Devoted dachshund-lover establishes fund to improve the lives of dogs Relationships with her dachshunds comforted Friedl Summerer throughout her life, from a war-torn childhood to the passing of three husbands, and throughout her golden years in New York City.
Born in Germany in 1918, Friedl Summerer grew up in Austria, where she began life as a budding actress. World War II soon brought her career to a crashing halt, and she narrowly escaped the Holocaust by fleeing to Paris and eventually settling in New York City.
“She had three passions: dogs, children, and public broadcasting,” said Imssy Klebe, a close friend of Summerer. “She could not have children, though she always wanted to. She was extremely devoted to her dogs. All through her life she had dachshunds, which she loved in particular. I walked many evenings with her and her dachshund Sissy. She was particularly close with Sissy.”
Dr. Lewis Berman ’57 served as Sissy’s veterinarian, and Summerer left a generous portion of her estate to Cornell’s College of Veterinary Medicine, where Berman received his training.
“She knew Cornell conducted research and patient care to help prolong the lives of dogs and wanted to support those efforts,” said Klebe.
Summerer passed on April 16, 2010, leaving a bequest in honor of Sissy for more than $2.2 million to the College, to be used for direct canine care.
The Sissy Summerer Canine Care fund will help the College and the Department of Clinical Sciences support lecturer positions that have direct impact on canine patient care and student training. The fund currently supports Dr. Andi Looney, an anesthesiologist in the Pain Management Service committed to providing care and comfort to canine companions, and Dr. Brian Collins in the Community Practice Service, part of Cornell’s distinctive training program that enables veterinary students to begin practicing their hands-on skills as first-year students.
“This endowment has a very real impact on the delivery of canine patient care, which runs the gamut from routine vaccinations to advanced end-of-life care,” said Dr. Margaret McEntee, chair of the Department of Clinical Sciences. “It will also expand our ability to train future veterinarians by providing significant hands-on experience in the Cornell University Hospital for Animals through the Community Practice Service as a core component of the veterinary curriculum. This is a great opportunity for them, and I think is invaluable for their training as future veterinarians.”
A conversation with Dr. Santiago Peralta, veterinary dentist, oral surgeon, and
new Lecturer in the Department of Clinical Sciences’ Section of Dentistry.
What path led you to your new position?
I grew up and studied in Colombia, South America, and graduated with a veterinary degree from La Salle University in 1999. In Botoga I worked in private practice for seven years and became interested in dentistry and oral surgery. As my interest grew, I decided to pursue further study in this specialty and completed a 3-year residency in veterinary dentistry at UC Davis between 2006-2009. Returning home, I resumed private practice until coming to Cornell in Summer 2011.
What will you offer as part of the dentistry service?
We offer state of the art dental and oral care for animal patients. Our service deals with small and large animals, and my focus will be small animals, mostly dogs and cats. I also have experience with exotic pets such as rabbits, chinchillas, and guinea pigs, as well as zoo animals including tigers, hyenas, orangutans, and more.
Our most common dental treatments deal with periodontal disease (gum disease), the most prevalent disease of animals. Other advanced dental procedures we offer include endodontics (root canals) to fractured teeth, orthodontics to correct bite abnormalities, oral surgery following facial trauma or to remove tumors.
What innovations do you bring to CUHA?
I’ve helped move our service from hand instrumentation techniques to more precise rotary root canal instrumentation techniques that provide more reliable results, higher success rates, and lower anesthesia times. These newer techniques come together with safer and more effective materials that allow success rates of therapy similar to that seen in humans.
Do you have research plans?
My main research interest involves tooth resorption, a common cat and dog disease in which the teeth degrade and disappear. Nobody has figured out why, and that is a question I’d like to pursue. I am also interested in research concerning oral tumors and oral radiology.
What do you like about your job so far?
I like the academic culture, and the opportunity to provide real clinical instruction. Interacting with students and other specialists offers a stimulating educational environment where everyone has something to learn. The opportunity to help out the community, clients, and local veterinarians is very rewarding.
Why is dentistry important and how can owners help?
Dental disease can lead not only to oral discomfort and pain, but can dramatically affect the general health of an animal. It can cause inflammation and infection that can spread to other organs or turn the blood toxic through permanent bacterial infection. Pets may stop eating, bleed from the mouth, and show discomfort.
Animals are very stoic in nature; they are good at hiding pain. Owners underestimate dental disease and often don’t realize their pets are suffering from it until it’s too late. Owners can help by bringing pets in for yearly routine oral exams, yearly or biyearly professional dental treatment. Toothbrushing is the only way to prevent periodontal disease. Just like in humans, it should be done every day.
Oral hygiene is very important for pets, and the magnitude of disease is difficult to appreciate until after treatment. The improvement in a pet’s demeanor following treatment can be amazing to see.
Toxoplasma gondii parasites can invade your bloodstream, break into your brain and prompt behavioral changes from recklessness to neuroticism. These highly contagious protozoa infect more than half the world’s population, and most people’s immune systems never purge the intruders.
Cornell researchers recently discovered how T. gondii evades our defenses by hacking immune cells, making it the first known parasite to control its host’s immune system. Immunologists from the College of Veterinary Medicine published the study Sept. 8 in PLoS-Pathogens, describing a forced partnership between parasite and host that challenges common conceptions of how pathogens interact with the body.
“Toxoplasma is an especially promiscuous parasite,” said Eric Denkers, professor of immunology. “It infects nearly all warm-blooded species, most nucleated cell types and much of the human population. Although it lives in vital brain and muscle tissues, it usually causes no obvious reaction. Infection can seriously harm people with weak immune systems, yet most hosts experience no overt symptoms because Toxoplasma has found a way to coerce cooperation.”
Famous for its manipulative powers, T. gondii has been shown to alter the brain chemistry of rodents so that they fearlessly pursue cats. Cats eat the rodents, delivering the parasites to their breeding ground in feline intestines. Similar manipulations have surfaced in human studies linking T. gondii infections to behavioral and personality shifts, schizophrenia and population variations, including cultural differences and skewed sex ratios. Denkers’ study maps T. gondii’s newfound ability to manipulate cells in the immune system at the molecular level.
“We found that Toxoplasma quiets its host’s alarm system by blocking immune cells from producing certain cytokines, proteins that stimulate inflammation,” said Denkers. “Cytokines are double-edged swords: They summon the immune system’s reinforcements, but if too many accumulate they can damage the body they’re trying to defend. An unregulated immune response can kill you.”
When immune cells meet intruders, they release cytokines that summon more immune cells, which produce more cytokines, rapidly causing inflammation. T. gondii must allow cytokines to trigger enough of an immune response to keep its own numbers in check and ensure host survival. But too many cytokines cause an overwhelming immune response that could damage the host or eliminate the parasites.
“Toxoplasma hijacks immune cells to enforce a mutually beneficial balance,” Denkers said. “Until recently we thought it walled itself away inside cells without interacting with its environment. It’s now clear that the parasite actively releases messages into cells that change cell behavior.”
To prove this, Barbara Butcher, a senior research associate working with Denkers, exposed immune cells in the lab to bacterial factors that typically stimulate the release of inflammatory cytokines.
“Cells infected with Toxoplasma produced no messages to trigger inflammation,” Denkers said. “Our colleagues at Stanford University found that Toxoplasma produces a specific protein called ROP16 to suppress inflammatory responses. Collaborating with parasitologists at Dartmouth Medical School, we found that Toxoplasma sends ROP16 to infiltrate communication channels in immune cells, causing them to lower cytokine production.
“We are excited to have found the first non-bacterial pathogen able to exert this kind of control,” said Denkers. “If Toxoplasma can do this, maybe other parasites can too. This is the first case where the whole process of immune system manipulation is close to being completely mapped out at the molecular level.”
That map may help steer future investigations into how pathogens interact with hosts, unveiling the inner workings of a spectrum of infectious diseases.
Carly Hodes ’10 is a communication specialist at the College of Veterinary Medicine.
Original Press Release:
Cornell University College of Veterinary Medicine news
Herpesviruses are thrifty reproducers — they only send off their most infectious progeny to invade new cells. Two Cornell virologists recently have discovered how these viruses determine which progeny to release.
The College of Veterinary Medicine researchers report in the Aug. 23 (108:34) issue I of the Proceedings of the National Academy of Sciences on the mechanisms of this quality-control system, which helps streamline viral reproduction to optimize its spreading.
The virologists identified proteins in the nuclear membranes of infected cells that control which viral products exit. This map could be used to identify new targets for future drugs that would hamper viral reproduction by clogging inspection pathways to trap viruses in the cells they first infect.
“When a herpesvirus hijacks a cell, it turns the nucleus into a viral production factory,” said Joel Baines, the James Law Professor of Virology, who co-authored the study with postdoctoral research associate Kui Yang. “It makes protein shells called capsids, stuffs them with viral DNA and ships them out of the nuclear membrane to infect new cells. But errors in the assembly line leave some capsids empty, without DNA, and shipping these is a waste of resources.”
When capsids bud from the nuclear membrane, they take pieces of it with them, forming protective lipid envelopes that let them move to new cells. Empty capsids can’t reproduce, so the virus only allows capsids with DNA through. How the membrane could determine whether the capsid had DNA or not was a mystery until Yang and Baines mapped its method.
“We found clamplike proteins on the surface of herpesvirus capsids that hold them together and keep them from bursting when they’re stuffed full of DNA,” said Baines. “Those with DNA have far more of these than empty capsids. We also found a protein complex living in the host cell’s nuclear membrane that binds to these structural support proteins, selecting DNA-filled capsids to pull through the membrane. Thus the virus releases only its most infectious particles.”
This streamlining process has helped herpesvirus species spread prevalently and permanently across all animal species. Eight of the 25 known viruses in the herpes family regularly infect humans, posing a leading cause of human viral infection.
Once in a body, herpesvirus stays for life. It can flare up at any time, causing symptoms and diseases, ranging from infected sores to brain inflammation, birth defects and cancers of the nose, throat and lymphatic system. Though usually not fatal, herpes can prove dangerous to patients with weak immune systems, such as those with HIV/AIDS or infants who contract HIV/AIDS from their mothers.
There is no cure for herpes, but Baines’ map illustrates a viral reproduction system that can be subverted.
“Take away either component, the capsid’s clamplike proteins or the membrane’s inspector proteins, and nothing escapes the host cell,” said Baines. “This opens the door to developing drugs that could block the interactions between these protein complexes, covering the binding sites to clog the system so that no viral particles get through. This would significantly slow or even stop the virus’s spread between cells. Our lab is now working on even more detailed maps of these proteins’ exact interaction sites that will help drug developers pinpoint precise targets to thwart viral reproduction.”
The research was supported, in part, by the National Institutes of Health.
Carly Hodes ’10 is a communication specialist at the College of Veterinary Medicine.
Growing embryos face a tight squeeze when it’s time to pack internal organs. A new study published in Nature Aug. 4 shows how simple mechanical forces between neighboring types of tissue help organs take shape and grow.
The work is among the first to uncover how an embryo develops from groups of cells into distinctly shaped organs. Though the research largely focuses on the mid-gut in chicken embryos, the findings are relevant to other vertebrates and the formation of other organs, including the heart. Such insights into how organs form could aid efforts to diagnose and prevent birth defects and diseases.
The research reveals how a vertebrate digestive system — a tube up to five times longer than the frame housing it — fits inside the body by packing itself into an organized bundle of intestinal coils. This formation, the researchers report, hinges on the growth of the dorsal mesentery, a bridge of artery-packed tissue anchoring the gut tube.
“Until now the dorsal mesentery seemed to offer only structural support; no one talked about its possible functions,” said developmental biologist Natasza Kurpios, assistant professor of molecular medicine at Cornell’s College of Veterinary Medicine and a first author with Thierry Savin and Amy Shyer of Harvard, where Kurpios conducted the study before she came to Cornell in 2009. “In adults, it’s a thin piece of tissue suspending the intestines and guiding arteries to them. But in embryos, we found that its properties aid construction by pulling back the gut and forcing it to loop.”
Using tiny surgical scissors Kurpios separated the looping gut tube from the dorsal mesentery.
“The gut instantaneously un-looped into a straight tube and the mesentery contracted like a relaxed rubber band,” said Kurpios. “Clearly the mesentery was under tension and the gut-mesentery connection had exerted tension on both that affected each other’s shape. We measured the organs’ growth rates throughout development and found that the gut tube grows far faster than the mesentery: nearly four-fold in chickens. The gut wants to grow, the slower mesentery holds it back, so the gut loops.”
At Harvard, Savin built a simple physical model using a latex sheet (to act as the mesentery) stitched to a rubber tube (to act as the intestine) to mimic the mechanical forces that create the gut looping. Experimenting with different physical properties in the two materials, Savin and colleagues developed a formula predicting the looping patterns based on the thickness and elasticity of the latex and the radius of the rubber tube.
Kurpios and her colleagues then applied the model to animals, finding that in chickens, quail, zebra finches and mice the model predicted the patterns and properties correctly. “We’ve found a simple physical explanation for what had seemed like a complex biological mystery,” Kurpios said.
By uncovering the basic mechanisms for how organs form, researchers may now begin to understand such developmental deformations as intestinal malrotation — which may cause knotting of tissue that blocks circulation — a birth defect in one in 500 newborns that can lead to death.
With the help of a newly funded grant from the March of Dimes, Kurpios says her Cornell lab is completing new research that identifies a hierarchy of specific genes responsible for gut development. “People have not understood how you can go from groups of cells to the actual shape of organs,” she said. “We are now uncovering that link.”
Other co-authors include Clifford Tabin and L. Mahadevan, both at Harvard. The research was funded by the National Science Foundation, National Institutes of Health and the MacArthur Foundation.
Carly Hodes is a writer at Cornell’s College of Veterinary Medicine.
Original press release:
Cornell University College of Veterinary Medicine news
Professor emeritus continues serving the community and the profession
If Noah’s ark sails again it could make a fruitful boarding stop in the office of Howard Evans, BS ’44, PhD ’50. A microcosm of biodiversity, this miniature museum is decked floor to ceiling with animal specimens from across the globe. Yet it models only a brief sample of the expansive zoological knowledge Evans holds. This professor emeritus is a proficient anatomist whose life is rich with stories of worldwide adventures, a tireless fascination for how life is built across kingdoms, and an equal delight in sharing this beauty with others.
“Everyone should know some anatomy because it’s the basis of how animals act and what they do,” said Evans. Since joining the Veterinary College’s Department of Anatomy in 1950, he has taught thousands of veterinarians the inside story of how animals work, with courses spanning species from farm to domestic to exotic.
With a joy in teaching as indiscriminate as his joy in nature, he advised Cornell’s undergraduate zoology club, served on 37 graduate committees, and spent 20 summers teaching the AQUAVET program for aspiring aquatic specialists. This generous collaborative spirit extended to his colleagues at the College, where he served as Secretary of the Faculty for twelve years and chaired the department of Anatomy for ten.
He has served the profession’s future through over 160 publications, including his seminal text, Miller’s Anatomy of the Dog, which he and Sandy deLahunta are currently updating to a new full-color edition. He has edited several anatomy journals, and served as consultant for anatomy programs in universities including Tufts, University of Georgia, UC Davis, and international universities in Grenada, South Africa, Zimbabwe, Taiwan, and Japan.
For Evans, retirement means more time for teaching. “Leading trips for Cornell Adult University (CAU) has been good fun, and gave me the chance to collect more specimens for Cornell’s Museum of Vertebrates,” said Evans. Since retiring in 1986 Evans has led scores of Cornell alumni across the world in over a dozen educational expeditions through CAU. Traveling to New Guinea, Australia, Tanzania, Kenya, and more, his recent Antarctic expedition introduced him to the Gentoo penguin skeleton now adorning his desk.
With bins brimming full of tangible treasures including stuffed animals, bones, fossils, and more, Evans now takes his show on tour. The energetic 88-year-old regularly presents on natural history topics across Cornell, including at Alice Cook House, where he is a Faculty Fellow and frequently dines with undergraduate residents. He and his wife, Erica, continue yearly pilgrimages to teach fish structure at Cornell’s Shoals Marine Lab, and he still gives anatomy lectures at the College.
His natural treasures and world of experience fascinate children at local elementary schools, where his visits are in high demand. Twice a week in the fall he gives classrooms a taste of nature’s spectacular show and tell.
“Teachers try to encourage kids to ask questions. But when they get excited about nature they just love to tell stories,” Evans laughed. As a storytelling scientist gifted at both these arts, Evans can relate.
Two experts from Cornell are teaming up to tackle salmonella contamination in produce, thanks to a $500,000 grant from the Agriculture and Food Research Initiative through the U.S. Department of Agriculture (USDA).
Cornell was one of 24 institutions to receive such grants to reduce food-borne illnesses and deaths from microbial contamination. Craig Altier, a salmonella specialist at the Animal Health Diagnostic Center at Cornell’s College of Veterinary Medicine, will work with Greg Martin, Cornell professor of plant pathology and plant-microbe biology and an expert on tomato disease resistance at the Cornell-affiliated Boyce Thompson Institute for Plant Research, to investigate how salmonella interacts with tomatoes with the hope of finding ways to stop its spread.
“My lab explores how salmonella interacts with animal intestinal tracts,” said Altier, associate professor of population medicine and diagnostic science. “Bacteria are very frugal creatures; they turn genes on and off only when they need to. They only turn on the genes that make animals sick when they know they’re in an animal, and we want to know how this process works in plants. We will look at which bacterial genes turn on when salmonella enters a tomato and try to figure out how to intervene.”
Unwittingly sharing our food with unseen organisms sends thousands to the hospital each year. Some 50 million Americans get sick every year after consuming food-poisoning pathogens, according to the U.S. Centers for Disease Control and Prevention, and 3,000 of those cases are fatal. Salmonella bacteria pose the biggest food-borne health threat in the United States. While the quest for cleaner food reduced cases of many food-borne pathogens during the past 15 years, salmonella infections continue to rise.
Altier will grow mutant strains of salmonella in his lab to study how the bacteria affect tomatoes when they lack certain genes. He will take strains to Martin’s lab to test them on tomato plants while Martin studies the plants’ immune responses. After running them through the course of infection, Altier will remove the salmonella from the plants to analyze in his lab.
“A number of recent salmonella outbreaks started with contaminated produce,” said Martin. “My lab studies how the tomato immune system acts against certain bacterial pathogens, and this new project will test whether the plant immune system interferes with salmonella’s ability to survive on leaves and fruits. If it does, we may be able to breed new varieties that suppress salmonella growth, which could have implications for lessening salmonella contamination in many different crop plants.”
From molecular blueprints to bacterial cities, Holger Sondermann explores biological architecture
What do sink scum, dental plaque, and streambed slime have in common? They are all biofilms, billions of bacteria banded together into a resilient community. Beyond clogging your drain, these colonies can turn equipment such as catheters, implants, and heart valves into biomedical hazards. When growing inside the body, biofilms can cause infectious diseases affecting urinary tracts infections, gingivitis, listeriosis in dairy cattle, and the infections associated with the deadly incurable lung disease cystic fibrosis.
But moving from solo life to social life requires communication. Holger Sondermann, structural biologist and student of cellular communication pathways, was determined to find out how Bacteria organize.
“Biofilms cause the majority of all chronic infectious diseases,” said Sondermann. “Once formed, they are extremely difficult to disperse. Knowing how these bacteria aggregate will help us find ways to stop them, but there was a void of information with regard to their signaling mechanisms.”
What happens when a lone bacterium decides it’s had enough of the single’s scene? Like any good Facebook user, it sends out friend requests. Discovering a social networking tool much like those we use online, Sondermann found how bacteria form biofilms by sending invitations to their neighbors. A receptor protein called VpsT accepts the request, and prepares the individual for community life.
“The next step is learning to modulate this pathway,” said Sondermann. “This could inform hospital instrument design, guiding the creation of materials that repel biofilm formation. Understanding how they grow will be crucial in developing future therapies to disperse biofilms and treat chronic infectious diseases. In the case of bovine Listeria infections, understanding these mechanisms could help improve food safety.”
Unveiling such molecular machinery requires probing proteins at the most basic level to uncover their structure. In his second line of research, Sondermann seeks the biophysical blueprints of cell signaling proteins in the brain.
“When they work right, these proteins help telling nerves what to do. When they don’t, they are associated with neurodegenerative diseases such as paraplegias, neuropathies, schizophrenia, and Huntingtons,” said Sondermann. “Our goal is to find how they are normally built in order to see what physically changes when their mutations lead to neurological diseases. Seeing these differences shows us what is physically going wrong, and may lead to better diagnostic tools for neurological disorders.”
A 2008 Pew Scholar in the Biomedical Sciences and Robert N. Noyes Assistant Professor in Life Science and Technology, Sondermann received tenure in November 2010.
“I hope to continue our lab’s work while expanding our collaborations,” said Sondermann. “We have partnered with faculty at the Dartmouth Medical School and University of California, Santa Cruz on the biofilm project, using complementary approaches and exchanging new knowledge. I also hope to intensify my interactions with colleagues in the College of Veterinary Medicine who are interested in infectious diseases, to explore how our research program can fit into the broader mission of the college to improve health across species.”
Romping through summer fields seems like a harmless pleasure for dogs, horses and humans alike. But just one bite from the wrong tick can rob an animal of that pastime. The bacteria Borrelia burgdorferi catch rides with certain species of ticks and can cause Lyme disease in animals the ticks bite. Catching the disease early is paramount because it becomes progressively harder to fight as the bacteria conduct guerilla warfare from hiding places in the joints, nervous tissues and organs of their hosts.
A new test for Lyme disease in horses and dogs, developed by researchers at the Animal Health Diagnostic Center (AHDC) at the College of Veterinary Medicine at Cornell, will improve our understanding of the disease and pinpoint time of infection, opening possibilities for earlier intervention and more effective treatment plans.
“We’ve offered Lyme disease testing for years,” said Bettina Wagner, the Harry M. Zweig Associate Professor in Equine Health and lead developer of the test, “but we have recently been able to improve our techniques with the multiplex testing procedure. The new test exceeds its predecessors in accuracy, specificity and analytical sensitivity.”
The multiplex procedure, which can detect three different antibodies produced in response to the bacteria associated with Lyme disease using a single test on the sample, eliminates the need for separate tests. In addition, it requires smaller samples and answers more questions about the disease. Multiplex technology has been used for the last decade, but the AHDC is the first veterinary diagnostic laboratory to use it to test for Lyme disease.
Different kinds of antibodies can be found in the body at different stages of infection. The new test can distinguish and measure these differences, giving more information about the timing of the disease.
The bacteria that cause Lyme disease are particularly difficult to detect, according to Wagner, because after infection they tend to hide where they can’t be found. They bury in the joints of dogs, causing arthritis or lameness. Serious kidney disease has also been associated with Lyme infections in dogs. In humans and horses, they also burrow into the nervous system, in the spine or the brain, causing pain, paralysis or behavioral changes. By the time such clinical signs appear, the bacteria are usually not in circulation anymore.
“Now we can distinguish between infection and vaccination and also between early and chronic infection stages,” Wagner said. “That was not possible before. You were able to say whether an animal was infected, but not when it was infected, or how far the infection had developed.”
The test and information the test provides can help veterinarians make advanced decisions about treatment. After the long treatment period ends, veterinarians usually conduct follow-up testing to see if it was successful.
Catherine Hackett, DVM, Ph.D., has been selected as the winner of the 2010 Storm Cat Career Development Award. The $15,000 award is presented to an early-stage scientist with an interest in a career in equine research.
Selected from numerous competitors, Hackett’s research will focus on equine stem cells in a project entitled “Temporal Analysis of Mesechymal Progenator Cells.” The research will be overseen by Dr. Lisa Fortier, a distinguished researcher, recipient of multiple Grayson-Jockey Club Research Foundation grants, and frequent recipient of Zweig funding.
“My project investigates characteristic cell surface traits of cell populations in bone marrow, particularly the cells that can form tissues such as cartilage, bone, and muscle,” said Hackett. “I look at the surface of different cell types to determine what type of mature cells they will become, such as blood or bone cells. I also study how these surface properties change over time in culture as the cells grow and respond to culture conditions.”
For patients waiting for stem cell therapy, it can take time (e.g. four to eight weeks) for cultured stem cells to divide enough times to reach clinically useful numbers. Hackett hopes to find ways to both decrease the time needed in culture before cells are ready to be implanted and to improve the ability of cells to form the correct tissue
“Stem cells from bone marrow have been used in horses to help heal injuries to tendons, cartilage, and joints, improving repair and changing the patient’s immune response to transplantation of cells or tissues from a different donor,” said Hackett. “The same applications are being investigated in humans to treat similar types of injuries as those seen in the horse. The properties of mesenchymal stem cells are still poorly understood, and we hope our research into their characteristics and behavior can help find ways to improve their clinical utility and function.”
The award is named for the Thoroughbred stallion Storm Cat, which stood at Overbrook Farm in Kentucky. Overbrook is owned by the family of Lucy Young Hamilton, a Foundation board of directors member who personally underwrites the Career Development Award.