Neema Yazdani is one of two graduate students selected for the 2015 “Outstanding Graduate Student Travel Award” for the 17th Annual International Behavioral and Neural Genetics Society (IBANGS) Meeting in Uppsala, Sweden. Neema is a third year PhD candidate and Program in Biomolecular Pharmacology student in the Laboratory of Addiction Genetics under the mentorship of Camron D. Bryant, Ph.D., Assistant Professor of Pharmacology and Psychiatry. As a recipient of this award, Neema is invited to present his research as an oral presentation titled, “Hnrnph1 is a quantitative trait gene for methamphetamine sensitivity”. Neema’s efforts in generating and phenotyping TALENs-targeted Hnrnph1 knockout mice combined with striatal transcriptome analysis via RNA-seq led to the identification of Hnrnph1 as a novel quantitative trait gene involved in the stimulant response to methamphetamine. His transcriptome results suggest that Hnrnph1 could regulate the neural development of the mesocorticolimbic circuitry which would have widespread implications for understanding the etiology of a variety of neurobiological disorders involving a dysregulation of dopamine transmission.
Dr. Carol Walsh Presents BUSDM Dental Pharmacology Integrated Problem Session to ADEA Annual Meeting
Carol Walsh, Ph.D., Pharmacology Vice Chair for Education, presented a description of the innovative Integrated Problem Sessions of the BUSDM Dental Pharmacology course at a symposium held March 9 at the American Dental Education Association (ADEA) annual meeting in Boston. The symposium, organized by Aldo Leone, D.M.D.,Associate Dean for Academic Affairs at BUSDM, was entitled “Igniting Minds through Student Self-directed Group Learning: Integrated Problem Sessions” and included presentations by Dr. Leone, Drs. Whitney and Pessina from the Anatomy and Neurobiology Department, and Dr. Sarita-Reyes from the Pathology Department. The presenters were honored by special recognition of the symposium by the Chair of the ADEA Board of Directors.
University-wide Graduate Program for Neuroscience Receives BU Provost’s CEIT Interdisciplinary Course Development Grant
Congratulations go to Shelley J. Russek, Ph.D., Professor Pharmacology & Experimental Therapeutics and Biology, and the University-wide Graduate Program for Neuroscience (GPN) on being awarded the Boston University Provost’s Center for Excellence and Innovation in Teaching (CEIT) Interdisciplinary Course Development Grant. As GPN Director, Shelley spearheads a university-wide team of outstanding faculty who do an exceptional job in preparing graduate students for careers in neuroscience.
GPN is a University-wide Ph.D. degree granting program uniting the graduate training faculty of the BU Charles River Campus and the BU Medical Campus to serve as the nexus point for all neuroscience training missions at Boston University.
Neil J. Ganem, Ph.D., Assistant Professor of Pharmacology & Experimental Therapeutics and Medicine at the Boston University School of Medicine, has received a 2014 Smith Family Foundation Award for Excellence in Biomedical Research.
This prestigious, highly competitive three-year award of $300,000 is intended to help launch the careers of newly independent biomedical researchers. Since 1992, the program has funded 130 investigators for a total investment of $23 million. Applications focus on all fields of basic biomedical science as well as research in physics, chemistry and engineering. Applicants, who are nominated by their institutions, must be full-time faculty at nonprofit academic, medical, or research institutions.
Dr. Ganem received his Ph.D. from the Geisel School of Medicine at Dartmouth and was a postdoctoral fellow at the Dana-Farber Cancer Institute/Harvard Medical School. His research focuses on the causes and consequences of chromosomal instability, broadly defined as the persistent acquisition of both numerical and structural chromosomal aberrations. Chromosomal instability is a hallmark of solid cancers and is known to facilitate tumor initiation, progression, and relapse. The Smith Family Foundation Award will support Dr. Ganem’s research to examine how cancer cells adapt to abnormal chromosomal content.
Boston University Medical Campus is located in the historic South End of the capital city of Massachusetts. Well-known for the high quality of teaching, research, and community service, the school provides an exceptional learning environment for its students in the heart of the city.
Article originally posted on BestMedicalDegrees.com.
Junior faculty arrive at Boston University full of ambition and with a head full of ideas, but they often have relatively little money for research. So being awarded a Peter Paul Career Development Professorship can feel like winning the lottery; winners receive an annual stipend of $40,000 for three years to pursue their research interests.
For some, it can even seem too good to be true.
“Once I received the email, I asked if they had the right Professor Gonzales,” says Ernest Gonzales, a School of Social Work assistant professor of human behavior. Gonzales, who had no idea that he had been nominated for the award, says the reply from the provost’s office was immediate: “Yes, Ernest, it’s you!”
Peter Paul Professorships were also awarded to Rachel Flynn, a School of Medicine assistant professor of pharmacology and experimental therapeutics, and to Jacob Bor, a School of Public Health assistant professor of global health at the Center for Global Health & Development. University trustee Peter Paul (GSM’71) created the professorships named for him in 2006 with a $1.5 million gift, later increased to $2.5 million. Jean Morrison, BU provost, and President Robert A. Brown select recipients from faculty who are holding their first professorship, have arrived within the last two years, and have been recommended by deans and department chairs.
“It is a privilege to witness the development of talented young scholars into outstanding teachers and researchers,” says Morrison. “From the discovery of novel new cancer treatments and effective approaches to the HIV epidemic to improving conditions for an aging workforce, Professors Bor, Flynn, and Gonzales are fulfilling—and in many ways exceeding—the promise we saw in them when they joined the BU community. We are enormously proud of the important work they’re performing and excited to help advance their research careers.”
Gonzales, who earned a doctorate from Washington University in St. Louis, arrived at the University in July 2013. He is still thinking about how to use the award. He currently juggles several interdisciplinary research projects that focus on productive aging, structural discrimination in and outside of the workforce, and “unretirement”—the practice of retirees returning to work.
His initial findings suggest that the groups most vulnerable to ageism are workers under 30 and those 55 and older. Employees who fall within these ranges face social exclusion and questions about their professionalism or competence. Gonzales is also examining how early life experiences can predict difficult work trajectories later in life. Someone who enters the workforce at 17 with a high school diploma will likely work more physically demanding jobs—such as construction and manufacturing—that wear on their bodies and make it difficult to remain in the workforce long-term.
Gonzales also compares US practices to those in European countries, like Germany, where Chancellor Angela Merkel’s government recently enacted a policy that allows people who have worked 45 years to retire with full benefits. He believes these individuals will relax, recuperate, and eventually return to the workforce—a theory he’s calling “Triple R.”
“I think we have a lot to learn from other nations,” says Gonzales, who would like to conduct cross-national research to see how this and other productive aging policies affect workers’ health and economic standing, with the eventual goal of proposing policy and legislation in the United States.
Flynn, who earned a doctoral degree in cancer biology from the University of Massachusetts Medical School, has been at BU since June 2013. She studies the role telomeres, repetitive DNA sequences that cap the ends of chromosomes, play in cancer development. Each time a cell divides, Flynn says, it loses a chunk of telomere instead of more essential genes further upstream. When telomeres get too short, cells either stop growing or die.
“That is the aging process,” she says. But cancer cells have a way to “highjack this mechanism. When a telomere starts to get shorter, cancer outsmarts it” by reactivating the mechanism that keeps it growing forever.
Telomeres maintain their length using two pathways. Flynn’s lab studies the pathway used by osteosarcoma and glioblastoma—rare and lethal cancers of the bone and brain—and hopes to identify novel treatments that would target this highjacked pathway to better manage the cancers.
So far, Flynn has seen promising results. One compound she’s testing in vitro doesn’t just stop cancer cells from growing, but completely obliterates them—and with minimal effects to surrounding healthy cells. The next step is to test the compound in mouse models.
“If it works as well as it does in a dish, it’ll be amazing,” she says.
Flynn will use the award to hire lab personnel and to buy reagents. “It’s a tremendous opportunity to represent Peter Paul and have money to build my lab,” she says, “but the real goal is to raise the bar, to elevate cancer research at BU.”
Bor, who earned a doctorate at the Harvard University School of Public Health, came to BU in September 2013. He applies the tools of microeconomic models and natural experiments to the field of public health.
“Economics puts an emphasis on the individual; each person is making the best decision for themselves,” Bor says. “At least, that’s the theory.” He looks at decision-making and behavior in a larger economic context to determine what effects they have on health.
Across southern Africa, there’s an elevated HIV infection rate for young women. There are also “high levels of transactional sex,” Bor says. “Maybe if we can expand the choice set of young women so that they can make the best decisions for themselves, we can give them economic opportunities to avoid these relationships.”
In Botswana, he says, the government changed the structure of secondary school so that young women were encouraged to attend. The move resulted in a decrease in HIV infections within that population, he says.
With the award, Bor plans to recruit more doctoral students and research assistants to tackle the papers he’s been dreaming of writing, especially on questions related to South Africa’s HIV treatment program.
“The goal is to rigorously turn these out,” Bor says, “and the faster we do so, the better monies are allocated and the more lives can be saved.”Original article posted on BU Today.
Joon Y. Boon, a graduate student in the Department of Pharmacology & Experimental Therapeutics in the joint Biomolecular Pharmacology and Biomedical Neuroscience Prorgam, has won the Perdana Scholar Award from the Malaysian Department of Education.
This prestigious honor, awarded to Malaysian national students studying in the United States, “aims to identify, document, promote, and award Malaysian students who have excelled in areas such as academic, leadership, sports, entrepreneurship, inventions, and research.” The Perdana Award specifically honors a student who has attained the highest overall level of achievement.
Joon will fly to New York City later this month to receive the award in person from Malaysian Prime Minister Najib. Hat’s off to Joon Y. and her mentor for this amazing achievement! Congratulations!
The Laboratory of Cancer Cell Biology has identified the tumor suppressor mechanism that prevents the oncogenic growth of cells harboring an abnormal number of chromosomes. The study, published in the journal Cell, was led by Neil J. Ganem, PhD.
Tetraploid cells, which are a common byproduct of cell division failure, are genomically unstable and have the capacity to facilitate tumorigenesis. Recent estimates suggest that ~40% of all solid tumors have undergone a transient tetraploid intermediate at some point during their evolution, suggesting that tetraploidy plays significant roles in both the development and/or progression of human malignancies. Given the potentially oncogenic consequences of tetraploidy, it is not surprising that tumor suppression mechanisms have evolved that prevent the proliferation of these cells. However, unlike other common cellular insults that trigger cell cycle arrest, such as DNA damage, the mechanisms governing cell cycle arrest in response to tetraploidy have been poorly defined.
To understand the mechanism of growth arrest in tetraploid cells, Dr. Ganem and colleagues combined genome-wide RNAi screening and in vitro evolution approaches to comprehensively identify all of the genes required to stall the growth of tetraploid cells. Collectively, these data revealed that the Hippo tumor suppressor pathway is specifically activated in tetraploid cells, both in vitro and in vivo, and that this is the pathway that prevents tetraploid proliferation. The authors pinpointed that defects in the cytoskeleton of tetraploid cells represented the initial trigger for Hippo pathway activation. Notably, analysis of a broad spectrum of human cancers revealed that near-tetraploid tumors frequently adapt to overcome Hippo signaling, suggesting that inactivation or bypass of this pathway may be a prerequisite for the development of high-ploidy tumors. “This work may help guide the development of new therapies that specifically target tumor cells with abnormal numbers of chromosomes, while sparing the normal healthy cells from which they originated,” explained corresponding author Dr. Ganem, PhD, Assistant Professor of Pharmacology & Experimental Therapeutics and Medicine in the Shamim and Ashraf Dahod Breast Cancer Research Laboratories at BUSM.
The study was highlighted with a preview article in Cell and by the journals Science Signaling, Cancer Discovery, and Nature Reviews Cancer. The article can be read online at: http://www.cell.com/cell/abstract/S0092-8674(14)00820-4.
With sadness I share that Terrell Gibbs, PhD, associate professor of Pharmacology & Experimental Therapeutics, died Friday, August 15, at M.D. Anderson Cancer Center in his home state of Texas. A member of the BUSM faculty for 24 years, Dr. Gibbs received his undergraduate degree in biology from MIT and his doctoral training in pharmacology from Harvard Medical School. He pursued his interests in neuropharmacology, first at Downstate Medical Center in the Department of Anatomy & Cell Biology at SUNY Health Science Center in Brooklyn, NY, and then at Boston University working in close collaboration with Pharmacology Chair Dr. David Farb.
Dr. Gibbs’ research involved elucidation of the molecular mechanisms of modulation of GABAergic function by benzodiazepines and neurosteroids and of CNS abnormalities such as autism. His discoveries were revealed in more than 45 publications and many abstracts presented at the Society of Neuroscience Annual Meetings.
A recent recipient of the Excellence in Education and Mentoring Award from the Neurosteroid Congress, he played a key role in the design and implementation of the curriculum for the Biomolecular Pharmacology Predoctoral Training Program at Boston University and guided innumerable PhD candidates. He taught medical, dental, and master’s degree students at BU the principles of pharmacology and the actions of drugs affecting the peripheral and central nervous system. All medical students over the past 23 years have learned the principles of pharmacodynamics under his tutelage.
His interest in pharmacologic research in many areas and rational evaluation of evidence of drug efficacy and safety were hallmarks of his approach as an educator and served as an outstanding role model for both students and faculty.
Dr. Gibbs also was renowned for his expertise in the martial arts, which he occasionally practiced on the Talbot Green.
He will be greatly missed by his students and his faculty and staff colleagues.
He is survived by his step-mother, brother and sister, half-sister and half-brother, and nieces and nephews.
To make a donation in memory of Dr. Gibbs please click here.
Researchers at Boston University School of Medicine (BUSM) have uncovered important clues about a biochemical pathway in the brain that may one day expand treatment options for cognitive deficits seen in schizophrenia. The study, published online in the journal Molecular Pharmacology, was led by faculty members David H. Farb, PhD, Terrell T. Gibbs, PhD, and Shelley J. Russek, PhD in thedepartment of pharmacology & experimental therapeutics at BUSM.
Patients with schizophrenia suffer from a life-long condition that can produce cognitive deficits, delusions, disordered thinking, and breaks with reality. A number of treatments are available for the treatment of schizophrenia, but many patients do not respond to these therapies or experience side effects that limit their use. There is no current treatment for the cognitive deficits experienced in schizophrenia.
The healthy brain is made up of billions of cells including the primary signaling cells called neurons, that are responsible for managing everything the body does: including movement, eating behavior, and memory formation. These neurons acts like a miniature computer and are controlled by substances called neurotransmitters that, like bits in a computer chip, may be “turned on” or “turned off” depending on the specific signals being integrated. Neurotransmitters latch onto a cell via a specific receptor, like a key fits into a lock.
In schizophrenia, it is thought that certain neurons don’t “turn on” as well when exposed to a certain neurotransmitter, the amino acid glutamate, may not be sensed by one of its key receptors (the NMDA receptor) whose diminished function may be the possible culprit for these sluggish cells. It is thought that this deficit can at least partially be responsible for symptoms seen in schizophrenics.
Currently the therapeutic means for making these cells more “sensitive” to glutamate can be toxic to the brain.
In this study, researchers discovered that another, naturally occurring steroid within the brain, known as PregS, may be able to bypass this toxic effect, and “turn on” neuron communication safely through a novel mechanism. The implication is that a deficit in the amount of this novel steroid may underlie deficits in signaling and that stimulation using therapeutics that elevate its levels in the brain may decrease or eradicate some of the debilitating symptoms seen in schizophrenia.
Although still in the early stages, further research in this area may be instrumental in the identification and development of treatments not only for schizophrenia, but also for other neurological conditions, such as age-related decreases in memory and learning ability.