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Kara S. Tanaka MD Veronica R. Andaya BA Steven W. Thorpe MD Kenneth R. Gundle MD James B. Hayden MD Yee-Cheen Duong MD Raffi S. Avedian MD David G. Mohler MD Lee J. Morse MD Melissa N. Zimel MD Richard J. O'Donnell MD Andrew Fang MD Robert Lor Randall MD Tina H. Tran BS Christin New BA Rosanna L. Wustrack MD other members of Study Group FORCE 《Journal of surgical oncology》2023,127(1):148-158
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Dongbing Lai Emma C. Johnson Sarah Colbert Gayathri Pandey Grace Chan Lance Bauer Meredith W. Francis Victor Hesselbrock Chella Kamarajan John Kramer Weipeng Kuang Sally Kuo Samuel Kuperman Yunlong Liu Vivia McCutcheon Zhiping Pang Martin H. Plawecki Marc Schuckit Jay Tischfield Leah Wetherill Yong Zang Howard J. Edenberg Bernice Porjesz Arpana Agrawal Tatiana Foroud 《Alcoholism, clinical and experimental research》2022,46(3):374-383
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Lei Yang You-Ling Shi Yan Ma Wei-Wei Ren Guang-Ming Pang Jiao Liu 《APMIS : acta pathologica, microbiologica, et immunologica Scandinavica》2022,130(1):43-52
Krüppel-like factor 16 (KLF16), a member of the Krüppel-like factor (KLF) family, has been extensively investigated in multiple cancer types. However, the role of KLF16 in oral squamous cell carcinoma (OSCC) remains unknown. Thus, we conducted this study to investigate its related mechanism. KLF16 expression in OSCC cell lines was quantified by western blotting. Then, OECM1 and OC3 cells were divided into Blank, siCtrl, siKLF16#1 and siKLF16#2 groups. Subsequently, cell proliferation was detected using 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assays, cell migration and invasion were detected with wound healing and Transwell assays, and cell cycle distribution and cell apoptosis were detected via flow cytometry. KLF16, p21, CDK4, Cyclin D1 and p-Rb expression was detected by western blotting. Finally, xenograft models were established in nude mice to observe the in vivo effects of KLF16 on OSCC. KLF16 protein expression was upregulated in OSCC cells. Compared to the cells in the Blank group, the OECM1 and OC3 cells in the siKLF16#1 group and siKLF16#2 group exhibited a sharp decrease in proliferation but a remarkable increase in apoptosis. Moreover, the proportion of cells in the G0/G1 phase notably increased and that in the S phase decreased, with evident decreases in cell invasion and migration. Moreover, KLF16, cyclin-dependent kinase 4 (CDK4), Cyclin D1 and p-Rb protein expression was upregulated, but p21 expression was downregulated. The mice in the siKLF16#1 and siKLF16#2 xenograft model groups exhibited slower tumour growth and smaller tumours with evident downregulation of Ki67 expression compared to the mice in the Blank group. KLF16 expression was upregulated in OSCC cells, and interfering with KLF16 led to cell cycle arrest, inhibited OSCC cell growth and promoted cell apoptosis. 相似文献
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本文通过对特发性肺纤维化急性发作病因病机的分析,认为其病因为外邪或内伤引动肺络虚火,从阳化热,病机为“肺热”、“络瘀”;并结合其病因病机,探究归纳《温病条辨》中清络法和中药复方清络饮在论治特发性肺纤维化急性发作时的理论基础,为临床中论治特发性肺纤维化急性发作,改善患者症状提供新方法,为肺络病证治体系构建及应用提供新思路。 相似文献
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K. Jean Forney PhD Jenny H. Jo MA Gabriella Pucci BS Christopher R. France PhD 《The International journal of eating disorders》2021,54(12):2223-2228
Fear is central to conceptualizations of weight and shape-focused eating disorders. The current study will examine the reliability and validity of a test meal paradigm that varies perceptions of fat content to manipulate fear. Undergraduate women with elevated eating pathology (N = 96) will be randomized to one of three test meal conditions: two “low” fat yogurts, two “high” fat yogurts, or one “high” fat and one “low” fat yogurt. In actuality, all yogurts will have the same fat content. Supporting reliability, we hypothesize that self-reported fear and electrodermal activity (psychophysiological index of fear-related arousal) will exhibit good test–retest reliability over a 48-hr period in the “high” fat/“high” fat and “low” fat/“low” fat conditions. Supporting construct validity, self-reported fear and electrodermal activity will be elevated during the “high” versus “low” fat condition and responses to the “high" fat condition will correlate with fear of food, eating, and weight gain. Supporting discriminant validity, self-reported disgust and anger will be comparable in the “high” and “low” fat conditions and will exhibit weak correlations with trait measures of disgust and anger. This experimental paradigm will allow researchers to manipulate fear in order understand the mechanisms by which fear maintains eating pathology. 相似文献