Midsummer Nights' Science 2015

Midsummer Nights' Science is an annual lecture series that explores key advances in genomics and medicine. This lecture series is held each summer, and is free and open to the general public. Midsummer Nights' Science at the Broad Institute takes place at 415 Main Street (formerly 7 Cambridge Center), in Kendall Square in Cambridge.

2015 Lecture Schedule:

Wednesday, July 8, 6-7pm
Immune mechanisms of synapse loss in health and disease[ video ]


How synapses are eliminated in the developing and diseased brain remains a mystery. During development, synaptic pruning is required for precise wiring, and emerging evidence implicates immune-related molecules and immune cells called microglia. This talk reviews research on how these pathways regulate the formation, refinement, and elimination of specific axons and synapses during development. The discoveries suggest ways of protecting synapses in neurodegenerative and psychiatric disorders involving synapse loss.

Beth Stevens
Beth Stevens is an assistant professor at Harvard Medical School in the FM Kirby Neurobiology Program at Boston Children’s Hospital. She is also a member of the Broad Institute and the Stanley Center for Psychiatric Research. Her research investigates the mechanisms by which synaptic connections in the brain are formed and eliminated in health and disease.

Stevens received her Ph.D. in neuroscience in 2003 from the University of Maryland, College Park. She performed her dissertation research at the National Institute of Child Health and Human Development (NICHD) in the area of neuron-glia interactions. During her postdoctoral work with Ben Barres at Stanford University, she discovered that the classical complement cascade, part of the innate immune system, mediates the pruning of inappropriate synaptic connections in the developing brain.

In 2008, Stevens established her independent laboratory in the Neurobiology Program at Boston Children’s Hospital, where she is using a combination of live imaging, molecular, biochemical, and neuroanatomical approaches to investigate the molecular mechanisms by which immune molecules and immune cells called microglia prune synapses in health and disease. Her recent work demonstrates immune-related pruning pathways mediate aberrant synapse loss and dysfunction in neurodegenerative diseases (e.g., Alzheimer’s and Huntington’s disease) and neurodevelopmental disorders, including autism. Stevens hasbeen the recipient of several awards including the Presidential Early Career Award for Scientists and Engineers, Ellison Medical Foundation New Scholar Award, and John Merck Scholar Award.
 

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Wednesday, July 15, 6-7pm
Understanding and controlling malaria through evolution[ video ]


Malaria is a disease of seemingly gratuitous complexity, caused by Plasmodium parasites which must complete intricate phases of their life cycle in two very different hosts: vertebrates and mosquitoes. Understanding the adaptations that facilitate and maintain the relationships between the members of this co-evolutionary triangle can give us insight into the fascinating biology of malaria, and also provide keys to controlling or eventually eliminating this disease. Daniel Neafsey, associate director of the Broad’s Genomic Center for Infectious Disease, will describe how recent developments in genome sequencing are giving us new perspectives on malaria, a disease that has been called the strongest known force of evolutionary selection in the recent history of the human genome.

Dan Neafsey
Daniel Neafsey joined the Broad in 2004 and is now associate director of the Broad Institute’s Genomic Center for Infectious Disease, where he leads a group that focuses on the genomics of malaria parasites and mosquito vectors. He is excited by the potential for new technology and bioinformatic approaches to turn the tide against disease like malaria. Neafsey’s current projects involve the application of comparative genomic and population genetic analyses to Plasmodium malaria parasites and Anopheles mosquitoes to study population structure, natural selection, and genomic factors underlying parasite and vector phenotypes that impact public health. Neafsey’s interests also include the use of pathogen polymorphism data to inform vaccine design and understand vaccine efficacy; analysis of drug resistance mechanisms and evolution; the use of clinical genotyping data to interpret disease transmission dynamics; and the development of new genomic protocols and informatic tools to address key questions in infectious disease and global health.

Before joining the Broad, Neafsey received his B.A. at Loyola University (Chicago) and completed his Ph.D. at Harvard University, with a focus on population genetics and genome size evolution of pufferfish (a short-lived model organism for genome studies and exceedingly minor threat to public health). He received the Broad’s inaugural Excellence Award in Science/Engineering in 2013.

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Wednesday, July 22, 6-7pm
Understanding our genes, with big help from small RNAs [ video ]



While we've had the parts list of the human genome (the 3 billion As, Cs, Gs, and Ts that make up our genetic code) for over a decade, the functions of most genes remains obscure. Yet knowing what genes do is critical for understanding how their dysfunction leads to disease and thus how to develop therapeutic interventions. In this talk, Doench, a senior group leader in the Broad’s Genetic Perturbation Platform, will describe how scientists “break” genes in order to discern their function, using tools re-purposed from the ancient and ongoing evolutionary struggle between organisms and deviant nucleic acids such as viruses. He will also show how the application of these tools can provide insight into biological problems, with an example from recent work focused on malaria.

John Doench
John G. Doench is a senior group leader in the Genetic Perturbation Platform at the Broad Institute. He develops and applies the latest approaches in functional genomics -- including RNAi, ORF, and CRISPR technologies -- to understand the function of genes and how gene dysfunction leads to disease. Doench collaborates with researchers across the Broad, the Boston community, and the world to develop faithful biological models and execute genetic screens.

Prior to joining the Broad in 2009, Doench did his postdoctoral work at Harvard Medical School and received his Ph.D. from the biology department at MIT. A history major at Hamilton College, John deeply values the broad-minded thinking and focus on written and oral presentation skills that are critical to a liberal arts education.

John lives in Jamaica Plain with his wife and daughter, where he enjoys coaching soccer, cheering on the Red Sox and Patriots, and avoiding imminent death while navigating the streets of Boston on a bicycle.

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Wednesday, July 29, 6-7pm
Finding gene mutations that protect against heart attack
and developing medicines that mimic themRegister


Heart attack is now the leading cause of death in the world. However, remarkably few medicines (e.g., aspirin, statins, and antihypertensive agents) are proven to prevent a first heart attack because most medicines fail during the drug development process. I will review an approach researchers are taking to overcome this problem: namely, leveraging the human genome as a tool for prioritizing molecular therapeutic targets for drug development. I will describe an opportunity to leverage the genome’s natural successes by: (1) scouring it for mutations that protect against disease with minimal adverse effects; and (2) developing medicines that mimic them.

Sekar Kathiresan
Sekar Kathiresan, a clinical cardiologist and human geneticist, is the director of preventive cardiology at Massachusetts General Hospital, an associate member in the Broad Institute’s Program in Medical and Population Genetics, and an associate professor of medicine at Harvard Medical School.

Sekar seeks to discover the genes responsible for inter-individual differences in risk for myocardial infarction and use this information to understand biological mechanisms and to improve preventive cardiac care.

He received his B.A. in history and graduated summa cum laude from the University of Pennsylvania in 1992. He received his M.D. from Harvard Medical School in 1997. Sekar completed his clinical training in internal medicine and cardiology at MGH. He served as Chief Resident in Internal Medicine at MGH in 2002-2003. He pursued research training in cardiovascular genetics through a combined experience at the Framingham Heart Study and the Broad Institute of MIT and Harvard. In 2008, he joined the research faculties of the MGH Cardiovascular Research Center and the MGH Center for Human Genetic Research. Sekar lives with his wife and three children in Newton, MA. His passions include Pittsburgh Steelers football and U.S. politics.


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