Three-dimensional boundary layers on a 6:1 spheroid at an incidence of 10 deg have been calculated at two Reynolds numbers. At the lower Reynolds number, the boundary layer is predominantly laminar, but at the higher Reynolds number it includes laminar, transitional, and turbulent-flow regions. Comparisons have been made with the previously existing data. The results clearly deomonstrate the capabilities and limitations of firstorder boundary-layer theory.
Comprehensive calculations of laminar and turbulent boundary layers in a plane of symmetry are made to explore the influence of mean-flow convergence and divergence. Comparisons are made with the experimental results presented in Part I, and with some previous data, to assess the gross effects of convergence and divergence on boundary-layer development and to evaluate the performance of a conventional turbulence model in the presence of the associated extra rates of strain.
Most eukaryotic cells have mitochondrial networks that can change in shape, distribution, and size depending on cellular metabolic demands and environments. Mitochondrial quality control is critical for various mitochondrial functions including energy production, redox homeostasis, intracellular calcium handling, cell differentiation, proliferation, and cell death. Quality control mechanisms within mitochondria consist of antioxidant defenses, protein quality control, DNA damage repair systems, mitochondrial fusion and fission, mitophagy, and mitochondrial biogenesis. Defects in mitochondrial quality control and disruption of mitochondrial homeostasis are common characteristics of various kidney cell types under hyperglycemic conditions. Such defects contribute to diabetes-induced pathologies in renal tubular cells, podocytes, endothelial cells, and immune cells. In this review, we focus on the roles of mitochondrial quality control in diabetic kidney disease pathogenesis and discuss current research evidence and future directions.
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