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Background: Browning of white adipose tissues (WAT) is recognized as a novel way to combat obesity and its related comorbidities. Thus, a lot of dietary agents contributing to browning of WAT have been identified. Objective: In this study, we try to explore the mechanism of the browning of WAT induced by resveratrol (Res) in 3T3-L1 adipocytes. Methods: The levels of cell viability and lipid accumulation were evaluated under different concentrations of Res. Cell signaling pathway analysis was performed to investigate the possible mechanisms of the WAT browning effect of Res in 3T3-L1 cells. Results: We found that Res induced the brown fat-like phenotype by activating protein expressions of brown adipocyte-specific markers, such as peroxisome proliferator-activated receptor gamma (PPAR-γ), peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α), and uncoupling protein 1 (UCP1). Besides, Res reduced lipid accumulation, as shown by Oil Red O staining. The increased small lipid droplets implied that Res-treated 3T3-L1 adipocytes had some features of brown adipocytes. The brown fat-like phenotype in 3T3-L1 adipocytes induced by Res was possibly mediated by activation of mammalian target of rapamycin (mTOR), as brown adipocyte-specific markers were decreased by rapamycin, an inhibitor of mTOR and the MHY1485 treatment, an activator of mTOR, showed the similar effect of Res on browning markers. Conclusions: Res induced brown-like adipocyte phenotype in 3T3-L1 adipocytes partly via mTOR pathway, which provided new insights into the utilization of Res to prevent obesity and related comorbidities. [ABSTRACT FROM AUTHOR]

The first present an equivalent definition of relative generalized Hamming weights of a linear code and its subcodes, and we develop a method using finite projective geometry. Making use of the equivalent definition and the projective-geometry method, all of the relative generalized Hamming weights of a 3-dimensional q-ary linear code and its subcodes will be determined. [ABSTRACT FROM AUTHOR]

The weight hierarchies of a linear [n, k ; q] code C satisfying the Near-Chain condition are studied, almost all the weight hierarchies of such code are determined. [ABSTRACT FROM AUTHOR]

Nowadays, the application of MEMS is more and more important. With the development of microstructure technology, higher requirements are also placed on measurement methods. However, the current measurement methods cannot meet these requirements due to their own limitations. We developed a method based on the temporal microscopic speckle interferometry, which has advantages of real-time, full field, high-precision, and nondestructive. The interferometer based on Linnik microscopic structure is built up. The corresponding displacement measuring experiments have been performed, and the measurement errors are <0.05 µm. The experimental results demonstrate the validity of our homemade device. [ABSTRACT FROM AUTHOR]

Previously, we confirmed that C-C chemokine receptor 7 (CCR7) promotes cell proliferation via the extracellular signalregulated kinase (ERK) pathway, but its role in apoptosis of non-small cell lung cancer (NSCLC) cell lines remains unknown. A549 and H460 cells of NSCLC were used to examine the effect of CCL21/CCR7 on apoptosis using flow cytometry. The results showed that activation of CCR7 by its specific ligand, exogenous chemokine ligand 21 (CCL21), was associated with a significant decline in the percent of apoptosis. Western blot and real-time PCR assays indicated that activation of CCR7 significantly caused upregulation of anti-apoptotic bcl-2 and downregulation of pro-apoptotic bax and caspase-3, but not p53, at both protein and mRNA levels. CCR7 small interfering RNA significantly attenuated these effects of exogenous CCL21. Besides, PD98059, a selective inhibitor of MEK that disrupts the activation of downstream ERK, significantly abolished these effects of CCL21/CCR7. Coimmunoprecipitation further confirmed that there was an interaction between p-ERK and bcl-2, bax, or caspase-3, particularly in the presence of CCL21. These results strongly suggest that CCL21/CCR7 prevents apoptosis by upregulating the expression of bcl-2 and by downregulating the expression of bax and caspase-3 potentially via the ERK pathway in A549 and H460 cells of NSCLC. [ABSTRACT FROM AUTHOR]