Emory Medicine, Winter 1999 - In Brief

Magnets that lift dark moods
CFAR - It's official
Joint venture with Columbia/HCA
42 acres (GMHI purchase)
On-off switches for gastro distress
Turning up the heat on eye tumors
Understanding cell cycle checkpoints
A pill for cystic fibrosis?
Setting the gold standard
New pieces of the food puzzle
Thymus transplants in pediatric AIDS
Building new bone
New inroads in circulation
People of note
The dean's pitch


In Brief


The future looks brighter for people who can't relieve their depression with medication. Their dark moods may lift after treatment with therapeutic magnets.

In a School of Medicine study, 56% of patients ages 22 to 65 and 23% of those over 65 responded favorably to an experimental treatment known as rapid-rate transcranial magnetic stimulation (rTMS). The study is the largest to date using rTMS and the first to evaluate its use in older patients with depression. Emory subjects were tested at Wesley Woods Geriatric Center using equipment loaned by the Atlanta Veterans Affairs Medical Center. Emory psychiatrist William McDonald and neurologist Charles Epstein are collaborating on this research.

During rTMS treatment, the doctor places a powerful magnetic coil close to the left prefrontal cortex, the portion of the brain believed to improve a depressed patient's mood. For a few seconds, an electromagnetic field is induced over the area, which apparently stimulates neurons to fire more effectively. Patients sit or lie down during the short procedure, which requires no anesthesic or sedation. The only discomfort: Most patients feel mild tightening of the scalp muscles, and a small percentage report headaches that go away when stimulation ends.

Rapid-rate TMS offers several advantages over electroconvulsive therapy (ECT). The experimental treatment is noninvasive and potentially more convenient. Patients could receive daily treatments during their lunch hour for a few weeks. In comparison, patients treated with ECT require general anesthesia, given intravenously. After treatment, patients cannot drive for several hours and usually miss a day of work.

Research at Emory and other sites studying rTMS also has shed light on the neuroanatomy of depression. Patients with early-onset depression have deficits in neuronal transmission, primarily in the outer, or cortical, areas of the brain, while patients with late-onset depression (age 50 or older) have deficits in the deeper, subcortical regions. As expected, people with early-onset depression benefit more from rTMS because it stimulates only the cortical areas.

Also, older patients who experienced depression early in life responded to rTMS at three times the rate of older patients with late-onset depression. Fortunately, patients with late-onset depression who have had little success with antidepressant medication respond favorably to ECT about 80% to 90% of the time, McDonald says.

Now, the researchers must look for possible risks as they determine the best way to give rTMS and to manage patients who receive it long term.

Magnets that lift dark moods



The NIH has designated the Emory/Atlanta Center for AIDS Research (CFAR) an official NIH CFAR site. The designation comes with a three-year, $2.3 million grant for Emory University, the AIDS Research Consortium of Atlanta (ARCA), and their primary collaborators. NIH recently designated five new sites nationwide in addition to 11 existing centers.

The Emory/Atlanta CFAR represents an unprecedented collaborative effort among academic, public health, government, and private AIDS researchers and clinicians, according to director and principal investigator of the new CFAR James Curran, dean of the Rollins School of Public Health and former director of the AIDS program at the Centers for Disease Control and Prevention. Major participants include Emory's schools of medicine, public health, and nursing, Yerkes Regional Primate Research Center, ARCA, Emory Hospitals, Grady Hospital, the Atlanta Veterans Affairs Medical Center, and Morehouse School of Medicine.

It's official


Last November, Emory Healthcare announced a joint venture agreement with Columbia/HCA Healthcare Corporation, which will allow Emory to expand its clinical services throughout metro Atlanta, specifically in eight Atlanta-area hospitals and five surgery centers owned by Columbia/HCA.

The agreement provides for the creation of a limited liability company (LLC) overseen by a board jointly governed by Emory Healthcare and Columbia/HCA. Through the LLC, Emory is responsible for clinical management and quality assurance in the 13 facilities, while Columbia/HCA will manage day-to-day operations.

The eight hospitals of which Emory assumes clinical management and quality assurance oversight are Cartersville Medical Center, Dunwoody Medical Center, Eastside Medical Center, Metropolitan Hospital, Northlake Regional Medical Center, Parkway Medical Center, Peachtree Regional Hospital, and West Paces Medical Center. These hospitals - all JCAHO accredited, one with commendation - will provide patient care under the umbrella of Emory Healthcare. Of the physicians practicing there, 92% are board eligible or board certified. Each hospital will retain its employees and medical staffs. New signage and published materials will reflect the addition of Emory Healthcare to the local name.

The agreement also extends to five ambulatory surgery centers: Atlanta Outpatient Surgery Center, Atlanta Outpatient Specialty Services, Atlanta Outpatient Peachtree Dunwoody, Marietta Surgical Center, and Northlake Surgical Center. Like the hospitals, these centers will retain their local employees and medical staffs.

None of the existing Emory Healthcare facilities (Emory University Hospital, Crawford Long Hospital, Wesley Woods Center and Geriatric Hospital, and a joint interest in Emory Adventist Hospital in Smyrna) are included in the arrangement. Also excluded are hospitals or facilities owned by Columbia/HCA elsewhere in Georgia. Columbia/HCA retains complete interest and control of its facilities outside Atlanta, and Emory Healthcare retains complete interest and control of all its own clinics and hospitals.

In 1994, Emory considered a very different arrangement with Columbia/HCA, signing letters of intent to create two joint ventures. This new proposal, however, has striking differences. For one, Emory is not selling or relinquishing control of any of its facilities, and two, Emory will have responsibility for medical management in the eight metro Atlanta hospitals owned by Columbia/HCA.

In addition, many aspects have changed at Columbia/ HCA and in market conditions in Atlanta in the past five years. The leadership at Emory believes that Columbia/HCA is a much stronger organization than it was five years ago, with new leadership and goals. The new LLC will be unaffected by a federal investigation of Columbia/HCA's past practices. The organization has committed significant resources to meeting all federal and state compliance and regulatory requirements as it refocuses its businesses with new management.

This agreement greatly broadens the community's access to care under the Emory umbrella, giving community physicians easier access to Emory services as well. It also helps implement Emory's goal of evolving from a specialty center to providing a full spectrum of care. According to Michael M.E. Johns, executive vice president for health affairs and CEO of Emory Healthcare, Emory is "dedicated to making the full range of Emory's exceptional health care services easily accessible throughout metropolitan Atlanta."

Joint venture with Columbia/HCA

This agreement gives community physicians easier access to Emory services.


This summer, the state of Georgia approved Emory's purchase of the 42-acre Georgia Mental Health Institute, located within a mile of the main campus on Briarcliff Road, to use for a variety of academic, education, research, and scientific activities. Emory co-developed the facility with the state more than 30 years ago and has administered programs on the property since then.

According to Emory President William M. Chace, Emory's first step is to create a master plan to address appropriate uses for the area, to insure it meets similar aesthetic standards as the main campus, and to consider the concerns of the surrounding neighborhood.

One of the keystones of Emory's planning is a multidisciplinary biotechnology development center in conjunction with Georgia Tech. New and promising early-stage medical and related technologies can be "incubated" and nurtured at this center, with support from the public and private sector to develop clinically useful therapies and diagnostics.

Among the numerous advantages to such a center, says Emory Vice President for Research Dennis Liotta, is "creating strong bridges between our universities and local industry, improving the success rate of new biotechnology ventures, and fully capitalizing on the scientific and business resources that already exist at Emory, Georgia Tech, and Georgia's other research universities."

42 acres



Emory pathologist James Madara has found a potential way to manipulate natural on-off switches in the body that may eventually allow physicians to regulate and treat chronic inflammatory diseases of the intestine. He has developed a lab model that demonstrates the molecular interactions between white blood cells called polymorphonuclear leukocytes (PMN) and the epithelial cells that line the intestinal wall. He and other scientists recently discovered that epithelial cells play an active role in intestinal inflammation. When epithelial cells recognize pathogens, they release substances that "invite" PMN to migrate across the intestinal epithelial barrier. As PMN cross the barrier, the barrier breaks down, allowing other pathogens to enter. The epithelial cells then initiate a signaling pathway, alerting other intestinal cells to secrete fluids and electrolytes, which cause diarrhea. Madara is testing new compounds in mice to regulate epithelial cell-PMN reactions and control inflammation.
On-off switches for gastro distress


Twenty-three out of 24 patients in an Emory Eye Center study are tumor-free thanks to a laser treatment using heat therapy.

Data from the study show that transpupillary thermotherapy (TPTT) effectively manages small choroidal melanoma (2.6 mm or smaller in thickness). During the procedure, retina surgeons Thomas Aaberg Jr. and Antonio Capone Jr. heat a tumor in 1/10-second bursts with an infrared diode laser. The laser destroys the melanoma cells' metabolism.

In the past, patients with intraocular tumors often were treated with radiation, but this is not without drawbacks. "Radiation collapses the tumor mass and can kill the tumor, but it often kills vision as well," says Capone, the study's principal investigator. "With the laser, we can destroy the tumor with surgical precision."

Side effects are infrequent among TPTT patients, who have participated in the Eye Center study for up to 30 months. TPTT also helps children with retinoblastoma.

'We still don't know the procedure's effectiveness on tumor-related mortality over the long term," reports Capone. "We still need to follow these patients for five or 10 more years."

Turning up the heat on eye tumors


Study results thus far indicate that laser heat therapy is effective against tumors such as choroidal melanoma. Courtesy of Ray Swords, Emory Eye Center.


Suppose you're repairing a hole in your roof, but before you can finish, other holes appear. You can't patch the holes fast enough before the roof caves in.

The same scenario applies to human cells, which constantly need to repair DNA damage caused by UV light, chemicals, man-made sources like gamma radiation, and oxygen by-products. They're adept at these repairs if they have time to make them.

About eight years ago, scientists discovered safety mechanisms in the cell cycle called "checkpoint arrests." These checkpoints allow cells to stop dividing long enough to repair themselves before continuing to replicate.

"If damage to a cell's genome goes unrepaired or is incorrectly repaired, genetic instability may result, which may be the first step to accumulating genetic changes that eventually lead to cancer," explains Wolfram Siede, a Winship Cancer Center investigator. "The human P53 gene, for example, which is altered in 50% of cancer cells, is one of the regulators of checkpoint arrest."

Using a yeast model, which already has a completely sequenced genome, Siede studies several genes that regulate checkpoint arrests. By analyzing mutants of these genes and their proteins, he hopes to learn what makes cells stop at checkpoints, what constitutes the signal to stop, and how the signal is transmitted from the damaged DNA to the cell-cycle regulating molecules.

The mutant yeast genes are models for cancer cells. At least one of these genes has a human homologue, the gene responsible for ataxia telangiectasia (AT), an inherited syndrome that causes early death, a proclivity to cancer, and a sensitivity to radiation treatment.

"Understanding why a cancer cell fails to use repair checkpoints goes to the molecular origins of cancer," says Siede, who will use this knowledge to test and develop therapeutic agents.

Understanding cell cycle checkpoints



Cancer researcher Wolfram Siede studies yeast cells to learn about "checkpoint arrests" - safety mechanisms in the cell cycle that allow cells to stop dividing long enough to repair DNA damage. When mutant cells try to keep on replicating without taking time for repair, the result correlates to the abnormalities seen in cancer cells.


Testing continues on CPX, a promising new drug for patients with cystic fibrosis (CF).

Co-investigators Nael McCarty (physiology) and Mark Weatherly (pediatrics) are directing Phase II clinical trials of CPX at the Egleston Cystic Fibrosis Center at Emory, the nation's first cooperative-care center dedicated to CF treatment. SciClone Pharmaceuticals, Inc. is sponsoring the trials for patients ages 18 to 45 at Emory, Rainbow Babies & Children's Hospital in Cleveland, the University of Iowa, and the University of Washington in Seattle.

CPX is one of three new drugs believed to circumvent a defective protein, the cystic fibrosis transmembrane regulator (CFTR). Found in cells that control chloride and sodium flow, CFTR causes an imbalance in the body's salt and water content and creates the sticky mucus that coats CF patients' lungs.

"We are very excited about the potential of CPX for CF patients, since it addresses the cellular defect exhibited in the largest portion of all CF patients in the country," McCarty says. Two other new drugs - phenylbutyrate and Duramycin - also appear to correct salt and water imbalance in the lungs. These drugs, along with CPX, are the first therapies to address CF's cause rather than just its symptoms. They comprise a new category of treatment strategies termed "gene-assist" therapies, which treat the cellular defect instead of trying to replace the defective gene.

Research sponsored by the Cystic Fibrosis Foundation and the NIH led to the recent discovery that CPX - which comes from the same drug compound family as caffeine - stimulates airway cells in two ways. First, it causes cells to process more CFTR protein into the fully functional form. Second, it stimulates those proteins to work harder. Both effects appear to circumvent the cellular defect caused by the mutation, without actually fixing the genetic mutation itself.

If CPX testing proves successful, it would be a lifetime maintenance medication administered in pill form.

A pill for cystic fibrosis?



Pediatrician Mark Weatherly (at left, with a cystic fibrosis patient) is co-directing Phase II trials of a CF drug that is among the first therapies to address the disease's cause, rather than just its symptoms.


In the research world, it's hard to beat praise from a Nobel laureate. Writing in a recent issue of Science, Nobel laureate Peter Doherty touted Emory researchers for "triggering a revolution" in understanding virus-specific T cell responses by developing accurate methods to measure them.

Using novel assays described as the new "gold standard" for measuring specific immune responses to viruses, the researchers found that the response of CD8+ T cells, which provide the front line of protection against viruses, is considerably larger and much more targeted to specific viral antigens than previously believed.

Although it is well known that T cells multiply in response to viral infection, it has been difficult to measure the number of cells and exactly what they are responding to. The most common assay used to measure the response, the limiting dilution analysis (LDA) has led scientists to believe that only a small fragment (1% to 5%) of activated CD8+ T cells are responding to specific viral antigens and that most of the T cell response is a general, nonspecific one.

Georgia Research Alliance Scholar Rafi Ahmed and fellow investigators John Altman and Kaja Murali-Krishna used three assays to test the CD8+ T cell response to lymphocytic choriomeningitis virus (LCMV) in mice. They found that more than 70% of the activated CD8+ T cells responded to specific antigens of LCMV - a number they described as "remarkably high" and that was 20 to 100 times greater than numbers based on LDA.

Based on these results, the team calculated that virus-specific CD8+ T cells can expand rapidly, more than 30,000 fold (about 15 divisions) in one week, with an estimated doubling time of six to eight hours during the peak phase of the response.

Reported in last February's issue of Immunity, this research should prove important for vaccine development "because you want a vaccine to induce a good response, and this research allows us to see directly what a good response is," says Ahmed, who also directs Emory's Vaccine Center.

Ahmed believes the findings about virus-specific responses most likely will apply to viral infections in general, including Epstein-Barr virus, HIV, and human T cell leukemia virus type 1, all of which are characterized by massive increases in the number of CD8+ T cells. "It is likely that most of the expanded CD8+ T cells in these infections are also specific to those particular viruses," Ahmed says.

One of the assays used in the study, tetramer staining, was developed by Altman as a researcher at Stanford. In this technique, small peptides of the virus are placed inside an MHC (major histocompatability complex) Class I molecule. MHC Class I molecules are proteins that "present" pathogens to T cell receptors, which in turn recognize the pathogens and attack them. A tetramer consists of four MHC molecules containing particular viral peptides. Labeled tetramers are then applied to a mixture of white blood cells and bind only to those CD8+ T cells specific for the MHC 'molecules plus viral peptide' combination.

"The beauty of tetramer technology is that it can be applied to study T cell responses to any pathogen, from influenza to HIV to malaria," says Altman. "And tetramers give you both a more accurate and a much more rapid picture of the immune response." In his Science article, Doherty states that tetramer staining is "set to be the gold standard" for quantifying virus-specific CD8+ T cells.

Emory researchers also tested the CD8+ T cell response using sensitive assays that measure the production of interferon-gamma, a cytokine produced by virus-specific T cells that is important in controlling infection. The interferon-gamma assay also demonstrates a strong, virus-specific response by CD8+ T cells.

After the initial CD8+ T cell viral response, about 95% of T cells die; the remainder persist to become memory cells poised to respond to future invasion by the same virus. The assays used in the Emory study were also able to detect memory CD8+ T cells specific to LCMV more than one year after infection.

Altman's findings have confirmed this prediction for HIV infection, and he continues to investigate the CD8+ T cell response to HIV in patients on antiretroviral therapy. This work was supported by the NIH and the American Cancer Society.

Setting the gold standard for measuring immune responses to viruses



Could your appetite for food be related to the craving an addict feels for cocaine? Neuroscientists at Yerkes Regional Primate Research Center believe so.

According to results of a study reported in Synapse, the researchers discovered a novel neurotransmitter that helps control food intake and seems partially responsible for feelings of satiety. Eventually, the finding may be used to develop medications for obesity.

The neurotransmitter is called CART peptide, short for cocaine and amphetamine regulated transcript, and its role in feeding was found during rat studies on the effects of cocaine on the brain. Yerkes neuroscientist Pastor Couceyro was one of the first to notice that CART messenger RNA increased in a specific area of the brain when cocaine was administered.

"We tested the CART peptide to see if it could be responsible for appetite loss because CART is associated with cocaine, and cocaine reduces food intake," says colleague Mike Kuhar, a Georgia Research Alliance Scholar and chief of the Neuroscience Division at Yerkes. "Also, CART peptides are found in regions of the brain that control food intake."

When researchers injected the CART peptide into the brains of normal rats, food intake dropped as much as 30%. The peptide was present in high levels in the hypothalamus, meaning that "CART apparently is involved in a variety of physiologic processes, not just in cocaine addiction," says Yerkes researcher Phil Lambert, who completed the behavioral part of the study.

Lambert then tried the flip side of the experiment: blocking the brain's naturally occurring CART peptides by injecting antibodies, which bind to the peptides and render them nonfunctional. Without CART peptides to put the brakes on appetite, the rats' feeding increased. "This antibody data makes us think CART is responsible, at least partially, for making you feel sated - whether it's after eating or perhaps after cocaine use," Lambert says.

He also found that CART interacts anatomically and functionally with neuropeptide Y (NPY), a neurotransmitter known to be a strong hunger stimulant. "We may be completing more of the food-intake picture," says Kuhar. "Although NPY has been well characterized as a catalyst for hunger, agents that mediate satiety are not fully identified. This seems to be a part of the puzzle."

To find more clues, the team is working to identify the precise structure of CART peptides and explore their role in managing body weight.

Kuhar and his colleagues believe CART peptides can also reveal much about the mechanisms of addiction and possibly even stress-related disorders because of their location in areas of the brain involved in stress.

New pieces of the food puzzle



Electron micrograph of the segment of the brain involved in addiction: the small dots within the larger circle contain "CART" peptide, a neurotransmitter that helps control food intake. Courtesy of Yoland Smith, Yerkes Primate Center.


While the thymus becomes virtually nonfunctional in older age, in children it serves the important function of producing T lymphocytic immune cells. In particular, it produces the CD4+ helper T cells that are depleted by AIDS as well as CD8+ cytotoxic T cells, both of which help the body develop a resistance to HIV and other organisms.

In a study of thymus transplants in four children with advanced AIDS, one of the children has now survived for more than four years and has no visible symptoms of the disease.

Andre J. Nahmias, director of infectious diseases in the Department of Pediatrics, believes that thymic transplants may be particularly useful for preventing opportunistic infections in a subgroup of HIV-infected infants with severe thymus dysfunction (about 15% of children with HIV).

"We have proven that the methodology of thymic transplants is simple, requiring only one day of hospitalization and little use of potentially harmful drugs to prevent rejection of the graft," Nahmias says. "No graft-vs-host rejection has occurred, and the main problem has been poor virus control and sometimes poor compliance."

Thymus transplants in pediatric AIDS


Pieces of thymus being prepared for transplant.


An Emory researcher's discovery has attracted the attention of a Memphis company that specializes in bone disorders.

Sofamor Danek Group, Inc. will develop products for potential use in bone growth, regeneration, or repair, and in gene therapy. The products will use the LIM Mineralization Protein-1 (LMP-1) gene, identified by orthopaedist Scott D. Boden, director of the Emory Spine Center. He first reported the gene and its protein products in 1997.

Cell culture and early animal studies suggest the LIM-1 gene is key to the body's ability to build new bone. Technology to grow new bone has enormous potential for orthopaedic patients, including those who undergo spinal fusions. As many as 40% of spinal fusions may fail to form adequate bone.

"The repair of fractures, reconstruction after trauma or infection, and removal of tumors all would be greatly enhanced with genetic tools to precisely control bone healing," says Boden, who conducted his research at the Atlanta Veterans Affairs Medical Center. "Eventually, we hope to re-engineer the gene to treat osteoporosis."

In June, Boden received the Volvo Award for Low Back Pain Research at the annual meeting of the International Society for Study of the Lumbar Spine, where he reported on animal studies using LMP-1 gene therapy to generate spine fusions.

He says, "Our demonstration of successful local gene therapy for spine fusion, along with ongoing work by others with intra-articular and intra-discal gene transfer, should reinforce the message that orthopaedic surgery is poised to enter the era of gene therapy."

Building new bone



Spine Center director Scott Boden is working with a company to develop and market products to help grow new bone.


Results of the first human trial to create new blood vessels in heart patients caused a stir last winter when they appeared in the journal Circulation. According to the authors of the German study, new microvessels had formed in the damaged heart muscles of all 20 patients who received a new compound for angiogenesis.

Emory School of Medicine and Beth Israel Hospital in Boston hope to achieve similar results in CHIRON, a study of adults with advanced, multivessel coronary artery disease. CHIRON is measuring the safety and tolerability of recombinant basic fibroblast growth factor (bFGF), a protein that triggers new vessel growth. Thus far, researchers have administered bFGF directly into an ischemic region of the heart muscle by injection or during cardiac catheterization. During the second half of the Phase I study, they gave bFGF to patients intravenously to compare the effects with the first method. The study involves 26 patients at Emory and 26 at Beth Israel, all of whom have at least one occluded coronary artery.

"We believe this type of treatment has the potential to become an option for patients with ischemic heart disease, who, for any number of reasons, may not qualify for angioplasty or bypass surgery," says cardiologist R. Wayne Alexander. "This use of the tools of modern biology may provide relief for patients to whom we previously had little to offer."

But there may be a catch. Angiogenesis research began with cancer investigators interested in the microvessels that form to nourish tumors. A recent New York Times article reported on a possible cancer treatment that uses drugs to keep new vessels from forming. So what would happen in the case of a heart patient who also had cancer cells? Would the angiogenesis drug for healing the heart also cause the cancer to grow?

"That's definitely one of our fears," says Emory cardiologist Nicolas Chronos. "We're screening all of our patients very extensively, including mammograms and pap smears for women and PSAs for men."

Naturally, angiogenic therapy will require further, careful study. Still, researchers are optimistic that stimulating new blood vessel growth may help heal broken hearts.

New inroads in circulation



People of Note


When recently we set ambitious goals for the direction medical research at Emory will take in the next millennium, we knew the school would need an equally ambitious research leader to ensure attainment of these goals," says Dean Thomas J. Lawley. "Robert Rich is just such a person. He is recognized internationally for his contributions to immunology research; he has been called upon by public and private institutions to help guide national science policy, and as vice president and dean of research at Baylor College of Medicine, he has proven himself a supportive and inspirational leader to academic medical researchers."

Rich assumed responsibilities in September as executive associate dean for research at the School of Medicine. In this role he oversees Emory's basic science and clinical research programs and guides implementation of the medical school's unfolding strategic plan for research.

A native of Kansas, Rich received his MD from the University of Kansas and completed an internship and residency in internal medicine at the University of Washington, Seattle. He then pursued postdoctoral fellowships at the National Institute of Allergy and Infectious Diseases and at Harvard. In 1973, Rich joined the faculty at Baylor and served there for the next 25 years, rising through the ranks to professor, vice president, and dean of research. In 1995 he was named Distinguished Service Professor at Baylor.

A major player at the national science policy level, Rich serves as adviser to the National Institutes of Health (NIH) and Association of American Medical Colleges. His research - which focuses on the biology and genetics of T cell function - has been continuously supported by NIH since 1974. He has received an NIH MERIT award, served as program director of an NIH training grant in immunology, and served, from 1977-1991, as a Howard Hughes Medical Institute investigator.





Robert Rich


Robert Rich, MD, is the medical school's new executive associate dean for research

Following a year-long, national search, Emory has hired a chief fund-raising professional to shape strategic development objectives for The Robert W. Woodruff Health Sciences Center - including the schools of medicine, public health, and nursing, Emory Hospitals, and Yerkes Regional Primate Research Center. That person is John Blohm, who was named senior associate vice president for health sciences development in August.

Blohm works closely with Michael Johns, executive vice president for health affairs, and with the university's office of Institutional Advancement. He oversees alumni relations in the health sciences, acquisition of major gifts, prospect development, and efforts of other development executives working in key components of the health sciences.

Blohm comes to Emory from the University of Alabama at Birmingham, where he served as associate vice president for major fund development and managed the university's development staff, with primary responsibility for major gifts.

"It took a while to find the right person, but we are convinced we've done just that," says Johns. "It's a good match in every way. John Blohm has the energy, vision, and experience we need to take the Woodruff Health Sciences Center to a new level of support. He knows who we are and where we've been and is convinced that opportunities for growth here are strong."

For his part, Blohm says one of the first things he intends to do is to rebuild the medical school's development program, missing a director since the death of Bonnie Brown Johnson in the spring of 1997. He also hopes to more closely involve the leadership and faculty of the medical school in the important work of fund-raising. "I think it's a privilege to be able to support something in which you truly believe," he says. "It's equally a privilege to help potential donors - alumni, patients, or citizens concerned about health issues or excited by research - to learn about things at Emory which match their own interests."


John Blohm


John Blohm, senior associate vice president for health sciences development

The medical school's brand-new Department of Urology will be guided by a veteran urologic oncologist recruited from Johns Hopkins. Fray F. Marshall - a urology leader at Hopkins for nearly 25 years - is one of the nation's top urologic surgeons and clinical researchers in urologic cancers.

"The Division of Urology at Emory, under the leadership of Sam Graham, attained a national reputation for clinical excellence," says Dean Thomas J. Lawley. "Following Dr. Graham's recent departure to join his brother in private practice, we began searching for a replacement of top rank. It soon became evident we would be unable to attract such a person until the division was granted full departmental status."

That request was granted by the university in early September, allowing the dean to finalize efforts to bring Marshall to Emory by the end of the fall semester.

"I consider Fray - as does most of the medical community - to be this country's outstanding scholar-physician in academic urology," Lawley says. "He was our first choice by far as someone who could build on the excellence of our existing clinical programs within the pediatric, adult, and elderly populations; who could strengthen the successful programs we already have in prostate cancer, incontinence, and cryosurgery; and who could develop first-rate programs in teaching and basic scientific research."

David Blake, associate director of Emory's Woodruff Health Sciences Center, was a colleague of Marshall's at Hopkins for more than 20 years. "The Department of Urology that Fray Marshall and Department Chair Patrick Walsh built at Hopkins is the most successful and well respected one in the country," says Blake. "A clear benchmark of departmental excellence is to look at the number of physicians who have gone through a particular program and now head up departments at other health care centers. In the field of urology, Drs. Walsh and Marshall have been most successful in that regard."

Fray Marshall earned his MD at the University of Virginia in 1969. He completed an internship and assistant residency in surgery at the University of Michigan, Ann Arbor, and a residency in urology at Massachusetts General Hospital. He joined the Hopkins faculty in 1975, rising to the rank of professor of urology in 1986 and professor of oncology in 1995. He was the incumbent holder of Hopkins' Bernard L. Schwartz Distinguished Professorship in Urologic Oncology.

Fray Marshall


Fray Marshall, MD, chair of the medical school's recently established Department of Urology


Last August, Dean Thomas J. Lawley momentarily realized his childhood dream of becoming a baseball star when he threw out the first pitch in a game between the Atlanta Braves and the San Francisco Giants. The event was to inaugurate Emory Healthcare's second year of providing health services for Turner Field.
The dean's pitch

 


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