Harold F. Sims
Washington University in St. Louis
53 Papers
586 Citations
Harold F. Sims is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Mitochondrion & Phospholipase. The author has an hindex of 31, co-authored 52 publications.
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Papers
A Fetal Fatty-Acid Oxidation Disorder as a Cause of Liver Disease in Pregnant Women
Jamal A. Ibdah,Michael J. Bennett,Piero Rinaldo,Yiwen Zhao,Beverly Gibson,Harold F. Sims,Arnold W. Strauss +6 more
TL;DR: A small number of women diagnosed with acute fatty liver of pregnancy and the HELLP syndrome (hemolysis, elevated liver-enzyme levels, and a low platelet count) also have low iron levels, which are normal during pregnancy.
454
Molecular Heterogeneity in Very-Long-Chain Acyl-CoA Dehydrogenase Deficiency Causing Pediatric Cardiomyopathy and Sudden Death
Amit M. Mathur,Harold F. Sims,Deepika Gopalakrishnan,Beverly Gibson,Piero Rinaldo,Jerry Vockley,George Hug,Arnold W. Strauss +7 more
TL;DR: Infantile CM is the most common clinical phenotype of VLCAD deficiency, and although mortality at presentation is high, both the metabolic disorder and cardiomyopathy are reversible.
157
Very-Long-Chain Acyl-Coenzyme A Dehydrogenase Deficiency in Mice
Vernat Exil,Richard L. Roberts,Harold F. Sims,Jacqueline E. McLaughlin,Robert A. Malkin,Carla D. Gardner,Gemin Ni,Jeffrey N. Rottman,Arnold W. Strauss +8 more
TL;DR: It is concluded that mice with VLCAD deficiency have altered expression of a variety of genes in the fatty acid metabolic pathway from birth, reflecting metabolic feedback circuits, with progression to ultrastructural and physiological correlates of the associated human disease in the absence of stress.
138
Molecular cloning of rat cardiac troponin I and analysis of troponin I isoform expression in developing rat heart.
TL;DR: During fetal and neonatal development, slow skeletal and cardiac troponin I isoforms are coexpressed in the rat heart and regulated in opposite directions, and the degree of primary sequence differences in these isoforms may result in important functional differences in the neonatal myocardium.
103
Reversible high affinity inhibition of phosphofructokinase-1 by acyl-CoA: a mechanism integrating glycolytic flux with lipid metabolism.
TL;DR: It is demonstrated that fatty acyl-CoA modulates phosphofructokinase activity through both covalent and noncovalent interactions to regulate glycolytic flux and enzyme membrane localization via the branch point metabolic node that mediates lipid flux through anabolic and catabolic pathways.
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