Tag Archives: Alvin Terry

Provost’s Perspective: New Leadership

First of all, let me take a moment to welcome everyone to the campus of Georgia Regents University and the start of the new academic year. Not only am I excited to see our returning students and the energy they bring as they pursue their academic goals, I am deeply honored that so many freshmen and their families have entrusted their university experience to GRU. More and more, we’re becoming a destination of choice for the best and brightest, not just here in the CSRA, but also in Georgia, the nation and even the world.

The start of the fall semester is also a time to reconnect with the faculty and staff who have chosen GRU as the place to put their special skills to use. We know there is great demand for the level of talent we’re recruiting across all our ranks, and I am grateful that so many wonderful colleagues continue to commit their time and expertise to GRU.

Of course, the excitement that came earlier this summer with Dr. Brooks Keel being tapped as the next president of GRU and CEO of GRHealth has been palpable. Dr. Keel has a thorough understanding of biomedical research, a track record of visionary leadership and a history with our legacy institutions that is second to none. As I’ve watched him meet with deans and faculty, students and staff, I’ve been impressed by his warmth and his ability to connect with the people within those positions.

It is indeed an exciting time to be at GRU.

And Dr. Keel is not the only new face who will have an impact on our organization. Indeed, we have recruited several talented individuals to fill other key roles in our university.

Undoubtedly, the person blessed with the best name is Dr. Quincy Byrdsong, our inaugural vice president for academic planning and strategic initiatives. Coming to us from Virginia Commonwealth University, he will be quarterbacking those complex initiatives that require great coordination and interaction with the colleges and different structural units. He will aid us all in ensuring that we have rigor and structure around our academic planning. Though we’ve always been conscious of that need, we feel he is perfectly suited to help colleges, departments, and faculty start framing the academic planning process even earlier, allowing us to consider the “what ifs” surrounding the development of, say, a particular program or major before the time comes to pitch it to those at a higher administration level.

Quincy also will take over some of the operational units that we see as being key to our strategic initiatives. Most visibly, as chief diversity officer, Quincy will also have responsibility for the Office of Diversity and Inclusion, an office that is very important to me personally and one that continues to be a national model. While the vice president for academic planning and strategic initiatives is new to GRU, it was developed to fulfill a number of critical functions for the institution, and it actually helped streamline our leadership ranks, since three previous positions – two active and one we were searching for – are being filled by this one role.

Dr. Zach Kelehear, our new dean of the College of Education, has only been on the job since July 1, but already he has started making strong, important connections throughout the community by reaching out to the schools, principals and superintendents in our regional education service area. Not only that, but his interaction with the faculty is already creating valuable and innovative ideas. The University of South Carolina’s loss is definitely our gain. And, if you want to start a conversation and see a gleam in Zach’s eyes, just ask him about another of his passions – beekeeping.

Speaking of the College of Education, former dean Dr. Cindi Chance continues to “fail retirement” and has agreed to return and offer her special leadership abilities to the Confucius Institute as its director. Her intense interest in global education in general and China in particular make her a natural to guide the Confucius Institute to the next stage of its existence at GRU.

I also want to take this opportunity to say a special thank you to Dr. Joe Tsien, for his pivotal work in developing and launching the Confucius Institute as its founding director. With the Institute now on strong footing, Joe, a world-renowned neuroscientist, felt it was a perfect time to focus more fully on his true passion – doing basic research in brain science.

We’re also proud that Joanne Sexton has moved into the role of Cyber Institute director. Not only does she have experience as an information technology expert for the U.S. Navy, but she has a deep understanding of our cyber education initiatives. The new institute is certainly in good hands.

And over in the Hull College of Business, we have the transition of Dean Marc Miller into the newly created role of executive director for economic development and entrepreneurial engagement. Entrepreneurship, economic development and community engagement are increasingly important institutional priorities, and we look forward to significant advances through Marc’s work in his new role. The national search for business dean will begin in the next few weeks, and I very much appreciate Mark Thompson’s service as interim dean until the position is filled.

Research administration is fortunate to have a familiar face in a new role – Dr. Alvin Terry joins SVP for Research Michael Diamond and adds strength to this critical unit as associate vice president for basic sciences. Alvin provides administrative oversight for lab animal services, as well as a number of other critical responsibilities.

And as an example of our continuing emphasis on enhancing student services at all levels, we’re happy to welcome David Barron, who, as associate vice president for enrollment services, will be over recruitment, admissions and financial aid, areas which are absolutely essential to our success.

This list is in no way comprehensive, nor does it adequately describe the intentional eye with which we’re considering our challenges. It’s simply a brief selection from a very long list of great people doing great things at our institution, and I hope to highlight more as the months go on. Please know that everyone’s efforts are valued and everyone’s dedication to our shared goal is admired. The success of Georgia Regents University requires all of us to give our best, and I’m confident our students, our patients and our community will receive no less.

Changes in research leadership announced

Earlier this month, Provost Gretchen Caughman and Senior Vice President for Research Michael Diamond announced some leadership changes in research.

Dr. Alvin Terry was appointed as the inaugural associate vice president for basic science research. In this role, his responsibilities will include the Division of Laboratory Animal Services and working with the senior vice president for research to provide oversight, management and growth of GRU’s research enterprise, providing oversight to GRU’s basic science core facilities and supporting the planning and implementation of GRU’s basic science research missions.

He will continue in his current position of chair of the Department of Pharmacology and Toxicology.

Effective Aug. 1, Dr. Michael Brands will be the new chair of the GRU Institutional Animal Care and Use Committee (IACUC), taking over from Dr. David Stepp.

In addition to other institutional and society service work, Brands has served on the Animal Care and Experimentation Committee and the Science Policy Committee for the American Physiological Society, served on the IACUC at Mississippi, and served on the IACUC at GRU from 2000 through 2006 and from 2010 to the present.

Nicotine metabolite amplifies action of the primary chemical messenger for learning and memory

Nicotine’s primary metabolite supports learning and memory by amplifying the action of a primary chemical messenger involved in both, researchers report.

“This is the first hint of what the mechanism of the metabolite cotinine might be,” said Dr. Alvin V. Terry, Chairman of the Department of Pharmacology and Toxicology at the Medical College of Georgia at Georgia Regents University and corresponding author of the study in The Journal of Pharmacology and Experimental Therapeutics.

While the findings show therapeutic promise for a metabolite once thought to be inactive, cotinine’s benefits don’t hold up across all learning and memory systems so Terry is already looking at analogues that would be even more broadly effective and equally safe.

The new findings indicate cotinine makes brain receptors more sensitive to lower levels of the messenger acetylcholine, which are typical in Alzheimer’s, and may boost effectiveness, at least for a time, of existing therapies for Alzheimer’s and possibly other memory and psychiatric disorders.

The neurotransmitter acetylcholine is produced by cholinergic neurons, a target in diseases such as Alzheimer’s. The first sign of damage is these brain cells start pulling back the axons that connect them, then they die, Terry said. Most Alzheimer’s drugs, including the widely used Aricept, or donepezil, help patients maintain higher levels of acetylcholine longer by blocking an enzyme that breaks it down. “This could be an extra boost,” Terry said.

Nicotine has long been known to aid learning and memory, but it’s also highly addictive with a host of side effects from nausea and vomiting to increasing blood pressure and heart rate. The side effects reflect nicotinic receptors’ presence in other areas of the brain and body and explain why its therapeutic use has essentially been limited to helping smokers quit, Terry said.

The body doesn’t make nicotine or cotinine but when the body is exposed to nicotine, from smoking, chewing tobacco or gum, or wearing slow-release patches, the liver converts it to less noxious metabolites, primarily cotinine, that can be easily eliminated in the urine. In fact, insurance physicals often include a urine test for cotinine to ensure that a potential client is a non-smoker.

Working with Switzerland research and development company HiQScreen, Terry’s research team looked at frog cells with human DNA in them that enabled them to see if a compound binds with a receptor and what kind of response it generates. They found a narrow range of cotinine concentrations that amplify the effect of the natural neurotransmitter acetylcholine.

“It works in conjunction with acetylcholine to improve learning and memory,” Terry said. Cotinine activated some of the same receptors. In related studies in rats, they also found cotinine has a synergistic effect with the commonly used Alzheimer’s drug Aricept or donepezil, which, as with most drugs for the disease, work to improve acetylcholine survival by blocking an enzyme that breaks it down. The researchers noted that it did not take a deficit in cholinergic activity, as might be found in Alzheimer’s or advanced age, to make the duo effective, a finding which potentially widens its therapeutic potential.

“It’s like a booster,” Terry said. “The holy grail is to keep acetylcholine receptors functioning.” Cotinine essentially had no effect on wide range of other pharmaceutical targets including receptors for other neurotransmitters such as dopamine and serotonin.

Cotinine was also helpful in some models that predict antipsychotic behavior, called prepulse inhibition. Patients with Alzheimer’s as well as psychiatric conditions such as schizophrenia may have trouble controlling themselves on many different levels. “One of the things that gets people put in a nursing home very commonly is psychiatric outbursts,” Terry said. “As your brain degenerates, Alzheimer’s is not just a disease of cognition. Some patients hallucinate, some have delusions, as well as aggressive behavior sometimes,” Terry said.

Cotinine has already been shown by Terry and others to be generally protective of brain cells. When brain cells are placed in a dish with amyloid, the infamous brain plaque found in Alzheimer’s, cotinine keeps them from being killed.

Terry and longtime collaborator, the late Dr. Jerry Buccafusco, found in the early 1990s that despite the short half-life of nicotine – about a half hour – monkeys taking the drug continued to benefit from memory improvements days later. That had them wondering if possibly some longer-lasting nicotine metabolite could help explain the unexpected, lasting effect. They began looking at nicotine’s major metabolite, cotinine, which has a half-life of about 18 hours, and were among the first scientists to document its positive effects in the brain.

“The body pretty much views nicotine as a poison, something unnatural that needs to be eliminated,” Terry said. “It’s a classic reaction where nicotine is converted to cotinine through an oxidative process in your liver.”

Even when purified nicotine just sits on a shelf for a few months, a natural oxidation process occurs that will convert a percentage of it to cotinine, just not as efficiently as the liver, he said. “Where there is oxygen around, there is going to be a very small amount of it formed anyway. But the liver is much more efficient at making that conversion.”

Nicotinic receptors in the brain and elsewhere got their name because nicotine was the first substance scientists found that binds to them but they are actually one of two receptor types in the body for the neurotransmitter acetylcholine.

The research was supported by the National Institutes of Health. MCG Research Scientist Patrick M. Callahan is a study co-author

Protein called YAP gives blood vessels strength, shape

Drs. Yong Wang  (foreground) and Jiliang Zhou

AUGUSTA, Ga. – A protein known to promote cancer appears to give the blood vessels strength and shape, researchers report.

When yes-associated protein, or YAP, is deleted from vascular smooth muscle cells during development, the protein makes thin-walled blood vessels that over-dilate in response to the usual pressure of blood flow, said Dr. Jiliang Zhou, vascular biologist at the Medical College of Georgia at Georgia Regents University.

“The thickness of the arterial wall decreases from three or four layers of smooth muscle cells to one or two layers,” said Zhou, corresponding author of the study featured on the cover of the American Heart Association journal, Circulation Research.

The researchers also found that YAP appears to manage vascular smooth muscle cells by controlling expression of the cell cycle arrest gene, Gpr132. During growth, YAP suppresses this suppressor then, when blood vessels walls are the right size, YAP expression decreases and Gpr132 expression increases.

“The balance shifts,” Zhou said. When the scientists deleted YAP in mice, Gpr132 expression increased and cell proliferation decreased. Conversely, knocking down Gpr132 expression increases vascular smooth muscle cell proliferation.

The study required deleting YAP from both vascular smooth muscle cells and heart cells – technology does not enable more selective removal – so the mice also were born with significant heart defects, confirming the protein’s key role in heart formation. YAP’s absence has been shown to cause, for example, ventricular septal defects, a common congenital heart defect in which a persistent hole between the right and left ventricle can lead to heart failure.

The mice in this study died shortly after birth from significant heart and vascular defects. Zhou suspects that less severe alterations in YAP may also produce aneurysms, weak points in the vascular system that often go undetected before rupturing, with benign to lethal results depending on their size and location. He and his colleagues are working on a method to selectively manipulate YAP levels in smooth muscle cells to further pursue their role in aneurysms and, ideally, find a way to easily identify and treat them.

“If you completely disrupt YAP function, you are not going to survive,” Zhou said. “But you also may experience a dose-dependent defect so your arterial walls are thinner and you can survive development but may be prone to aneurysms as an adult.”

showed that YAP plays a role in the re-narrowing, or restenosis, of the carotid artery after treatment to avoid a stroke. Those studies were published in the AHA journal Arteriosclerosis, Thrombosis, and Vascular Biology.

They found that physical injury resulting from inserting a catheter to clear the artery then inserting a stent to help keep the artery open led to YAP-mediated creation of new plaque over just two weeks in rats, which likely translates to a couple of years in humans.

“It’s a double-edged sword. You remove the plaque but you somehow create the new stress to the tissue and the smooth muscle cells respond by building plaque again,” Zhou said. Coating stents with drugs such as rapamycin, an immunosuppressive drug given to kidney transplant patients, appears to reduce or at least delay restenosis.

Zhou is working with Dr. Alvin V. Terry Jr., Chairman of the MCG Department of Pharmacology and Toxicology, to develop an anti-YAP drug that could provide another layer of protection. He’s also working with MCG Vascular Surgeon Gautam Agarwal to look at carotid artery plaque removed from patients to see if YAP, along with known culprits such as a high-fat, high-cholesterol diet, also has a role in its initial formation. YAP’s role in restenosis prompted Zhou to explore its role in normal blood vessel wall formation.

Zhou noted that YAP likely plays a similar role in blood vessel formation throughout the body and he suspects it also has a role in endothelial cells, which comprise the innermost layer of blood vessels. YAP is also known to help determine organ size; in fact, when it’s overexpressed in, for example, the liver for only a week, the organ can grow five times its usual size.

Because of YAP’s varying roles. drugs to control it will require localized delivery, which is another reason Zhou likes the idea of coating stents. YAP was originally identified in the fruit fly.

GRU Postdoctoral Fellow Yong Wang is the study’s first author. The research was funded by the National Institutes of Health.