The BUSM Pediatric Interest Group has been selected to receive the inaugural...
Barry M. Manuel, MD, Associate Dean for Continuing Medical Education from 1980 to 2014 and Professor of Surgery from 1982 to 2014 at BUSM, has been honored by the Massachusetts Medical Society with its 2015 Award for Distinguished Service to the Massachusetts Medical Society. The honor is given each year to a member of the Society who has made a lasting contribution to the practice of medicine over a lifetime and who has made significant contributions to the goals of the Society.
The award, one of the most prestigious given by the Society, will be presented to Dr. Manuel at the Society’s Annual Meeting May 1 at the Seaport Hotel in Boston. It is the second major recognition from the Society given to Dr. Manuel. In 2010, he was honored with the organization’s Lifetime Achievement Award.
A member of the Medical Society since 1962, Dr. Manuel has a long and distinguished record of service with the organization. He was the Society’s 1990-1991 President, following terms as President-Elect and Vice President. He has been a member of its House of Delegates, its Board of Trustees, and many of the organization’s committees, including the Committees on Administration and Management, Finance, Professional Liability, and Occupational Health, all of which he chaired at various times over the years.
His activity in organized medicine also extended to the national level. He was a member of the Board of Governors of the American College of Surgeons from 1979-1985, was Chairman of the Board of Governors Committee on Professional Liability, Chairman of the Regents Committee on Patient Safety, and was elected president of the College’s Massachusetts Chapter in 1982-1983. He was also a member of the Massachusetts delegation to the American Medical Association for six years.
Dr. Manuel was also Chairman of the Board for 12 years of Coverys (formerly ProMutual Medical Professional Insurance Company), one of the largest medical malpractice carriers in the U.S. and upon retirement there was honored with the title of Chairman Emeritus. He also founded and served for seven years as Chairman of the Professional Liability Foundation, Ltd., an organization composed of all healthcare providers in Massachusetts dedicated to reforming the tort system. He was also honored with the title of Chairman Emeritus upon his retirement.
Dr. Manuel has spoken extensively in this country and abroad on the reform of the national system dealing with medical errors. He has published many articles on the subject in peer- reviewed literature and conducted many postgraduate courses on Professional Liability and Patient Safety for the American College of Surgeons. He has published editorials on health policy, professional liability and patient safety in leading U.S. newspapers and has written book chapters and co-edited a book on Patient Safety.
While at BUSM, Dr. Manuel was Executive Director of the Alumni Association for more than 35 years and was Faculty Councilor to Alpha Omega Alpha, the National Honor Medical Society for 23 years. He has served as a member or chairman of many medical school committees. He also served as a member of the school’s Executive Committee and the Dean’s Committee throughout his tenure.
Upon his retirement on June 30th of this year, he will be confirmed with the titles of Associate Dean, Emeritus and Professor of Surgery, Emeritus, and the Office of Continuing Medical Education will be renamed the Barry M. Manuel Office of Continuing Medical Education at BUSM.
A graduate of BUSM, Dr. Manuel has previously been recognized by the school with its Distinguished Alumnus Award and by the American College of Surgeons with its Distinguished Service Award, the highest award presented by the College of Surgeons. He is a resident of Belmont.
BUSM students hold staff appreciation lunch
BUSM students held a thank you lunch in the Hiebert Lounge on April 1 for BUSM support staff. Organized by SCOMSA, the event was an opportunity for students to express their deep appreciation for the important work of staff at the School.
“Support staff don’t always get the recognition they deserve for their hard work,” said Jaime Stull, second-year medical student and vice chair of SCOMSA. “They keep the School running, and we wanted to take the time to let them know how much we appreciate all that they do.”
“It is very kind of the students to do this for us,” said Jim Munroe, Director of Facilities Operations. “This was a tough winter and some of our staff worked 60-hour weekends. It’s great to know that the students appreciate our work.”
In appreciation for their dedication and patience during the unusually harsh winter, Deans Karen Antman, Sandro Galea and Jeffrey Hutter invited Boston University Medical Campus staff and faculty to the Equinox Celebration of Spring on Wednesday, March 18, in the Hiebert Lounge.
Photos courtesy David Keough (BUMC Educational Media) and BUSM Communications.
Boston University’s (BU) Biomedical Laboratory and Clinical Sciences (BLCS) Program and the Center for Regenerative Medicine (CReM) were awarded grants from the Massachusetts Life Sciences Center as part of a $17M package targeted for capital projects, equipment and supplies.
“We are delighted that both the Center for Regenerative Medicine (CReM) at Boston Medical Center (BMC) and Boston University School of Medicine as well as the Biomedical Laboratory and Clinical Sciences (BLCS) Program have received this honor from the Massachusetts Life Science Center,” said Karen Antman, MD, dean of Boston University School of Medicine and provost of Boston University Medical Campus. “Their investments in these programs will help patients with pulmonary hypertension, cystic fibrosis, and acute lung injury as well as provide students with the necessary equipment as they train for careers in the biotechnology field,” she added.
CReM was awarded $1.7 M to launch an expansive Lung Regeneration Initiative (LRI) as part of their Center for Regenerative Medicine. The goal of the LRI is the clinical application of recent BU-led discoveries in stem cell research, such as the treatment of lung diseases with personalized therapeutics, as well as the ultimate reconstitution of diseased lung epithelia in patients with emphysema. The LRI also aims to define and launch treatments for pulmonary fibrosis, pulmonary hypertension, cystic fibrosis and acute lung injury from inhaled pathogens.
The BLCS Program, which is offered by BU’s Metropolitan College in collaboration with the School of Medicine, received $180,000 in funding to enhance the quality of the training and add to the competencies of the students. The funding from MLSC will enable the BLCS program to obtain essential equipment: a small bioreactor, an HPLC protein chromatography unit and a small bench top fluorescence activated cell analyzer, as well as to implement an electronic laboratory information and management system to train students for the changing environment for record keeping in the biotech industry.
David Salant, MD, professor of Pathology and Laboratory Medicine at Boston University School of Medicine (BUSM) has been named as the 2015 recipient of The Donald W. Seldin Award. The Award recognizes excellence in clinical nephrology.
“Dr. Donald Seldin is one of the giants of Nephrology and his legacy is reflected in the successes of many of his former trainees that have gone on to become leaders themselves,” said Salant. “Receiving the Seldin Award is a singular honor.”
Salant, who also serves as chief, Section of Nephrology at Boston Medical Center, is supported by grants from the National Institutes of Health (NIH). He has conducted extensive research on immune disorders of the kidneys. “My research has focused on how the kidneys are damaged when our own immune system goes awry and makes antibodies that attack critical components of the kidneys,” he said.
Salant will receive the award at the National Kidney Foundation’s (NKF) Spring Clinical Meetings held March 25-29 in Dallas, Texas. The National Kidney Foundation (NKF) is the leading organization in the U.S. dedicated to the awareness, prevention and treatment of kidney disease.
The Federation of Pediatric Organizations (FOPO) has selected Boston University School of Medicine Professor and Chair Emeritus of the Department of Pediatrics Barry S. Zuckerman MD as the 2015 recipient of the Joseph W. St. Geme, Jr. Leadership Award. Dr. Zuckerman will receive this award April 25 at the Pediatric Academic Societies Meeting in San Diego.
FOPO is a national non-profit organization whose mission is to promote optimal health for children by uniting the efforts and expertise of its member organizations to accomplish shared goals.
Created in honor of St. Geme to recognize a pediatrician who is a role model for others to emulate as a clinician, an educator, and/or an investigator, recipients have had a record of broad and sustained contributions to pediatrics that have had or will have a major impact on child health. Most importantly, the award recognizes those individuals who have “created a future.”
Zuckerman is recognized for his tireless efforts to understand how social and environmental factors adversely impact children, and to create practical, scalable and sustainable tools that allow pediatric practitioners to intervene to improve developmental outcomes. In addition to his role at BUSM, Zuckerman is Professor of Public Health at Boston University School of Public Health. He has authored 250 publications, more than 130 of them peer-reviewed, and edited 12 books, including a leading book on Developmental and Behavioral Pediatrics, now in its third edition. His leadership and mentorship lead to the creation of Medical Legal Partnerships for Children, HealthLeads, Reach Out and Read and Healthy Steps, all of which focus on improving outcomes in our most vulnerable patients. This body of work has changed the face of pediatric practice, particularly in the places that care for our most vulnerable children.
MED neurologist on battered brains, tangled tau, and the future of sports
For Ann McKee, every brain tells a story. And sometimes it’s a tragic one. McKee, a School of Medicine professor of neurology and pathology, is the director of neuropathology for the Veterans Affairs New England Health Care System and also directs BU’s Chronic Traumatic Encephalopathy Center. Chronic traumatic encephalopathy (CTE) is a degenerative brain disease found in athletes with a history of repetitive brain trauma. McKee first identified its telltale mark—tiny tangles of a protein called tau, clustered around blood vessels—in the dissected brain of a boxer who had been diagnosed with Alzheimer’s disease.
Although most people associate CTE with professional football players, McKee has found it in the brains of soccer, hockey, rugby, and baseball players as well. Her research has alerted the public to the long-term dangers of repetitive hits in sports and raised tough questions about safety. McKee was invited to speak about this growing public health concern at the annual meeting of the American Association for the Advancement of Science, the world’s largest general scientific society, held February 2015 in San Jose, Calif. She told BU Today the story behind her discovery of CTE, and what it might mean for the future of sports.
BU Today: You’re a world expert on tau protein, which has been implicated in Alzheimer’s, CTE, and other brain diseases. Have you studied tau your whole career?
McKee: Yes. I love tau.
It’s beautiful, the way it collects throughout the nervous system and just sort of fills up the nerve cell. It’s always been quite lovely to look at, visually captivating. I mean, how crazy is that? But it’s true.
When you started studying tau, you were studying Alzheimer’s disease?
I was interested in Alzheimer’s, but I also worked on PSP (progressive supernuclear palsy), and something called corticobasal degeneration.
Those are not so famous.
No, they’re not so famous. But I got very involved in defining what these individual diseases looked like. It’s like being at the Smithsonian and being really interested in one collection of pottery or something. And once you start understanding it, you start seeing all these differences, and it’s like, Whoa!
Do you remember the first time you saw a brain with CTE?
Yes. It was phenomenally interesting. The first case was Paul Pender, a professional boxer here in the Boston area. He had twice been world champion. That was my first time seeing it under the microscope. I looked at the slide and it was like, Oh, my God. This is so amazing. I’ve never seen anything like this. It just blew my mind. That was 2003.
How did it look different than, say, a brain with Alzheimer’s?
Alzheimer’s disease has these beta amyloid plaques that look like small puffs of smoke throughout the brain. You have to have these plaques in fairly high numbers to make the diagnosis of Alzheimer’s disease. In most cases, and certainly below the age of 50, CTE doesn’t have any plaques. The other difference is the tau pattern. Tau clusters in little tangles, and in CTE they’re always around blood vessels. So the blood vessels are a clue to the origins of CTE—we think it might be damage to the vessels and leakiness of the vessels that’s causing it.
How did you end up with this boxer’s brain?
He was a veteran and died at the Bedford VA with a diagnosis of Alzheimer’s disease. And there was no amyloid, so it was like, well, it’s not Alzheimer’s disease. And the tau pattern was so unusual that I asked my technician to do this very old technique that people used to use in neuroanatomy before everything was automated. It’s difficult—you cut the brain very slowly in these big sections that contain the whole hemisphere, then you have to stain it while it’s floating in water, and then you have to very painstakingly lay it all out on the slide. It was amazing, because it allowed you to see the landscape of the brain. So it’s phenomenally informative. It allows you to see nuances that you can’t really appreciate with tinier, thinner specimens. The technique contributed to our recognition that this was really something quite extraordinary. This was something really different.
That was 2003. Was CTE a known disease?
Not really. It was primarily called dementia pugilistica and most people thought it affected only boxers. Then, in 2008, I had the opportunity to look at a football player who had had some cognitive issues, and it was like, Oh, my God, another one. And what I couldn’t believe was that the football player was 45. If you’re used to studying neurodegenerative diseases, 45 is incredibly young. So after that case, we started the center and started collecting more brains. The next brain we got was from a football player who died at the age of 45, too. And it was the same disease. It was like, What? Holy Christmas.
And you now have 240 brains in the CTE bank. Are most of them football players?
Yes. We have more football players in the bank than any other sport. But we have boxers, we have hockey players, we have a few soccer players, a couple of rugby players. We have military.
When CTE started coming into the public perception, it was just about the NFL. Now it’s getting bigger and bigger.
That’s exactly right. We’ve seen it in all these professional players, but we’re finding it in nonprofessional players, college players. And I think, from the public health perspective, that’s what’s really important.
Are there implications for kids’ sports?
There’s a lot of interest now in heading in soccer, because that would be something easy to take out. It wouldn’t destroy the game, especially at the lower levels. But also in football, which is such a hugely popular sport, we need to understand the risks for young athletes and reevaluate whether or not young kids should even be playing this game. Their bodies are immature, their necks aren’t very well developed, they’re not very coordinated. Plus, they’re literally walking bobbleheads with big heads, thin necks, and small bodies. Your brain is adult-size by age four, and it’s relatively heavy for those little bodies. The only good thing is, they’re low to the ground.
What surprises you most about CTE?
The thing that is shocking to me, and continues to be shocking, are the 25-year-olds who have died with this disease. Not because of it—it’s usually a suicide or an accidental death. I can’t say that CTE caused their suicide. But for me, it’s shocking to see neurodegenerative disease in a 25-year-old. It’s horrible. And it’s undeniable. We’ve seen it in enough 20-somethings now that you can’t escape this. It’s a shock to think, that guy looks so young, and he’s dead. And he’s dead with this.
A version of this story appears on the BU Research website.
This BU Today story was written by Barbara Moran. She can be reached at firstname.lastname@example.org.
Deborah A. Frank, MD, BUSM inaugural Professor in Child Health and Well-Being, Pediatrics, has been named to the National Commission on Hunger by the U.S.Congress. Frank is director of the Grow Clinic for Children at Boston Medical Center (BMC) and founder and principal investigator of Children’s HealthWatch, a network of pediatric and public health researchers working to improve child health. A highly respected national authority, she has testified before both the United States and Massachusetts legislatures on the growing national problem of hunger and its effects on children. Learn more at https://hungercommission.rti.org/.
Deeper understanding of telomeres may lead to targeted cancer treatments
By a quirk of biology, every time an adult cell divides, a bit of DNA gets lopped off the end of the double helix. This seems like a recipe for disaster—imagine a crazed librarian ripping the last chapter off a book every time it got checked out. Soon, the book would be useless. So would truncated DNA, if not for structures called telomeres, long sequences of repetitive base pairs—the same meaningless TTAGGG over and over—that cap each end of our DNA. Every time a cell divides, it’s a bit of telomere that gets chopped off, rather than vital genes.
But biologists have long understood telomeres to be a double-edged sword. When they get too short, cells stop dividing. We see this as aging: hair turns gray, skin sags. But some cells are able to keep their telomeres long, effectively becoming immortal and dividing forever. Sometimes, the immortal cells become a cancer.
Now, scientists led by Rachel L. Flynn, a Boston University School of Medicine (MED) assistant professor of pharmacology and experimental therapeutics and medicine, have found a new way to kill certain cancers by targeting mechanisms of telomere elongation. The research, funded by the National Institutes of Health, the Foster Foundation, and the Karin Grunebaum Cancer Research Foundation, and published in the January 15, 2015, issue of Science, may lead to new therapies for certain rare and deadly cancers that often appear in children.
Cells that are able to lengthen their telomeres, and thereby divide indefinitely, use two known methods to do so. The more common is to use an enzyme called telomerase, which is active in embryonic stem cells but repressed as cells become specialized. The less common method, and the one Flynn studies, is called ALT, for alternative lengthening of telomeres. The ALT pathway is most prevalent in certain cancers, including pediatric osteosarcoma, a bone cancer, and glioblastoma, a type of brain cancer.
“In terms of the possible clinical applications, this research could be a game changer,” says Karen Antman, MD, provost of BU Medical Campus and dean of Boston University School of Medicine. “This exciting finding could allow us to target any cancer that uses the ALT pathway to maintain telomeres. Such cancers are often resistant to common treatment options and have a poor prognosis.”
The ALT pathway, though discovered almost two decades ago, is still poorly understood, says Flynn. “We know that ALT is a mechanism that relies on recombination—one telomere basically hijacks another and uses it to replicate and elongate itself,” she says. “But we didn’t know how the pathway was maintained until now.”
Flynn’s paper suggests how cancer cells may be able to maintain the ALT pathway—by depending on an enzyme called ATR kinase. This enzyme is what’s known as a “master regulator,” says Flynn. In a normal cell, it recognizes DNA damage when a cell is preparing to divide, and leads to either DNA repair or cell death. ALT cancer cells are constantly undergoing DNA repair at the telomere and are more reliant on ATR kinase activity than other cancer cells. Therefore, ATR promotes immortality by helping telomere elongation. Attack this enzyme, says Flynn, and you stop the cancer cell in its tracks.
“When you take ATR kinase out of the picture, it shuts down a whole chain of events,” says Flynn. “The cancer cell tries to promote telomere elongation, but it can’t, and the cell dies.”
There are several drugs already on the market that act as ATR kinase inhibitors, but none are used individually to treat these types of cancers. “The cool thing about these drugs is that the cancer cells actually die incredibly fast as opposed to just slowing down cell growth,” Flynn says. She also notes that since the drugs only affect cancer cells using the ALT pathway, normal cells should be left unharmed.
Flynn’s next step is to get the existing drugs into clinical testing for targeted use. She is working with a group at Massachusetts General Hospital who will test it on mice with glioblastomas. Eventually, she hopes, her work will lead to a new treatment for these deadly diseases.
“The dream is that this research will eventually give kids with devastating cancers an option for individualized treatment, something that will hopefully improve outcomes,” says Flynn.
This BU Today article was written by Barbara Moran. She can be reached at email@example.com.
A version of this story was originally published in BU Research.
Emelia J. Benjamin, MD, ScM, professor of Medicine at BUSM, professor of Epidemiology at BU School of Public Health, co-Principal Investigator of the Framingham Heart Study and attending cardiologist at Boston Medical Center, has been selected as the recipient of the prestigious 2015 American Heart Association (AHA) Paul Dudley White Award.
The award, named in honor of one of Boston’s most revered cardiologists, Dr. Paul Dudley White, a founding father of the AHA, is given annually to a Massachusetts physician who has made a distinguished contribution to the Association’s mission of building healthier lives, free of cardiovascular disease and stroke. Benjamin will receive the award at the Boston AHA Heart Ball on May 2. Last year BUSM faculty member Dr. Gary Balady, received the award.
Benjamin is an associate editor for Circulation, and she also volunteers as vice chair of the Heart Disease and Stroke Statistics annual publication. She is a current member of the Council Operations and the Research committees, and past chair of the Functional Genomics and Translational Biology Council, and the Genomics & Translational Biology, Epidemiology and Observational/Epidemiology Research Study Section. In 2012 and 2013 she received the AHA’s Women in Cardiology and Functional Genomics and Translational Biology national mentoring awards, respectively.
Benjamin focuses on cardiovascular genetic epidemiology, and has made major contributions in the areas of atrial fibrillation, inflammation, vascular function and echocardiography.