These common, chronic and disabling mental illnesses are complex, involving abnormal behaviors that vary in expression. They have also lacked the kind of quantitative tests that enable precise diagnosis. While science has demonstrated that the single biggest risk factor for both schizophrenia and bipolar disorder is genetic, it has not been able to design tools for exploring how the genetics relates to the evolution of the disease in people.  But just in the last two years, with the sequencing of the human genome and maps of human genetic variation, ignorance has given way to major findings.<br><br>

In schizophrenia and bipolar disease, researchers have discovered that gene deletions and duplications (called copy number variants) cause significant brain circuit mischief.  They’ve also learned there are gene variants common to both diseases, as well as clusters of genes that malfunction.  Scolnick describes diverse research at MIT, proceeding at a “breakneck pace,” that uses this genetic information “to delve into the malfunctioning of brain circuits.” <br><br>

Scientists have applied functional magnetic resonance imaging to compare the brains of ordinary people and schizophrenia patients, and discovered that the schizophrenic’s brain in a resting state is hyperactive. Other researchers found that schizophrenics generate the gamma brainwaves involved with higher mental activities in a different manner than control subjects.<br><br>

Another MIT lab has begun to manipulate specific brain circuits using optical technology -- shining different wavelengths of light at special interneurons that regulate the firing of other neurons, and which are postulated to have a critical role in the malfunctioning of schizophrenics’ brains.  Two other MIT labs are examining the biochemical disruptions due to altered genes, and developing “safe, specific chemical inhibitors” that might yield potential treatments for schizophrenia and bipolar illnesses.  In Japan, researchers are growing stem cells into brain cells, which may lead to precise experiments that relate genetic problems to malfunctions in brain wiring.  Indeed, adding up this research, a central biochemical pathway central to the pathogenesis of psychogenic illness seems to be emerging, knowledge that “can be exploited to understand illness and to find drug treatments.”

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			<title><![CDATA[Alzheimer’s Disease: Current State and Hope for the Future]]></title>
			<pubDate>Fri, 12 Jun 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/679</guid>
			<link>http://mitworld.mit.edu/video/679</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill01154picowerbrainspt3tsaialzheimers04may2009.jpg"  alt="" />Measured in human suffering, and by statistics, Alzheimer’s Disease (AD) presents a formidable specter: with incidence approaching 30 million worldwide and growing rapidly, it is now the sixth leading cause of death in the US.  As life expectancy lengthens, AD is anticipated to triple in prevalence over the next few decades. The disease is found in nearly 50% of people age 85 and older. Triply higher medical costs are incurred by seniors with AD. These daunting facts give urgency and weight to molecular neuroscientist <b>Li-Huei Tsai’s</b> research.<br><br>
Tsai begins her presentation with an historical perspective of Alzheimer’s, first documented in 1901 in Germany as “strange behavioral symptoms and loss of short-term memory.” Post-mortem examination of a patient’s brain showed “the hallmark pathological lesions: amyloid plaques and neurofibrillary tangles.” Telltale manifestations include “forgetfulness, …confusion, disorganized thinking, impaired judgment,” difficulty expressing oneself, spatial and temporal disorientation, and incapacity in daily activities. Family members must often quit jobs to provide round-the-clock care. In the advanced disease, becoming bedridden engenders chronic infections, secondary conditions, and eventual demise.<br><br>
Definitive clinical diagnosis can be elusive. Imaging techniques with radioactive tracers, using a compound that selectively binds with amyloid plaques, help to identify AD. Tsai describes several cognitive tests developed by fellow MIT researchers to aid in confirming the disease. One method assesses retention of verbal facts and geometric figures. Another diagnostic tool is functional MRI, pinpointing brain areas activated upon exposure to new versus repeated scenes, a challenge for memory. Both approaches reveal notable distinctions between AD patients and control subjects.<br><br>
“Currently there is no treatment that can prevent, delay or reverse Alzheimer’s Disease,” says Tsai. FDA approved drugs that act upon neurotransmitters postpone cognitive deterioration by only a few months.<br><br>
Using a transgenic mouse model, Tsai’s pioneering research seeks to target compounds that can preferentially manipulate proteins to assume a desired structure. Resulting cellular differentiation into neurons could help correct deficits of AD by augmenting brain volume in specific regions, thereby enhancing learning and memory.<br><br>
Just as experimental mouse subjects perform better with “environmental enrichment…by keeping them very physically engaged,” Tsai recounts that “people with higher education, more active lifestyles” benefit cognitively as they age. As to the respective contributions of genetic and environmental factors, she believes “it’s really a combination.” Though treatment for Alzheimer’s will not be solely pharmaceutical, Tsai hopes to identify chemical compounds to ameliorate the characteristic brain atrophy that robs one of vitality and dignity.
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			<title><![CDATA[Introduction/Overview of Brain Disorders]]></title>
			<pubDate>Tue, 09 Jun 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/677</guid>
			<link>http://mitworld.mit.edu/video/677</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill01152picowerbrainspt1hockfieldsuroverview04may2009.jpg"  alt="" />In their symposium introduction, <b>Susan Hockfield</b> and <b>Mriganka Sur</b> place MIT at the forefront of a revolution in neuroscience.  Hockfield, a neuroscientist by training, recaps the evolution of the discipline at MIT, from its 1964 start in the Department of Psychology to the more recent establishment of the Department of Brain and Cognitive Sciences.  These changes mirror the transformation of a field in which, says Hockfield, “at first you could do little more than make qualitative observations about behavior and only speculate about causes, to one that can examine brain function at the level of molecules and cell circuits; that can conduct quantitative experiments with genetically targeted model systems and can directly observe the living human brain in action.”<br><br>

We are now poised “for the first time in human history to deliver scientifically designed, rational therapies for some crippling disorders of the brain.”  Hockfield credits MIT’s progress to “meta-experiments,” specifically collaborations among scientists and engineers, and the generosity of patrons.<br><br>

Mriganka Sur and his colleagues believe “the vast majority of brain disorders have their roots in brain wiring gone awry,” so a solution to such disorders lies in understanding the wiring, and its associated functions.  MIT gets at these questions from many angles of research, including the genetic underpinnings of brain development, the architecture of synaptic pathways and networks, and the brain’s response to environmental stimuli.  MIT addresses research problems through a “unique interdisciplinary effort” comprising molecular biology, neuron and cognitive science, and computation. What’s more, researchers have united behind a singular mission --  a “wish to make a difference in the world” --  which involves a specific focus on addressing such brain disorders and diseases as dyslexia, Alzheimer’s, schizophrenia, and autism.   “There is not one other entity like this anywhere else,” says Sur, who believes MIT’s potential for future impact is “virtually limitless.”
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			<title><![CDATA[The Autistic Neuron]]></title>
			<pubDate>Tue, 09 Jun 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/678</guid>
			<link>http://mitworld.mit.edu/video/678</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill01153picowerbrainspt2bearautism04may2009.jpg"  alt="" />This self-described “basic neuroscientist” confesses he never thought he’d give a talk on autism, but as <b>Mark Bear</b> recounts, decades of research in the basics are now paying off with important insights into the etiology and treatment of brain disorders, including autism.  <br><br>

Bear provides a primer on this developmental disorder, noting that its roots are biological, it is highly heritable, and astonishingly prevalent: one in 150 people express some of the symptoms of autism.  These fall on a spectrum, from severely reduced social behavior, abnormal language, repetitive movements, seizures and mental retardation, to the milder Asperger’s Syndrome, where individuals are often academically successful, but socially awkward.  Particularly significant to Bear: Autism’s underlying genetic changes manifest themselves in problematic communication between neurons. <br><br>

To unravel autism, researchers are examining its clinical heterogeneity, “genetic risk architecture,” and how it alters brain connections and function. One of the difficulties in approaching autism is that a variety of genetic mutations can result in autistic behaviors, and only a few of these mutations have been identified.  Bear himself has been probing the single gene disorder, Fragile X syndrome (responsible for about 5% of the cases “of full-blown autism.”)  In Fragile X, the FMR1 gene is silenced, leading to a missing protein that serves as a key regulator of brain proteins involved in neuron communication.  Without FMR1, “the brakes are missing,” and there’s excessive protein synthesis leading to altered brain function. <br><br>

Bear hypothesized that it might be possible to correct Fragile X by bringing the system back in balance.  He created mice models of the disease, and found that by reducing the number of neurotransmitter receptors that respond to the excessive brain proteins, he could ameliorate or correct Fragile X defects.  These receptors are “druggable targets,” and, says Bear, “if the treatment works in fly, fish or mouse, it better work in humans or Darwin was wrong.”<br><br>

Based on this work, drug companies are devising compounds to test in human clinical trials of Fragile X syndrome. In addition, Bear notes, colleagues have discovered that other mutations connected with autism also involve protein regulation problems.  “This gets us excited, because it looks like a common pathway that causes synaptic dysfunction in different diseases that may ultimately manifest as autism. If that’s the case, then treatment for the disorder may be efficacious in multiple disorders.”
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			<title><![CDATA[The Evolution of Trichromatic Color Vision]]></title>
			<pubDate>Sun, 17 May 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/669</guid>
			<link>http://mitworld.mit.edu/video/669</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill01132mcgovernscolnickcolorvisionnathans27apr2009.jpg"  alt="" />Sometime around 100 million years ago, when the continents of Africa and South America were still in touch, a female primate -- one of our ancestors -- was born with the capacity to see in vivid color.  <b>Jeremy Nathans</b> describes the fortuitous genetic event that gave rise to this evolutionary leap, and links an ancient biological timeline to his very current research in human color vision.<br><br>

Nathan’s talk, spanning eons and disciplines, starts with Isaac Newton’s astonishing 17th century experiments into the physics of colored light, and his prescient guess that the human brain could somehow translate colors the way it interpreted sound vibrations.  The physiology behind vision didn’t coalesce until the 19th century, when a picture emerged of photoreceptor cells, with rods for night vision and cones for color.  20th century science finally cracked the photochemical mechanism behind light sensing.<br><br>

In the 1980s, Nathans became interested in “making a dent in the area of identifying (genetic) sequences of the visual pigments.”  He describes how he isolated the DNA behind the light sensors responsible for human color vision -- the short(S), medium (M) and long (L) wavelength receptors.  He also discovered a diversity of genetic variations in normal, trichromatic  vision.  Indeed, he says the sequences lend themselves to all sorts of “mischief,” which can result in what’s commonly described as color blindness. When genes for the M or L pigments are not expressed, humans lose various degrees of color discrimination.  When Nathans shows a picture of fruit from the perspectives of those with normal and abnormal color vision,  it’s clear how “trichromats” enjoy an advantage in detecting ripe foods, or just enjoying scenery.  <br><br>  

From his genetic research, Nathans became interested in how <u>some</u> mammals made the leap from dichromatic to trichromatic vision.  Simple creatures such as honey bees and tropical fish are blessed with better color vision than humans, but among mammals, only a subset of primates have moved to trichromatic vision. Lower mammals lack one of the three dimensions for color vision. Nathans conjectured a “happy accident” on the X chromosome in primates likely resulted in the genes for the additional dimension.  In a groundbreaking experiment to “recreate in a mouse the first step in the evolution of trichromatic color vision,” Nathans knocked into the mouse genome a human L pigment gene in place of its M pigment gene, resulting in an animal with the capacity for distinguishing colors a normal mouse could not.  “This argues,” concludes Nathans, “that acquisition of a new dimension of color vision is not so difficult after all.”
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			<title><![CDATA[Transitioning from the Space Shuttle to the Constellation System]]></title>
			<pubDate>Wed, 13 May 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/668</guid>
			<link>http://mitworld.mit.edu/video/668</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill01158mitwaerospacerantnasagerstenmaier15apr2009.jpg"  alt="" /><b>William Gerstenmaier </b> knows the U.S. space program inside out -- both literally and figuratively.  As a 30-plus year veteran of NASA, Gerstenmaier has managed the operational dimensions of the space shuttle, international space station, and other space flight missions.  For this talk, he dissects a problem that recently grounded the shuttle, coming at it from the perspective of both an engineer, and a top-level manager with responsibility to the highest levels of government.<br><br>

Gerstenmaier presents his case “as it unfolded,” for a behind-the-scenes view of how NASA keeps its aging shuttles aloft.  His account begins in 2008, after a shuttle flight revealed something wrong with flow control valves essential to the shuttle’s hydrogen system.  These valves are connected in a closed loop to the main engines, via a 170-foot length of pipe, through all manner of twists and turns, and frequently subjected to very high pressures.  Gerstenmaier describes the series of tests his engineering teams performed, over long days, weekends and holidays, to determine what precisely had gone wrong, and the risks posed by potentially faulty equipment.  <br><br>

NASA engineers ruled out wiring problems, but discovered during an “x-ray of the plumbing” a chunk missing from one of the valves. They examined the problem from a structural dynamics standpoint: could the “flow through the plumbing” have made the valves vibrate violently?  The same valves had been in use since 1981, but perhaps a “failure associated with an extremely resonant condition that could occur periodically” was responsible. <br><br>

Gerstenmaier’s team shot particles through a simulated piping system and then used a scanning electron microscope to detect valve damage.  They also analyzed historical failure data, which suggested that valve cracks might be a “high cycle fatigue problem,” and could therefore possibly occur during any flight. Gerstenmaier felt bound to “ground the fleet,” until engineers figured out a way of screening for damage in the valves pre flight.  <br><br>

A flash of unorthodox thinking led engineers (unbeknownst to Gerstenmaier) to buy a common bolt tester, which permitted them to get a comprehensive picture of the valves in working shuttles without removing or damaging them.  After running numbers around flight risk, and many discussions with his engineers, Gerstenmaier felt they’d arrived at a rationale to resume flying.<BR><BR>

Says Gerstenmaier, “I can tell you, I wasn’t looking out the window in Florida. At the shuttle launch, I was looking at data of the flow control valves and watching the pressures …  I knew what I needed to look at in terms of the data.  An engineer’s tendency comes through.”

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			<title><![CDATA[]]></title>
			<pubDate>Fri, 03 Apr 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video</guid>
			<link>http://mitworld.mit.edu/video</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/1238788829-mitwstill01144killianleccomplexityorgearthsysbras30mar2009.jpg"  alt="" />]]></description>
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			<title><![CDATA[]]></title>
			<pubDate>Fri, 03 Apr 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video</guid>
			<link>http://mitworld.mit.edu/video</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/1238789155-mitwstill01144killianleccomplexityorgearthsysbras30mar2009.jpg"  alt="" />]]></description>
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			<title><![CDATA[Planet Water: Complexity and Organization in Earth Systems]]></title>
			<pubDate>Fri, 03 Apr 2009 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/658</guid>
			<link>http://mitworld.mit.edu/video/658</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/1238791409-mitwstill01144killianleccomplexityorgearthsysbras30mar2009.jpg"  alt="" />Rafael Bras, a professor of civil and environmental engineering who pioneered the field of hydrologic science, is MIT&#39;s James R. Killian Jr. Faculty Achievement Award winner for 2008-2009.

If he doesn’t have the whole world in his hands, <b>Rafael Bras</b> certainly grasps more pieces of the gigantic puzzle than most of us.  Often credited with launching the science of hydrology -- the study of water’s crucial role in Earth systems -- Bras has developed passions for pretty much the rest of the Earth sciences as well.  In this fond, valedictory lecture to MIT (he’s recently taken the post of Dean of Engineering at UC Irvine), Bras describes some of the research problems that have long fascinated him. <br><br>

Bras enjoys wrapping his mind around big things, such as the size of the world’s oceans, whose numbers are in the billions of cubic kilometers.  What interests Bras even more are the ways huge amounts of water cycle from the atmosphere as rain, into the soil, as runoff to the sea, and back again.  He says “a lot of what we depend on is the result of differences between large numbers. It is those differences between very large numbers that makes it so uncertain, variable and so sensitive to our intervention or changes.”<br><br>

The physics behind the various water cycles involves vast and continuous transfers of energy: rain changes soil moisture, which changes the amount of radiation the earth reflects, which affects evaporation, which changes the convection potential energy, which impacts cloudiness, which leads again to rain. It’s a “very nonlinear, very interacting cycle,” says Bras, which is “elegant and quite pretty.”  Bras helped lay out the models for these cycles. His studies describe how nature seems to prefer extremes like flood and drought, and how in river basins all over the world, nature favors fractal organization and minimal energy expenditure. <br><br>

Other observation and modeling projects may have consequences for the future of the planet:  A nine-year study of an Amazon region that sampled cloud cover from a satellite every three hours demonstrated that deforested regions produce shallow clouds less likely to produce rain, while deeply forested regions generate deep clouds.  He has been captivated for the last 10 years by “the intertwined dance between vegetation, landscape hydrology and radiation,” how soil moisture accommodates certain kinds of plants, which then change the properties of soil, which changes the drainage capability of water, which over time alters entire landscapes.  Concludes Bras, “This beautiful trip through hydrology has been made exciting by all these things I did not know, which came through the exercise of research, trying things and finding things. It is all a result of chance and necessity; things adjust themselves.”
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			<title><![CDATA[Science Policy and the Obama Administration: Advice to a New President]]></title>
			<pubDate>Sat, 24 Jan 2009 00:00:00 -0500</pubDate>
			<guid>http://mitworld.mit.edu/video/639</guid>
			<link>http://mitworld.mit.edu/video/639</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitw01063cisstarrkastnersciencepolicy19nov2008.jpg"  alt="" />The mood of gloom has eased somewhat within the science community, with the advent of a new presidential administration, and <b>Marc Kastner</b> captures the mix of hopefulness and trepidation among his peers around the enormous challenges the nation faces in coming years.<br><br>

Kastner describes four areas “in order of increasing difficulty” the new president must address: <br><br>

The president’s first move should be to increase the prestige of science in government, by giving the science advisor a more important role, listening carefully to career scientists in government agencies, and encouraging rather than punishing them for speaking out.<br><br>

Second, Kastner advises expanding basic research on energy and environment.  The U.S. imports $700 billion worth of oil per year, placing the nation “in jeopardy economically and politically,” says Kastner.  Clean energy is likely to be a huge industry, and if the U.S. is to lead worldwide, it must begin to master a cluster of technologies that together pose our best chance of beating climate change.<br><br>

We need a huge infusion of R&D money in such thorny areas as: carbon sequestration (we don’t yet know if CO<sub>2</sub> can be efficiently and safely injected into underground pore space); electrical storage, where we need a five-fold improvement in battery technology to produce an all-electric car that can run for 200 miles; solar energy, where current solar cells are made from materials that are too costly, and not yet efficient enough. While federal and private energy research has been declining, the International Energy Agency estimates the world will require $17 trillion dollars to stabilize CO<sub>2</sub>emissions between now and 2050.<br><br>

The third order of business involves biology: Having teased apart the DNA molecule and mapped the genome, we now stand ready for a third revolution in life science, says Kastner.  This will involve the convergence of biology with mathematics, physics and engineering. Says Kastner: “The gigantic amount of data being generated by rapid sequencing requires new approaches: biology needs theory for the first time, needs integrating ideas to explore information and come up with clarity.”<br><br>

The final and perhaps toughest job involves stabilizing science funding.  Over the past 20 years, math, physical science and engineering funding have remained flat.  In the life sciences it doubled (partly due to 9/11), then declined.  While “it’s wonderful to give more money to science,” rapid increases over short times have often been followed by sharp dips, creating major research disruptions. Plus, says Kastner, it’s unhealthy to fund one area and not the rest.  “Different sciences reinforce each other and the scientific enterprise cannot do well if only one field is supported and the others are not.”
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			<title><![CDATA[20-Ton Canaries: The Great Whales of the North Atlantic  (Keynote)]]></title>
			<pubDate>Fri, 05 Dec 2008 00:00:00 -0500</pubDate>
			<guid>http://mitworld.mit.edu/video/620</guid>
			<link>http://mitworld.mit.edu/video/620</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitw01084mitseagrantgreatwhalesdolin15oct2008.jpg"  alt="" />This two-part lecture provides a brief illustrated journey through our whaling past, and the heart-breaking current story of the North Atlantic right whale.  <br><br>

Using many slides, author <b>Eric Jay Dolin </b> recaps highlights from his recent book, <i>Leviathan.</i> Among the tidbits, we learn that Captain John Smith (of Jamestown fame) came to Maine and Massachusetts in 1614 to hunt for whales (with a sideline in gold and silver).  It was a bust, like some of his other ventures.  The next settlers had more luck, harvesting dead whales that drifted ashore. Through the next century, colonists mastered offshore whaling, and ultimately more than half the income New England earned from selling products to England was derived from whales.<br><br>

With breaks during the American Revolution and the War of 1812, New Englanders built up the whaling industry steadily: By 1846, there were 735 American whaling ships (out of 900 worldwide) earning 70,000 people their living. $70 million was invested in whaling infrastructure, and 60 coastal cities and towns rose from whale harvesting.  It was the fifth largest industry in the U.S., providing the clean-burning candles favored by Ben Franklin and baleen for ladies’ hoops and stays. <br><br>

It was also a dangerous, bloody and stinking vocation, involving years at sea, death by fin or rope, and hours over a boiling rendering vat. Populations of whales sank drastically, and whalers searched farther for their prey.  West Coast whalers chased bowheads into the Arctic and were trapped by ice. Ultimately, the American whaling industry “sailed into oblivion” with the discovery of oil in Titusville, PA, the Civil War, and the evaporation of the baleen-based corset market – done in by new Paris fashions. <br><br>

The tiny, remaining population of North Atlantic right whales – perhaps 350 --  is known to researchers “better than any other mammal in the world,” says <b>Michael Moore.</b>  Their continued existence depends on our “walking a tightrope between commerce and conservation.”    Perhaps this individual knowledge adds to the poignancy of his account:  Whales tracked and photographed since they were babies are spotted now with fishing rig wrapped around their fins, or hack marks cut into their bodies by ship propellers.<br><br>

The “trajectory” for these animals does not look good:  from 1986 to 2005, biologists counted 50 dead right whales. This does not include those animals that simply sank out of sight after they died. Moore is quietly indignant: death by fishing rope constriction is awful, lasting for months in some cases.  “There’s the conservation piece,” he says, “and the extreme animal welfare issue.” There’s also the matter of deteriorating habitat and dwindling food supply, toxic contaminants, and noise. <br><br>

The only hope for these creatures lies in measures that reduce the chances that whales get fouled in fishing gear, and that slow down boats in the lanes favored by whales up and down the East Coast.  More mitigation must be done to achieve animal welfare and sustainable global ecology while satisfying human needs, maintains Moore.
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			<title><![CDATA[The Lightness of Being: Mass, Ether, and the Unification of Forces: Anticipating a New Golden Age]]></title>
			<pubDate>Wed, 03 Dec 2008 00:00:00 -0500</pubDate>
			<guid>http://mitworld.mit.edu/video/618</guid>
			<link>http://mitworld.mit.edu/video/618</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitw01079authorswilczeklightnessofbeing16oct2008.jpg"  alt="" />Listening to Frank Wilczek describe his research, one might not recognize simple English words, for they assume unfamiliar meanings in the context of physics. The deceptive lexicon of particles, forces and equations includes “up,” “down,” “flavor,” “color,” “strange,” “everything,” and the compelling “beautiful.” Rigorous science is conveyed in poetry and metaphor.<br><br>

The springboard for this presentation is the final chapter of Wilczek’s new book, <i>The Lightness of Being: Mass, Ether, and the Unification of Forces</i>. For a sense of history, he first touches on breakthroughs of the 20th century that gave rise to conceptual revolutions: 1910 – theory of relativity; 1925 – quantum mechanics; 1970 – standard model of normal matter. He then broaches current exploration in particle physics and the promise residing in the Large Hadron Collider (LHC) near Geneva.<br><br>

Just as Wilczek finds “standard model” too modest a designation for what it represents in physics – redubbing it “core theory” – likewise he upgrades the archaic notion of “ether,” more precisely naming it “the grid” to connote the essential structural material of the universe. As to examining the oxymoronic “dynamic void,” Wilczek explains that “to see something, you must disturb it.”<br><br>

LHC experiments seek to give substance to the calculations of unified field theory, the quest to combine harmoniously the four fundamental interactions – gravity, electromagnetism, weak force, strong force. The LHC is the logical successor, extending the capability of the human eye, to Leeuwenhoek’s 17th century optical microscope and Rosalind Franklin’s 1952 x-ray images of DNA. As “an ultrastroboscopic nanomicroscope,” it advances <i>seeing</i> to new extremes of scale and resolution (temporally and spatially).<br><br>

Through a virtual recreation of Big Bang conditions in a tunnel of 27 kilometers circumference, investigators endeavor to understand the nature of innermost space…as Wilczek terms it, “the deep structure of reality.” He intends no paradox in saying that the LHC will take pictures of “what appears to our senses as nothingness.” He emphasizes that the LHC is grand not only in concrete size but also “in every aspect of engineering and concept,” touting its distributed computing facilities at 100 sites around the globe as “the Internet on steroids.”<br><br>

As a theoretical scientist, Wilczek hopes highly energized, accelerated protons will collide to reveal new subatomic particles, bolster the unification of forces, and confirm his postulate of supersymmetry. As a curious human, he embraces this massive effort with profound wonder and gratitude. In closing, he offers that “If you’re willing to make the investment to expand your mind, it’s an exciting time to be a thinking being!”<br><br>
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			<title><![CDATA[Energy: The Past Must Not Be Prologue]]></title>
			<pubDate>Wed, 19 Nov 2008 00:00:00 -0500</pubDate>
			<guid>http://mitworld.mit.edu/video/615</guid>
			<link>http://mitworld.mit.edu/video/615</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/1227221535-mitwstill01088miteishultz15oct2006.jpg"  alt="" />There are few people who have spent as much time wielding high-level influence in Washington as <b>George Shultz,</b> and  in such a variety of roles (Secretary of Labor, Treasury and State, plus the Office of Management and Budget, among others).  So the MIT Energy Initiative has much to gain from a friend with this kind of distinguished government record.<br><br>

Shultz discusses our nation’s “roller coaster” energy ride. He harks back fondly to Dwight Eisenhower, who thought if the U.S. imported more than 20% of its oil, “we would be headed for trouble in national security.”  Eisenhower instituted an oil import quota program, many viewed as the “OPEC of its day,” says Shultz. Prices stood at a whopping $3 per barrel.  Then came the oil shocks of the ‘70s – the Arab oil embargo, the Iranian revolution and the Iran-Iraq war.  The U.S. faced rationing and prices that landed at $40/barrel by decade’s end.  During each of these price spikes, there was a “kerfuffle” that subsided rapidly, says Shultz. We never learned our lesson. <br><br>

Shultz sees the U.S. at a momentous crossroads that he views, this time, with optimism. “Powerful constituencies are involved in this, all oddly pointing in the same direction.”  National and economic security and climate change are converging to force our hand.  Shultz envisions the next administration taking on a host of actions: a “stable tax regime” for wind and solar power; carbon capture and transformation (rather than the iffy sequestration); implementation of nuclear power, if we can “come to grips with the nuclear fuel cycle issue;” ending the “dumb policy” of corn-based ethanol subsidies; and finding a better car battery.<br><br>

These things seem doable, says Shultz. He adds to his wishlist “a wedge” -- something that would keep the price of crude oil at $70 or above, to help people working on alternative fuels.  And there’s also need for a carbon tax (preferred by economists to cap and trade).  But “the big enchilada” for Shultz is “investing heavily in basic research.”  If you’re going to subsidize something, he says, support activities that “will get results that will pay off for us.”  Shultz acknowledges the kind of partisanship and game-playing that take place in Washington around wise energy policy and science. He offers advice for people in the scientific community who wish to gain the ear of politicians:  “Get people in there who are fun to talk to, and when the president thinks they’re coming to the Oval Office, he’ll look forward to it, and enjoy it and get some education.”
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			<title><![CDATA[A New Age of Exploration: From Earth to Mars]]></title>
			<pubDate>Thu, 25 Sep 2008 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/601</guid>
			<link>http://mitworld.mit.edu/video/601</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill-01026-alumni-tech-day-2008-newman-07jun2008.jpg"  alt="" />Happily for human spaceflight, <b>Dava Newman</b> and her students enjoy working in such laboratories as NASA’s “Vomit Comet.” Newman’s work aims to provide a better understanding of how humans can withstand the rigors of space missions.  Her decades studying human physiology and performance in extreme environments may prove key not just to the success of reaching Mars this century, but to improving the quality of life for people disabled by disease or accident on Earth.<br><br>

Studies of astronauts in flight, training on Earth, and on long engagements at the International Space Station, reveal “significant physiological deconditioning,” Newman says.  Microgravity produces musculo-skeletal loss, especially in the vertebrae and leg bones, as bipeds become “more like snakes, using a swimming type of motion.”  Muscles also atrophy from 20-30%.   It’s possible some of this loss could be restored once on the moon (where people are 1/6th their weight), or on Mars (3/8th their Earth weight). But Newman wants to do something about these conditions before humans reach these destinations.<br><br>

She’s working on such countermeasures as unique spaceflight exercises, special drugs, human augmentation, next-generation spacesuits, and creating artificial gravity. She shows a nifty, pedal-powered artificial gravity device on which an astronaut spins, to combat deleterious physiological effects.  Newman says it takes the brain around 30 days to adapt to zero gravity, and to switch back to Earth gravity. Our astronauts don’t get the hang of being home right away. Says Newman, “The funny thing is when a crew comes back, and they let go of their toothbrush and it just falls down.”  <br><br>

Newman provides a fast history of the spacesuit (including a giant, white spherical ball from the ‘60s and a shrink-wrap version from the &#39;70s), before introducing her bio suit, the result of many experiments, including hanging people from the ceiling, to simulate moon walking.  Her outfit comes with a mechanical counter pressure system, and biosensors to maximize mobility and minimize energy consumption.  Newman hopes to modify this gear into a smart suit to help children with cerebral palsy achieve more normal locomotion.<br><br>

What fires Newman up the most is exploration, something she’s passionate about, having circumnavigated the globe on a 1 1/2 year voyage. Mars is within reach --“We’re up to the task” -- but we may have to accept that maybe everyone doesn’t come back alive, says Newman. Yet, “what’s it worth if we can really find evidence for the origins of life three to four billion years ago on Mars.  That’s huge!”
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			<title><![CDATA[Precision Cosmology]]></title>
			<pubDate>Mon, 22 Sep 2008 00:00:00 -0400</pubDate>
			<guid>http://mitworld.mit.edu/video/600</guid>
			<link>http://mitworld.mit.edu/video/600</link>
			<description><![CDATA[<img vspace="4" hspace="4" border="1" align="right" src="http://mitworld.mit.edu/thumbs/video/home/mitwstill-01025-alumni-tech-day-2008-hockfield-tegmark-07jun2008.jpg"  alt="" />Buzz Lightyear has nothing on <b> Max Tegmark, </b> who takes his alumni audience on a dizzying tour of the universe and beyond.<br><br>

Before Tegmark begins, MIT President <b>Susan Hockfield</b> highlights some newsworthy Institute milestones and initiatives, including breaking ground on a new cancer research center that will bring together engineering and life sciences; and pioneering work on new energy solutions, with a focus on harnessing light from the sun.  Since federal funding for research has diminished, says Hockfield, MIT is increasingly pursuing philanthropy to move these key ventures into their next phase.  She also describes a banner year for MIT admissions, in spite of turmoil nationally in higher education applications and financial aid; and a record for 2008 Alumni fund giving.<br><br>

In his “little ride” from Earth into the far reaches of space and time, Max Tegmark demonstrates the success of new technologies such as orbiting space telescopes and super computer number crunching that enable scientists to test their theories of the universe.  Tegmark remarks, “30 years ago, cosmology was largely viewed as somewhere out there between philosophy and metaphysics. You could speculate over a bunch of beers about what happened, and then you could go home, because there wasn’t a whole lot else to do.” But “now we’re so spoiled, with a few clicks of the mouse, we can zoom out ‘til the whole galaxy is just a little dot, and other dots are not stars but other galaxies.”  <br><br>

Tegmark illustrates not just our planet’s place in space, but the layout of the entire known cosmos as well, relying in particular on the Sloan Digital Sky Survey, and NASA satellite maps, which help animate 3D renderings of the universe over time. Scientists are closing in on a “consistent picture of how the universe evolved from the earliest moment to the present,” expanding, cooling and clumping over its 14-billion-year history. Tegmark pays tribute to MIT colleague Alan Guth, whose inflation theory predicts not just a really big universe, but an infinite one, with parallel universes.  As fantastic a concept as this appears, Tegmark says, “I feel inflation is testable.”  Scientists can increasingly take the measure of a vast cosmos, with real numbers. <br><br>

Tegmark hopes to “map everything in the observable universe” with the help of the Fast Fourier Transform Telescope, which he likens to a “giant sea of cheap radio antennas hooked into a computer.” Next stop on the cosmologist’s infinite voyage: getting to the bottom of dark matter and dark energy, and trying to figure out whether our universe will expand forever, or end with a “crunch.” 
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