Xiaoying Qiao

Abstract Genetic mutations causing Complex I (CI) dysfunction lead to the accumulation of NADH in the mitochondrial matrix due to impaired oxidation. An elevated NADH/NAD⁺ ratio feedback-inhibits key enzymes of the tricarboxylic acid (TCA) cycle, reducing metabolic flux, while concurrent electron transport chain (ETC) blockade exacerbates reactive oxygen species (ROS) generation and oxidative stress.

You are already at the latest version As machine learning pipelines grow to handle massive datasets, the computational cost of data processing and feature engineering becomes a primary bottleneck. Traditional pipelines often process all available data uniformly, leading to inefficiencies when large portions of the data contribute little to model improvement.

Introduction Myocardial infarction (MI) is a major cause of global morbidity and mortality that affects nearly 800,000 patients each year in the United States alone.1 Cardiac wound healing after MI is a complex and multiphase process that begins with necrosis and apoptosis of cardiomyocytes due to ischemic injury with or without reperfusion followed by the formation of a fibrotic scar.2 The acute phase of this process involves an inflammatory response and degradation of the extracellular...