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Hydrodynamic sorting of microchip particles in microchannels is essential in microfluidic systems used for applications requiring particle-based multiplexing. Understanding the forces acting on the particle, as well as the dependencies of the forces on channel and fluid flow parameters, allows for prediction of the flow conditions needed to initiate particle movement, or lift-off. This study presents the experimental characterization of the lift-off of a single, flat-plate, non-neutrally buoyant microchip particle initially sedimented near the inlet of straight, rectangular microfluidic channels of different channel sizes and solvents at moderate Archimedes number of 191 to 2820. The critical shear Reynolds number, corresponding to the minimum required for lift-off, was found to increase with larger Archimedes number and the relationship was found to exhibit particle-channel size dependency. The observed critical lift-off for the flat-plate particle was lower than that predicted using a previous generalized lift-off model based on modified particle Reynolds and Archimedes numbers which may be explained by entrance effects and fluid film lubrication pressure under the particle. Numerical evaluations of the hydrodynamic forces acting on the particle revealed that electrostatic forces are significant. A remodified Archimedes number, based on the channel width, particle diameter, and solvent relative permittivity, is introduced as a correction to the generalized lift-off model to account for hydrodynamics and electrostatics affecting the lift-off of a flat-plate particle. This model is in good agreement with the generalized particle lift-off model and allows for prediction of flat-plate particle lift-off in microfluidic channels for a moderate range of Archimedes numbers. 

Metabolic adaptations are essential for survival. The mitochondrial calcium uniporter plays a key role in coordinating metabolic homeostasis by regulating mitochondrial metabolic pathways and calcium signaling. However, a comprehensive analysis of uniporter-regulated mitochondrial pathways has remained unexplored. Here, we investigate consequences of uniporter loss and gain of function using uniporter knockout cells and fibrolamellar carcinoma (FLC), which we demonstrate to have elevated mitochondrial calcium levels. We find that branched-chain amino acid (BCAA) catabolism and the urea cycle are uniporter-regulated pathways. Reduced uniporter function boosts expression of BCAA catabolism genes and the urea cycle enzyme ornithine transcarbamylase. In contrast, high uniporter activity in FLC suppresses their expression. This suppression is mediated by the transcription factor KLF15, a master regulator of liver metabolism. Thus, the uniporter plays a central role in FLC-associated metabolic changes, including hyperammonemia. Our study identifies an important role for the uniporter in metabolic adaptation through transcriptional regulation of metabolism and elucidates its importance for BCAA and ammonia metabolism.