By: Dr. Tomasz Kościółek and Bryn Taylor
University of California San Diego
19 Jun 2018
Summary
The Microbiome Immunity Project researchers—from Boston, New York, and San Diego—met in person a few weeks ago to make plans that include a 3D map of the protein universe and other far-ranging uses for the data from the project.
The research team members pictured above are (from left to right): Vladimir Gligorijevic (Simons Foundation’s Flatiron Institute), Tommi Vatanen (Broad Institute of MIT and Harvard), Tomasz Kosciolek (University of California San Diego), Rob Knight (University of California San Diego), Rich Bonneau (Simons Foundation’s Flatiron Institute), Doug Renfrew (Simons Foundation’s Flatiron Institute), Bryn Taylor (University of California San Diego), Julia Koehler Leman (Simons Foundation’s Flatiron Institute). Visit the project’s Research Participants page for additional team members.
During the week of May 28, researchers from all Microbiome Immunity Project (MIP) institutions (University of California San Diego, Broad Institute of MIT and Harvard, and the Simons Foundation’s Flatiron Institute) met in San Diego to discuss updates on the project and plan future work.
Our technical discussions included a complete overview of the practical aspects of the project, including data preparation, pre-processing, grid computations, and post-processing on our machines.
We were excited to notice that if we keep the current momentum of producing new structures for the project, we will double the universe of known protein structures (compared to the Protein Data Bank) by mid-2019! We also planned how to extract the most useful information from our data, store it effectively for future use, and extend our exploration strategies.
We outlined three major areas we want to focus on over the next six months.
Structure-Aided Function Predictions
We can use the structures of proteins to gain insight into protein function—or what the proteins actually do. Building on research from MIP co-principal investigator Richard Bonneau’s lab, we will extend their state-of-the-art algorithms to predict protein function using structural models generated through MIP. Using this new methodology based on deep learning, akin to the artificial intelligence algorithms of IBM, we hope to see improvements over more simplistic methods and provide interesting examples from the microbiome (e.g., discover new genes creating antibiotic resistance).
Map of the Protein Universe
Together we produce hundreds of high-quality protein models every month! To help researchers navigate this ever-growing space, we need to put them into perspective of what we already know about protein structures and create a 3D map of the “protein universe.” This map will illustrate how the MIP has eliminated the “dark matter” from this space one structure at a time. It will also be made available as a resource for other researchers to explore interactively.
Structural and Functional Landscape of the Human Gut Microbiome
We want to show what is currently known about the gut microbiome in terms of functional annotations and how our function prediction methods can help us bridge the gap in understanding of gene functions. Specifically, we want to follow up with examples from early childhood microbiome cohorts (relevant to Type-1 diabetes, or T1D) and discuss how our methodology can help us to better understand T1D and inflammatory bowel disease.
The future of the Microbiome Immunity Project is really exciting, thanks to everyone who makes our research possible. Together we are making meaningful contributions to not one, but many scientific problems!
“World Community Grid (WCG) brings people together from across the globe to create the largest non-profit computing grid benefiting humanity. It does this by pooling surplus computer processing power. We believe that innovation combined with visionary scientific research and large-scale volunteerism can help make the planet smarter. Our success depends on like-minded individuals – like you.”
WCG projects run on BOINC software from UC Berkeley.
My BOINC
“Download and install secure, free software that captures your computer’s spare power when it is on, but idle. You will then be a World Community Grid volunteer. It’s that simple!” You can download the software at either WCG or BOINC.
Summary
The FightAIDS@Home – Phase 2 researchers are making plans to write a paper and to test new compounds as part of the continuing search for new and better treatments.
No image caption or credit.
Background
Researchers all over the world have been making advances in the battle against HIV/AIDS for many years. However, AIDS-related complications still affect far too many people. UNAIDS estimates that 36.7 million people were living with HIV in 2016. And while AIDS-related deaths have decreased significantly since their peak in 2005, approximately 1 million people died of causes related to AIDS in 2016. (See the UNAIDS website for more statistics.)
HIV continues to be a challenge because it quickly mutates in ways that make existing drug treatments ineffective. FightAIDS@Home joined World Community Grid more than a decade ago with the simple but challenging goal of finding new treatments for HIV. During Phase 1 of the project, the team identified thousands of potentially promising candidates to be confirmed experimentally in the lab. However, because it’s cost and time prohibitive to lab test all the potential candidates, Phase 2 was created to prioritize the candidate compounds by evaluating them with more accurate methods.
Current Work
Our team is processing the current type of work units through World Community Grid as quickly as possible. Once these work units are completed, we plan to write a paper about the process, including its strengths, limitations, and lessons learned.
We are also planning to use World Community Grid’s computing power to analyze new compounds that are important to our work with the HIVE Center at the Scripps Research Institute. This work will begin after we run a sample of these new compounds on our own grid computing network.
Thank You
We appreciate everyone who continues to donate their computing power to the search for better anti-HIV treatments. We also encourage everyone to opt in to Phase 2 of the project—the more quickly we can run through the current work units, the sooner we can move ahead to new compounds.
“World Community Grid (WCG) brings people together from across the globe to create the largest non-profit computing grid benefiting humanity. It does this by pooling surplus computer processing power. We believe that innovation combined with visionary scientific research and large-scale volunteerism can help make the planet smarter. Our success depends on like-minded individuals – like you.”
WCG projects run on BOINC software from UC Berkeley.
My BOINC
“Download and install secure, free software that captures your computer’s spare power when it is on, but idle. You will then be a World Community Grid volunteer. It’s that simple!” You can download the software at either WCG or BOINC.
The 3D bioprinter designed by Khademhosseini has two key components: a custom-built microfluidic chip (pictured) and a digital micromirror.Amir Miri.
A UCLA bioengineer has developed a technique that uses a specially adapted 3D printer to build therapeutic biomaterials from multiple materials. The advance could be a step toward on-demand printing of complex artificial tissues for use in transplants and other surgeries.
“Tissues are wonderfully complex structures, so to engineer artificial versions of them that function properly, we have to recreate their complexity,” said Ali Khademhosseini, who led the study and is UCLA’s Levi James Knight, Jr., Professor of Engineering at the UCLA Samueli School of Engineering. “Our new approach offers a way to build complex biocompatible structures made from different materials.”
The technique uses a light-based process called stereolithography, and it takes advantage of a customized 3D printer designed by Khademhosseini that has two key components. The first is a custom-built microfluidic chip — a small, flat platform similar in size to a computer chip — with multiple inlets that each “prints” a different material. The other component is a digital micromirror, an array of more than a million tiny mirrors that each moves independently.
The researchers used different types of hydrogels – materials that, after passing through the printer, form scaffolds for tissue to grow into. The micromirrors direct light onto the printing surface, and the illuminated areas indicate the outline of the 3D object that’s being printed. The light also triggers molecular bonds to form in the materials, which causes the gels to firm into solid material. As the 3D object is printed, the mirror array changes the light pattern to indicate the shape of each new layer.
The process is the first to use multiple materials for automated stereolithographic bioprinting — an advance over conventional stereolithographic bioprinting, which only uses one type of material. While the demonstration device used four types of bio-inks, the study’s authors write that the process could accommodate as many inks as needed.
The researchers first used the process to make simple shapes, such as pyramids. Then, they made complex 3D structures that mimicked parts of muscle tissue and muscle-skeleton connective tissues. They also printed shapes mimicking tumors with networks of blood vessels, which could be used as biological models to study cancers. They tested the printed structures by implanting them in rats. The structures were not rejected.
The study’s other authors include first author Amir Miri, who was a postdoctoral scholar at Harvard Medical School when the study was conducted and is now at Rowan University. The co-senior author is Yu Shrike Zhang of Brigham and Women’s Hospital and Harvard Medical School. The other authors are from University of Santiago de Compostela, Spain; Sharif University of Technology, Iran; and UC San Diego.
Khademhosseini, who joined UCLA in November 2017, has faculty appointments in bioengineering and in chemical and biomolecular engineering, as well as in the David Geffen School of Medicine at UCLA. He is the director of the Center for Minimally Invasive Therapeutics and an associate director of the California NanoSystems Institute.
The study was funded by the Office of Naval Research and the National Institutes of Health.
For nearly 100 years, UCLA has been a pioneer, persevering through impossibility, turning the futile into the attainable.
We doubt the critics, reject the status quo and see opportunity in dissatisfaction. Our campus, faculty and students are driven by optimism. It is not naïve; it is essential. And it has fueled every accomplishment, allowing us to redefine what’s possible, time after time.
This can-do perspective has brought us 12 Nobel Prizes, 12 Rhodes Scholarships, more NCAA titles than any university and more Olympic medals than most nations. Our faculty and alumni helped create the Internet and pioneered reverse osmosis. And more than 100 companies have been created based on technology developed at UCLA.
Experiments at SLAC’s Linac Coherent Light Source show the promise of using X-ray free-electron lasers to better understand the structure and function of amyloid fibrils, tiny protein strands that play a role in diseases like Alzheimer’s and Parkinson’s. In this illustration, X-ray light penetrates a sample of amyloid fibrils placed on the honeycomb-like carbon lattice of graphene, a new method that produces cleaner data because the thin graphene virtually disappears from view. (Greg Stewart/SLAC)
SLAC/LCLS
To learn more about diseases such as Alzheimer’s and Parkinson’s, scientists have zeroed in on invisibly small protein filaments that bunch up to form fibrous clusters called amyloids in the brain: How do these fibrils form and how do they lead to disease?
Until now, the best tools for studying them have generated limited views, largely because the fibrils strands are so complex and tiny, just a few nanometers thick.
Now an international research team has come up with a new method with potential for revealing the structure of individual amyloid fibrils with powerful beams of X-ray laser light. They describe it in a report published today in Nature Communications.
In experiments conducted at the Linac Coherent Light Source (LCLS) at the Department of Energy’s SLAC National Accelerator Laboratory, the scientists placed up to 50 fibrils at a time on a layer of graphene, whose carbon atoms are arranged in a honeycomb-like pattern, and hit them with bursts of X-ray laser light. The graphene, it turned out, was almost transparent to the X-rays, and this allowed them to probe the structures of the delicate fibrils without picking up significant extraneous signals from the graphene layer in individual snapshots.
While the team did not uncover the complete fibril structure, they said the innovative method they developed at LCLS opens up a promising path for amyloid studies using X-ray free-electron lasers, or XFELs, such as LCLS.
Carolin Seuring, a scientist at the Center for Free-Electron Laser Science (CFEL) at DESY in Germany and principal author of the paper, said the results suggest this technique could even be used to determine the structure of individual fibrils.
“There is a common consensus that it is not the amyloid fiber alone, but rather the protofilaments composing the fiber and the process of fibril formation that are toxic to the cell,” she said. “XFEL-based experiments have the potential to overcome the challenges we’ve faced in better understanding amyloid fibrils.”
The Problem with Amyloids
While amyloid fibrils are believed to play a major role in the development of neurodegenerative diseases, scientists have recently discovered that they also have other functions, Seuring said.
“The ‘feel-good hormone’ endorphin, for example, can form amyloid fibrils in the pituitary gland,” she said. “They dissolve into individual molecules when the acidity of their surroundings changes, after which these molecules can fullfil their purpose in the body. Other amyloid proteins, such as those found in post-mortem brains of patients suffering from Alzheimer’s, accumulate as amyloid fibrils in the brain, and cannot be broken down and therefore impair brain function in the long term.”
Accurate information about the structure of amyloid fibrils can inform scientists about their function, she added.
“Our aim is to understand the role of the formation and structure of amyloid fibrils in the body and in the development of neurodegenerative diseases,” Seuring said.
One barrier to studying amyloid fibrils is that they cannot be grown as crystals, which are the conventional targets for structural studies using X-rays. And because individual amyloid fibrils are so small, they don’t produce a measurable signal when exposed to X-rays. Scientists typically line up millions of fibrils parallel to each other to amplify the signal, but information about their individual differences is lost in the process.
“A major part of our understanding about amyloid fibrils is derived from nuclear magnetic resonance and cryo-electron microscopy data,” Seuring said. But these methods are also of limited value for seeing individual differences between amyloid fibrils or observing their formation. “The structural analysis of amyloids is complex and examining them using existing methods is hampered by differences between the fibrils within a single sample,’” she said “Being able to look at the individual components of the sample would make it possible to determine the 3D structure of one type of fibril at a time.”
The New Approach
Earlier attempts to study fibrils at X-ray lasers delivered them into the path of the beam in jets of fluid. Switching to a solid graphene carrier gave the team two advantages, according to CFEL’s Henry Chapman, a professor at the University of Hamburg and a lead scientist at DESY.
Because graphene is just one layer of atoms thick, it leaves hardly a trace in the diffraction patterns formed by X-rays scattering off the fibrils, which are used to determine their structures, he said. And the regular structure of the graphene encourages the fibrils to all line up in the same direction.
This allows diffraction patterns to be obtained from fewer than 50 amyloid fibrils. Based on the results, the team hopes to eventually get patterns from single fibrils. To get to that goal, new methods of exposing a single fibril to the XFEL beam will need to be developed, according to Seuring: “With enough snapshots, a full 3D data set of a single fibril should be possible.”
The exceptionally bright and narrowly focused beam at LCLS’s Coherent X-ray Imaging instrument was also key to the team’s success in taking data from such a small number of fibrils, according to SLAC staff scientist Mengning Liang.
Intense X-ray pulses at XFELs limit the exposure of delicate samples to damaging X-rays. In this study, the fibrils were exposed for only a few femtoseconds, or millionths of a billionth of a second. Before the molecules are destroyed, information about their structure can be read by detectors.
“Fibrils are a third category of samples that can be studied with the ‘diffract before destroy’ method at XFELs, in addition to single particles and crystals,” Liang said. “In some regards, fibrils fit between the other two: they have regular, recurring variations in structure like crystals, but without the rigid crystal structure.”
The scientists tested their method on samples of well-studied tobacco mosaic virus filaments and smaller amyloid fibrils, some of which are associated with certain types of cancer. The tests produced structural data with a high degree of accuracy: The resolution in the diffraction images was almost on the scale of a single atom.
“It is amazing that we are essentially carrying out the same experiments as Rosalind Franklin did on DNA in 1952, which led to the discovery of the double helix, but now we are reaching the level of single molecules,” says Chapman.
SLAC is a multi-program laboratory exploring frontier questions in photon science, astrophysics, particle physics and accelerator research. Located in Menlo Park, California, SLAC is operated by Stanford University for the DOE’s Office of Science.
The APOE gene, the strongest genetic risk factor for Alzheimer’s disease, may play a more prominent role in disease development among women than men, according to new research from the Vanderbilt Memory and Alzheimer’s Center.
The research confirmed recent studies that carrying the APOE ε4 allele has a greater association with Alzheimer’s disease among women compared to men, and went one step further by evaluating its association with amyloid and tau levels.
The study published May 7 in JAMA Neurologyadds to mounting evidence that the higher prevalence of Alzheimer’s disease among women may not simply be a consequence of living longer.
Almost two-thirds of Americans with Alzheimer’s are women. The research, based on a meta-analysis of both cerebral spinal fluid (CSF) samples from study volunteers from four datasets and autopsy findings from six datasets of Alzheimer-diseased brains, is the most robust evidence to date that the APOE gene may play a greater role in women than men in developing Alzheimer’s pathology, said Timothy Hohman, PhD, assistant professor of Neurology and the study’s lead author.
“In Alzheimer’s disease, we have not done enough to evaluate whether or not sex is a contributing factor to the neuropathology,” Hohman said. “We haven’t fully evaluated sex as a biological variable. But there is good reason to expect in older adulthood that there would be hormonal differences between the sexes that could impact disease.”
The study looked at whether APOE in men and women was primarily associated with the amyloid pathway — the proteins that form plaques in the brain — or with the tau pathway — the proteins that form tangles in the brain.
The association with the amyloid pathway was the same in men and women. However, the APOE association was much greater for women with the tau pathway. This is opposite of what researchers expected because of APOE’s established role in amyloid processing.
“The prevailing hypothesis of disease in Alzheimer’s is that amyloid comes online first and downstream is where we see tau changes that ultimately drive neurodegenerative changes,” Hohman said.
Further analysis revealed that the sex difference with tau levels was present in amyloid-positive individuals — those with higher levels of amyloid plaque as determined by their CSF amyloid levels. The research suggests that APOE may modulate risk for neurodegeneration in a sex-specific manner, particularly in the presence of amyloidosis.
The greater association with tau occurred in CSF samples, but not with the autopsy datasets.
The reason for the contradiction between CSF samples and autopsy datasets could be because Braak staging — the method for quantifying the degree of tau tangle pathology at autopsy — measures a different aspect of tau pathology than what is measured in CSF .
“The way Braak staging works is you are actually looking at where in the cortex you see tangles at autopsy,” Hohman explained. “So it is not a measure of how many tangles are there. It is a measure of where those tangles are located.”
Another possibility is that CSF tau may be an indicator of a more general neurodegenerative process that is not specific to tangle pathology.
“This study is at least moving toward bringing sex as a biological variable into our analyses and thinking about sex differences. Do we see differences in disease that could tell us something about the biology of the disease and could help both sexes in terms of coming up with treatment approaches? I think that the right treatment approach for a female above the age of 65 may end up being different than what it is for a male. Really the only way to find out is to look.”
The research was supported by the National Institutes of Health, the Alzheimer’s Disease Genetics Consortium (funded by the National Institute on Aging) and the Vanderbilt Memory and Alzheimer’s Center.
Commodore Cornelius Vanderbilt was in his 79th year when he decided to make the gift that founded Vanderbilt University in the spring of 1873.
The $1 million that he gave to endow and build the university was the commodore’s only major philanthropy. Methodist Bishop Holland N. McTyeire of Nashville, husband of Amelia Townsend who was a cousin of the commodore’s young second wife Frank Crawford, went to New York for medical treatment early in 1873 and spent time recovering in the Vanderbilt mansion. He won the commodore’s admiration and support for the project of building a university in the South that would “contribute to strengthening the ties which should exist between all sections of our common country.”
McTyeire chose the site for the campus, supervised the construction of buildings and personally planted many of the trees that today make Vanderbilt a national arboretum. At the outset, the university consisted of one Main Building (now Kirkland Hall), an astronomical observatory and houses for professors. Landon C. Garland was Vanderbilt’s first chancellor, serving from 1875 to 1893. He advised McTyeire in selecting the faculty, arranged the curriculum and set the policies of the university.
For the first 40 years of its existence, Vanderbilt was under the auspices of the Methodist Episcopal Church, South. The Vanderbilt Board of Trust severed its ties with the church in June 1914 as a result of a dispute with the bishops over who would appoint university trustees.
kirkland hallFrom the outset, Vanderbilt met two definitions of a university: It offered work in the liberal arts and sciences beyond the baccalaureate degree and it embraced several professional schools in addition to its college. James H. Kirkland, the longest serving chancellor in university history (1893-1937), followed Chancellor Garland. He guided Vanderbilt to rebuild after a fire in 1905 that consumed the main building, which was renamed in Kirkland’s honor, and all its contents. He also navigated the university through the separation from the Methodist Church. Notable advances in graduate studies were made under the third chancellor, Oliver Cromwell Carmichael (1937-46). He also created the Joint University Library, brought about by a coalition of Vanderbilt, Peabody College and Scarritt College.
Remarkable continuity has characterized the government of Vanderbilt. The original charter, issued in 1872, was amended in 1873 to make the legal name of the corporation “The Vanderbilt University.” The charter has not been altered since.
The university is self-governing under a Board of Trust that, since the beginning, has elected its own members and officers. The university’s general government is vested in the Board of Trust. The immediate government of the university is committed to the chancellor, who is elected by the Board of Trust.
The original Vanderbilt campus consisted of 75 acres. By 1960, the campus had spread to about 260 acres of land. When George Peabody College for Teachers merged with Vanderbilt in 1979, about 53 acres were added.
wyatt centerVanderbilt’s student enrollment tended to double itself each 25 years during the first century of the university’s history: 307 in the fall of 1875; 754 in 1900; 1,377 in 1925; 3,529 in 1950; 7,034 in 1975. In the fall of 1999 the enrollment was 10,127.
In the planning of Vanderbilt, the assumption seemed to be that it would be an all-male institution. Yet the board never enacted rules prohibiting women. At least one woman attended Vanderbilt classes every year from 1875 on. Most came to classes by courtesy of professors or as special or irregular (non-degree) students. From 1892 to 1901 women at Vanderbilt gained full legal equality except in one respect — access to dorms. In 1894 the faculty and board allowed women to compete for academic prizes. By 1897, four or five women entered with each freshman class. By 1913 the student body contained 78 women, or just more than 20 percent of the academic enrollment.
National recognition of the university’s status came in 1949 with election of Vanderbilt to membership in the select Association of American Universities. In the 1950s Vanderbilt began to outgrow its provincial roots and to measure its achievements by national standards under the leadership of Chancellor Harvie Branscomb. By its 90th anniversary in 1963, Vanderbilt for the first time ranked in the top 20 private universities in the United States.
Vanderbilt continued to excel in research, and the number of university buildings more than doubled under the leadership of Chancellors Alexander Heard (1963-1982) and Joe B. Wyatt (1982-2000), only the fifth and sixth chancellors in Vanderbilt’s long and distinguished history. Heard added three schools (Blair, the Owen Graduate School of Management and Peabody College) to the seven already existing and constructed three dozen buildings. During Wyatt’s tenure, Vanderbilt acquired or built one-third of the campus buildings and made great strides in diversity, volunteerism and technology.
The university grew and changed significantly under its seventh chancellor, Gordon Gee, who served from 2000 to 2007. Vanderbilt led the country in the rate of growth for academic research funding, which increased to more than $450 million and became one of the most selective undergraduate institutions in the country.
On March 1, 2008, Nicholas S. Zeppos was named Vanderbilt’s eighth chancellor after serving as interim chancellor beginning Aug. 1, 2007. Prior to that, he spent 2002-2008 as Vanderbilt’s provost, overseeing undergraduate, graduate and professional education programs as well as development, alumni relations and research efforts in liberal arts and sciences, engineering, music, education, business, law and divinity. He first came to Vanderbilt in 1987 as an assistant professor in the law school. In his first five years, Zeppos led the university through the most challenging economic times since the Great Depression, while continuing to attract the best students and faculty from across the country and around the world. Vanderbilt got through the economic crisis notably less scathed than many of its peers and began and remained committed to its much-praised enhanced financial aid policy for all undergraduates during the same timespan. The Martha Rivers Ingram Commons for first-year students opened in 2008 and College Halls, the next phase in the residential education system at Vanderbilt, is on track to open in the fall of 2014. During Zeppos’ first five years, Vanderbilt has drawn robust support from federal funding agencies, and the Medical Center entered into agreements with regional hospitals and health care systems in middle and east Tennessee that will bring Vanderbilt care to patients across the state.
studentsToday, Vanderbilt University is a private research university of about 6,500 undergraduates and 5,300 graduate and professional students. The university comprises 10 schools, a public policy center and The Freedom Forum First Amendment Center. Vanderbilt offers undergraduate programs in the liberal arts and sciences, engineering, music, education and human development as well as a full range of graduate and professional degrees. The university is consistently ranked as one of the nation’s top 20 universities by publications such as U.S. News & World Report, with several programs and disciplines ranking in the top 10.
Cutting-edge research and liberal arts, combined with strong ties to a distinguished medical center, creates an invigorating atmosphere where students tailor their education to meet their goals and researchers collaborate to solve complex questions affecting our health, culture and society.
Vanderbilt, an independent, privately supported university, and the separate, non-profit Vanderbilt University Medical Center share a respected name and enjoy close collaboration through education and research. Together, the number of people employed by these two organizations exceeds that of the largest private employer in the Middle Tennessee region.
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Anis Contractor, PhD, professor of Physiology and senior author of a study published in Molecular Psychiatry.
An FDA-approved drug can reverse an ionic imbalance in neurons that leads to hyper-excitability in mice modeling an autism-related genetic disorder, according to a Northwestern Medicine study published inMolecular Psychiatry.
These findings suggest that the sensory hypersensitivity experienced by patients with Fragile X syndrome, a syndromic autism, may be caused by elevated intracellular chloride in neurons during early development, according to Anis Contractor, PhD, professor of Physiology and senior author of the study.
“Some children with Fragile X syndrome or autism have changes in sensory processing, similar to the mouse model,” Contractor said. “The mouse models give us a window into the human disorder. Although mouse brain development is not a completely faithful model of humans, there certainly are parallels.”
While most genetic mutations that cause autism are very rare — and most cases of autism spectrum disorder are not linked to a genetic cause — children with Fragile X syndrome have a well-defined mutation in a gene on the X chromosome, so Fragile X syndrome is used as a laboratory model for certain aspects of autism, including sensory hypersensitivity.
“A lot of patients don’t like loud sounds or don’t like to be touched,” Contractor said. “When I talk to parents of children with Fragile X, some tell me these sensory issues lead to many other problems, because the kids are withdrawn or socially isolated.”
Prior studies in Contractor’s lab established the role of intracellular chloride in certain symptoms of Fragile X syndrome: While it is important for neurotransmitter signaling, high chloride concentration in neural cells can also cause abnormal excitation, shifting the timing of important developmental critical periods.
These critical periods are phases of early brain development where essential neural circuitry is formed; shifting them earlier or later affects how the brain is wired, as can be seen in the sensory cortex of mouse models. In normal mice, activity in a single whisker activates a single cluster of cells, relaying information about the force and direction in which the whisker was moved.
However, in mice with Fragile X syndrome, activity from a single whisker activates multiple clusters of cells, creating hyper-excitability.
“The activity bleeds to other clusters of cells, activating more cells than it normally would,” he said.
To investigate if this hyper-excitability could be reversed, Contractor and his colleagues treated mice for two weeks after birth with bumetanide, a drug originally used for hypertension.
“It’s actually not used very much anymore, because there are better drugs on the market now. But in addition to its effect on blood pressure it can affect neuronal chloride transporters and the influx of chloride into the cell,” Contractor said.
In mice with the Fragile X mutation, Contractor found it returned the concentration of intracellular chloride back to normal in neurons, shifting the critical periods back to their correct timing and leading to more typical synapse development.
“We found that if we gave this drug early in development, it not only corrected the development of synapses during the early critical period, it also corrected the sensory problems we saw in adult mice,” Contractor said. “It is possible that correcting chloride or correcting neurotransmitter signaling in humans could also have the same effect.”
In fact, a high concentration of intracellular chloride could be associated with a variety of developmental disorders, not just Fragile X syndrome and autism, according to Contractor.
“We think it actually might be a more general mechanism, it’s been shown to play a role in Down syndrome and childhood epilepsies as well,” Contractor said. “People are interested in this chloride mechanism in a whole host of neurodevelopmental disorders.”
Contractor is also a professor in the Department of Neurobiology in the Weinberg College of Arts and Sciences. Qionger He, PhD, a former postdoctoral fellow in Contractor’s laboratory, was first author of the study. Feinberg co-authors include Jeffrey Savas, PhD, assistant professor in the Ken & Ruth Davee Department of Neurology and of Medicine and Pharmacology, Sam Smukowski, staff member in the Savas Laboratory and Jian Xu, PhD, research assistant professor of Physiology.
The authors also collaborated with Carlos Portera-Cailliau, MD, PhD, associate professor of Neurology at the University of Southern California-Los Angeles, and other members of his research group.
On May 31, 1850, nine men gathered to begin planning a university that would serve the Northwest Territory.
Given that they had little money, no land and limited higher education experience, their vision was ambitious. But through a combination of creative financing, shrewd politicking, religious inspiration and an abundance of hard work, the founders of Northwestern University were able to make that dream a reality.
In 1853, the founders purchased a 379-acre tract of land on the shore of Lake Michigan 12 miles north of Chicago. They established a campus and developed the land near it, naming the surrounding town Evanston in honor of one of the University’s founders, John Evans. After completing its first building in 1855, Northwestern began classes that fall with two faculty members and 10 students.
Twenty-one presidents have presided over Northwestern in the years since. The University has grown to include 12 schools and colleges, with additional campuses in Chicago and Doha, Qatar.
Northwestern is recognized nationally and internationally for its educational programs.
From left to right, Associate Professor Axel Guenther, Navid Hakimi and Richard Cheng have created the first ‘skin printer’ that forms tissues in situ for application to wounds (photo by Liz Do)
University of Toronto researchers have developed a handheld 3D skin printer that deposits even layers of skin tissue to cover and heal deep wounds. The team believes it to be the first device that forms tissue in situ, depositing and setting in place, within two minutes or less.
Credit: University of Toronto
The research, led by PhD student Navid Hakimi under the supervision of Associate Professor Axel Guenther of the Faculty of Applied Science & Engineering, and in collaboration with Dr. Marc Jeschke, director of the Ross Tilley Burn Centre at Sunnybrook Hospital and professor of immunology at the Faculty of Medicine, was recently published in the journal Lab on a Chip.
For patients with deep skin wounds, all three skin layers – the epidermis, dermis and hypodermis – may be heavily damaged. The current preferred treatment is called split-thickness skin grafting, where healthy donor skin is grafted onto the surface epidermis and part of the underlying dermis.
Split-thickness grafting on large wounds requires enough healthy donor skin to traverse all three layers, and sufficient graft skin is rarely available. This leaves a portion of the wounded area “ungrafted” or uncovered, leading to poor healing outcomes.
Although a large number of tissue-engineered skin substitutes exist, they are not yet widely used in clinical settings.
“Most current 3D bioprinters are bulky, work at low speeds, are expensive and are incompatible with clinical application,” explains Guenther.
The research team believes their in-situ skin printer is a platform technology that can overcome these barriers, while improving the skin-healing process – a major step forward.
The handheld skin printer resembles a white-out tape dispenser – except the tape roll is replaced by a microdevice that forms tissue sheets. Vertical stripes of “bio ink,” made up of protein-based biomaterials including collagen, the most abundant protein in the dermis, and fibrin, a protein involved in wound healing, run along the inside of each tissue sheet.
“Our skin printer promises to tailor tissues to specific patients and wound characteristics,” says Hakimi. “And it’s very portable.”
The handheld device is the size of a small shoe box and weighs less than a kilogram. It also requires minimal operator training and eliminates the washing and incubation stages required by many conventional bioprinters.
The researchers plan to add several capabilities to the printer, including expanding the size of the coverable wound areas. Working with Jeschke’s team at Sunnybrook Hospital, they plan to perform more in vivo studies. They hope that one day they can begin running clinical trials on humans, and eventually revolutionize burn care.
Established in 1827, the University of Toronto has one of the strongest research and teaching faculties in North America, presenting top students at all levels with an intellectual environment unmatched in depth and breadth on any other Canadian campus.
Established in 1827, the University of Toronto has one of the strongest research and teaching faculties in North America, presenting top students at all levels with an intellectual environment unmatched in depth and breadth on any other Canadian campus.
The prevalence of autism spectrum disorder at 11 surveillance sites was one in 59 among 8-year-olds in 2014, according to a new U.S. Centers for Disease Control and Prevention report, a 15 percent increase from the most recent report two years ago and the highest prevalence since the CDC began tracking ASD in 2000.
Consistent with previous reports, boys were four times more likely to be identified with ASD than girls. The rate is one in 38 among boys (or 2.7 percent) and one in 152 among girls (or 0.7 percent). Researchers at the Johns Hopkins Bloomberg School of Public Health contributed to the report.
ASD is a developmental disorder characterized by social and communication impairments, combined with limited interests and repetitive behaviors. Early diagnosis and intervention are key to improving learning and skills. Rates have been rising since the 1960s, but researchers do not know how much of this rise is due to an increase in actual cases. There are other factors that may be contributing, such as increased awareness, screening, diagnostic services, treatment and intervention services, better documentation of ASD behaviors, and changes in diagnostic criteria.
For this new report, the CDC collected data at 11 regional monitoring sites that are part of the Autism and Developmental Disabilities Monitoring Network in the following states: Arizona, Arkansas, Colorado, Georgia, Maryland, Minnesota, Missouri, New Jersey, North Carolina, Tennessee, and Wisconsin. (A report with individual state findings is available online [CDC]).The Maryland monitoring site is based at the Bloomberg School in Baltimore.
This is the sixth report by the ADDM Network, which has used the same surveillance methods for more than a decade. Estimated prevalence rates of ASD in the U.S. reported by previous data were:
One in 68 children in the 2016 report that looked at 2012 data
One in 68 children in the 2014 report that looked at 2010 data
One in 88 children in the 2012 report that looked at 2008 data
One in 110 children in the 2009 report that looked at 2006 data
One in 150 children in the 2007 report that looked at 2000 and 2002 data
“The estimated overall prevalence rates reported by ADDM at the monitoring sites have more than doubled since the report was first published in 2007,” says Li-Ching Lee, a psychiatric epidemiologist with the Bloomberg School’s departments of Epidemiology and Mental Health and the principal investigator for Maryland-ADDM. “Although we continue to see disparities among racial and ethnic groups, the gap is closing.”
Autism spectrum disorder prevalence was reported to be approximately 20 to 30 percent higher among white children as compared with black children in previous ADDM reports. In the current report, the difference has dropped to 7 percent. In addition, approximately 70 percent of children with ASD had borderline, average, or above average intellectual ability, a proportion higher than that found in ADDM data prior to 2012.
Some trends in the latest CDC report remain similar, such as the greater likelihood of boys being diagnosed with ASD, the age of earliest comprehensive evaluation, and presence of a previous ASD diagnosis or classification. Specifically, non-white children with ASD are being identified and evaluated at a later age than white children. The majority of children identified with ASD by the ADDM Network (80 percent) had a previous ASD diagnosis or a special educational classification.
In Maryland, the prevalence of ASD was higher than in the network as a whole. An estimated one in 50 children (2 percent) was identified as having ASD—one in 31 among boys and one in 139 among girls. The data were derived from health and special education records of children who were 8 years old and living in Baltimore County in 2014.
Lee notes, similar to previous reports, the vast majority of children identified with ASD in Maryland had a developmental concern in their records by age 3 (92 percent), but only 56 percent of them received a comprehensive evaluation by that age.
“This lag may delay the timing for children with ASD to get diagnosed and to start receiving needed services,” says Lee, an associate director of the school’s Wendy Klag Center for Autism and Developmental Disabilities.
The causes of autism are not completely understood; studies show that both environment and genetics may play a role. The CDC recommends that parents track their child’s development and act quickly to get their child screened if they have a concern, and has made available online a free checklist and information resource for parents, physicians, and child care providers.
We’ve been doing some thinking — quite a bit, actually — about all the things that go on at Johns Hopkins. Discovering the glue that holds the universe together, for example. Or unraveling the mysteries of Alzheimer’s disease. Or studying butterflies in flight to fine-tune the construction of aerial surveillance robots. Heady stuff, and a lot of it.
In fact, Johns Hopkins does so much, in so many places, that it’s hard to wrap your brain around it all. It’s too big, too disparate, too far-flung.
We created the Hub to be the news center for all this diverse, decentralized activity, a place where you can see what’s new, what’s important, what Johns Hopkins is up to that’s worth sharing. It’s where smart people (like you) can learn about all the smart stuff going on here.
At the Hub, you might read about cutting-edge cancer research or deep-trench diving vehicles or bionic arms. About the psychology of hoarders or the delicate work of restoring ancient manuscripts or the mad motor-skills brilliance of a guy who can solve a Rubik’s Cube in under eight seconds.
There’s no telling what you’ll find here because there’s no way of knowing what Johns Hopkins will do next. But when it happens, this is where you’ll find it.
The Johns Hopkins University opened in 1876, with the inauguration of its first president, Daniel Coit Gilman. “What are we aiming at?” Gilman asked in his installation address. “The encouragement of research … and the advancement of individual scholars, who by their excellence will advance the sciences they pursue, and the society where they dwell.”
The mission laid out by Gilman remains the university’s mission today, summed up in a simple but powerful restatement of Gilman’s own words: “Knowledge for the world.”
What Gilman created was a research university, dedicated to advancing both students’ knowledge and the state of human knowledge through research and scholarship. Gilman believed that teaching and research are interdependent, that success in one depends on success in the other. A modern university, he believed, must do both well. The realization of Gilman’s philosophy at Johns Hopkins, and at other institutions that later attracted Johns Hopkins-trained scholars, revolutionized higher education in America, leading to the research university system as it exists today.
[This post is dedicated to all of my readers whose lives and children have been affected by Austism in all of its many forms.]
25 Apr, 2018
Scott LaFee
Jan Zverina
Genes inherited from both parents contribute to development of autism in children.
Courtesy Unsplash/Brittany Simuangco.
One percent of the world’s population lives with autism spectrum disorder (ASD), and the prevalence is increasing by around ten percent each year. Though there is no obvious straight line between autism and any single gene, genetics and inherited traits play an important role in development of the condition.
In recent years, researchers have firmly established that gene mutations appearing for the first time, called de novo mutations, contribute to approximately one-third of cases of autism spectrum disorder (ASD).
Early symptoms. Children with ASD may avoid eye contact, have delayed speech, and fail to demonstrate interest. Courtesy Unsplash.
In a new study [Science], an international team led by scientists at University of California San Diego (UCSD) School of Medicine have identified a culprit that may explain some of the remaining risk: rare inherited variants in regions of non-coding DNA.
The newly discovered risk factors differ from known genetic causes of autism in two important ways. First, these variants do not alter the genes directly but instead disrupt the neighboring DNA control elements that turn genes on and off, called cis-regulatory elements or CREs. Second, these variants do not occur as new mutations in children with autism, but instead are inherited from their parents.
“For ten years we’ve known that the genetic causes of autism consist partly of de novo mutations in the protein sequences of genes,” said Jonathan Sebat, a professor of psychiatry, cellular and molecular medicine and pediatrics at UCSD School of Medicine and chief of the Beyster Center for Genomics of Psychiatric Genomics. “However, gene sequences represent only 2 percent of the genome.”
Autism affects 1 in 68 children
Boys are four times more likely than girls to have autism
Symptoms usually appear before age 3
Autism varies greatly; no two people with autism are alike
There is currently no cure for autism
Early intervention is key to successful treatment
____________________________________________________
To investigate the other 98 percent of the genome in ASD, Sebat and his colleagues analyzed the complete genomes of 9,274 subjects from 2,600 families. One thousand genomes were sequenced in San Diego at Human Longevity Inc. (HLI) and at Illumina Inc.
DNA sequences were analyzed with the Comet supercomputer at the San Diego Supercomputer Center (SDSC).
SDSC Dell Comet supercomputer at San Diego Supercomputer Center (SDSC)
These data were then combined with other large studies from the Simons Simplex Collection and the Autism Speaks MSSNG Whole Genome Sequencing Project.
“Whole genome sequence data processing and analysis are both computationally and resource intensive,” said Madhusudan Gujral, an analyst with SDSC and co-author of the paper.
Using SDSC’s Comet, processing and identifying specific structural variants from a single genome took about 2½-days.
“Since Comet has 1,984 compute nodes and several petabytes of scratch space for analysis, tens of genomes can be processed at the same time,” added SDSC scientist Wayne Pfeiffer. “Instead of months, with Comet we were able to complete the data processing in weeks.”
The researchers then analyzed structural variants, deleted or duplicated segments of DNA that disrupt regulatory elements of genes, dubbed CRE-SVs. From the complete genomes of families, the researchers found that CRE-SVs that are inherited from parents also contributed to ASD.
HPC for the 99 percent. The Comet supercomputer at SDSC meets the needs of underserved researchers in domains that have not traditionally relied on supercomputers to help solve problems. Courtesy San Diego Supercomputer Center.
“We also found that CRE-SVs were inherited predominantly from fathers, which was a surprise,” said co-first author William M. Brandler, PhD, a postdoctoral scholar in Sebat’s lab at UCSD and bioinformatics scientist at HLI.
“Previous studies have found evidence that some protein-coding variants are inherited predominantly from mothers, a phenomenon known as a maternal origin effect. The paternal origin effect we see for non-coding variants suggests that the inherited genetic contribution from mothers and fathers may be qualitatively different.”
Sebat said current research does not explain with certainty what mechanism determines these parent-of-origin effects, but he has proposed a plausible model.
“There is a wide spectrum of genetic variation in the human population, with coding variants having strong effects and noncoding variants having weaker effects,” he said. “If men and women differ in their capacity to tolerate such variants, this could give rise to the parent-of-origin effects that we see.”
Science Node is an international weekly online publication that covers distributed computing and the research it enables.
“We report on all aspects of distributed computing technology, such as grids and clouds. We also regularly feature articles on distributed computing-enabled research in a large variety of disciplines, including physics, biology, sociology, earth sciences, archaeology, medicine, disaster management, crime, and art. (Note that we do not cover stories that are purely about commercial technology.)
In its current incarnation, Science Node is also an online destination where you can host a profile and blog, and find and disseminate announcements and information about events, deadlines, and jobs. In the near future it will also be a place where you can network with colleagues.
You can read Science Node via our homepage, RSS, or email. For the complete iSGTW experience, sign up for an account or log in with OpenID and manage your email subscription from your account preferences. If you do not wish to access the website’s features, you can just subscribe to the weekly email.”
A Vanderbilt team took the next leap forward in using a little-known bacteria to stop the spread of deadly mosquito-borne viruses such as Zika and dengue.
Wolbachia are bacteria that occur widely in insects and, once they do, inhibit certain pathogenic viruses the insects carry. The problem with using Wolbachia broadly to protect humans is that the bacteria do not normally occur in mosquitoes that transmit Zika and dengue. So success in modifying mosquitoes relies on the bacteria’s cunning ability to spread like wildfire into mosquito populations.
Wolbachia do so by hijacking the insect reproductive system in a process called cytoplasmic incompatibility, or CI. This makes the sperm of infected fathers lethal to eggs of uninfected mothers. However, if infected fathers mate with infected mothers, the eggs live, and the infected mothers carrying Wolbachia will also infect all her offspring with it. Then those offspring pass on Wolbachia to the next generation, and so on, until they eventually replace all of the resident mosquitoes. As Wolbachia spreads in the population, the risk of dengue and Zika virus transmission drops.
How that sperm and egg hijacking worked in infected fathers and mothers remained a mystery for decades, until Associate Professor of Biological Sciences Seth Bordenstein and his team helped solve it. They set out to dissect the number and types of genes that Wolbachia use to spread with the long-term goal of harnessing that genetic ability for protecting humans against diseases transmission.
“In this new study, we’ve dissected a simple set of Wolbachia genes that replicate how Wolbachia change sperm and egg” Bordenstein said. “There are two genes that cause the incompatibility, and one of those same genes rescues the incompatibility. Engineering mosquitoes or Wolbachia for expression of these two genes could enhance or cause the spread of Wolbachia through target mosquito populations.”
Wolbachia spreads itself by hijacking the insect reproductive system in a process called cytoplasmic incompatibility, or CI. (J. Dylan Shropshire/Vanderbilt University)
In a previous study last year Nature, the team identified the two genes in Wolbachia — named cytoplasmic incompatibility factors cifA and cifB — and learned that they modify the sperm to kill eggs. Now they solved the other half of the genetic mystery: cifA single-handedly can protect embryos from death.
“It’s a microbial encryption and de-encryptyion system that ensures Wolbachia spread through insect populations so they can adequately block the transmission of viruses and ultimately save lives” Bordenstein said.
Coauthors of the paper include Ph.D. student and National Science Foundation Graduate Research Fellow J. Dylan Shropshire and Vanderbilt undergraduates Emily Layton and Helen Zhou.
Vanderbilt University has filed patent applications on this new finding and seeks industry partners for further development through its Center for Technology Transfer and Commercialization.
This work was supported by National Institutes of Health (NIH) awards R01 AI132581 and R21 HD086833, National Science Foundation award IOS 1456778, a National Science Foundation Graduate Research Fellowship, and Vanderbilt University Medical Center Cell Imaging Shared Resources (supported by NIH grants CA68485, DK20593, DK58404, DK59637 and EY08126).
Commodore Cornelius Vanderbilt was in his 79th year when he decided to make the gift that founded Vanderbilt University in the spring of 1873.
The $1 million that he gave to endow and build the university was the commodore’s only major philanthropy. Methodist Bishop Holland N. McTyeire of Nashville, husband of Amelia Townsend who was a cousin of the commodore’s young second wife Frank Crawford, went to New York for medical treatment early in 1873 and spent time recovering in the Vanderbilt mansion. He won the commodore’s admiration and support for the project of building a university in the South that would “contribute to strengthening the ties which should exist between all sections of our common country.”
McTyeire chose the site for the campus, supervised the construction of buildings and personally planted many of the trees that today make Vanderbilt a national arboretum. At the outset, the university consisted of one Main Building (now Kirkland Hall), an astronomical observatory and houses for professors. Landon C. Garland was Vanderbilt’s first chancellor, serving from 1875 to 1893. He advised McTyeire in selecting the faculty, arranged the curriculum and set the policies of the university.
For the first 40 years of its existence, Vanderbilt was under the auspices of the Methodist Episcopal Church, South. The Vanderbilt Board of Trust severed its ties with the church in June 1914 as a result of a dispute with the bishops over who would appoint university trustees.
kirkland hallFrom the outset, Vanderbilt met two definitions of a university: It offered work in the liberal arts and sciences beyond the baccalaureate degree and it embraced several professional schools in addition to its college. James H. Kirkland, the longest serving chancellor in university history (1893-1937), followed Chancellor Garland. He guided Vanderbilt to rebuild after a fire in 1905 that consumed the main building, which was renamed in Kirkland’s honor, and all its contents. He also navigated the university through the separation from the Methodist Church. Notable advances in graduate studies were made under the third chancellor, Oliver Cromwell Carmichael (1937-46). He also created the Joint University Library, brought about by a coalition of Vanderbilt, Peabody College and Scarritt College.
Remarkable continuity has characterized the government of Vanderbilt. The original charter, issued in 1872, was amended in 1873 to make the legal name of the corporation “The Vanderbilt University.” The charter has not been altered since.
The university is self-governing under a Board of Trust that, since the beginning, has elected its own members and officers. The university’s general government is vested in the Board of Trust. The immediate government of the university is committed to the chancellor, who is elected by the Board of Trust.
The original Vanderbilt campus consisted of 75 acres. By 1960, the campus had spread to about 260 acres of land. When George Peabody College for Teachers merged with Vanderbilt in 1979, about 53 acres were added.
wyatt centerVanderbilt’s student enrollment tended to double itself each 25 years during the first century of the university’s history: 307 in the fall of 1875; 754 in 1900; 1,377 in 1925; 3,529 in 1950; 7,034 in 1975. In the fall of 1999 the enrollment was 10,127.
In the planning of Vanderbilt, the assumption seemed to be that it would be an all-male institution. Yet the board never enacted rules prohibiting women. At least one woman attended Vanderbilt classes every year from 1875 on. Most came to classes by courtesy of professors or as special or irregular (non-degree) students. From 1892 to 1901 women at Vanderbilt gained full legal equality except in one respect — access to dorms. In 1894 the faculty and board allowed women to compete for academic prizes. By 1897, four or five women entered with each freshman class. By 1913 the student body contained 78 women, or just more than 20 percent of the academic enrollment.
National recognition of the university’s status came in 1949 with election of Vanderbilt to membership in the select Association of American Universities. In the 1950s Vanderbilt began to outgrow its provincial roots and to measure its achievements by national standards under the leadership of Chancellor Harvie Branscomb. By its 90th anniversary in 1963, Vanderbilt for the first time ranked in the top 20 private universities in the United States.
Vanderbilt continued to excel in research, and the number of university buildings more than doubled under the leadership of Chancellors Alexander Heard (1963-1982) and Joe B. Wyatt (1982-2000), only the fifth and sixth chancellors in Vanderbilt’s long and distinguished history. Heard added three schools (Blair, the Owen Graduate School of Management and Peabody College) to the seven already existing and constructed three dozen buildings. During Wyatt’s tenure, Vanderbilt acquired or built one-third of the campus buildings and made great strides in diversity, volunteerism and technology.
The university grew and changed significantly under its seventh chancellor, Gordon Gee, who served from 2000 to 2007. Vanderbilt led the country in the rate of growth for academic research funding, which increased to more than $450 million and became one of the most selective undergraduate institutions in the country.
On March 1, 2008, Nicholas S. Zeppos was named Vanderbilt’s eighth chancellor after serving as interim chancellor beginning Aug. 1, 2007. Prior to that, he spent 2002-2008 as Vanderbilt’s provost, overseeing undergraduate, graduate and professional education programs as well as development, alumni relations and research efforts in liberal arts and sciences, engineering, music, education, business, law and divinity. He first came to Vanderbilt in 1987 as an assistant professor in the law school. In his first five years, Zeppos led the university through the most challenging economic times since the Great Depression, while continuing to attract the best students and faculty from across the country and around the world. Vanderbilt got through the economic crisis notably less scathed than many of its peers and began and remained committed to its much-praised enhanced financial aid policy for all undergraduates during the same timespan. The Martha Rivers Ingram Commons for first-year students opened in 2008 and College Halls, the next phase in the residential education system at Vanderbilt, is on track to open in the fall of 2014. During Zeppos’ first five years, Vanderbilt has drawn robust support from federal funding agencies, and the Medical Center entered into agreements with regional hospitals and health care systems in middle and east Tennessee that will bring Vanderbilt care to patients across the state.
studentsToday, Vanderbilt University is a private research university of about 6,500 undergraduates and 5,300 graduate and professional students. The university comprises 10 schools, a public policy center and The Freedom Forum First Amendment Center. Vanderbilt offers undergraduate programs in the liberal arts and sciences, engineering, music, education and human development as well as a full range of graduate and professional degrees. The university is consistently ranked as one of the nation’s top 20 universities by publications such as U.S. News & World Report, with several programs and disciplines ranking in the top 10.
Cutting-edge research and liberal arts, combined with strong ties to a distinguished medical center, creates an invigorating atmosphere where students tailor their education to meet their goals and researchers collaborate to solve complex questions affecting our health, culture and society.
Vanderbilt, an independent, privately supported university, and the separate, non-profit Vanderbilt University Medical Center share a respected name and enjoy close collaboration through education and research. Together, the number of people employed by these two organizations exceeds that of the largest private employer in the Middle Tennessee region.
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