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Events

The National Institutes of Health (NIH) campuses host a variety of events that inform, challenge, and unite the biomedical research community. IRP investigators lead or participate in many of these events, and they regularly present their work at scientific conferences at the NIH and around the world. We invite you to learn about (and possibly join us in) some of our upcoming events. Unless otherwise noted, times listed are Eastern Standard Time (EST).

Tuesday, January 24, 2017, 4:00 pm to 6:00 pm

Building 50 Conference Room

The next Demystifying Medicine course is “New Approach to Atherosclerosis from Studies of Chronic Granulomatous Disease” by John Gallin, M.D. (NIAID).  Course materials are posted at https://demystifyingmedicine.od.nih.gov. Note: materials may not be available until a week before the lecture. No registration is needed if not for credit.

The 2017 Demystifying Medicine Series, which is jointly sponsored by FAES and NIH, includes the presentation of patients, pathology, diagnosis and therapy in the context of major disease problems and current research.  Primarily directed toward Ph.D. students, clinicians and program managers, the course is designed to help bridge the gap between advances in biology and their application to major human diseases.  Each session includes clinical and basic science components presented by NIH staff and invitees. All students, fellows and staff are welcome, as well.

Wednesday, January 25, 2017, 3:00 pm to 4:00 pm (reception to follow)

Masur Auditorium, NIH Clinical Center (Bldg. 10)

Join us for "Human pluripotent stem cells in understanding genetic cardiovascular disease and effects of drugs" by Christine L. Mummery, Ph.D. Dr. Mummery is Director of the Dorris Neuroscience Center and Hahn Professor of Neuroscience at The Scripps Research Institute.

Derivation of many different cell types from human pluripotent stem cells (embryonic stem cells or HESCs and induced pluripotent stem cells or hiPS cells) is an area of growing interest both for potential cell therapy and as a platform for drug discovery and toxicity. Most particularly, the recent availability of methods to introduce specific disease mutations into human pluripotent stem cells and/or to derive these cells as hiPS cells by reprogramming from any patient of choice, are creating unprecedented opportunities to create disease models “in a dish” and study ways to treat it or slow down its rate of development. We produce isogenic pairs of hiPSC lines to compare diseased and corresponding healthy cardiomyocytes and vascular endothelial cells and identify disease related phenotypes and mechanisms. We have shown in hiPSC-cardiomyocytes that mutations in ion channel genes can accurately predict changes in cardiac electrical properties and reveal drug sensitivities observed in patients. Similar studies will be described using vascular endothelial cells from hPSC. Relevant in all cases is the development of appropriate bioassays in which to measure disease phenotypes which may be highly cell type specific dependent. For heart cells, this might be electrical activity or contractions force; for vascular cells, responses to fluid flow flow and inflammation. Various approaches to this will be presented.

Friday, January 27, 2017, 12:00 pm to 1:00 pm

Wilson Hall, Building 1

Next up in the Director’s Seminar Series is “Molecular mechanisms of synapse assembly and maturation” by Mihaela Serpe, Ph.D., of the NICHD Unit on Cellular Communication.

From the speaker: “The purpose of our research is to elucidate molecular mechanisms that regulate cell-cell communication during development. We focus on two related questions: 1) how are tissues patterned and correctly connected by long-range signals, and 2) how cells structures and functions are coordinated at short-range with those of their neighbors. TGF-beta factors modulate long-range signaling during patterning, but also ensure short-range communication at specialized cell-cell interaction zones, for example the neuromuscular junction (NMJ). We use the Drosophila model system and a variety of molecular and biochemical approaches to study genes that modulate the function of TGF-beta-type signals. Highly conserved throughout the animal kingdom, TGF-beta family of signaling factors have the ability to function as morphogens, that is to specify cell fate in a concentration-dependent manner. In addition, these signaling factors provide a mechanism for coupling a cell to its neighbors and to its environment, so that the cell has the necessary plasticity to respond appropriately to changes around it, in its environment, or even to its own state.”