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Biology subjects

Yoon, S. J.

Publications and source records attributed to Yoon, S. J..

4 recordsLinked to original sources

An ensemble of Gleditsia sinensis Lam. and gut microbiota against alcoholic liver disease

Gleditsia sinensis Lam. (GSL) is a medicinal herb and a noticeable resource of possessing hepatic protective agents such as alcoholic liver disease (ALD). At present, it has been documented that gut microbiota (GM) is related directly to etiology of ALD. Nevertheless, the bioactive molecules in GSL, favorable GM, targets, and key mechanism(s) against ALD are yet to be revealed. Hence, we integrated the significant four components to clarify the nuanced pathogenesis with help of network pharmacology (NP) concept. We retrieved significant metabolites via gutMGene and constructed GSL or GM-Signaling pathways-Targets-Metabolites (GGSTM) networks. Finally, molecular docking test (MDT) was performed to verify the key findings. The gutMGene suggested that 16 GM and 6 metabolites were related to the two signaling pathways through GGSTM networks. Both MDT and frontier molecular orbitals (FMO) theory revealed the most stable conformers: equol from Lactobacillus paracasei JS1 on IL6, Bauer-7-en-3-one, and Urs-12-en-3-one from GSL on PPARA, PPARD, and PPARG, respectively. In conclusion, this study sheds light on the combinatorial effects of GM, and GSL in treating ALD via systems biology concept.

systems biology↗

Mitochondrial Function is Preserved Under Cysteine Starvation via Glutathione Catabolism in NSCLC

Cysteine metabolism occurs across cellular compartments to support diverse biological functions and prevent the induction of ferroptosis. Though the disruption of cytosolic cysteine metabolism is implicated in this form of cell death, it is unknown whether the substantial cysteine metabolism resident within the mitochondria is similarly pertinent to ferroptosis. Here, we show that despite the rapid depletion of intracellular cysteine upon loss of extracellular cystine, cysteine-dependent synthesis of Fe-S clusters persists in the mitochondria of lung cancer cells. This promotes a retention of respiratory function and a maintenance of the mitochondrial redox state. Under these limiting conditions, we find that mitochondrial glutathione sustains the function of the Fe-S proteins critical to oxidative metabolism. This is achieved through CHAC1 catabolism of the cysteine-containing tripeptide within the mitochondrial matrix. We find that disrupting Fe-S cluster synthesis under cysteine restriction protects against the induction of ferroptosis, suggesting that the preservation of mitochondrial function is antagonistic to survival under starved conditions. Overall, our findings implicate mitochondrial cysteine metabolism in the induction of ferroptosis and reveal a novel mechanism of mitochondrial resilience in response to nutrient stress.

cancer biology↗

The Origin Of Cysteine and its Catabolism in Mammalian Tissues and Tumors

Cysteine plays critical roles in cellular biosynthesis, enzyme catalysis, and is an essential contributor to redox metabolism. While cultured cells are highly dependent on exogenous cystine for proliferation and survival, how diverse tissues obtain and use cysteine in vivo has not been characterized. We comprehensively interrogated cysteine metabolism in normal murine tissues and the cancer that arise from them using stable isotope 13C-serine and 13C-cystine tracing. We found that de novo cysteine synthesis was highest in normal liver and pancreas and absent in lung tissue. In tumors, cysteine synthesis was either inactive or downregulated during tumorigenesis. By contrast, cystine uptake and metabolism to downstream metabolites was a universal feature of normal tissues and tumors. Differences in cysteine catabolism were evident across tumor types, including glutathione synthesis. Thus, cystine is a major contributor to the cysteine pool in tumors and cysteine catabolic pathways are differentially active across tumor types.

cancer biology↗

Real-time spectroscopic photoacoustic/ultrasound (PAUS) scanning with simultaneous fluence compensation and motion correction for quantitative molecular imaging

For over two decades photoacoustic (PA) imaging has been tested clinically, but successful human trials have been minimal. To enable quantitative clinical spectroscopy, the fundamental issues of wavelength-dependent fluence variations and inter-wavelength motion must be overcome. Here we propose a new real-time, spectroscopic photoacoustic/ultrasound (PAUS) imaging approach using a compact, 1-kHz rate wavelength-tunable laser. Instead of illuminating tissue over a large area, the fiber-optic delivery system surrounding an US array sequentially scans a narrow laser beam, with partial PA image reconstruction for each laser pulse. The final image is then formed by coherently summing partial images at a 50-Hz video rate. This scheme enables (i) automatic laser-fluence compensation in spectroscopic PA imaging and (ii) inter-wavelength motion correction using US speckle tracking, which have never been shown before in real-time systems. The 50-Hz video rate PAUS system is demonstrated in vivo using a murine model of drug delivery monitoring.

bioengineering↗