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The Virtual Summer Research Program: supporting future physician-scientists from underrepresented backgrounds
- Briana Macedo, Briana Christophers, Rio Barrere-Cain, Yentli Soto Albrecht, Michael C. Granovetter, Rachit Kumar, Dania Daye, Elizabeth Bhoj, Lawrence Brass, Jose Alexandre Rodrigues
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- Journal:
- Journal of Clinical and Translational Science / Volume 6 / Issue 1 / 2022
- Published online by Cambridge University Press:
- 22 August 2022, e120
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- Article
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- Open access
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Introduction:
Physician-scientist training programs expect applicants to have had extensive research experience prior to applying. Even at the best of times, this leaves individuals from underserved and underrepresented backgrounds at a competitive disadvantage, especially those remote from major academic centers. The COVID-19 pandemic exacerbated that disadvantage by closing research laboratories and suspending summer research opportunities.
Methods:The Virtual Summer Research Program (VSRP) was designed to combat this shortfall by helping participating students become better informed and better prepared for applying to MD/DO–PhD programs. 156 participants were recruited from historically black colleges and universities and from national organizations for underrepresented trainees. Participants were paired with medical school faculty members and current MD/DO–PhD students from 35 participating institutions. The program lasted for at least 4 weeks and included a short research project, interactive sessions, journal clubs, social events, and attendance at a regional American Physician Scientists Association conference.
Results:In follow-up surveys, participants reported improvements in their science-related skills and in their confidence in becoming a physician-scientist, applying to training programs, and navigating mentorship relationships. A follow-up study completed one year later indicated that participants felt they had benefited from an enhanced skill set, long-term relationships with their mentors, and connections to the physician-scientist community at large.
Discussion:The results suggest that VSRP met its primary goals, which were to provide a diverse group of trainees with mentors, provide skills and resources for MD/DO–PhD application and matriculation and to support the development of longitudinal relationships between VSRP mentees and APSA. VSRP provides an approach that can be applied at an even larger scale when the constraints caused by a global pandemic have lifted.
3 - Mechanisms of platelet activation
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- By Lawrence F. Brass, Timothy J. Stalker, University of Pennsylvania, Philadelphia, PA, USA
- Edited by Paolo Gresele, Università degli Studi di Perugia, Italy, Valentin Fuster, Mount Sinai School of Medicine, New York, Jose A. Lopez, Seattle University, Clive P. Page, King's College London, Jos Vermylen, Katholieke Universiteit Leuven, Belgium
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- Book:
- Platelets in Hematologic and Cardiovascular Disorders
- Published online:
- 15 October 2009
- Print publication:
- 13 December 2007, pp 37-52
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Summary
INTRODUCTION
Platelets evolved as a means of responding to injuries that produce holes in a high-pressure circulatory system and, to a great extent, the attributes acquired by platelets through evolution reflect the demands placed upon them. To be maximally useful and minimally harmful, circulating platelets must be able to sustain repeated contact with the normal vessel wall without premature activation, recognize the unique features of a damaged wall, cease their forward motion upon recognition of damage, adhere to the vessel wall despite the forces produced by continued blood flow, and stick (cohere) to each other, forming a stable plug of the correct size that can remain in place until it is no longer needed. Pathologic thrombus formation occurs when diseases or drugs subvert the mechanisms designed to allow platelets to respond as rapidly as possible to injury.
Although much has been discovered about the mechanisms that underlie normal platelet activation, a considerable amount still remains to be learned. Platelets have been the subject of fruitful investigation for most of the past 50 years. However, a number of technical breakthroughs within the past 10 years have moved the field along considerably. Among these are the widespread use of genetically modified mice, the availability of improved methods for studying platelet function in vitro and in vivo under flow conditions and in real time, a better understanding of signaling mechanisms in general, and the development of methods that allow megakaryocyte (MK) maturation and platelet formation to be studied ex vivo.
8 - Platelet receptors for thrombin
- from PART I - PHYSIOLOGY
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- By Lawrence F. Brass, Departments of Medicine and Pharmacology, and the Center for Experimental Therapeutics at the University of Pennsylvania, Philadelphia, USA, Marina Molino, Istituto di Ricerche Farmacologiche Mario Negri, Consorzio Mario Negri Sud, Santa Maria Imbaro, Italy, Peter J. O'Brien, Departments of Medicine and Pharmacology, and the Center for Experimental Therapeutics at the University of Pennsylvania, Philadelphia, USA, Mark Kahn, Departments of Medicine and Pharmacology, and the Center for Experimental Therapeutics at the University of Pennsylvania, Philadelphia, USA
- Edited by Paolo Gresele, Università degli Studi di Perugia, Italy, Clive P. Page, Valentin Fuster, Jos Vermylen, Universiteitsbibliotheek-K.U., Leuven
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- Book:
- Platelets in Thrombotic and Non-Thrombotic Disorders
- Published online:
- 10 May 2010
- Print publication:
- 30 May 2002, pp 113-126
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Summary
Introduction
Thrombin is one of the most potent agonists that platelets will encounter in vivo, but unlike most of the others it is a protease. For years after thrombin was shown to be a platelet activator as well as an effector in the clotting cascade, the precise mechanism by which it activates platelets remained obscure. Binding studies demonstrated high affinity interactions with several sites on the platelet surface, including glycoprotein (GP) Ibα, but efforts to establish that any of these constituted a receptor in the signalling sense were not entirely successful. Substrates on the platelet surface for proteolytic cleavage by thrombin were also identified, including GP V, but cleavage of these sites did not appear to be required for platelet activation by thrombin. Before discussing the receptors that have been identified, it is worth considering what some of the criteria might be for establishing a protein as a true signalling receptor for thrombin. Such criteria would include (i) demonstrating its presence on the platelet surface, (ii) showing that it was a substrate for thrombin or closely associated with a substrate for thrombin, (iii) demonstrating an association of the candidate receptor with mediators or effectors for intracellular signalling cascades, (iv) showing that expression of the candidate receptor could render a cell that was otherwise unresponsive to thrombin capable of responding, and (v) showing that blocking, dismantling or otherwise removing the candidate receptor would reduce platelet responses to thrombin.