Caltech Professor Pamela Bjorkman Elected To National Academy of Sciences

Pamela Bjorkman, professor of and executive officer for biology at the California Institute of Technology, is one of 72 American scientists elected this year to membership in the National Academy of Sciences (NAS). The announcement was made earlier this month in Washington at the 138th annual meeting of the academy.

Bjorkman, who has been on the Caltech faculty since 1989, focuses much of her research on molecules involved in cell-surface recognition, particularly molecules of the immune system. Investigators in her lab use a combined approach, including X-ray crystallography to determine three-dimensional structures, molecular biological techniques to produce proteins and to modify them, and biochemistry to study the properties of the proteins.

Much of the Bjorkman lab's efforts has involved proteins known as class I MHC, as well as very similar proteins—or homologues—that have a number of functions aside from an immunological role. In a 1999 study, for example, Bjorkman and her colleagues determined the three-dimensional structure of a protein that causes cachexia, a wasting syndrome in cancer and AIDS patients. The discovery provided the scientific basis for possible future strategies for controlling cachexia and/or treatment of obesity.

A native of Portland, Oregon, Bjorkman earned her bachelor's degree from the University of Oregon in 1978 and her doctorate from Harvard University in 1984. Afterward, she held postdoctoral positions at Harvard and the Stanford University School of Medicine.

She is an investigator of the Howard Hughes Medical Institute and has been a Pew Scholar in the biomedical sciences, an American Cancer Society Postdoctoral Fellow, and an American Society of Histocompatibility and Immunogenetics Young Investigator.

She has been the recipient of the William B. Coley Award for Distinguished Research in Fundamental Immunology, the Gairdner Foundation International Award for achievements in medical science, and the Paul Ehrlich and Ludwig Darmstaedter Award.

Bjorkman's election to the National Academy of Sciences brings to 67 the number of living Caltech professors and professors emeritus who have earned the prestigious honor. The National Academy, established in 1863 by President Lincoln, acts as an advisory body for the federal government on scientific matters.

Contact: Robert Tindol (626) 395-3631

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Caltech President Honored for Pioneering Work Leading to Cancer Therapy

PASADENA, Calif. — David Baltimore, the president of the California Institute of Technology, was one of five scientists to receive the 13th annual Warren Alpert Foundation Scientific Prize today, May 1, for research that ultimately led to a new groundbreaking cancer therapy.

The prize, awarded at a ceremony at Boston's Four Seasons Hotel, recognizes the significance of STI571, a new cancer therapy that has shown remarkable effectiveness against chronic myelogenous leukemia (CML) in clinical trials.

Created by understanding the fundamental mechanisms by which CML occurs, STI571 was cited by Dr. Francis Collins, director of the National Human Genome Research Institute, as an early example of the kind of rational drug design that will stem from human genome studies. At a recent lecture at Harvard Medical School he stated that the STI571 clinical trials have shown "pretty dramatic results and ones which we hope will be repeated in other disorders as we get this kind of molecular understanding of what's gone awry in disease."

Phase I clinical trials of STI571 have produced encouraging results for patients with CML, a form of cancer characterized by rising white blood cell counts. Currently approved treatments are aggressive and difficult for patients to tolerate. A person with CML, which affects an estimated 5,000 Americans each year, typically dies within five years. With STI571, however, clinical investigators report that so far, 51 of 53 patients who received the highest dose in one study have gone into remission with few and modest side effects.

In addition to serving as president of Caltech, Baltimore continues his work as a biology professor with an active research lab on campus. Baltimore and Owen N. Witte, MD, Howard Hughes Medical Institute investigator, and professor of microbiology, immunology and molecular genetics at UCLA and the Jonsson Cancer Center, were honored by the Alpert Foundation for the basic science investigations that characterized the genetic pathway to CML.

For their preclinical work that led to the creation of STI571, the Alpert Foundation presented the award to Alex Matter, MD, head of oncology research, Novartis Pharma AG, and Nicholas B. Lydon, PhD, formerly of Novartis and now vice president for small molecule drug discovery at Amgen, Inc. Brian J. Druker, MD, professor of medicine at Oregon Health Sciences University, was recognized for both his preclinical work and clinical trial investigations. The foundation will divide a $150,000 award among the winners.

CML is caused by a genetic anomaly triggered by the rearrangement of chromosomes nine and 22, forming what is called the Philadelphia chromosome. A molecular consequence of this anomalous chromosome is the Bcr-Abl gene, whose product is a member of the tyrosine kinase family of proteins, which play a central role in a variety of cellular processes. Bcr-Abl's cancer-causing properties were identified and characterized by Drs. Baltimore and Witte.

The presence of Bcr-Abl in 95 percent of CML patients made this molecule a particularly attractive target for the design of a selective kinase inhibitor. Matter, an early champion of kinase inhibitor research at Novartis, recruited Lydon to take on the effort of identifying Bcr-Abl inhibitors. Lydon, while working on this effort, began collaborating with Druker, whom he had met years earlier when Druker was an oncology fellow studying kinases in the 1980s at the Dana Farber Cancer Institute, a Harvard Medical School teaching affiliate. They ultimately identified STI571, and in 1998, after curing mice, the drug was taken into clinical trials, and today Druker continues to take a lead role in the development of STI571 for CML. The drug works by blocking Bcr-Abl's ability to transfer phosphate groups to acceptor proteins, a key process in signaling the continued growth of the tumor cells.

Recently, STI571 has also shown effectiveness against gastrointestinal stromal tumors (GISTs), which occur in an estimated 2,000 Americans each year. GISTs originate in the stomach or small intestine in cells that form the organs' connective tissue. Patients with malignant GISTs that cannot be removed by surgery generally die within a year or two of diagnosis. Researchers found that STI571 blocked another tyrosine kinase, KIT, the flawed protein found in GISTs, and one patient has shown significant shrinkage in tumor size.

The foundation's Scientific Advisory Committee comprises physicians and scientists from Harvard Medical School and the Massachusetts Institute of Technology and is chaired by Harvard Medical School dean Joseph B. Martin, MD, PhD. Each year the committee recognizes creative research that has dramatically affected the human condition.

Chelsea, Massachusetts, native Warren Alpert, chairman of Warren Equities, established the Alpert Prize in 1987 after reading an article about the University of Edinburgh's Kenneth Murray, who had developed a vaccine for hepatitis B. Alpert decided he would like to reward such far-reaching breakthroughs. He called Murray to tell him he had won a prize, then set about creating the foundation. To choose subsequent recipients, he asked Dr. Daniel Tosteson, then dean of Harvard Medical School, to convene a panel of experts to select and honor renowned scientists from around the world. Nominations are invited from scientific leaders nationwide.

In 1950, Warren Alpert, a first generation American, started his business with, as he tells it, $1,000 and a used car. Today Warren Equities and its subsidiaries, which market petroleum, food, and spirits and engage in transportation and real estate investments, generate approximately $900 million in annual volume and have more than 2,100 employees in 11 states. Forbes listed Warren Equities number 225 on its most recent list of the nation's largest privately held companies. Alpert is Warren Equities' sole owner and the foundation's sole benefactor.

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Owls perform a type of multiplicationin locating ground prey in dark, study shows

Owls have long been known for their stunning ability to swoop down in total darkness and grab unsuspecting prey for a midnight snack.

In the April 13 issue of the journal Science, neuroscientists from the California Institute of Technology report that an owl locates prey in the dark by processing two auditory signal cues to "compute" the position of the prey. This computation takes place in the midbrain and involves about a thousand specialized neurons.

"An owl can catch stuff in the dark because its brain determines the location of sound sources by using differences in arrival time and intensity between its two ears," says Mark Konishi, who is Bing Professor of Behavioral Biology at Caltech and coauthor of the Science paper.

For example, if a mouse on the ground is slightly to the right of a flying owl, the owl first hears the sound the mouse makes in its right ear, and a fraction of a second later, in its left ear. This information is transmitted to the specialized neurons in the midbrain.

Simultaneously, the owl's ears also pick up slight differences in the intensity of the sound. This information is transmitted to the same neurons of the midbrain, where the two cues are multiplied to provide a precise two-dimensional location of the prey.

"What we did not know was how the neural signals for time and intensity differences were combined in single neurons in the map of auditory space in the midbrain," Konishi says. "These neurons respond to specific combination of time and intensity differences. The question our paper answers is how this combination sensitivity is established."

"The answer is that these neurons multiply the time and intensity signals," he says.

Thus, the neurons act like switches. The neurons do not respond to time or intensity alone, but to particular combinations of them.

The reason the neural signals are multiplied rather than added is that, in an addition, a big input from the time pathway alone might drive the neuron to the firing level. In a multiplication, however, this possibility is less likely because a multiplication reduces the effects of a big input on one side.

It's not clear how the owl perceives the location of the mouse in the third dimension, Konishi says, but it could be that the owl simply remembers how far it is to the ground or how much noise a mouse generally makes, and somehow adds this information into the computation.

The lead author of the Science paper is José Luis Peña, a senior research fellow in biology at Caltech.

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Baxter Awards Caltech Professor $250,000

PASADENA, Calif.— The BioScience business of Baxter Healthcare Corporation, Hyland Immuno, has awarded $250,000 to a California Institute of Technology faculty member to continue his protein design research.

Glendale-based Baxter Hyland Immuno awarded the unrestricted grant to Dr. David Tirrell, the Ross McCollum - William H. Corcoran Professor of Chemistry and Chemical Engineering. Tirrell is also division chair for the Chemistry and Chemical Engineering Division at Caltech.

Tirrell's research addresses the design and synthesis of novel proteins and protein-like materials for applications in biology, biotechnology and medicine. He and his coworkers use biological cells to make proteins, just as nature does, but the cells are reprogrammed to produce specific materials that are targeted toward important biomedical technologies.

"I am delighted by this award, which will allow us to move our research forward much more rapidly," said Tirrell. "The link to Baxter will also help us connect our programs more directly to important clinical problems."

Said Norbert Riedel, PhD, president of Hyland Immuno's recombinant business, "One of our keys to growth is the collaboration with world-class academic research centers like Caltech. We are pleased to provide this grant to Dr. Tirrell to further his important work in protein design."

Founded in 1891, Caltech has an enrollment of some 2,000 students, and an academic staff of about 275 professorial faculty and 130 research faculty. The Institute has more than 19,000 alumni. Caltech employs a staff of more than 2,100 on campus and 4,800 at JPL. Over the years, 28 Nobel Prizes and four Crafoord Prizes have been awarded to faculty members and alumni. Forty-seven Caltech faculty members and alumni have received the National Medal of Science; and eight alumni (two of whom are also trustees), two additional trustees, and one faculty member have won the National Medal of Technology. Since 1958, 13 faculty members have received the annual California Scientist of the Year award. On the Caltech faculty there are 78 fellows of the American Academy of Arts and Sciences; and on the faculty and Board of Trustees, 70 members of the National Academy of Sciences and 48 members of the National Academy of Engineering.

Baxter Healthcare Corporation is the principal U.S. subsidiary of Baxter International Inc. (NYSE:BAX), a global medical products and services company that focuses on critical therapies for people with life-threatening conditions. Baxter's medical products and services include blood therapies, medication delivery and renal therapy, and are used by healthcare providers and their patients in more than 100 countries. The Hyland Immuno business of Baxter Healthcare Corporation develops and produces therapeutic proteins from plasma and through recombinant methods to treat hemophilia, immune deficiencies, and other blood-related disorders. Hyland Immuno's portfolio of therapies includes coagulation factors, immune globulins, albumin, wound management products and vaccines.

Contact: Deborah Williams-Hedges (626) 395-3227 debwms@caltech.edu

Visit the Caltech Media Relations Web site at: http://www.caltech.edu/~media

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Caltech Professor Awarded Wolf Foundation Prize for Insights Into the Life Cycle of Cells

PASADENA, Ca.-For his discovery of a critical protein system that regulates normal cell division and many other biological processes, the California Institute of Technology's Alexander Varshavsky has been named the co-recipient of the 2001 Wolf Foundation Prize in Medicine.

Varshavsky, the Smits Professor of Cell Biology at Caltech, will share the award with Avram Hershko of the Technion-Israel Institute of Technology. The Wolf Prize was established in 1978, and is designed to promote science and art for the benefit of mankind. Specifically, the pair is being honored for the discovery of the "ubiquitin system of intracellular protein degradation and the crucial functions of this system in cellular regulation." The prize includes an honorarium of $100,000 that will be split between the two awardees.

Proteins are biology's blue-collar workers. They are the catalysts that jump-start the various reactions of cellular life, telling cells when it's time to divide, change into other cell types, or die, and monitoring the timing of such events. When its specific job is done, it's often critical that a particular protein should be destroyed and thereby cease functioning.

Ubiquitin is a small protein that attaches itself to other proteins within a cell, marking them for degradation (or destruction) by proteases, still another kind of specialized protein. Ubiquitin is, well, ubiquitous in all organisms other than bacteria; hence its name. Using both mouse cells and baker's yeast as model organisms, Varshavsky proved that ubiquitin is essential for protein degradation in living cells. His laboratory also showed that the ubiquitin system plays major roles in a number of biological processes, including cell growth and division, DNA repair, and responses to stress. Subsequent work by numerous laboratories uncovered many other functions of this remarkable system, including its multiple roles in the functioning of the brain (for example, memory formation), in the development of most organs in the body, and in the regulation of general metabolism.

Conversely, malfunctions of the ubiquitin system often allow the cell's mechanisms to run amok. Therefore, these malfunctions play major roles in many human diseases, including cancer, bacterial and viral infections, and neurodegenerative syndromes like Parkinson's and Alzheimer's diseases. Varshavsky's work on the ubiquitin system was instrumental in making possible the current efforts to devise new classes of drugs to attack such diseases.

Varshavsky is a member of the National Academy of Sciences, the American Academy of Arts and Sciences, and the American Academy of Microbiology. His other honors include the 1998 Merit Award from the National Institutes of Health; the 1998 Novartis-Drew Award in Biomedical Science; the 1999 Gairdner International Award from Canada's Gairdner Foundation; the 2000 Sloan Prize from the General Motors Cancer Research Foundation; the 2000 Albert Lasker Award in Basic Medical Research from the Lasker Foundation; and the 2001 Merck Award, from the American Society for Biochemistry and Molecular Biology.

 

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Baxter Awards Caltech Professor $250,000

PASADENA, Calif.— The Hyland Immuno division of Baxter Healthcare Corporation has awarded $250,000 to a California Institute of Technology faculty member to continue his protein design research.

Glendale-based Baxter Hyland Immuno awarded the unrestricted grant to Dr. David Tirrell, the Ross McCollum – William H. Corcoran Professor of Chemistry and Chemical Engineering. Tirrell is also division chair for the Chemistry and Chemical Engineering Division at Caltech.

Tirrell's research addresses the design and synthesis of novel proteins and protein-like materials for applications in biology, biotechnology and medicine. He and his coworkers use biological cells to make proteins, just as nature does, but the cells are reprogrammed to produce specific materials that are targeted toward important biomedical technologies.

"I am delighted by this award, which will allow us to move our research forward much more rapidly," said Tirrell. "The link to Baxter will also help us connect our programs more directly to important clinical problems."

Said Norbert Riedel, PhD, president of Hyland Immuno's recombinant business, "One of the reasons Baxter is in Southern California is the opportunity to collaborate with world-class academic research centers like Caltech. We are pleased to provide this grant to Dr. Tirrell to further his important work in protein design."

Baxter Healthcare Corporation is the principal U.S. subsidiary of Baxter International Inc. (NYSE:BAX), a global medical products and services company that focuses on critical therapies for people with life-threatening conditions. Baxter's medical products and services include blood therapies, medication delivery and renal therapy, and are used by healthcare providers and their patients in more than 100 countries. The Hyland Immuno business of Baxter Healthcare Corporation develops and produces therapeutic proteins from plasma and through recombinant methods to treat hemophilia, immune deficiencies, and other blood-related disorders. Hyland Immuno's portfolio of therapies includes coagulation factors, immune globulins, albumin, wound management products and vaccines.

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CONTACT: Jill Perry, Media Relations Director (626) 395-3226 jperry@caltech.edu

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Researchers progress toward mutating a mousefor studying Parkinson's disease

Some inventors hope to build a better mousetrap, but California Institute of professor of biology Henry Lester's grand goal is to build a better mouse.

Not that the everyday laboratory mouse is inappropriate for a vast variety of biological and biomedical research. But for Parkinson's disease research, it has become clear that a strain of mutant mice with "slight" alterations would be a benefit in future medical studies. And not only would the mutant mice be useful for Parkinson's, but also for studies of anxiety and nicotine addiction.

Though Lester and his colleagues Johannes Schwarz and Cesar Labarca have not yet produced the mouse they envision, they have already achieved encouraging results by altering the molecules that form the receptors for nicotine in the mouse's brain. If they can just make these receptors overly sensitive in the right amount, they reason, the mice will develop Parkinson's disease after a few months of life.

Two earlier strains of mice were not ideal, but nonetheless convinced the Lester team members they were on the right track. One strain of mice suffered from nerve-cell degeneration too quickly, developing ion channels that opened literally before birth. These overly sensitive receptors essentially short-circuited some nerve cells. These mice usually do not survive birth, and never live long enough to reproduce.

Another strain developed modest nerve-cell degeneration in about a year, which is a long time in a mouse's life as well as a long time for a research project to wait for its test subjects. Lester wants the "Goldilocks mouse," with neurons that die "not before birth—that's too fast. Not at a year—that's too slow and incomplete. With a mouse strain that degenerates in three months, we could generate and test hypotheses several times per year."

Though they haven't achieved the "Goldilocks mouse" yet, the strain of mice developing modest degeneration after a year is particularly interesting. Tests showed that they were quite anxious, but tended to be calmed down by minuscule doses of nicotine. For reasons not entirely understood, humans who smoke are less likely to develop Parkinson's disease later in life, pointing to the likelihood that a mouse with hypersensitive nicotine receptors will be a good model for studying the disease.

In fact, the Lester team originally set out to build the strain of mice in order to study nicotine addiction and certain psychiatric diseases that might involve acetylcholine, a natural brain neurotransmitter that is mimicked by nicotine. The work in the past has been funded by the California Tobacco-Related Disease Research Program, the National Institute of Mental Health, and the National Institute of Neurological Disorders and Stroke (NINDS).

Once they had some altered mice, Schwarz (a neurologist who works with many Parkinson's patients) realized that the dopamine-containing nerve cells were dying fastest. The death of these cells is also a cause of Parkinson's disease. Because present mouse models for Parkinson's research are unsatisfactory, the researchers applied for and soon received funding from the National Parkinson Foundation, Inc. (NPF). Not only did the researchers receive the funding from the NPF, but they also were named recipients of the Richard E. Heikkila Research Scholar Award, which is presented for new directions in Parkinson's research.

"The Heikkila award is gratifying recognition for our new attempts to develop research at the intersection of clinical neuroscience and molecular neuroscience here at Caltech," says Lester.

Dr. Yuan Liu, program director at NINDS, says the Lester team's research is important not only because it is the first genetic manipulation of an ion channel that might lead to a mammalian model for Parkinson's disease, but also because the research is a pioneering effort in an emerging field called "channelopathy."

"Channelopathy addresses defects in ion channel function that causes diseases," Liu says. "Dr. Lester is one of the pioneers working in this field.

"We're excited about this development," she says, "because Parkinson's is a disease that affects such a large number of people—500,000 in the US. The research on Parkinson's is one of the research highlights that the NINDS is addressing."

The first results of the Lester team's research are reported in the current issue of the journal Proceedings of the National Academy of Sciences (PNAS).

In addition to Labarca, a member of the professional staff in the Caltech Department of Biology, and Schwarz, a visiting associate, the collaborators include groups led by professors James Boulter of UCLA and Jeanne Wehner of the University of Colorado.

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Caltech Professor Receives Ellison Award

PASADENA, Calif.—Giuseppe Attardi, the California Institute of Technology's Grace C. Steele Professor of Molecular Biology, has received the Ellison Medical Foundation Senior Scholar Award. The award is for $935,584 over four years.

Attardi's work encompasses research in the area of aging and in the detection of DNA that affects the aging processes. He is responsible for the discovery and development of new genetic research techniques that are used by laboratories internationally.

Attardi's career spans nearly a half century, including 35 years at Caltech. Prior to joining the Caltech faculty in 1963, Attardi was an assistant professor in histology and general embryology at the University of Padua, Italy. He received his MD from the University of Padua in 1947.

Throughout his career, Attardi has received numerous distinguished honors and awards.

The Ellison Medical Foundation is a nonprofit corporation that was established by a gift from Mr. Lawrence J. Ellison to support basic biomedical research on aging, relevant to understanding aging processes and age-related diseases and disabilities. The Ellison Medical Foundation stimulates basic biomedical research in multiple disciplines including molecular genetics, cell cycle regulation, cellular differentiation, genetic epidemiology, immunology, gene/environment and gene/gene interactions, metabolism, endocrinology, signal transduction, and integrative physiology. Through various award mechanisms, including the Senior Scholar and New Scholar Awards programs, the foundation fosters research by means of grants-in-aid to investigators at universities and laboratories within the United States.

Contact: Deborah Williams-Hedges (626) 395-3227 debwms@caltech.edu

Visit the Caltech Media Relations Web site at: http://www.caltech.edu/~media

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Odor recognition is a patterned, time-dependent process, research shows

PASADENA, Calif.-When Hamlet told the courtiers they would eventually "nose out" the hidden corpse of Polonius, he was perhaps a better neurobiologist than he realized. According to research by neuroscientists at the California Institute of Technology, the brain creates and uses subtle temporal codes to identify odors.

This research shows that the signals carried by certain neuron populations change over the duration of a sniff such that one first gets a general notion of the type of odor. Then, the wiring between these neurons performs work that leads to a more subtle discrimination, and thus, a precise recognition of the smell.

In the February 2 issue of the journal Science, Caltech biology and computation and neural systems professor Gilles Laurent and his colleague, postdoctoral scholar Rainer W. Friedrich, now at the Max Planck Institute in Heidelberg, Germany, report that the neurons of the olfactory bulb respond to an odor through a complicated process that evolves over a brief period of time. These neurons, called mitral cells because they resemble miters, thepointed hats worn by bishops, are found by the thousands in the olfactory bulb of humans.

"We're interested in how ensembles of neurons encode sensory information," explains Laurent, lead author of the study. "So we're less interested in where the relevant neurons lie, as revealed by brain mapping studies, than in the patterns of firing these neurons produce and in figuring out from these patterns how recognition, or decoding, works."

The researchers chose to use zebrafish in the study because these animals have comparatively few mitral cells and because much is already known about the types of odors that are behaviorally relevant to them. The Science study likely applies to other animals, including humans, because the olfactory systems of most living creatures appear to follow the same basic principles.

After placing electrodes in the brain of individual fish, the researchers subjected them sequentially to 16 amino-acid odors. Amino acids, the components of proteins, are found in the foods these fish normally go after in their natural environments.

By analyzing the signals produced by a population of mitral cells in response to each one of these odors, the researchers found that the information they could extract about the stimulus became more precise as time went by. The finding was surprising because the signals extracted from the neurons located upstream of the mitral cells, the receptors, showed no such temporal evolution.

"It looks as if the brain actively transforms static patterns into dynamic ones and in so doing, manages to amplify the subtle differences that are hard to perceive between static patterns," Laurent says.

"Music may provide a useful analogy. Imagine that the olfactory system is a chain of choruses-a receptor chorus, feeding onto a mitral-cell chorus and so on-and that each odor causes the receptor chorus to produce a chord.

"Two similar odors evoke two very similar chords from this chorus, making discrimination difficult to a listener," Laurent says. "What the mitral-cell chorus does is to transform each chord it hears into a musical phrase, in such a way that the difference between these phrases becomes greater over time. In this way, odors that, in this analogy, sounded alike, can progressively become more unique and more easily identified."

Applied to our own experience, this result could be described as follows: When we detect a citrus smell in a garden, for example, the odor is first conveyed by the receptors and the mitral cells. The initial firing of the cells allows for little more than the generic detection of the citrus nature of the smell.

Within a few tenths of a second, however, this initial activity causes new mitral cells to be recruited, leading the pattern of activity to change rapidly and become more unique. This quickly allows us to determine whether the citrus smell is actually a lemon or an orange.

However, the individual tuning of the mitral cells first stimulated by the citrus odor do not themselves become more specific. Instead, the manner in which the firing patterns unfold through the lateral circuitry of the olfactory bulb is ultimately responsible for the fine discrimination of the odor.

"Hence, as the system evolves, it loses information about the class of odors, but becomes able to convey information about precise identity," says Laurent. This study furthers progress toward understanding the logic of the olfactory coding.

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New research shows that the ears can sometimes trick the eyes

Though it seems to follow common sense that vision is the most dominant of the human senses, a new study by California Institute of Technology researchers shows that auditory signals can sometimes trick test subjects into misinterpreting what they have seen.

In a new study appearing in the Dec. 14 issue of the journal Nature, Caltech psychophysicists Ladan Shams, Yukiyasu Kamitani, and Shinsuke Shimojo report that auditory information can alter the perception of accompanying visual information, even when the visual input is otherwise unambiguous.

"We have discovered a visual illusion that is induced by sound," the authors write in the paper. Using a computer program that runs very short blips of light accompanied by beeps, the researchers asked test subjects to determine whether there was one or two flashes.

However, unknown to the subjects, the number of flashes mismatch that of beeps in some trials. When the subjects were shown the flash accompanied by one beep, everyone correctly stated that they had seen one flash. But when they were shown the flash with two very quick beeps spaced about 50 milliseconds apart, the subjects all erroneously reported that they had seen two flashes.

What's more, test subjects who were told that there was actually only one flash still continued to perceive two flashes when they heard two beeps.

According to Shimojo, a professor of biology at Caltech, the effect works only if the beeps are very rapid. When they are, "there's no way within the time window for vision to tell whether there's a single or double flash," he says.

According to Shams, a postdoctoral scholar working in Shimojo's lab and lead author of the paper, the results contribute to a shift in our view of visual processing from one "that is independent of other modalities, toward one that is more intertwined with other modalities, and can get as profoundly influenced by signals of other modalities as it influences them."

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