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Tebon, Peyton J. ; Wang, Bowen ; Markowitz, Alexander L. ; Davarifar, Ardalan ; Tsai, Brandon L. ; Krawczuk, Patrycja ; Gonzalez, Alfredo E. ; Sartini, Sara ; Murray, Graeme F. ; Nguyen, Huyen Thi Lam ; et al ( , Nature Communications)
Abstract High throughput drug screening is an established approach to investigate tumor biology and identify therapeutic leads. Traditional platforms use two-dimensional cultures which do not accurately reflect the biology of human tumors. More clinically relevant model systems such as three-dimensional tumor organoids can be difficult to scale and screen. Manually seeded organoids coupled to destructive endpoint assays allow for the characterization of treatment response, but do not capture transitory changes and intra-sample heterogeneity underlying clinically observed resistance to therapy. We present a pipeline to generate bioprinted tumor organoids linked to label-free, time-resolved imaging via high-speed live cell interferometry (HSLCI) and machine learning-based quantitation of individual organoids. Bioprinting cells gives rise to 3D structures with unaltered tumor histology and gene expression profiles. HSLCI imaging in tandem with machine learning-based segmentation and classification tools enables accurate, label-free parallel mass measurements for thousands of organoids. We demonstrate that this strategy identifies organoids transiently or persistently sensitive or resistant to specific therapies, information that could be used to guide rapid therapy selection.
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Rege, Shraddha D. ; Royes, Luiz ; Tsai, Brandon ; Zhang, Guanglin ; Yang, Xia ; Gomez‐Pinilla, Fernando ( , Molecular Nutrition & Food Research)
Scope The action of brain disorders on peripheral metabolism is poorly understood. The impact of traumatic brain injury (TBI) on peripheral organ function and how TBI effects can be influenced by the metabolic perturbation elicited by fructose ingestion are studied.
Methods and Results It is found that TBI affects glucose metabolism and signaling proteins for insulin and growth hormone in the liver; these effects are exacerbated by fructose ingestion. Fructose, principally metabolized in the liver, potentiates the action of TBI on hepatic lipid droplet accumulation. Studies in isolated cultured hepatocytes identify GH and fructose as factors for the synthesis of lipids. The liver has a major role in the synthesis of lipids used for brain function and repair. TBI results in differentially expressed genes in the hypothalamus, primarily associated with lipid metabolism, providing cues to understand central control of peripheral alterations. Fructose‐fed TBI animals have elevated levels of markers of inflammation, lipid peroxidation, and cell energy metabolism, suggesting the pro‐inflammatory impact of TBI and fructose in the liver.
Conclusion Results reveal the impact of TBI on systemic metabolism and the aggravating action of fructose. The hypothalamic‐pituitary‐growth axis seems to play a major role in the regulation of the peripheral TBI pathology.