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Thursday, January 31st, 2019
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| 10:45a |
SuperUROP: Showcasing students' research work in progress If one overarching message emerged from the 2018 SuperUROP Showcase, it was this: MIT undergraduates can do just about anything.
The lively poster session, which marked the halfway point in the annual Advanced Undergraduate Research Opportunities Program (SuperUROP), featured more than 130 poster presentations by students on topics ranging from DNA-based memory storage to adaptive flight control and from image recognition to the automated correction of grammatical errors in Japanese.
Capping the event was the SuperUROP Community Dinner, which featured a keynote address by Tom Leighton PhD ’81, the CEO and co-founder of Akamai, a $2.5 billion technology company that was born at MIT. Leighton’s talk, “The Akamai Story: From Theory to Practice,” was designed to inspire the undergraduates in attendance. It centered, as Leighton put it, on “taking a UROP project and forming a company and having some success with it.”
SuperUROP builds on the success of MIT’s flagship UROP program. While traditional UROP experiences last just one term, SuperUROP involves research projects spanning the full academic year and includes a two-term class on conducting and presenting research, including writing journal-style papers as their final assignments.
Typically, the impact of SuperUROP experience extends well beyond the course, says Anantha Chandrakasan, dean of the School of Engineering and Vannevar Bush Professor of Electrical Engineering and Computer Science.
“We expect to see the results of many of these projects presented at major conferences and published in top journals,” says Chandrakasan, who founded SuperUROP when he was head of the Department of Electrical Engineering and Computer Science (EECS). “We are also thrilled to see our former SuperUROP scholars move on to top PhD programs and making impact in industry.”
“The fact that it’s year-long is crucial,” says EECS senior Faraaz Nadeem, who is trying to automate the transcription of music featuring multiple instruments, a task he finds quite time-consuming. “The extra time and the way the class is structured, with deadlines, is pretty helpful.”
Launched in 2012 within EECS, SuperUROP later expanded to the full School of Engineering, and in 2017 began supporting research involving the School of Humanities, Arts, and Social Sciences (SHASS). Nadeem is among this year’s nine CS+HASS Undergraduate Research and Innovation Scholars, who work on projects combining computer science with the humanities, arts, and social sciences.
“SHASS is so excited to have students involved in SuperUROP,” says Agustín Rayo, associate dean of SHASS, who attended the December 2018 poster session. “I think our undergraduates are really at the vanguard.”
This year, SuperUROP also included eight scholars funded by the School of Engineering and the MIT Quest for Intelligence, a campus-wide initiative launched in February 2018 to advance human understanding of intelligence.
“The research goes beyond EECS. We have a really broad spectrum,” says Piotr Indyk, the Thomas D. and Virginia W. Cabot Professor of EECS and one of three faculty members who teach the SuperUROP class 6.UAR (Seminar in Advanced Undergraduate Research) with the support of eight teaching assistants.
EECS faculty member Thomas Heldt, who has served as an advisor for several SuperUROP students in the past few years, pointed out that the year-long program enables undergraduates to really dig into their topics.
“Usually it’s a more meaningful experience than a regular UROP because we’re working with students for nine months and there’s a formal program of classwork,” noted Heldt, who is the W.M. Keck Career Development Professor in Biomedical Engineering and an associate professor of electrical and biomedical engineering. “The experience is fantastic.”
Students agree.
“This is usually something graduate students would do,” says Patrick Tornes, a senior in mechanical engineering and School of Engineering/Quest scholar who is creating adaptive controls for drones so that the devices can better navigate the variable conditions of the real world. “It’s really awesome to be able to work on this as an undergraduate. In the spring, I’m looking forward to implementing the controller on a hexacopter and seeing how it actually performs.”
EECS senior Sky Shin, also a School of Engineering/Quest scholar, says SuperUROP is helping her decide what path to take in her future.
“I think [SuperUROP is] testing how I’ll fit in grad school,” says Shin, who is working in the Computational Cognitive Science Group to enable computers to classify images based on just a few examples. “This is very extensive research.”
The poster session gave students the chance to practice presenting technical material to a technical audience — one of the key skills taught in the SuperUROP program, says Dina Katabi, the Andrew & Erna Viterbi Professor of EECS and another 6.UAR instructor. “This is a very different class from anything other universities do. It’s a class that believes that research and presentation should go hand in hand,” she says.
Austin Garrett, a senior double-majoring in EECS and physics, says the SuperUROP class assignments — from developing a research topic to creating a poster and giving a presentation — have been useful in helping him plan his research.
“I’ve realized how difficult it is to develop a project,” says Garrett, a School of Engineering/Quest scholar whose research goal is to embed an intuitive understanding of physics into artificial intelligence. “It’s easy to get lost in the sea of possibilities.”
What many students say they like best about SuperUROP, however, is the chance to pursue independent research in an area that really interests them. “I’ve been given a lot of freedom in how I approach the problem. It’s really self-driven,” says Alex Kimn, a senior double-majoring in EECS and physics and another School of Engineering/Quest scholar. Kimn is using neural modeling to address grammatical errors to aid students of Japanese — work motivated by his interest in education.
Ronit Langer, a junior in EECS, meanwhile, has pursued her interest in “how we can take biological knowledge and, using computer science, develop things that can be deployed to help people.” Specifically, she’s trying to develop a protein sensor that will alert first responders to the presence of fentanyl, a powerful synthetic opioid, in possible drug-overdose cases. “What I’ve been able to accomplish in one semester is inspiring,” says Langer, a CS+HASS scholar.
The December showcase gave just a taste of things to come; students will next present the results of their research at the April 2019 SuperUROP Showcase poster session. However, it was clear that MIT undergraduates have the potential to produce great work, as Leighton underscored in his keynote dinner presentation.
As Leighton recounted the story of Akamai’s founding at MIT, its meteoric rise during the dot.com era, and its near total collapse in 2001, he attributed much of the company’s success to the work of MIT students. Teams of students worked to get the company launched and later helped it rebound from disaster, he said.
“We got through it, led by people just like you: MIT undergraduates.” | | 11:00a |
Bacteria promote lung tumor development, study suggests MIT cancer biologists have discovered a new mechanism that lung tumors exploit to promote their own survival: These tumors alter bacterial populations within the lung, provoking the immune system to create an inflammatory environment that in turn helps the tumor cells to thrive.
In mice that were genetically programmed to develop lung cancer, those raised in a bacteria-free environment developed much smaller tumors than mice raised under normal conditions, the researchers found. Furthermore, the researchers were able to greatly reduce the number and size of the lung tumors by treating the mice with antibiotics or blocking the immune cells stimulated by the bacteria.
The findings suggest several possible strategies for developing new lung cancer treatments, the researchers say.
“This research directly links bacterial burden in the lung to lung cancer development and opens up multiple potential avenues toward lung cancer interception and treatment,” says Tyler Jacks, director of MIT’s Koch Institute for Integrative Cancer Research and the senior author of the paper.
Chengcheng Jin, a Koch Institute postdoc, is the lead author of the study, which appears in the Jan. 31 online edition of Cell.
Linking bacteria and cancer
Lung cancer, the leading cause of cancer-related deaths, kills more than 1 million people worldwide per year. Up to 70 percent of lung cancer patients also suffer complications from bacterial infections of the lung. In this study, the MIT team wanted to see whether there was any link between the bacterial populations found in the lungs and the development of lung tumors.
To explore this potential link, the researchers studied genetically engineered mice that express the oncogene Kras and lack the tumor suppressor gene p53. These mice usually develop a type of lung cancer called adenocarcinoma within several weeks.
Mice (and humans) typically have many harmless bacteria growing in their lungs. However, the MIT team found that in the mice engineered to develop lung tumors, the bacterial populations in their lungs changed dramatically. The overall population grew significantly, but the number of different bacterial species went down. The researchers are not sure exactly how the lung cancers bring about these changes, but they suspect one possibility is that tumors may obstruct the airway and prevent bacteria from being cleared from the lungs.
This bacterial population expansion induced immune cells called gamma delta T cells to proliferate and begin secreting inflammatory molecules called cytokines. These molecules, especially IL-17 and IL-22, create a progrowth, prosurvival environment for the tumor cells. They also stimulate activation of neutrophils, another kind of immune cell that releases proinflammatory chemicals, further enhancing the favorable environment for the tumors.
“You can think of it as a feed-forward loop that forms a vicious cycle to further promote tumor growth,” Jin says. “The developing tumors hijack existing immune cells in the lungs, using them to their own advantage through a mechanism that’s dependent on local bacteria.”
However, in mice that were born and raised in a germ-free environment, this immune reaction did not occur and the tumors the mice developed were much smaller.
Blocking tumor growth
The researchers found that when they treated the mice with antibiotics either two or seven weeks after the tumors began to grow, the tumors shrank by about 50 percent. The tumors also shrank if the researchers gave the mice drugs that block gamma delta T cells or that block IL-17.
The researchers believe that such drugs may be worth testing in humans, because when they analyzed human lung tumors, they found altered bacterial signals similar to those seen in the mice that developed cancer. The human lung tumor samples also had unusually high numbers of gamma delta T cells.
“If we can come up with ways to selectively block the bacteria that are causing all of these effects, or if we can block the cytokines that activate the gamma delta T cells or neutralize their downstream pathogenic factors, these could all be potential new ways to treat lung cancer,” Jin says.
Many such drugs already exist, and the researchers are testing some of them in their mouse model in hopes of eventually testing them in humans. The researchers are also working on determining which strains of bacteria are elevated in lung tumors, so they can try to find antibiotics that would selectively kill those bacteria.
The research was funded, in part, by a Lung Cancer Concept Award from the Department of Defense, a Cancer Center Support (core) grant from the National Cancer Institute, the Howard Hughes Medical Institute, and a Margaret A. Cunningham Immune Mechanisms in Cancer Research Fellowship Award. | | 1:59p |
Technique could boost resolution of tissue imaging as much as tenfold Imaging deep inside biological tissue has long been a significant challenge. That is because light tends to be scattered by complex media such as biological tissue, bouncing around inside until it comes out again at a variety of different angles. This distorts the focus of optical microscopes, reducing both their resolution and imaging depth. Using light of a longer wavelength can help to avoid this scattering, but it also reduces imaging resolution.
Now, instead of attempting to avoid scattering, researchers at MIT have developed a technique to use the effect to their advantage. The new technique, which they describe in a paper published in the journal Science, allows them to use light scattering to improve imaging resolution by up to 10 times that of existing systems.
Indeed, while conventional microscopes are limited by what is known as the diffraction barrier, which prevents them focusing beyond a given resolution, the new technique allows imaging at “optical super-resolution,” or beyond this diffraction limit.
The technique could be used to improve biomedical imaging, for example, by allowing more precise targeting of cancer cells within tissue. It could also be combined with optogenetic techniques, to excite particular brain cells. It could even be used in quantum computing, according to Donggyu Kim, a graduate student in mechanical engineering at MIT and first author of the paper.
In 2007, researchers first proposed that by shaping a wave of light before sending it into the tissue, it is possible to reverse the scattering process, focusing the light at a single point. However, taking advantage of this effect has long been hampered by the difficulty of gaining sufficient information about how light is scattered within complex media such as biological tissue.
To obtain this information, researchers have developed numerous techniques for creating “guide stars,” or feedback signals from points within the tissue that allow the light to be focused correctly. But these approaches have so far resulted in imaging resolution well above the diffraction limit, Kim says.
In order to improve the resolution, Kim and co-author Dirk Englund, an associate professor in MIT’s Department of Electrical Engineering and Computer Science and the Research Laboratory of Electronics, developed something they call quantum reference beacons (QRBs).
These QRBs are made using nitrogen-vacancy (N-V) centers within diamonds. These tiny molecular defects within the crystal lattice of diamonds are naturally fluorescent, meaning they will emit light when excited by a laser beam.
What’s more, when a magnetic field is applied to the QRBs, they each resonate at their own specific frequency. By targeting the tissue sample with a microwave signal of the same resonant frequency as a particular QRB, the researchers can selectively alter its fluorescence.
“Imagine a navigator trying to get their vessel to its destination at night,” Kim says. “If they see three beacons, all of which are emitting light, they will be confused. But, if one of the beacons deliberately twinkles to generate a signal, they will know where their destination is,” he says.
In this way the N-V centers act as beacons, each emitting fluorescent light. By modulating a particular beacon’s fluorescence to create an on/off signal, the researchers can determine the beacon’s location within the tissue.
“We can read out where this light is coming from, and from that we can also understand how the light scatters inside the complex media,” Kim says.
The researchers then combine this information from each of the QRBs to create a precise profile of the scattering pattern within the tissue.
By displaying this pattern with a spatial light modulator — a device used to produce holograms by manipulating light — the laser beam can be shaped in advance to compensate for the scattering that will take place inside the tissue. The laser is then able to focus with super resolution on a point inside the tissue.
In biological applications, the researchers envision that a suspension of nanodiamonds could be injected into the tissue, much as a contrast agent is already used in some existing imaging systems. Alternatively, molecular tags attached to the diamond nanoparticles could guide them to specific types of cells.
The QRBs could also be used as qubits for quantum sensing and quantum information processing, Kim says. “The QRBs can be used as quantum bits to store quantum information, and with this we can do quantum computing,” he says.
Super-resolution imaging within complex scattering media has been hampered by the deficiency of guide stars that report their positions with subdiffraction precision, according to Wonshik Choi, a professor of physics at Korea University, who was not involved in the research.
“The researchers have developed an elegant method of exploiting quantum reference beacons made of the nitrogen vacancy center in nanodiamonds as such guide stars,” he says. “This work opens up new venues for deep-tissue super-resolution imaging and quantum information processing within subwavelength nanodevices.”
The researchers now hope to explore the use of quantum entanglement and other types of semiconductors for use as QRBs, Kim says. | | 11:59p |
Biologist Adam Martin studies the mechanics of tissue folding Embryonic development is tightly regulated by genes that control how body parts form. One of the key responsibilities of these genes is to make sure that tissues fold into the correct shapes, forming structures that will become the spine, brain, and other body parts.
During the 1970s and ’80s, the field of embryonic development focused mainly on identifying the genes that control this process. More recently, many biologists have shifted toward investigating the physics behind the tissue movements that occur during development, and how those movements affect the shape of tissues, says Adam Martin, an MIT associate professor of biology.
Martin, who recently earned tenure, has made key discoveries in how tissue folding is controlled by the movement of cells’ internal scaffolding, known as the cytoskeleton. Such discoveries can not only shed light on how tissues form, including how birth defects such as spina bifida occur, but may also help guide scientists who are working on engineering artificial human tissues.
“We’d like to understand the molecular mechanisms that tune how forces are generated by cells in a tissue, such that the tissue then gets into a proper shape,” Martin says. “It’s important that we understand fundamental mechanisms that are in play when tissues are getting sculpted in development, so that we can then harness that knowledge to engineer tissues outside of the body.”
Cellular forces
Martin grew up in Rochester, New York, where both of his parents were teachers. As a biology major at nearby Cornell University, he became interested in genetics and development. He went on to graduate school at the University of California at Berkeley, thinking he would study the genes that control embryonic development.
However, while in his PhD program, Martin became interested in a different phenomenon — the role of the cytoskeleton in a process called endocytosis. Cells use endocytosis to absorb many different kinds of molecules, such as hormones or growth factors.
“I was interested in what generates the force to promote this internalization,” Martin says.
He discovered that the force is generated by the assembly of arrays of actin filaments. These filaments tug on a section of the cell membrane, pulling it inward so that the membrane encloses the molecule being absorbed. He also found that myosin, a protein that can act as a motor and controls muscle contractions, helps to control the assembly of actin filaments.
After finishing his PhD, Martin hoped to find a way to combine his study of cytoskeleton mechanics with his interest in developmental biology. As a postdoc at Princeton University, he started to study the phenomenon of tissue folding in fruit fly embryonic development, which is now one of the main research areas of his lab at MIT. Tissue folding is a ubiquitous shape change in tissues to convert a planar sheet of cells into a three-dimensional structure, such as a tube.
In developing fruit fly embryos, tissue folding invaginates cells that will form internal structures in the fly. This folding process is similar to tissue folding events in vertebrates, such as neural tube formation. The neural tube, which is the precursor to the vertebrate spinal cord and brain, begins as a sheet of cells that must fold over and “zip” itself up along a seam to form a tube. Problems with this process can lead to spina bifida, a birth defect that results from an incomplete closing of the backbone.
When Martin began working in this area, scientists had already discovered many of the transcription factors (proteins that turn on networks of specific genes) that control the folding of the neural tube. However, little was known about the mechanics of this folding.
“We didn’t know what types of forces those transcription factors generate, or what the mechanisms were that generated the force,” he says.
He discovered that the accumulation of myosin helps cells lined up in a row to become bottle-shaped, causing the top layer of the tissue to pucker inward and create a fold in the tissue. More recently, he found that myosin is turned on and off in these cells in a dynamic way, by a protein called RhoA.
“What we found is there’s essentially an oscillator running in the cells, and you get a cycle of this signaling protein, RhoA, that’s being switched on and off in a cyclical manner,” Martin says. “When you don’t have the dynamics, the tissue still tries to contract, but it falls apart.”
He also found that the dynamics of this myosin activity can be disrupted by depleting genes that have been linked to spina bifida.
Breaking free
Another important cellular process that relies on tissue folding is the epithelial-mesenchymal transition (EMT). This occurs during embryonic development when cells gain the ability to break free and move to a new location. It is also believed to occur when cancer cells metastasize from tumors to seed new tumors in other parts of the body.
During embryonic development, cells lined up in a row need to orient themselves so that when they divide, both daughter cells remain in the row. Martin has shown that when the mechanism that enables the cells to align correctly is disrupted, one of the daughter cells will be squeezed out of the tissue.
“This has been proposed as one way you can get an epithelial-to-mesenchymal transition, where you have cells dissociate from native tissue,” Martin says. He now plans to further study what happens to the cells that get squeezed out during the EMT.
In addition to these projects, he is also collaborating with Jörn Dunkel, an MIT associate professor of mathematics, to map the network connections between the myosin proteins that control tissue folding during development. “That project really highlights the benefits of getting people from diverse backgrounds to analyze a problem,” Martin says. |
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