Human genetic and metabolite variation reveals that methylthioadenosine is a prognostic biomarker and an inflammatory regulator in sepsis
Liuyang Wang(Duke University), Emily Ko(Duke University), James J. Gilchrist(Centre for Human Genetics), Kelly J. Pittman(Duke University), Anna Rautanen(Centre for Human Genetics), Matti Pirinen(Centre for Human Genetics), J. Will Thompson(Duke Medical Center), Laura G. Dubois(Duke Medical Center), Raymond J. Langley(University of South Alabama), Sarah L. Jaslow(Duke University), Raul Salinas(Duke University), Douglas Rouse(Duke University), M. Arthur Moseley(Duke University), Salim Mwarumba(Kenya Medical Research Institute), Patricia Njuguna(Kenya Medical Research Institute), Neema Mturi(Kenya Medical Research Institute), Kenyan Bacteraemia Study Group(Kenya Medical Research Institute), Thomas N. Williams(University of London), J. Anthony G. Scott(University of London), Adrian V. S. Hill(Centre for Human Genetics), Christopher W. Woods(Duke University), Geoffrey S. Ginsburg(Duke University), Ephraim L. Tsalik(Duke University), Dennis C. Ko(Duke University)
Cited by 58Open Access
Abstract
had prolonged survival when MTA was administered before infection, suggesting that manipulating MTA levels could regulate the severity of the inflammatory response. Our results demonstrate how combining genetic data, biomolecule measurements, and animal models can shape our understanding of disease and lead to new biomarkers for patient stratification and potential therapeutic targeting.
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