Sickle cell disease afflicts around a hundred thousand Americans, causing their red blood cells to harden, compress into the namesake C-shapes, clog small blood vessels and die off early (which, in turn, causes red blood cell shortages). However, some of the mechanisms at play in sickle cell disease have historically been poorly understood. Now, researchers from three universities and one hospital have applied supercomputing power to investigate those mechanisms.
Specifically, the researchers – led by Michael Graham, a professor of chemical and biological engineering at the University of Wisconsin–Madison – used supercomputing to simulate how sickle cells exert forces on the walls of blood vessels.
Graham had been hard at work on sickle cell disease (which particularly afflicts Black and Hispanic populations) for years prior to this research. Graham’s research group had found evidence suggesting that the healthier red blood cells might be pushing the sickle-shaped cells toward blood vessels’ walls, causing sickle cells to congregate at the margins and amplifying the damage caused by the sickle cells brushing against those same walls of their own accord.
To expand on this research, the team received a time allocation on Comet through the NSF‘s Extreme Science and Engineering Discovery Environment (XSEDE) resource-sharing system. Comet, hosted by the San Diego Supercomputer Center (SDSC), delivers 2.76 peak petaflops through its 1,944 Intel Haswell CPU nodes and its 72 Nvidia GPU nodes.
“We are grateful for being able to use supercomputers like Comet to help us better illustrate, and hopefully come closer to a cure for, sickle cell disease,” said Wilbur Lam, a physician and biomedical engineer at Emory University and the Georgia Institute of Technology who collaborated with Graham on the research.
Using Comet, the researchers simulated how the various blood cells deformed and collided with one another during blood flow through a vessel. They found that, indeed, the harder sickle cells were being pushed toward the boundaries of blood vessels, agitating healthy cells.
“Our new simulations showed how the motions of sickle cells near vessel walls generate large forces,” Graham said. “The forces caused by these sickle cells impact healthy cells on the blood vessel walls, which in turns causes inflammation.”
Graham cautioned that the simulations were heavily simplified when compared to the extremely complex human circulatory system. Still, he expressed excitement about the implications of the work.
“There’s still lots of work to be done, but it’s kind of an exciting direction for sure, and something that hadn’t been addressed previously,” Graham said.
To learn more about this research, visit these articles from SDSC and the University of Wisconsin — Madison.