University News

Chemistry Meets Computer, Data and Networking Technologies

Representatives of The National Science Foundation (NSF) has announced the first round of grants in "cyber-enabled chemistry," a program developed by its chemistry division to explore how researchers and educators in that field can fully exploit the potential of cyberinfrastructure.

The lead principal investigators for the four awards include two researchers in separate projects at the University of California, Berkeley, and one each at the University of Illinois at Urbana-Champaign and The Pennsylvania State University. The awards represent a combined investment of about $10 million over a 5-year period, including co-funding from NSF's former Division of Shared Cyberinfrastructure.

"Cyberinfrastructure" is an umbrella term meant to encompass the vast webs of computer, data and networking technologies that have infiltrated every aspect of modern life, and that are now beginning to revolutionize science and engineering research.

The goal of the cyber-enabled chemistry program--formally known as Chemistry Research Instrumentation and Facilities: Cyberinfrastructure and Research Facilities--is to ensure that chemists can take full advantage of that revolution. In particular, the program seeks to

• foster new chemical research and education activities through the use of grid computing, community databases, remote access to instrumentation, electronic support for geographically-dispersed collaborations, and other web- and grid-accessible services
• help teams of researchers assemble distributed expertise and resources into integrated virtual laboratories
• impact the day-to-day practice of chemistry though advances such as scientific portals, workflow management, computational modeling, and data and molecular visualization
• access the expertise and resources that cyberinfrastructure provides to greatly broaden participation in the chemical sciences, and to create a truly inclusive national and international community

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Franklyn G. Jenifer Named President Emeritus of U. T. Dallas

Franklyn G. Jenifer, the former president of The University of Texas at Dallas, was named president emeritus of that institution last week by the UT System Board of Regents.

Dr. Jenifer served as president of UT Dallas from 1994 to 2005. UT Dallas' enrollment increased more than 61 percent during his tenure -- from less than 8,500 students to nearly 14,000 -- and the campus has undergone a dramatic physical transformation as major new facilities have been constructed -- including buildings for the School of Management, the Erik Jonsson School of Engineering and Computer Science and the Callier Center for Communication Disorders as well as a Student Activity Center, athletic facilities and hundreds of student apartments.

Jenifer, a biologist, earned his bachelor's and master's degree from Howard University and his Ph.D. from the University of Maryland. He previously served as president of Howard University in Washington, D.C., as chancellor of higher education in Massachusetts, where he was responsible for 27 public colleges and universities with a total enrollment of approximately 180,000 students, and as vice chancellor of the New Jersey Department of Higher Education, a system composed of 32 public institutions of higher education with an enrollment of nearly a quarter-million students.

Jenifer began his career in academia at Rutgers University in New Jersey. He started as an assistant professor of biology at the Livingston College campus in New Brunswick in 1970, became an associate professor the following year and a full professor in 1976. He also served as chairperson of the biology department and as chairperson of the university senate. Later, he served as associate provost at Rutgers' Newark campus. 

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Scholars Awarded £100,000 in Research Prizes

Two young researchers at The University of Nottingham have been awarded prestigious prizes for their outstanding work. Dr. Mark Darlow of the Department of French and Francophone Studies, and Dr. Georgina Endfield of the School of Geography, have each been awarded £50,000 (US$87,000) Philip Leverhulme Prizes to further their research.

The two-year awards, made by the prestigious Leverhulme Trust, are for outstanding scholars whose work has already been recognized at an international level.

Darlow will use the prize money to complete a book on the theatre of the French Revolution. This will involve substantial work in archives in Paris, looking at the records of the government, the police, and theatres, as well as reactions in the contemporary press. His research will investigate how culture was turned into an instrument of education or propaganda by the state during the French Revolution, and to what extent politics permeated culture.

Endfield will focus on regional environmental and climate history, and socio-economic responses to extreme weather events such as droughts, flood events and hurricanes, primarily in Mexico and Southern Africa. She will also look at the cultural history of climate theory.

 The Leverhulme Trust, established at the wish of William Hesketh Lever, the first Viscount Leverhulme, makes awards for the support of research and education. The Trust emphasizes individuals and encompasses all subject areas.

The Philip Leverhulme Prizes commemorate the contribution to the work of the Trust made by Philip Leverhulme, the Third Viscount Leverhulme and grandson of the founder. Each year approximately 25 awards are given to scholars in UK institutions, across five subject areas.

Prize-winners each receive £50,000 over two years to pursue research in the way they judge to be most effective, with little or no constraints imposed by the Trust. The recipient can follow their own intellectual path and can develop their research on an ongoing basis depending on concepts and results as these emerge.

The key aim of the awards is to recognize and facilitate the work of outstanding young researchers — usually under the age of 36 — based in UK universities. Prize recipients are scholars who have already influenced the understanding of their field and gained an international standing, but of whom it is felt that their best research is yet to come.

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Sir Peter Crane Accepts Faculty Appointment in Geophysical Sciences

Sir Peter Crane, the director of the Royal Botanic Gardens, Kew, in England, has announced that he will resign his position there to accept a faculty appointment in the University of Chicago’s Department of Geophysical Sciences and the College effective July 1, 2006.

Crane returns to Chicago to devote more time to research, teaching and writing in plant science, evolutionary biology and conservation. Before his appointment at Kew in 1999, Crane spent 17 years in Chicago. A former curator in the geology department, vice president for academic affairs and then director of the Field Museum, he also served as a Professor in Geophysical Sciences and Lecturer in the Committee on Evolutionary Biology at the University of Chicago.

Crane’s appointment as the Marion and John Sullivan University Professor will bolster an already first-rank faculty in evolutionary paleobiology, said David Rowley, Professor and Chairman of the Geophysical Sciences Department.

Crane said that leaving Kew was a difficult decision, but he is delighted to be returning to the city where he built his career and still has family and many friends.

Declared a UNESCO World Heritage Site in 2003, Kew Gardens holds the world’s largest collection of living plants, with more than seven million specimens. Kew employs more than 650 scientists and other staff, and its Millennium Seed Bank project has developed partners in 17 nations to secure the long-term conservation of more than 20,000 plant species.

Kew’s vast, newly created electronic databases disperse knowledge throughout the scientific world, and its staff collaborates with local communities and specialists in more than 40 overseas countries on conservation and biodiversity projects. Back at Kew and its country estate, Wakehurst Place, attendance has increased during Crane’s tenure from 1.1 million in 1999-2000 to a projected 1.8 million in 2005-2006.

In addition to overseeing Kew’s operations, Crane has continued his own research, integrating studies of living and fossil plants to understand the large-scale patterns and processes of evolution. He is the author of more than 100 scientific publications, including several books on plant evolution.

He holds academic appointments in the Department of Botany at the University of Reading, the Department of Geology at Royal Holloway College, University of London, and the Department of Biological Sciences at Imperial College. He was elected to the Royal Society in 1998 and the National Academy of Sciences in 2001. He was knighted in 2004 for services to horticulture and conservation.

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U. T. Southwestern Physician-Researcher Wins International Award for Lipid Research

Dr. Helen Hobbs, director of the Eugene McDermott Center for Human Growth and Development and an investigator in the Howard Hughes Medical Institute at UT Southwestern Medical Center, has been awarded Germany's highly respected  Heinrich Wieland Prize for her research on lipids.

The prestigious international science award is given annually to an individual who has conducted outstanding research in the fields of biochemistry, chemistry and physiology of fats and lipids and its clinical importance.

Dr. Hobbs' research focuses on the genetics of lipid metabolism, such as inherited factors that play a role in determining the level of low-density lipoproteins (LDL), or "bad" cholesterol, in the blood. High LDL cholesterol is a major risk factor for heart disease, heart attack and stroke because it contributes to the buildup of plaque that clogs the walls of arteries. Dr. Hobbs' research has shown, for example, that at least one out of every 50 blacks has a variation in one particular gene that results in a 40 percent-lower level of LDL.

The award is named after German chemist Dr. Heinrich Otto Wieland (1877-1957), who won the Nobel Prize in 1927 for his work on bile acids. Dr. Hobbs' work provides new insights on how cholesterol gets into bile, which is the major method used by the human body to eliminate cholesterol. Dr. Hobbs will receive the award at a ceremony in Munich. She is the fifth faculty member to receive the award. Since the Heinrich Wieland Prize was first awarded in 1964, only the University of Heidelberg has had more recipients, with six.

Dr. Brown and Dr. Goldstein, chairman of molecular genetics, won the award in 1974 for their research on lipoprotein receptors and the genetic control of cholesterol metabolism. They shared the Nobel Prize in physiology or medicine in 1985 for their discovery of the underlying mechanisms of cholesterol metabolism, which led to the development of statin drugs to treat high cholesterol.

Dr. John Dietschy, professor of internal medicine, received the Wieland Prize in 1983 for his research into the regulation of cholesterol balance in tissues.

Dr. David Mangelsdorf, professor of pharmacology and biochemistry, won the award in 2003 for his research focusing on the mechanisms of nuclear receptor proteins, which serve as sensors in protecting human cells against unusually high and possibly toxic levels of lipids, such as cholesterol and fatty acids.

Dr. Hobbs also directs the Donald W. Reynolds Cardiovascular Clinical Research Center at UT Southwestern, which includes the Dallas Heart Study, a multiyear, multimillion dollar project aimed at learning more about the hidden causes of heart disease and finding new treatments. She holds the Eugene McDermott Distinguished Chair for the Study of Human Growth and Development and the Dallas Heart Ball Chair in Cardiology Research. In 2004 she was elected to the National Academy of Sciences' Institute of Medicine.

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Dr. Steven Goodman Named Editor-in-Chief of Experimental Biology and Medicine

Dr. Steven R. Goodman, who holds a chaired professorship and directs a research institute at The University of Texas at Dallas (UTD), was named editor-in-chief of Experimental Biology and Medicine, a leading journal in the biomedical research field.

Goodman will begin a three-year term, which is renewable for an additional three years, at the journal on July 1, 2006. He will continue in his current roles at UTD, where he is the C.L. and Amelia A. Lundell Professor of Life Sciences and director of the Institute of Biomedical Sciences and Technology (IBMST).

The peer-reviewed journal is published 11 times a year by the Society for Experimental Biology and Medicine, a not-for-profit scientific society founded in 1903 to promote investigation in the biomedical sciences by encouraging and facilitating interchange of scientific information among disciplines. The organization is based in Maywood, New Jersey.

Goodman joined UTD in 2001 to found the university’s Sickle Cell Disease Research Center. Eighteen months later, he established IBMST to provide added focus and effort to the university’s research and education initiatives in areas related to combating disease and improving health. The institute has created interdisciplinary teams of faculty members and researchers from UTD and other universities from such disparate fields as physics, chemistry, mathematics, computer science, engineering, nanotechnology and the biological sciences. The teams’ efforts are focused in four broad areas of research – diseases of the aging brain, blood disorders, molecular diagnostics and biomedical technology and bioengineering, security and defense.

Goodman earned a doctorate in biochemistry from St. Louis University Medical School and a bachelor of science degree in chemistry from the State University of New York at Stony Brook. He did post-doctoral research in cell biology at Harvard University and molecular biology at Harvard Medical School.

Goodman is the current president of the Association of Anatomy, Cell Biology and Neurobiology Chairs, a national biomedical sciences organization. He is also a professor of molecular and cell biology at UTD and an adjunct professor of cell biology.

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New System for Earthquake Early Warning

A University of California, Berkeley, seismologist has discovered a way to provide seconds to tens of seconds of advance warning about impending ground shaking from an earthquake.

While a few seconds may not sound like much, it is enough time for school children to dive under their desks, gas and electric companies to shut down or isolate their systems, phone companies to reroute traffic, airports to halt takeoffs and landings, and emergency providers to pinpoint probable trouble areas. Such actions can save lives and money.

An early warning system like this is possible thanks to the work of Richard Allen, UC Berkeley assistant professor of earth and planetary science, who in the last five years has demonstrated that within a few seconds of an earthquake rupture, he can predict the total magnitude of the quake and its destructive potential. In San Francisco, for example, Allen estimates that it's likely the city could receive 20 seconds' warning of an impending temblor.

Allen and his colleagues are now testing a system, ElarmS, that would make these predictions, and the researchers are working with the U.S. Geological Survey (USGS) to determine how accurate these warnings would be.

Allen and coauthor Erik L. Olson, a former graduate student at the University of Wisconsin, Madison, published their data on early earthquake ground motion predictions in the Nov. 10 issue of Nature.

Seismologists, especially those in the United States, have become increasingly pessimistic about being able to predict earthquakes. Experiments at the intensively monitored Parkfield, Calif., site have dampened enthusiasm that earthquake ruptures could be predicted hours or days before they happen. To reduce loss of life and property, earthquake-prone regions generally rely on a combination of advance preparation and post-earthquake assessment and notification between five and 10 minutes after a quake.

Allen's early warnings come after a quake rupture has already begun but before the shaking is felt tens of miles from the epicenter.

San Francisco , for example, sits about midway along the northern half of the 800-mile San Andreas fault. If a rupture occurs at the extreme northern end, it could take 80 seconds, traveling nearly 2 miles per second, to reach the city. An early warning system could provide a critical buffer for residents, businesses and emergency responders, even if the time isn't sufficient to evacuate a building.

The early warning information also would feed directly into the new active-response building designs that change the mechanical properties of a structure to let it ride out shaking and minimize damage both inside and out. Active response buildings are already operational in Japan, Allen said.

Two years ago, while at the University of Wisconsin, Allen reported differences in the frequency of seismic signals emanating from small and medium earthquakes during the first four seconds of the rupture, with the larger quakes showing lower frequency signals than the smaller quakes. The signal is part of the primary wave, or P wave, that is the first, though least destructive, wave to arrive after a rupture. Most people experience the P wave, which is a pressure wave that travels through rock like sound through air, as a jolt.

This P wave is followed by a secondary wave, or S wave, that shears the ground back and forth and up and down. Shortly after, more destructive surface waves arrive that jerk the ground sideways and later roll in like ocean waves.

In the current study, Allen shows that the relationship between P wave frequency and the total magnitude of the quake holds for major quakes, up to magnitude 8 and higher, as well as for medium and small quakes. Based on the correlation, he can predict the total magnitude of the quake to within 1 magnitude, and for a specific area, like the San Andreas Fault, to within half a magnitude. Magnitude is a measure of the total area that ruptures underground and the average amount of slip along the rupture. A half a magnitude amounts to a factor of 3 difference in ground motion.

Allen's findings conflict with the current model of earthquake rupture. The "cascade" model assumes that earthquake faults are made up of lots of different-sized patches, each under some degree of stress. When one of the patches is stressed enough to slip, the slip propagates to adjacent patches, which rupture in turn like falling dominoes. The rupture stops only when the stress propagating along the fault zone reaches a patch that is too solidly locked to slip.

Inherent in this model is the idea that the initiating rupture is the same for big and small quakes. Allen's findings suggest this is wrong. Instead, the rupture is different for large and small quakes from the beginning, and the initial rupture contains information that can be used to predict the final size.

He proposes that if the initial rupture generates a large "slip pulse" that travels continuously in all directions across the fault plane, the pulse can supply the necessary energy to propagate through patches that would not otherwise have ruptured. Only when the energy in the pulse drops to a level insufficient to overcome the grip of rock on rock does the rupture stop.

Allen's demonstration that this observation holds in earthquakes around the world, from California to Taiwan and Japan, provides a solid basis for constructing an early warning system. Once the magnitude of the quake has been estimated, computers can predict areas of serious ground shaking based on an understanding of a particular fault. Within five seconds, warnings could be sent to cities in the areas calculated to expect damaging ground motion.

Because humans couldn't respond fast enough, Allen said, these warnings would have to rely on computers programmed to respond to quakes of a certain magnitude.

The ElarmS system also could warn rescue and clean-up personnel of aftershocks, which can cause collapse of unstable debris.

As the rupture proceeds, Allen said, analysis of seismic waves can refine magnitude and ground motion estimates, finally merging into the standard shake map typically produced within minutes of the end of an earthquake.

The work was supported by the USGS, University of Wisconsin, Madison, and UC Berkeley.

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Discovery of Molecular Signature Will Aid in Treatment of Brain Tumors

Researchers at UCLA's Jonsson Cancer have identified key characteristics in certain deadly brain tumors that make them 51 times more likely to respond to a specific class of drugs than tumors in which the molecular signature is absent.

The discovery of the telltale molecular signature - the expression of a mutant protein and the presence of a tumor suppressor protein called PTEN - will allow researchers to identify patients who are likely to respond to the drug treatment before they undergo therapies that are not likely to work, said Dr. Paul Mischel, a UCLA associate professor of pathology and laboratory medicine and a Jonsson Cancer Center researcher.

Mischel and his colleagues write in an article in the Nov. 10 issue of the New England Journal of Medicine that the discovery could change the way doctors treat glioblastomas, the most common type of malignant brain tumor and one of the those lethal forms of cancer.

Between 8,000 and 10,000 new cases of glioblastoma will be diagnosed in Americans this year. Average survival is less than a year, according to the American Cancer Society. Although treatment may prolong life, most malignant brain tumors are not curable, making the search for better treatments even more urgent, Mischel said.

A protein called epidermal growth factor receptor (EGFR) is commonly amplified in glioblastoma, making it a prime focus for therapies. Drugs such as Tarceva and Iressa target EGFR, blocking the cell signals that drive amplification of the protein and speed cancer growth. A subset of glioblastoma patients responded to Tarceva and Iressa, but it was not clear what characteristics made them respond to these drugs. There had to be critical molecular factors that determined response, Mischel said.

He and his team set out to find the molecular determinants that indicated which patients would respond best to EGFR blockers. Previous UCLA research in brain and other cancers suggested that the key might be the interaction of the PTEN protein and a mutant protein called EGFRvIII. About half of patients with amplified EGFR also have this mutant protein.

The UCLA team and their collaborators studied a subset of 26 glioblastoma patients who either responded very well or very poorly to EGFR-blocking drugs and developed a way to test their brain tumor tissue for the presence of both the mutant and PTEN proteins. Mischel's team found that patients with both genetic variations were 51 times more likely to respond to EGFR blockers. They also lived five times longer after initiating therapy than those without the variation, surviving 253 days versus 50 days.

To confirm their promising work, Mischel and his team obtained tissue samples from 33 brain cancer patients treated at another facility without knowing who the responders were. They were able to replicate their results independently, confirming that those with both genetic variations were more likely to respond to EGFR-blocking drugs.

The study shows that glioblastoma patients can respond to targeted agents, and suggests that patients likely to benefit from treatment can be identified by molecular testing. The study also raised the possibility that patients whose tumors lack the genetic variations in the molecular signature could possibly be treated with drugs to make them more sensitive to EGFR blockers.

Of the 8,000 to 10,000 glioblastoma patients diagnosed each year, about 10 percent to 20 percent have the combination of the mutant and PTEN proteins, Mischel said. The next step is a prospective study determining the molecular signature of patients' tumors and directing those with the right protein combination to EGFR-blocking therapies. Mischel's team also is working to uncover the molecular signatures in the tumors of non-responders so they can determine what therapies might be most effective for them.

The study, Mischel said, also may have important implications in other cancers.

Mischel's research was funded in part by the National Institute of Neurological Disorders and Stroke, the National Cancer Institute, Accelerate Brain Cancer Cure, and UCLA's Jonsson Comprehensive Cancer Center, which comprises more than 240 researchers and clinicians engaged in research, prevention, detection, treatment and education. One of the nation's largest comprehensive cancer centers, the Jonsson Center is dedicated to promoting research and translating the results into leading-edge clinical studies. In July 2005, the Jonsson Cancer Center was named the best cancer center in the Western United States by U.S. News & World Report, a ranking it has held for six consecutive years.

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Targeting Brain Disorders

A team of researchers from Cambridge’s Department of Biochemistry and the California Institute of Technology have published a paper in the November 10 issue of Nature that brings scientists closer to understanding the way messages are passed around the brain. The research will have implications in the treatment of illnesses as far ranging as alcoholism and Alzheimers disease.

The research is looking at the 5-HT3 receptor, a member of a family of proteins which are found in the brain, and are the molecules of memory, learning, and thinking. They are the targets of drugs used to treat many disorders including Alzheimers disease, Parkinsons disease, schizophrenia, learning and attention deficits. The 5-HT3 receptor has a number of roles, one of which is in the way the brain responds to alcohol - blocking 5-HT3 receptors in human alcoholics reduces their drinking and causes them to enjoy alcohol less. There is also potential for the development of drugs that act at these receptors as a new way to treat Alzheimers disease, and to control addiction to drugs of abuse.

The team, headed by Dr Sarah Lummis in Cambridge and Professor Dennis Dougherty at CalTech, researches how the proteins work at the molecular level, to better understand what has gone wrong when they malfunction, and how drugs work on these proteins. The initial work could be relevant to many brain proteins, and could help have much more wide ranging implications for the treatment of diseases originating in the brain.