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311.
Summary As the nonparametric generalization of the one‐way analysis of variance model, the Kruskal–Wallis test applies when the goal is to test the difference between multiple samples and the underlying population distributions are nonnormal or unknown. Although the Kruskal–Wallis test has been widely used for data analysis, power and sample size methods for this test have been investigated to a much lesser extent. This article proposes new power and sample size calculation methods for the Kruskal–Wallis test based on the pilot study in either a completely nonparametric model or a semiparametric location model. No assumption is made on the shape of the underlying population distributions. Simulation results show that, in terms of sample size calculation for the Kruskal–Wallis test, the proposed methods are more reliable and preferable to some more traditional methods. A mouse peritoneal cavity study is used to demonstrate the application of the methods. 相似文献
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The trans-membrane transport of hydrocarbons is an important and complex aspect of the process of biodegradation of hydrocarbons by microorganisms. The mechanism of transport of 14C n-octadecane by Pseudomonas sp. DG17, an alkane-degrading bacterium, was studied by the addition of ATP inhibitors and different substrate concentrations. When the concentration of n-octadecane was higher than 4.54 μmol/L, the transport of 14C n-octadecane was driven by a facilitated passive mechanism following the intra/extra substrate concentration gradient. However, when the cells were grown with a low concentration of the substrate, the cellular accumulation of n-octadecane, an energy-dependent process, was dramatically decreased by the presence of ATP inhibitors, and n-octadecane accumulation continually increased against its concentration gradient. Furthermore, the presence of non-labeled alkanes blocked 14C n-octadecane transport only in the induced cells, and the trans-membrane transport of n-octadecane was specific with an apparent dissociation constant K t of 11.27 μmol/L and V max of 0.96 μmol/min/mg protein. The results indicated that the trans-membrane transport of n-octadecane by Pseudomonas sp. DG17 was related to the substrate concentration and ATP. 相似文献
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Hui Liu Xing‐Hua Zhang Ying‐Xin Li Xiang Li Cun‐Ku Dong De‐Yao Wu Cheng‐Chun Tang Shu‐Lei Chou Fang Fang Xi‐Wen Du 《Liver Transplantation》2020,10(25)
Catalyst support with good conductivity and stability is an eternal pursuit in the search for a high‐performance electrocatalyst. Here, an unusual catalyst support, laser‐modified boron nitride with C, O dopants (L‐BN), for the oxygen evolution reaction is reported. L‐BN exhibits unique advantages for electrocatalysis, namely, high corrosion resistance under oxidizing conditions, enhanced electrical conductivity arising from interlayer B–B dipolar interaction, and strong interaction with IrOx catalyst caused by N? C?N bonds. As an excellent substrate, L‐BN helps to achieve higher activity and stability than its carbon black counterpart. 相似文献
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Dongyan Zhou Jasper Fuk-Woo Chan Biao Zhou Runhong Zhou Shuang Li Sisi Shan Li Liu Anna Jinxia Zhang Serena J. Chen Chris Chung-Sing Chan Haoran Xu Vincent Kwok-Man Poon Shuofeng Yuan Cun Li Kenn Ka-Heng Chik Chris Chun-Yiu Chan Jianli Cao Chun-Yin Chan Zhiwei Chen 《Cell host & microbe》2021,29(4):551-563.e5
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318.
Yu-xiang Wang Xu Zhang Qing-yang Ma Lan-dian Hu Xi Zhang Yi Wang Lan Xu Chun-hao Yang Cun Tan Xiang-yin Kong Jian Ding Ling-hua Meng 《Cell death & disease》2021,12(1)
Phosphoinositide-3 kinase alpha-specific inhibitors (PI3Kαi) displayed promising potential for the treatment of esophageal squamous cell carcinoma (ESCC) with frequent activation in PI3K signaling. However, acquired resistance is likely to develop and limit the efficacy of PI3Kαi like other targeted therapies. To identify genomic adaptation to PI3Kαi, we applied whole-genome sequencing and detected gene mutation and amplification in four lines of ESCC cells established with adapted resistance to a novel PI3Kαi CYH33. Particularly, HRASG12S mutation was found in KYSE180C cells. Overexpression of HRASG12S in ESCC parental cells rendered resistance to CYH33. By contrast, down-regulation of HRASG12S restored the sensitivity of KYSE180C1 cells to CYH33, and combination of CYH33 and MEK162 displayed synergistic effect against KYSE180C1 cells and xenografts. Furthermore, elevated mTORC1, mitogen-activated protein kinase (MAPK), and c-Myc signaling pathways were found in resistant cells by RNA sequencing and combination of CYH33 and RAD001, MEK162, or OTX015 overcame the resistance to CYH33, which was accompanied with enhanced inhibition on S6, extracellular signal-regulated kinase 1 (ERK), or c-Myc, respectively. Overall, we characterized the adaptations to PI3Kαi in ESCC cells and identified combinatorial regimens that may circumvent resistance.Subject terms: Cancer therapeutic resistance, Oncogenes 相似文献
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