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https://www.selleckchem.com/products/mito-tempo.html Experiments are conducted on three datasets, including two SR tasks of Voxceleb and CN-celeb, and one LR task, NIST LRE 07. For SR, D-MONA improves on ResNet-34 results by at least 29% and 15% for Voxceleb1 and CN-celeb respectively. For the LR task, a large improvement is achieved over ResNet-34 of 21% for the challenging 3s utterance condition, 59% for the 10s condition and 67% for the 30s condition. It also outperforms the state-of-the-art deep bottleneck feature-DNN (DBF-DNN) x-vector system at all scales. Thyroid cancer is the most common malignancy in human endocrine system. Increasing evidence has indicated that p62 plays a key role in tumorigenesis. The roles and underlying molecular mechanisms of P62 in thyroid cancer, however, remain to be elucidated. The expression levels of P62 in thyroid tumor tissues and thyroid cancer cells were detected by western blotting and qRT-PCR. Then, the effects of up-regulation or down-regulation of P62 on thyroid cancer cell proliferation, migration, invasion, cell cycle and apoptosis were measured by CCK-8 assay, transwell assay, flow cytometry and transwell assay, respectively. In terms of the mechanism, P62 could stimulate thyroid cancer progression by the activation of nuclear factor-kappa B (NF-κB) signaling pathway. P62 was highly expressed in thyroid tumor tissues. Furthermore, high expression of p62 was observed in PTC cell lines, and especially in the K1 and TPC-1 cells. In vitro, the up-regulation of p62 promoted cell proliferation, migration, and invasion of thyroid cancer cells, whereas the knockdown of p62 resulted in the opposite effect. Knock-down of P62 increased the number of cells in the G0/G1 phase but reduced it in the S and G2/M phase. Moreover, we confirmed that overexpression of p62 inactivated NF-κB pathway with sequencing analysis and bioinformatics analysis. This research work suggested that p62 could promote PTC cell proliferation, migration, an

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