Displaying publications 41 - 42 of 42 in total

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  1. Feng W, Wang F, Han Y, Li G
    Heliyon, 2024 Mar 30;10(6):e27544.
    PMID: 38533080 DOI: 10.1016/j.heliyon.2024.e27544
    PURPOSE: The purpose of the study was to examine the impact of core strength training on the dynamic balance, agility, and dribbling ability of adolescent basketball players.

    METHODS: A randomized controlled between-subjects design was employed. Forty-four male adolescent basketball players (aged 14.41 ± 3.22 years) were randomly divided into two groups: the core strength training (CST) group and the conventional training (CT) group. The CST program included 1-h sessions, three times/week for 12 weeks. In contrast, the CT group provided a thorough physical training program that targeted general conditioning rather than focusing solely on core strength. Three measurements were used to evaluate performance in players: the Star Excursion Balance Test, the Illinois Agility Test, and the Dribbling Test conducted at T0 (week 0), T1 (week 6), and T2 (week 12), respectively.

    RESULTS: Compared to the CT group, the CST group showed a greater improvement (p  0.05).

    CONCLUSION: The 12-week CST program significantly improved dynamic balance, agility, and dribbling skills in adolescent basketball players, demonstrating its potential as a valuable training component. Future research should explore CST's impact on other sport-specific elements and its applicability to female players.

  2. Gao Y, Zhang W, Liu C, Li G
    Sci Rep, 2019 12 11;9(1):18844.
    PMID: 31827114 DOI: 10.1038/s41598-019-54289-6
    Resistance to tamoxifen is a major clinical challenge. Research in recent years has identified epigenetic changes as mediated by dysregulated miRNAs that can possibly play a role in resistance to tamoxifen in breast cancer patients expressing estrogen receptor (ER). We report here elevated levels of EMT markers (vimentin and ZEB1/2) and reduced levels of EMT-regulating miR-200 (miR-200b and miR-200c) in ER-positive breast cancer cells, MCF-7, that were resistant to tamoxifen, in contrast with the naïve parental MCF-7 cells that were sensitive to tamoxifen. Further, we established regulation of c-MYB by miR-200 in our experimental model. C-MYB was up-regulated in tamoxifen resistant cells and its silencing significantly decreased resistance to tamoxifen and the EMT markers. Forced over-expression of miR-200b/c reduced c-MYB whereas reduced expression of miR-200b/c resulted in increased c-MYB We further confirmed the results in other ER-positive breast cancer cells T47D cells where forced over-expression of c-MYB resulted in induction of EMT and significantly increased resistance to tamoxifen. Thus, we identify a novel mechanism of tamoxifen resistance in breast tumor microenvironment that involves miR-200-MYB signaling.
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