August 2020
Vol 6, Issue 35

About The Cover

Cover image expansion

ONLINE COVER Ruptured blood clots can be deadly, sometimes resulting in a life-threatening condition in which a piece of the clot travels downstream and blocks other vessels, preventing blood flow to tissues. Ruptured blood clots correlate with a 30% higher mortality rate in venous thromboembolism, a condition that affects 900,000 people in the U.S. alone each year. However, the mechanisms that lead to ruptures in fibrin, a protein involved in blood clotting, remain unknown. To measure the toughness of fibrin clots and determine the structural mechanisms that cause them to break, Tutwiler et al. stretched clots derived from human blood plasma in a strain-controlled tensile tester. The researchers tested clots of various lengths with or without edge cracks, finding that the fibrin gels could sustain much higher forces when did not have preexisting cracks than they could when a crack was already present. These observations led them to conclude that growth of a critical flaw, rather than diffuse damage, causes fibrin to fail. The findings may help inform personalized medical treatments and assist in the development of fibrin-based biomaterials. [CREDIT: VALERIE TUTWILER, RUSTEM I. LITVINOV, JOHN W. WEISEL, UNIVERSITY OF PENNSYLVANIA]