目的 调查分析ICU转出患者的陪床家属即照顾者的准备度对其迁移应激的影响作用。方法 纳入2020年1月—2022年12月在焦作市第二人民医院ICU住院治疗的患者家属106人为研究对象,以问卷调查法对患者及家属一般资料、家属准备度水平以及迁移应激水平进行数据分析。结果 ICU转出患者家属的照顾者准备度测试总分为（14.92±3.86）分,为中等水平,迁移应激总分为（57.21±5.88）分,为中度应激水平,照顾准备度与迁移应激呈负相关。结论 ICU转出患者家属的照顾者准备度水平不足,且与迁移应激水平呈负相关。

Objective To investigate and analyze the effect of readiness of accompanying family members,i.e．caregivers,on migration stress in patients transferred out of the ICU．Methods From January 2020 to December 2022,106 patients hospitalized in ICU were included in the study,general data of patients and their caregives,preparation level and migration stress level of caregives were investigated and analyzed by questionnaire survey．Results The caregivers of patients transferred out of the ICU had a total readiness test score of（14.92±3.86）,which was moderate level,and the total score of migration stress was（57.21±5.88）,which was moderate stress level,and was negatively correlated with readiness．Conclusions The readiness level of the caregivers of patients transferred out of the ICU is insufficient and negatively correlated with the migration stress level．

目的 本研究从细胞生物学角度检测二甲双胍对小鼠胰岛瘤MIN6的影响,并探讨此过程中包含的分子生物学机制。方法 MTT法检测不同浓度二甲双胍(1、2、5、10、20 mmol/L)对MIN6细胞活力的影响,细胞划痕实验检测二甲双胍对MIN6细胞迁移的影响,免疫印记实验检测此过程中细胞凋亡相关蛋白Bcl-2、Bax、caspase3表达的变化,及AMPK和JNK信号通路蛋白磷酸化水平的变化。结果 二甲双胍浓度大于10 mmol/L时可以抑制MIN6细胞的活力(P<0.01),降低其迁移能力(P<0.01),高浓度二甲双胍可以上调细胞内凋亡蛋白Bax(P<0.05)和p-AMPK的表达(P<0.05),降低抗凋亡蛋白Bcl-2的表达,增加caspase3剪切体(P<0.05)。同时,二甲双胍可以降低MIN6细胞内JNK信号通路的磷酸化水平(P<0.05)。结论 高浓度二甲双胍可以抑制MIN6细胞的增殖和迁移,其作用可能与降低了JNK信号的通路活化有关。

Objective This study aims to investigate the effect of metformin on proliferation and migration of MIN6 cells, and to explore the underlying mechanism. Methods The viability of MIN6 cells that were treated with various metformin (1,2,5,10 and 20 mmol/L) was detected by MTT assay. The migration of MIN6 cells was determined by wound-healing assay. Meanwhile, the proteins expression of Bcl-2, Bax, caspase3 and the phosphorylation of AMPK, JNK was detected by western bolt assay. Results The cell viability and the migration of MIN6 cells were decreased when the concentration of metformin above 10 mmol/L(P<0.01). The expression of apoptosis-related protein Bax(P<0.05) and p-AMPK(P<0.05)was up-regulated, anti-apoptosis-related protein Bcl-2 was down-regulated and cleaved caspase3 (P<0.05)was increased after high metformin treatment. At the same time, the phosphorylation of JNK was down-regulated by metformin(P<0.05). Conclusion High concertration of metformin may inhibit the proliferation and migration of MIN6 cells through suppressing the activation of JNK signaling pathway.