Monday, May 5, 2014
Moore 070

Teaching Statement Workshop - 2-Part Event

Monday, May 12, 2014
Center for Student Services 360 (Workshop Space)

Teaching Statement Workshop - 2-Part Event

Friday, April 4, 2014
Center for Student Services 360 (Workshop Space)

Spring TA Training

Tuesday, April 1, 2014
Center for Student Services 360 (Workshop Space)

Spring Head TA Lunch

Fighting Flies

Caltech biologists identify sex-specific brain cells in male flies that promote aggression

When one encounters a group of fruit flies invading their kitchen, it probably appears as if the whole group is vying for a sweet treat. But a closer look would likely reveal the male flies in the group are putting up more of a fight, particularly if ripe fruit or female flies are present. According to the latest studies from the fly laboratory of California Institute of Technology (Caltech) biologist David Anderson, male Drosophilae, commonly known as fruit flies, fight more than their female counterparts because they have special cells in their brains that promote fighting. These cells appear to be absent in the brains of female fruit flies.  

"The sex-specific cells that we identified exert their effects on fighting by releasing a particular type of neuropeptide, or hormone, that has also been implicated in aggression in mammals including mouse and rat," says Anderson, the Seymour Benzer Professor of Biology at Caltech, and corresponding author of the study. "In addition, there are some recent papers implicating increased levels of this hormone in people with personality disorders that lead to higher levels of aggression."

The team's findings are outlined in the January 16 version of the journal Cell.

At first glance, a fruit fly may seem nothing like a human being. But look much closer, at a genetic level, and you will find that many of the genes seen in these flies are also present—and play similar roles—in humans. However, while such conservation holds for genes involved in basic cellular functions and in development, whether it was also true for genes controlling complex social behaviors like aggression was far from clear.

"Our studies are the first, to our knowledge, to identify a gene that plays a conserved role in aggression all the way from flies to humans," explains Anderson, who is also a Howard Hughes Medical Institute investigator. If that is true for one such gene, it is also is likely true for others, Anderson says. "Our study validates using fruit flies as a model to discover new genes that may also control aggression in humans."

The less-complex nervous system of the fruit fly makes them easier to study than people or even mice, another genetic model organism. For this particular study, the research team created a small library consisting of different fly lines; in each line, a different set of specific neurons was genetically labeled and could be artificially activated, with each neuron type secreting a different neuropeptide. Forty such lines were tested for their ability to increase aggression when their labeled neurons were activated. The one that produced the most dramatic increase in aggression had neurons expressing a particular neuropeptide called tachykinin, or Tk.

Next, Anderson and his colleagues used a set of genetic tools to identify exactly which neurons were responsible for the effect on aggression and to see if the gene that encodes for Tk also controls aggressive behavior by acting in that cell.

"We had to winnow away the different cells to find exactly which ones were involved in aggression—that's how we discovered that within this line, there was a male-specific set of neurons that was responsible for increased aggressive behavior," explains Kenta Asahina, a postdoctoral scholar in Anderson's lab and lead author of the study. Male-specific neurons controlling courtship behavior had previously been identified in flies, but this was the first time a male-specific neuron was found that specifically controls aggression. Having identified that neuron, the team was then able to modify its gene expression. Says Asahina, "We found that if you overproduce the gene in that cell and then stimulate the cell, you get an even stronger effect to promote aggression than if you stimulate the cell without overproducing the gene."

In fact, combining cell activation and the overproduction of the neuropeptide, which is released when the cell is activated, caused the flies to attack targets they normally would not. For example, when the researchers eliminated cues that normally promote aggression in a target fly — such as pheromones — the flies containing the hyperactivated "aggression" neurons attacked those targets despite the absence of the cues.

Moreover, this combined activation of the cell and the gene produced such a strong effect that the researchers were even able to get a fly to attack an inanimate object—a fly-sized magnet—when it was moved around in an arena.

Such behavior had never been observed previously. "A normal fly will chase the magnet, but will never attack the magnet," Asahina explains. "By over-activating these neurons, we are able to get the fly to attack an object that displays none of the normal signals that are required to elicit aggression from another fly."

"These results suggest that what these neurons are doing is promoting a state of aggressive arousal in the fly," Anderson says. "This elevated level of aggressiveness drives the fly to attack targets it would normally ignore. I wouldn't anthropomorphize the fly and say that it has increased 'anger,' but activating these neurons greatly lowers its threshold for attack."

The finding that these neurons are present in the brains of male but not female flies indicates that this sex difference in aggressive behavior is genetically based. At the same time, Asahina stresses, finding a gene that influences aggression does not mean that aggression is controlled only by genes and always genetically programmed.

"This is a very important distinction, because when people hear about a gene implicated in behavior, they automatically think it means that the behavior is genetically determined. But that is not necessarily the case," he says. "The key point here is that we can say something about how the gene acts to influence this behavior—that is, is by functioning as a chemical messenger in cells that control this behavior in the brain. We've been able to study the problem of aggressive behavior at two levels, the cell level and the gene level, and to link those studies together by genetic experiments."

This research, Anderson says, has given his team a beachhead into the circuitry in the fly brain that controls aggression, a behavior that they will continue to try to decode.

"We have to use this point of entry to discover the larger circuit in which those cells function," Anderson says. "If aggression is like a car, and if more aggression is like a car going faster, we want to know if what we're doing when we trigger these cells is stepping on the gas or taking the foot off the brake. And we want to know where and how that's happening in the brain. That's going to take a lot of work."

Additional Caltech authors on the Cell paper, "Male-specific Tachykinin-expressing neurons control sex differences in levels of aggressiveness in Drosophila," are Kiichi Watanabe, Brian J. Duistermars, Eric Hoopfer, Carlos Roberto González, Eyrún Arna Eyjólfsdóttir, and Pietro Perona. Their work was supported by the National Institutes of Health, a grant from the Gordon and Betty Moore Foundation, the Japan Society for the Promotion of Science, and the Howard Hughes Medical Institute.

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Bacterial "Syringe" Necessary for Marine Animal Development

If you've ever slipped on a slimy wet rock at the beach, you have bacteria to thank. Those bacteria, nestled in a supportive extracellular matrix, form bacterial biofilms—often slimy substances that cling to wet surfaces. For some marine organisms—like corals, sea urchins, and tubeworms—these biofilms serve a vital purpose, flagging suitable homes for such organisms and actually aiding the transformation of larvae to adults.

A new study at the California Institute of Technology (Caltech) is the first to describe a mechanism for this phenomenon, providing one explanation for the relationship between bacterial biofilms and the metamorphosis of marine invertebrates. The results were published online in the January 9 issue of Science Express.

The study focused on a marine invertebrate that has become a nuisance to the shipping industry since its arrival in U.S. waters during the last half century: the tubeworm Hydroides elegans. The larvae of the invasive pest swim free in the ocean until they come into contact with a biofilm-covered surface, such as a rock or a buoy—or the hull of a ship. After the tubeworm larvae come in contact with the biofilm, they develop into adult worms that anchor to the surface, creating hard, mineralized "tubes" around their bodies. These tubes, which often cover the bottoms of ships, create extra drag in the water, dramatically increasing the ship's fuel consumption.

The tubeworms' unwanted and destructive presence on ships, called biofouling, is a "really bad problem," says Dianne Newman, a professor of biology and geobiology and Howard Hughes Medical Institute (HHMI) investigator at Caltech. "For example, biofouling costs the U.S. Navy millions of dollars every year in excess fuel costs," says Newman, who is also a coauthor of the study. And although researchers have known for decades that biofilms are necessary for tubeworm development, says Nicholas Shikuma, one of the two first authors on the study and a postdoctoral scholar in Newman's laboratory, "there was no mechanistic explanation for how bacteria can actually induce that process to happen. We wanted to provide that explanation."

Shikuma began by investigating Pseudoalteromonas luteoviolacea, a bacterial species known to induce metamorphosis in the tubeworm and other marine invertebrates. In earlier work, Michael G. Hadfield of the University of Hawai'i at Mānoa, a coauthor of the Science Express paper, had identified a group of P. luteoviolacea genes that were necessary for tubeworm metamorphosis. Near those genes, Shikuma found a set of genes that produced a structure similar to the tail of bacteriophage viruses.

The tails of these phage viruses contain three main components: a projectile tube, a contractile sheath that deploys the tube, and an anchoring baseplate. Together, the phage uses these tail components as a syringe, injecting their genetic material into host bacteria cells, infecting—and ultimately killing—them. To determine if the phage tail-like structures in P. luteoviolacea played a role in tubeworm metamorphosis, the researchers systematically deleted the genes encoding each of these three components.

Electron microscope images of the bacteria confirmed that syringe-like structures were present in "normal" P. luteoviolacea cells but were absent in cells in which the genes encoding the three structural components had been deleted; these genes are known as metamorphosis-associated contractile structure (mac) genes. The researchers also discovered that the bacterial cells lacking mac genes were unable to induce metamorphosis in tubeworm larvae. Previously, the syringe-like structures had been found in other species of bacteria, but in these species, the tails were deployed to kill other bacteria or insects. The new study provides the first evidence of such structures benefitting another organism, Shikuma says.

In order to view the three-dimensional arrangement of these unique structures within intact bacteria, the researchers collaborated with the laboratory of Grant Jensen, professor of biology and HHMI investigator at Caltech. Utilizing a technique called electron cryotomography, the researchers flash-froze the bacterial cells at very low temperatures. This allowed them to view the cells and their internal structures in their natural, "near-native" states.

Using this visualization technique, Martin Pilhofer, a postdoctoral scholar in Jensen's lab and the paper's other first author, discovered something unique about the phage tail-like structures within P. luteoviolacea; instead of existing as individual appendages, the structures were linked together to create a spiny array. "In these arrays, about 100 tails are stuck together in a hexagonal lattice to form a complex with a porcupine-like appearance," Shikuma says. "They're all facing outward, poised to fire," he adds. "We believe this is the first observation of arrays of phage tail-like structures."

Initially, the array is compacted within each bacterium; however, the cells eventually burst—killing the microbes—and the array unfolds. The researchers hypothesize that, at this point, the individual spines of the array fire outward into the tubeworm larva. Following this assault, the larvae begin their developmental transition to adulthood.

"It was a tremendous surprise that the agent that drives metamorphosis is such an elaborate, well-organized injection machine," says coauthor Jensen. "Who would have guessed that the signal is delivered by an apparatus that is almost as large as the bacterial cell itself? It is simply a marvelous structure, synthesized in a 'loaded' but tightly collapsed state within the cell, which then expands like an umbrella, opening up into a much larger web of syringes that are ready to inject," he says.

Although the study confirms that the phage tail-like structures can cause tubeworm metamorphosis, the nature of the interaction between the tail and the tubeworm is still unknown, Shikuma says. "Our next step is to determine whether metamorphosis is caused by an injection into the tubeworm larva tissue, and, then, if the mechanical action is the trigger, or if the bacterium is injecting a chemical morphogen," he says. He and his colleagues would also like to determine if mac genes and the tail-like structures they encode might influence other marine invertebrates, such as corals and sea urchins, that also rely on P. luteoviolacea biofilms for metamorphosis.

Understanding this process might one day help reduce the financial losses from P. luteoviolacea biofilm fouling on ship hulls, for example. While applications are a long way off, Newman says, it is also interesting to speculate on the possibility of leveraging metamorphosis induction in beneficial marine invertebrates to improve yields in aquaculture and promote coral reef growth.

The study, the researchers emphasize, is an example of the collaborative research that is nurtured at Caltech. For his part, Shikuma was inspired to utilize electron cryotomography after hearing a talk by Martin Pilhofer at the Center for Environmental Microbiology Interactions (CEMI) at Caltech. "Martin gave a presentation on another type of phage tail-like structures in the monthly CEMI seminar. I saw his talk and I thought that the mac genes I was working with might somehow be related," Shikuma says. Their subsequent collaboration, Newman says, made the current study possible.

The paper is titled "Marine tubeworm metamorphosis induced by arrays of bacterial phage tail-like structures." Gregor L. Weiss, a Summer Undergraduate Research Fellowship student in Jensen's laboratory at Caltech, was an additional coauthor on the study. The published work was funded by a Caltech Division of Biology Postdoctoral Fellowship (to N. Shikuma), the Caltech CEMI, the Howard Hughes Medical Institute, the Office of Naval Research, the National Institutes of Health, and the Gordon and Betty Moore Foundation.

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Caltech Cell Biologist Wins $3 Million Breakthrough Prize in Life Sciences

Alexander Varshavsky, Caltech's Howard and Gwen Laurie Smits Professor of Cell Biology, has been awarded one of six 2014 Breakthrough Prizes in Life Sciences. Varshavsky was honored for "his discovery of the critical molecular determinants and biological functions of intracellular protein degradation," according to the award citation.

Each of the laureates will receive $3 million, making the award, announced at a ceremony at NASA's Ames Research Center on December 12, one of the largest academic prizes in the world.

At the same ceremony, Caltech's John Schwarz, the Harold Brown Professor of Theoretical Physics, and Michael B. Green of the University of Cambridge were named winners of the 2014 Fundamental Physics Prize in recognition of the new perspectives they have brought to quantum gravity and the unification of the fundamental physical forces of the universe. They will share a $3 million award.

Caltech's Alexei Kitaev, Ronald and Maxine Linde Professor of Theoretical Physics and Mathematics, is a previous winner of the Fundamental Physics Prize.

The Breakthrough Prize in Life Sciences was instituted to recognize "excellence in research aimed at curing intractable diseases and extending human life," according to the Breakthrough Prize in Life Sciences Foundation website. Founding sponsors of the prize include Sergey Brin and Anne Wojcicki, Mark Zuckerberg and Priscilla Chan, Jack Ma and Cathy Zhang, and Yuri Milner.

The inaugural class of 11 prize winners, announced in February, served on the selection committee for the 2014 awards; Varshavsky and the other laureates will join the selection committee for future awardees.

Varshavsky was noted for the fundamental discovery, in the 1980s, of biological regulation by intracellular protein degradation and its central importance in cellular physiology. "Studies by my laboratory, at first at the Massachusetts Institute of Technology and later at Caltech, focused on the understanding of how and why cells destroy their own proteins to withstand stress, to grow and divide, to differentiate into new kinds of cells, and to do countless other things that make living organisms so astonishing and fascinating," Varshavsky says.

His work focuses on the design and biological functions of the ubiquitin system, a major proteolytic circuit in living cells. Ubiquitin is a small protein that is present in cells either as a free protein or as a part of tight (covalent) complexes with many other proteins. The association of ubiquitin with cellular proteins marks them for degradation or other metabolic fates. Through its ability to destroy specific proteins, the ubiquitin system plays a major role in cell growth and differentiation, DNA repair, regulation of gene expression, and many other biological processes.

"The field of ubiquitin has been expanding at an amazing pace and is now one of the largest arenas in biomedical science," Varshavsky says. "Both earlier and recent discoveries illuminate the ubiquitin system and protein degradation from many different angles and continue to foster our ability to tackle human diseases, from cancer, infections and cardiovascular illnesses to neurodegenerative syndromes and aging itself. I feel privileged having been able to contribute to the birth of this field and to partake in its later development.

"The Breakthrough Prize will support, in a major way, our studies at Caltech," Varshavsky adds. "I am most grateful to the Breakthrough Foundation, to its founders, and to its committee for the honor of this award."

"The Breakthrough Prize in Life Sciences recognizes Alex's truly pioneering discovery of ubiquitin-mediated protein degradation and its central role in both cellular function and dysfunction. His work has opened up completely new approaches to understanding and treating human disease," says Stephen Mayo, Bren Professor of Biology and Chemistry and the William K. Bowes Jr. Leadership Chair of the Division of Biology and Biological Engineering.

Varshavsky earned his BS from Moscow State University in 1970 and his PhD from the Institute of Molecular Biology in 1973. He has been Smits Professor at Caltech since 1992.

A member of the National Academy of Sciences, the American Academy of Arts and Sciences, the American Philosophical Society, and the Academia Europaea, Varshavsky has received many international prizes in biology and medicine, including the 2012 King Faisal International Prize for Science (Saudi Arabia), the 2011 Otto Warburg Prize (Germany); the 2008 Gotham Prize in Cancer Research; the 2006 Gagna Prize (Belgium); the 2006 Griffuel Prize (France); the 2005 Stein and Moore Award; the 2001 Horwitz Prize; the 2001 Merck Award; the 2001 Wolf Prize in Medicine (Israel); the 2000 Lasker Award in Basic Medical Research; and the 1999 Gairdner International Award (Canada).

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Kathy Svitil
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Probiotic Therapy Alleviates Autism-like Behaviors in Mice

Autism spectrum disorder (ASD) is diagnosed when individuals exhibit characteristic behaviors that include repetitive actions, decreased social interactions, and impaired communication. Curiously, many individuals with ASD also suffer from gastrointestinal (GI) issues, such as abdominal cramps and constipation.

Using the co-occurrence of brain and gut problems in ASD as their guide, researchers at the California Institute Technology (Caltech) are investigating a potentially transformative new therapy for autism and other neurodevelopmental disorders.

The gut microbiota—the community of bacteria that populate the human GI tract—previously has been shown to influence social and emotional behavior, but the Caltech research, published online in the December 5 issue of the journal Cell, is the first to demonstrate that changes in these gut bacteria can influence autism-like behaviors in a mouse model.

"Traditional research has studied autism as a genetic disorder and a disorder of the brain, but our work shows that gut bacteria may contribute to ASD-like symptoms in ways that were previously unappreciated," says Professor of Biology Sarkis K. Mazmanian. "Gut physiology appears to have effects on what are currently presumed to be brain functions."

To study this gut–microbiota–brain interaction, the researchers used a mouse model of autism previously developed at Caltech in the laboratory of Paul H. Patterson, the Anne P. and Benjamin F. Biaggini Professor of Biological Sciences. In humans, having a severe viral infection raises the risk that a pregnant woman will give birth to a child with autism. Patterson and his lab reproduced the effect in mice using a viral mimic that triggers an infection-like immune response in the mother and produces the core behavioral symptoms associated with autism in the offspring.

In the new Cell study, Mazmanian, Patterson, and their colleagues found that the "autistic" offspring of immune-activated pregnant mice also exhibited GI abnormalities. In particular, the GI tracts of autistic-like mice were "leaky," which means that they allow material to pass through the intestinal wall and into the bloodstream. This characteristic, known as intestinal permeability, has been reported in some autistic individuals. "To our knowledge, this is the first report of an animal model for autism with comorbid GI dysfunction," says Elaine Hsiao, a senior research fellow at Caltech and the first author on the study.

To see whether these GI symptoms actually influenced the autism-like behaviors, the researchers treated the mice with Bacteroides fragilis, a bacterium that has been used as an experimental probiotic therapy in animal models of GI disorders.

The result? The leaky gut was corrected.

In addition, observations of the treated mice showed that their behavior had changed. In particular, they were more likely to communicate with other mice, had reduced anxiety, and were less likely to engage in a repetitive digging behavior.

"The B. fragilis treatment alleviates GI problems in the mouse model and also improves some of the main behavioral symptoms," Hsiao says. "This suggests that GI problems could contribute to particular symptoms in neurodevelopmental disorders."

With the help of clinical collaborators, the researchers are now planning a trial to test the probiotic treatment on the behavioral symptoms of human autism. The trial should begin within the next year or two, says Patterson.

"This probiotic treatment is postnatal, which means that the mother has already experienced the immune challenge, and, as a result, the growing fetuses have already started down a different developmental path," Patterson says. "In this study, we can provide a treatment after the offspring have been born that can help improve certain behaviors. I think that's a powerful part of the story."

The researchers stress that much work is still needed to develop an effective and reliable probiotic therapy for human autism—in part because there are both genetic and environmental contributions to the disorder, and because the immune-challenged mother in the mouse model reproduces only the environmental component.

"Autism is such a heterogeneous disorder that the ratio between genetic and environmental contributions could be different in each individual," Mazmanian says. "Even if B. fragilis ameliorates some of the symptoms associated with autism, I would be surprised if it's a universal therapy—it probably won't work for every single case."

The Caltech team proposes that particular beneficial bugs are intimately involved in regulating the release of metabolic products (or metabolites) from the gut into the bloodstream. Indeed, the researchers found that in the leaky intestinal wall of the autistic-like mice, certain metabolites that were modulated by microbes could both easily enter the circulation and affect particular behaviors.

"I think our results may someday transform the way people view possible causes and potential treatments for autism," Mazmanian says.

Along with Patterson, Hsiao, and Mazmanian, additional Caltech coauthors on the paper, "Microbiota Modulate Behavioral and Physiological Abnormalities Associated with Neurodevelopmental Disorders," are Sara McBride, Sophia Hsien, Gil Sharon, Julian A. Codelli, Janet Chow, and Sarah E. Reisman. The work was supported by a Caltech Innovation Initiative grant, an Autism Speaks Weatherstone Fellowship, a National Institutes of Health/National Research Service Award Ruth L. Kirschstein Predoctoral Fellowship, a Human Frontiers Science Program Fellowship, a Department Of Defense Graduate Fellowship, a National Science Foundation Graduate Research Fellowship, an Autism Speaks Trailblazer Award, a Caltech Grubstake award, a Congressionally Directed Medical Research Award, a Weston Havens Foundation Award, several Callie McGrath Charitable Foundation awards, and the National Institute of Mental Health.

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Focusing on Faces

Researchers find neurons in amygdala of autistic individuals have reduced sensitivity to eye region of others' faces

Difficulties in social interaction are considered to be one of the behavioral hallmarks of autism spectrum disorders (ASDs). Previous studies have shown these difficulties to be related to differences in how the brains of autistic individuals process sensory information about faces. Now, a group of researchers led by California Institute of Technology (Caltech) neuroscientist Ralph Adolphs has made the first recordings of the firings of single neurons in the brains of autistic individuals, and has found specific neurons in a region called the amygdala that show reduced processing of the eye region of faces. Furthermore, the study found that these same neurons responded more to mouths than did the neurons seen in the control-group individuals.

"We found that single brain cells in the amygdala of people with autism respond differently to faces in a way that explains many prior behavioral observations," says Adolphs, Bren Professor of Psychology and Neuroscience and professor of biology at Caltech and coauthor of a study in the November 20 issue of Neuron that outlines the team's findings. "We believe this shows that abnormal functioning in the amygdala is a reason that people with autism process faces abnormally."

The amygdala has long been known to be important for the processing of emotional reactions. To make recordings from this part of the brain, Adolphs and lead author Ueli Rutishauser, assistant professor in the departments of neurosurgery and neurology at Cedars-Sinai Medical Center and visiting associate in biology at Caltech, teamed up with Adam Mamelak, professor of neurosurgery and director of functional neurosurgery at Cedars-Sinai, and neurosurgeon Ian Ross at Huntington Memorial Hospital in Pasadena, California, to recruit patients with epilepsy who had electrodes implanted in their medial temporal lobes—the area of the brain where the amygdala is located—to help identify the origin of their seizures. Epileptic seizures are caused by a burst of abnormal electric activity in the brain, which the electrodes are designed to detect. It turns out that epilepsy and ASD sometimes go together, and so the researchers were able to identify two of the epilepsy patients who also had a diagnosis of ASD.

By using the implanted electrodes to record the firings of individual neurons, the researchers were able to observe activity as participants looked at images of different facial regions, and then correlate the neuronal responses with the pictures. In the control group of epilepsy patients without autism, the neurons responded most strongly to the eye region of the face, whereas in the two ASD patients, the neurons responded most strongly to the mouth region. Moreover, the effect was present in only a specific subset of the neurons. In contrast, a different set of neurons showed the same response in both groups when whole faces were shown.

"It was surprising to find such clear abnormalities at the level of single cells," explains Rutishauser. "We, like many others, had thought that the neurological abnormalities that contribute to autism were spread throughout the brain, and that it would be difficult to find highly specific correlates. Not only did we find highly specific abnormalities in single-cell responses, but only a certain subset of cells responded that way, while another set showed typical responses to faces. This specificity of these cell populations was surprising and is, in a way, very good news, because it suggests the existence of specific mechanisms for autism that we can potentially trace back to their genetic and environmental causes, and that one could imagine manipulating for targeted treatment."

"We can now ask how these cells change their responses with treatments, how they correspond to similar cell populations in animal models of autism, and what genes this particular population of cells expresses," adds Adolphs.

To validate their results, the researchers hope to identify and test additional subjects, which is a challenge because it is very hard to find people with autism who also have epilepsy and who have been implanted with electrodes in the amygdala for single-cell recordings, says Adolphs.

"At the same time, we should think about how to change the responses of these neurons, and see if those modifications correlate with behavioral changes," he says.

Funding for the research outlined in the Neuron paper, titled "Single-neuron correlates of abnormal face processing in autism," was provided by the Simons Foundation, the Gordon and Betty Moore Foundation, the Cedars-Sinai Medical Center, Autism Speaks, and the National Institute of Mental Health. Additional coauthors were Caltech postdoctoral scholar Oana Tudusciuc and graduate student Shuo Wang.

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New Department of Medical Engineering Added by the Caltech Division of Engineering and Applied Science

Caltech's Division of Engineering and Applied Science (EAS) has added a new department to its roster: the Department of Medical Engineering (MedE). MedE joins EAS's existing departments of Aerospace; Applied Physics and Materials Science; Computing and Mathematical Sciences; Electrical Engineering; Environmental Science and Engineering; and Mechanical and Civil Engineering. Like these other departments, MedE pulls together faculty from a broad range of specialties, both within EAS and outside it, to create an interdisciplinary program that aims to aid collaboration and provide graduate education in a critical area of engineering that directly and positively impacts human health and well-being.

MedE was formed to take advantage of Caltech's commitment to basic science, using this focus as a stepping-stone to finding fresh avenues to developing diagnostic tools, medical devices, and treatment options, in an approach sometimes known as translational, or "bench-to-bedside," medicine. Ares Rosakis, Theodore von Kármán Professor of Aeronautics and Mechanical Engineering and Booth Leadership Chair of the EAS division, explains that the MedE department was formed "in response to the desire of many of our faculty and of local research hospitals and medical foundations to engage jointly in engineering-centric technology development efforts for medical applications." To that end, the MedE department is already partnering with the Keck School of Medicine of USC, UCLA's Geffen School of Medicine, City of Hope, the UCSF School of Medicine, and Huntington Memorial Hospital, among others.

Combined with the newly established Division of Biology and Biological Engineering at Caltech, MedE positions Caltech to become an even more dynamic force in the field of bioengineering. As Vice Provost and Hans W. Liepmann Professor of Aeronautics and Bioinspired Engineering Morteza Gharib explains, "Medical engineering is top-down. We look at the problems that are currently challenging to the field and try to come up with devices and techniques to help clinicians do their job better or make breakthroughs. Biological engineering is bottom-up. It tries to understand how biology works and then builds upon that to get to the point where it can contribute to the field. Basically we're looking at the same wall from two different sides." Bringing the two sides together, says Gharib, "will not only help coordinate scientific work at Caltech but will also give outsiders a more accurate impression of how we at Caltech are taking a multifaceted approach to the challenges of bioengineering across disciplines."

"Caltech really has an opportunity here," says Yu-Chong Tai, Anna L. Rosen Professor of Electrical Engineering and Mechanical Engineering and executive officer of the new MedE department. "There are more than 60 accredited biomedical engineering programs in the United States, and there are about 100 biomedical programs at various universities and institutes. A lot of the work we want to do has to rely on deep engineering, which is our strength at Caltech. That's why our intention is to build the Caltech medical engineering department in a way that is rooted in really first-class engineering, moving from that base toward medical applications."

The expertise the MedE faculty bring to the department is deep and varied. In the field of diagnostics, Tai's research uses microelectromechanical and nanoelectromechanical systems (MEMS/NEMS) technologies to produce high-performance liquid chromatography (HPLC) on a chip and blood labs on a chip. Similar technologies are deployed for therapeutic treatments, such as the creation of miniature or micro implant devices including spinal neural stimulators, ECG implants, retinal prosthetic devices, intraocular lenses, and increasingly precise drug delivery systems. Gharib is looking into the use of nanoscale carbon-tube medical adhesives and painless nanoscale needles, and is also exploring the hemodynamics and wave dynamics of large blood vessels and embryonic heart flow with an eye toward cardiovascular medical applications. Joel Burdick, Richard L. and Dorothy M. Hayman Professor of Mechanical Engineering and Bioengineering, has been focusing his expertise in robotics to help patients suffering from paralysis. He and his colleagues have developed a rehabilitation technology that could lead to the successful repair of paralyzing spinal-cord injuries. Azita Emami, Professor of Electrical Engineering, and her team are designing high-performance, low-power, minimally invasive implantable and wearable medical devices for neural recording, neural stimulation, and drug delivery.

The medical engineering department is currently offering MS and PhD degrees, seeking to train a new generation of engineers to close the gap between engineering and medicine. The MedE department will cooperate with existing research centers at Caltech such as the Donna and Benjamin M. Rosen Bioengineering Center and the Center for Bioinspired Engineering. To learn more about the MedE department, visit its website at http://www.mede.caltech.edu, or read an overview of the department's faculty and their ambitions for the new MedE program in the Fall 2013 issue of EAS's ENGenious magazine (http://eas.caltech.edu/engenious/ten/eas_feature).

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