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Conference on Physiology and Pathophysiology of Sickle Cell Disease


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Project Summary/Abstract The purpose of this proposal is to seek support for the American Physiological Society (APS) conference entitled Physiology and Pathophysiology of Sickle Cell Disease scheduled for November 6th to 8th, 2017 in Washington, DC. Sickle cell disease (SCD) refers to a group of autosomal recessive congenital disorders that affect hemoglobin, the protein that carries oxygen in red blood cells. Sickled hemoglobin distorts the shape of red blood cells causing them to lose flexibility and stick to vessel walls, reducing oxygen delivery to organs and tissues downstream. SCD is highly prevalent in African and Hispanic Americans. Complications of SCD are numerous and deadly, negatively affecting the function of nearly every organ system. Although we know the genetic cause, preventing and reversing its lethal consequences will require greater understanding of how SCD impacts basic physiology. The objectives of the conference are to convene an internationally recognized, interdisciplinary group of investigators to present and discuss current basic and clinical research findings about SCD; develop new ideas and directions for SCD research and clinical treatment; attract and develop early career investigators for careers in SCD research; and, encourage participation of investigators at all career levels with an emphasis on underrepresented minorities and women through a travel award program. The APS agreed to host this meeting because the topic is integrative and interdisciplinary in nature, providing a mechanism for APS to have broad exposure and recruitment opportunities to scientific communities beyond the regular APS membership. More importantly, it fosters the Society's mission to promote the discipline of physiology.
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R13HL138729

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Collapse start date
2017-09-01
Collapse end date
2018-08-31
RCMI CC is supported by the National Institute on Minority Health and Health Disparities, National Institutes of Health (NIH), through Grant Number U24MD015970. The contents of this site are solely the responsibility of the authors and do not necessarily represent the official views of the NIH

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