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- 저자 : Xuemei Su (검색결과 3 건)
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Numerical Analysis of the Wave Shape in Light Storage
Fenglin Li,Kim J. B.,Chae Min,Xuemei Su 한국물리학회 2006 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.49 No.1
We report a numerical analysis of the wave shape of light storage in a two-level degenerate atomic system considering the decay. The details of the probe field’s propagation will be shown, and a suggestion about measuring the decay between atomic levels will be made.?
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Classicality in Imaginary Weak Amplification
Tao Wang,Gang Li,Chang-Bao Fu,Rui Zhang,Xuemei Su,Qian-qian Bao 한국물리학회 2017 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.71 No.12
Weak ampli¯cation is an interesting phenomenon. In this paper we show an example that the imaginary weak ampli¯cation e®ect can be only related to the classical probability distribution of the measured quantity. A general result for any two orthogonal postselections and any meter state is also given.
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Hui Ran,Yao Lu,Qi Zhang,Qiuyue Hu,Junmei Zhao,Kai Wang,Xuemei Tong,Qing Su 대한당뇨병학회 2021 Diabetes and Metabolism Journal Vol.45 No.3
Background: Skeletal muscle is the largest tissue in the human body, and it plays a major role in exerting force and maintaining metabolism homeostasis. The role of muscle transcription factors in the regulation of metabolism is not fully understood. MondoA is a glucose-sensing transcription factor that is highly expressed in skeletal muscle. Previous studies suggest that MondoA can influence systemic metabolism homeostasis. However, the function of MondoA in the skeletal muscle remains unclear. Methods: We generated muscle-specific MondoA knockout (MAKO) mice and analyzed the skeletal muscle morphology and glycogen content. Along with skeletal muscle from MAKO mice, C2C12 myocytes transfected with small interfering RNA against MondoA were also used to investigate the role and potential mechanism of MondoA in the development and glycogen metabolism of skeletal muscle. Results: MAKO caused muscle fiber atrophy, reduced the proportion of type II fibers compared to type I fibers, and increased the muscle glycogen level. MondoA knockdown inhibited myoblast proliferation, migration, and differentiation by inhibiting the phosphatase and tensin homolog (PTEN)/phosphoinositide 3-kinase (PI3K)/Akt pathway. Further mechanistic experiments revealed that the increased muscle glycogen in MAKO mice was caused by thioredoxin-interacting protein (TXNIP) downregulation, which led to upregulation of glucose transporter 4 (GLUT4), potentially increasing glucose uptake. Conclusion: MondoA appears to mediate mouse myofiber development, and MondoA decreases the muscle glycogen level. The findings indicate the potential function of MondoA in skeletal muscle, linking the glucose-related transcription factor to myogenesis and skeletal myofiber glycogen metabolism.
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