Caltech Receives $10 Million to Establish Bren Professors Endowment

PASADENA-The Donald Bren Foundation of Newport Beach has awarded the California Institute of Technology a $10 million grant to establish named professorships to support Caltech's ambitious Biological Sciences Initiative.

The Bren Professors Endowment will provide support for scholarly activities in biology and related disciplines, which are focused on solving some of the toughest problems of the life sciences. This gift brings the Biological Sciences Initiative total to over $80 million. A three-year fundraising effort announced in May 1998, the Initiative aims to provide essential resources and people to explore new territory in the biological sciences through the kind of interdisciplinary approach at which Caltech excels.

"Caltech's focus on biological sciences will open a new area for its scholarly inquiry and research that promises endless possibilities to profoundly touch and improve our lives," said Bren, the chairman of The Irvine Company. "It pleases me to be able to encourage this initiative and the distinguished scholars who will carry it out."

The named professorship is the highest honor a university can confer upon a faculty member. It is a tool to recognize and reward achievements and for recruiting senior faculty to join a new institution. Ultimately, five senior faculty will be named new Bren Professors, joining Peter Dervan who holds the first Bren Professorship established at Caltech in 1988.

Initially, a portion of the $10 million grant will be used to establish the Bren Scholars Program, which will support new faculty identified by Caltech as scientific stars before they are recognized in the scientific community at large. The Bren Scholars Program will fund the expenses associated with initiating their research programs for a period of six years, thus launching them on a lifelong career, and maximizing their contributions to science and engineering. After six years, the endowment for the Bren Scholars Program will be added to the Bren Professors Endowment.

The Bren Foundation grant is being made in memory of Earle Jorgensen, Bren's stepfather, who died this August at the age of 101. He was a self-made Southern California steel pioneer, whose products fortified the area's economic boom and whose commitment to community included support for Ronald Reagan's campaigns for governor of California and president. He also served as a member of Reagan's "kitchen cabinet." Jorgensen was a Caltech trustee from 1957 to 1999.

"Earle's life spanned the 20th Century, and for 42 years, he brought his special energy, optimism, curiosity, and interest in science and engineering to the Caltech board - attending his last meeting as a Life Trustee after he had turned 100," said Bren who has been a Caltech trustee since 1983.

Caltech President David Baltimore said the grant will help Caltech reach its goals. "I think Don has focused his giving on the most important aspect of Caltech, which is the quality of our faculty," Baltimore said. "Bringing the very best people here is at the heart of Caltech's mission."

The Bren Foundation is a private philanthropic organization chartered by Donald Bren, the chairman of The Irvine Company, to further his lifetime interests in public and private education, scientific research, conservation, and the visual arts.

Since 1988, Bren's higher education philanthropy is making possible, over time, the creation of at least 20 endowed chairs that are being filled at U.C. Irvine, U.C. Santa Barbara, Caltech and Chapman University.

Founded in 1891, Caltech has an enrollment of some 2,000 students, and an academic staff of about 280 professorial faculty and 130 research faculty. The Institute has more than 19,000 alumni. Caltech employs a staff of more than 1,700 on campus and 5,300 at JPL.

Over the years, 28 Nobel Prizes and four Crafoord Prizes have been awarded to faculty members and alumni, including the Nobel Prize in chemistry awarded to Professor Ahmed Zewail earlier this month. Forty-four 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 77 fellows of the American Academy of Arts and Sciences; and on the faculty and Board of Trustees, 69 members of the National Academy of Sciences and 49 members of the National Academy of Engineering.


Mutations in the mitochondrial DNA of cells dramatically increase with aging, Caltech study shows

PASADENA-Certain effects of aging could be caused by mutations in the DNA molecules of the energy-producing engines of cells known as mitochondria, according to new research from the California Institute of Technology and the University of Milan.

The study, published in the October 22 issue of the journal "Science", describes the results of skin-cell biopsies of about 30 individuals in a variety of age groups. The study concludes that damage to mitochondrial DNA dramatically increases around the age of 65.

"It's not a magic number, but we see a clear trend," says Giuseppe Attardi, who is Grace C. Steele Professor of Molecular Biology at Caltech and leader of the team authoring the paper.

Attardi and his colleagues focused their efforts on the small structures in cells known as mitochondria. Every cell can have tens to hundreds of these structures, which play an important metabolic role in the energy production that allows the cell to do its work.

Each of the mitochondria has about 10 to 20 molecules of DNA, which means that a single cell can have hundreds or thousands of mitochondrial DNA molecules.

But mitochondrial DNA is known to be susceptible to mutations over the course of a lifetime. These mutations can be due to oxidative damage, some enzyme malfunction, or even the cell's own efforts to repair itself. But prior to the new study, molecular biologists had difficulty in detecting aging-related mutations.

Over a period of about five years, Attardi and his colleagues developed a technique for detecting aging-related mutations in the main control region of mitochondrial DNA. This provided a very reliable method for determining the percentage of mitochondrial DNA molecules in a cell that had actually undergone mutations.

With this technique, they then studied tissue samples provided by the National Institutes of Health (NIH) and the University of Milan from skin biopsies. These biopsies came from individuals ranging from a 20-week-old fetus to a 101-year-old subject, which allowed the researchers to determine the prevalence of mutations in different age groups.

The results showed virtually no aging-related mutations for any of the subjects under the age of 65. But a dozen or so individuals above the age of 65 showed a dramatic increase in mutations. And not only did the rate of mutations sharply increase with age, but individuals also showed a sharp increase in mutations if they passed the age of 65 between biopsies.

Overall, the researchers found that up to 50 percent of the mitochondrial DNA molecules had been mutated in subjects 65 or over.

Attardi says future study will be needed to ascertain the precise effects of the mutations and the relationship to the known characteristics of aging. In addition, the researchers would like to know how the original mutation "amplifies," or is established in thousands of other molecules.

Also, the precise mechanism of the mutations is not known at this time. And finally, the study was done only on skin cells, although Attardi says the effect may possibly be seen in other cells of the human body.

In addition to Attardi, the other authors are Yuichi Michikawa, a senior research fellow in biology at Caltech; and Franca Mazzucchelli, Nereo Bresolin, and Guglielmo Scarlato, all of the University of Milan.

Robert Tindol

A heart medication is found effectivein treating skin cancer, Caltech researchers discover

PASADENA-Researchers have discovered that one type of drug used for human heart disease can inhibit the growth of skin cancer cells.

The drug, known as BQ788, is proving effective in suppressing skin cancer in mice, and drugs of this type could have potential for ovarian and prostate tumors as well. In the September 28, 1999, issue of the Proceedings of the National Academy of Sciences, California Institute of Technology biology professor Paul Patterson and researchers Ronit Lahav and Garrett Heffner report that the drug can stop melanoma tumor growth and even reduce tumors in some cases.

Further, the drug seems to be effective both as a direct treatment of the tumor and when injected systemically into the animal. The latter result is particularly promising as it has the potential for also suppressing metastasis, or the spread of tumors to other organs, says Patterson.

"If you went to the doctor with a tumor on the skin, he would take it out immediately," says Patterson, who is executive officer for the Division of Biology at Caltech. "So the first line of treatment is to surgically excise the tumor, and if it's a superficial tumor, you essentially have a complete cure.

"But the worry is when the tumor has penetrated more deeply and already metastasized," he says. "We think this drug could turn out to be an effective way to stop cancer cells from spreading, or at least stop their growth if they have already spread."

The strategy is based on the targeting of "growth factors," or proteins that cells use to stimulate their growth. The cancerous state represents a reversal of healthy, mature cells to a state similar to that of embryonic cells. In other words, cancerous cells tend to multiply rapidly, just as cells do in a developing embryo.

Lahav, the lead author on the paper, reasoned that melanoma cancer cells perhaps use a growth factor similar to that employed by their precursor cells in the embryo. She showed that such a growth factor, called endothelin, acts on the embryonic cells, and is also made by the cancer cells. By serendipity, the heart drug BQ788 is an antagonist for the endothelin receptor B. Thus, BQ788 is a substance that disrupts the receptor from performing its function in the cell.

Lahav found that this drug can stop human melanoma cell growth when introduced into cell cultures. In fact, the drug not only makes the cells stop dividing, but it can also kill such cells.

When the drug was given to mice with tumors, tumor growth slowed dramatically, and in some cases even regressed.

"It works whether you inject it into the tumor or into the body cavity," Patterson says. "In about half the mice, the tumors actually shrank."

Patterson says there is reason to think this type of drug could also work on certain other cancers (ovarian, prostate) where runaway cell growth may also be controlled by the same growth factor, endothelin.

Ronit Lahav is a postdoctoral scholar from Israel, and Garrett Heffner is a Caltech sophomore who participated in this research the summer after graduating from high school.

Robert Tindol

Gene linked to human kidney disease is also responsible for mating in roundworms

PASADENA-For a male nematode, the LOV-1 gene couldn't be more aptly named. The millimeter-long roundworm, if its LOV-1 gene is functioning properly, has the eagerness to mate and the instincts to perform successfully.

But if the LOV-1 gene is disabled, the male nematode is truly clueless. The fact that "LOV" is an acronym for "location of vulva" pretty much says it all.

While there is no such single gene controlling sexual interest and instinct in humans, California Institute of Technology researchers who recently identified the LOV-1 gene say there is a similar human gene involved in a type of kidney disease.

In the Sept. 23 issue of the British journal Nature, Caltech researchers Paul Sternberg and Maureen Barr write of their discovery that the LOV-1 gene has a sensory role in nematodes. The human homolog (or counterpart) is PKD1, or polycystic kidney disease gene 1.

In other words, a male nematode that has this particular gene intact is able and willing to mate, while a human with the gene intact is disease-free. But if the genes are respectively knocked out, the nematode is sexually dysfunctional and the human is prone to autosomal dominant polycystic kidney disease, a serious disease that afflicts about one in 1,000 people and may ultimately result in renal failure.

"This is a surprise," says Sternberg, a biology professor at Caltech. "We can only speculate on what the connection might be."

PKD1 and a second gene, PKD2, account for about 95 percent of all cases of autosomal dominant polycystic kidney disease. These genes cause the human body to produce polycystin 1 and polycystin 2, which are thought to work somehow in concert at the molecular level.

In an analogous manner, the LOV-1 gene also seems to work in concert with the PKD-2 gene, which in nematodes is the counterpart of the PKD2 gene in humans. The fact that the genes in both humans and nematodes seem to work in pairs actually strengthens the likelihood that there is some underlying molecular relationship, Sternberg says.

Much of the lab work leading to this discovery was done by Maureen Barr, a postdoctoral scholar in Sternberg's lab who painstakingly watched in a microscope for male nematodes who were not successfully mating.

Barr then singled out the dysfunctional males and used standard genetic screening techniques and DNA sequencing analysis to identify the LOV-1 gene, which when mutated, is responsible for the lack of mating behavior.

While the researchers are not clear on why a gene involved in mating behavior in one species would be involved in disease in another, they say there could be a couple of possible explanations.

For one thing, the connection between the human gene and the worm gene might be very basic. Perhaps the gene is involved in setting up polarity of human kidney cells and polarity of worm neurons that govern sexual behavior.

In the case of the worm, the LOV-1 might actually act as part of a sensory signaling pathway responding to the presence of a mating partner by altering the electrical properties of the specific nerve cell that senses the mate.

Or perhaps the underlying relationship has to do with cell structure, Sternberg says. In this case, the LOV-1 protein might function as a molecular scaffold for other molecules, or promote the assembly of many molecules to create structures such as the sensory neuronal cilia.

Sternberg and Barr say the scientific goal of the study was to investigate ways in which genes influence behavior. But the findings could also serendipitously point to new avenues for research on autosomal dominant polycystic kidney disease.

"This is a mystery disease, so it could be that renal failure is just the first defect in a disease with broader manifestations," Sternberg says. In that case, improved knowledge at the molecular level could lead to different approaches in identifying treatments or even a cure.

"Here's a new way to study the basic mechanism," Sternberg says.

Robert Tindol

A unique class of neurons in humans and apes that may participate in cognition, volition, and self-awareness discovered by researchers

PASADENA-Clusters of large neurons found exclusively in the brains of humans and other primates closely related to humans may provide these species with enhanced capacities for solving hard problems, as well as for self-control and self-awareness.

In the April 27 issue of Proceedings of the National Academy of Science, neurobiologists Patrick Hof from Mount Sinai and John Allman from Caltech and their colleagues have found an unusual type of neuron, that is likely to be a recent evolutionary acquisition.

The neurons in question are spindle-shaped cells, which are almost large enough to be seen with the naked eye. Their location in the brain is in the frontal lobe near the corpus callosum, which connects the two halves of the brain.

Allman, the Hixon Professor of Psychobiology and professor of biology; Hof; and their team studied 28 different species of primates and found the spindle neurons only in humans and very closely related apes. The concentration of spindle neurons was greatest in humans, somewhat less in chimpanzees, still less in gorillas, and rare in orangutans.

According to Allman, "This declining concentration matches the degree of relatedness of these apes to humans." There were no spindle cells in gibbons, which are small apes, or in of any of the other 22 species of monkey or prosimian primates they examined. The spindle cells were also absent in 20 nonprimate species examined including various marsupials, bats, carnivores and whales.

The cells in question are found in an area of the brain already linked to psychiatric diseases. According to Allman, "In brain imaging studies of depressed patients, there is less neuronal activity in the region and the volume of the area is smaller. The activity of the area is increased in obsessive compulsive patients."

The activity of the area has been shown to increase with the difficulty of the cognitive task being performed. This suggests that the area enhances the capacity to do hard thinking. Activity is also increased when a subject withholds a response or focuses its attention, suggesting the area is involved in self-control.

Furthermore, the spindle neurons themselves are especially vulnerable to degeneration in Alzheimer's disease, which is characterized by diminished self-awareness. From this Allman suggests, "Part of the neuronal susceptibility that occurs in the brain in the course of age-related dementing illnesses may have appeared only recently during primate evolution."

Robert Tindol

Caltech biologists reveal structure of protein responsible for weight loss in cancer and AIDS patients

PASADENA-Caltech biologists have determined the three-dimensional structure of a protein that causes wasting in cancer and AIDS patients. The discovery could lead to new strategies for controlling weight loss in patients with devastating illnesses-and conversely, perhaps new strategies for fighting obesity.

The protein is commonly known as ZAG and is found in most bodily fluids. But researchers have been aware for some time that the protein is particularly abundant in patients who have cancer.

More recently, researchers have discovered that the protein is involved in the wasting syndrome known as cachexia, which is associated with both cancer and AIDS.

"This protein has something to do with fat metabolism," says Pamela Bjorkman, a professor of biology at Caltech and associate investigator of the Howard Hughes Medical Institute. Bjorkman and her team recently published a paper in the journal Science showing ZAG's structure.

One of the most noteworthy features of the structure is the resemblance between ZAG and a family of proteins known as class I major histocompatibility complex molecules, or MHC.

"MHC proteins have a large groove that binds a peptide derived from a pathogen," says Bjorkman, explaining that their new picture of the ZAG crystal shows an unexpected blob in the ZAG counterpart of the MHC peptide binding grove.

"It's not a peptide, but some organic molecule," she says. "We suspect that it is involved in the function of ZAG. If this compound is involved in breaking down lipids, then maybe you could design a drug that replaces it and interfere with lipid breakdown."

According to Bjorkman, other research shows that tumor cells themselves seem to stimulate the body to overproduce ZAG somehow, which in turn leads to the breakdown of body fat.

Thus, people suffering from cachexia don't lose body weight because they don't eat, but because the fat in their bodies is ultimately destroyed by an interaction involving ZAG.

An intervention to stop the wasting, then, might be to disrupt the overexpression of ZAG, and this might be accomplished with monoclonal antibodies or small molecules that bind to ZAG, she says.

The research appeared in the March 19 issue of Science, and was also the subject of an article in HHMI news, published by the Howard Hughes Medical Institute.

The other authors of the paper are Luis Sanchez and Arthur Chirino, both senior research fellows in Bjorkman's lab.

Robert Tindol

Alice Huang Receives Achievement Award

PASADENA—Alice S. Huang, senior councilor for external relations and faculty associate in biology at the California Institute of Technology, has been awarded the 1999 Achievement Award from the Chinese-American Faculty Association of Southern California for her outstanding contribution to microbiology research and for her dedicated leadership in higher education.

Huang was recognized at the association's 28th annual convention on February 27, at which she presented a keynote address titled "New Challenges for Chinese-American Activism."

Huang sits on the boards of AAAS, Johns Hopkins University, and the Health Effects Institute. She is also chair of the Foundation for Microbiology and chair of the Scientific Board of the Institute for Molecular and Cell Biology in Singapore. She is a member of the Food and Drug Administration Advisory Committee on Vaccines and Related Biological Products. She was previously dean for science at New York University and prior to that professor of microbiology and molecular genetics at Harvard Medical School.

Born in China, she grew up in the United States attending St. Mary's Hall, Burlington, New Jersey; the National Cathedral School, Washington, D.C.; and Wellesley College. She received BA, MA, and PhD degrees (microbiology, 1966) from Johns Hopkins University.

Dr. Huang has been recognized by the American Society for Microbiology with the Eli Lilly Award in Immunology and Microbiology (1977), followed by election as that society's president in 1988–1989. She has honorary doctorates of science from Wheaton College, Mt. Holyoke College, and the Medical College of Pennsylvania. She has served on the board of trustees of UMass and Shady Hill School. She is a fellow of the Academia Sinica in Taiwan (1991).

As an administrator Dr. Huang is particularly interested in education, in career mentoring, and in policy issues related to science and technology. Since coming to Caltech, where her husband David Baltimore is the president, Dr. Huang has joined the board of the Keck Graduate Institute of Applied Life Sciences, the Pacific Council on International Policy, and the Blue Ribbon Committee of the Los Angeles Music Center.

Dr. Huang resides in Pasadena, California, and has one daughter in New York City.

The Chinese-American Faculty Association was established 28 years ago with the purpose of promoting closer cultural and social ties among Chinese-American scholars in colleges and universities in Southern California. Today it has over 100 members. Previous annual convention speakers and achievement awardees include Caltech alumnus David Ho, former Caltech trustee Yuan Lee, and Caltech's Hoag Professor of Biophysical Chemistry Sunney Chan.

Sue Pitts McHugh
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Caltech Receives $1.4 Million for L. K. Whittier Gene Expression Center

PASADENA-The California Institute of Technology has received a $1,444,000 grant from the L. K. Whittier Foundation. The award is for support of the L. K. Whittier Gene Expression Center.

Led by Professor of Biology Barbara Wold, the L. K. Whittier Gene Expression Center will utilize unique resources already available at Caltech to initiate a large-scale human gene expression analysis. This breakthrough will be made in the growing field of "functional genomics," a field whose entire purpose is to make new medical and biological discoveries based on the DNA sequence of the human genome.

Mel Simon, chair of the Caltech Division of Biology and the Anne P. and Benjamin F. Biaggini Professor of Biological Sciences, has produced probes for all 40,000 known human genes. By combining this information with what scientists have already learned from the Human Genome Project, the center is expected to produce wide-ranging discoveries in both the medical and biological sciences.

"We hope to make the center a useful tool for all of the biologists on campus, and ultimately for scientists around the world, through our accumulated database of gene expression information," says Stephen Quake, assistant professor of applied physics and another collaborating scientist at the L. K. Whittier Gene Expression Center. "The interesting thing about the gene arrays is that they provide more data than any one person can analyze, and the aggregate sum of the data provides a powerful resource to answer a number of questions about gene function."

The L. K. Whittier Foundation, located in South Pasadena, was incorporated in 1955 by the late Leland Whittier and other members of the Whittier family. The Whittiers are descendants of Mericos H. Whittier, who was one of the first independent oil producers in California.

Founded in 1891, Caltech has an enrollment of some 2,000 students, and an academic staff of about 280 professorial faculty and 130 research faculty. The Institute has more than 19,000 alumni. Caltech employs a staff of more than 1,700 on campus and 5,300 at JPL.

Over the years, 27 Nobel Prizes and four Crafoord Prizes have been awarded to faculty members and alumni. Forty-four 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 75 fellows of the American Academy of Arts and Sciences; and on the faculty and Board of Trustees, 68 members of the National Academy of Sciences and 49 members of the National Academy of Engineering.

Caltech discovers genetic process for controlling plant characteristics

PASADENA-Caltech biologists have harnessed a gene communication network that controls the size and shape of a flowering land plant.

The discovery is a fundamental advancement in understanding the processes that make plants what they are. The knowledge could also lead to greater control over certain characteristics of plants such as fruit size and stem durability.

In the March 19 issue of the journal Science, Professor of Biology Elliot Meyerowitz and his colleagues explain how they have managed to control three genes found in the "shoot apical meristem." This structure is the source of all cells creating a plant's leaves, stems, and flowers, and is somewhat analogous to the stem cells in animals.

The shoot apical meristem-also known as SAM-begins as a portion of the seed comprising just a few hundred cells. Like stem cells, they are undifferentiated at first, but as the young organism develops, they diversify to create the cells that make up all the recognizable features. "These divide in highly specific patterns to make leaves and stems and flowers," says Meyerowitz, who specializes in the molecular biology of plants. "Everything you see above ground arises from these cells."

Working with the nondescript flowering plant known as Arabidopsis thaliana, the Meyerowitz team first cloned the genes that gave appearance to the plant. These genes, known as CLV1 and CLV3, turned out to reveal a communication network that the plant uses to make its various parts.

Meyerowitz and his team discovered that the Arabidopsis plant tends to grow differently when the genes are disrupted. For example, the normal plant is about six inches in height with a thin, fragile stem and a few white flowers at the top.

But when the genes are knocked out, the plant grows a much thicker stem and mutant flowers with extra organs of all types, especially stamens and carpels.

In effect, this means that the researchers are in control of the genetic mechanism that governs various characteristics of a plant. And since the effect is genetic, the mutated characteristics are passed along to future generations.

Meyerowitz says the discovery could be used to mutate certain plants of human benefit so that they would have more favorable traits. For example, wheat might be altered so that the stem would be stouter and more resistant to being blown over.

But many of these effects have been accomplished for centuries with selective breeding, he says.

"The difference between a cherry tomato and a big beefsteak tomato is just like the difference between a normal Arabidopsis plant and those mutant for CLV1 or CLV3," he says. "We're not sure if it's exactly the same gene because we haven't yet looked.

"So there are ways to make fruit bigger, for example, without understanding the process," he says. "But what we're trying to do is understand the process."

Also involved in the research are Jennifer Fletcher, a research fellow in biology at Caltech; Mark Running, a graduate of Caltech who is now at UC Berkeley; Rüdiger Simon of the Institut für Entwicklungsbiologie in Cologne, Germany; and Ulrike Brand, a grad student in Simon's lab.

Robert Tindol

U.S. Holocaust Memorial Museum architect to design Caltech's new Broad Center for Biological Sciences

PASADENA—James Freed, the architect who designed the United States Holocaust Memorial Museum, has been chosen to design the new Broad Center for the Biological Sciences on the Caltech campus.

Freed, a senior partner of the firm Pei Cobb Freed & Partners, was selected from four finalists to design the building, which is the cornerstone of a $100-million initiative to strengthen Caltech's research efforts in the biological sciences.

The building is named for Eli Broad, chairman and CEO of SunAmerica Inc. and a Los Angeles civic leader and philanthropist. Broad provided $18 million for the building's construction.

David Baltimore, president of Caltech and a member of the committee that selected Freed, said the Holocaust Museum especially shows the architect's genius in designing a magnificent building to benefit society within a well-established neighborhood of other buildings.

"We were impressed by his flexibility and his ability to design a structure that is at once modern and appropriate to a settled architectural style in its surrounding," Baltimore said. "We were also impressed that he could take our very sketchy program and turn it into a fascinating model."

"The work he has done shows a remarkable ability to translate a set of needs into a structure of elegance and clear functionality." Eli Broad said he is "very pleased with the selection of James Freed."

"His functional yet highly creative designs have greatly enhanced many of America's most important metropolitan areas," Broad said. "I have no doubt his design for the Broad Center for Biological Sciences will both reflect and enhance Caltech's heritage of academic excellence, innovation and creativity."

The Broad Center will be located on the northwest quadrant of the campus. Measuring 100,000 square feet, the building will include laboratories and offices for 10 to 12 new research teams, as well as conference rooms, a lecture hall, and a seminar room. The latest modular design elements will be used to allow the greatest flexibility for rearranging labs and offices to accommodate future needs at minimum cost.

The building will house several major new research facilities, including an Imaging Center and a Biomolecular Structures Lab. The Imaging Center will feature powerful new magnetic resonance imagers that, for the first time, will give Caltech scientists the capability to view noninvasively the brains of large mammals and humans while they carry out normal activities such as viewing objects and paying attention. The result will be a deeper understanding of the complex relationship between brain-cell activity and behavior, including the causes of mental illness.

The Biomolecular Structures Laboratory will house state-of-the-art electron microscopes and powerful computational tools for visualizing and analyzing the structures of the multimolecular assemblies critical to the functioning of the immune response and other important biological processes.

The selection committee asked that each finalist discuss his/her approach for making the building blend into the surroundings while at the same time "capturing the essence of modern-day technology," developing a design that would comport with Southern California's seismic code requirements, maintain an open modular concept of laboratory space while incorporating specialized facilities, enhance student and faculty life, and address community concerns for public space.

As design architect, Freed will work closely with the executive architectural firm SMP-SHG, which will be represented by Susan O'Connell as project manager and William Diefenbach as lead architect. The lab programming architectural firm will be Kornberg Associates, with Ken Kornberg as lead architect.


Robert Tindol


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