目的探讨镇静镇痛集束护理策略对ICU气管插管患者谵妄的影响。方法依据便利抽样法,选取2017年1—8月转入ICU的80例行气管插管患者,作为集束化组,在常规护理的同时进行规范化镇静镇痛集束护理措施。另取同期转入ICU的80例气管插管患者,作为对照组,行常规护理。记录患者性别、年龄、疾病诊断例数分布、使用镇静镇痛药的情况、急性生理和慢性健康评分(Acute Physiology and Chronic Health Evaluation,APACHEⅡ)、ICU住院时间、机械通气时间、谵妄发生率、谵妄类型(安静型、躁动型或混合型)及持续时间。结果 2组患者的性别构成、平均年龄、疾病诊断例数分布、使用镇静镇痛药的情况、APACHEⅡ评分、ICU住院时间和机械通气时间比较,差异均无统计学意义(P>0.05);集束化组谵妄的发生率及谵妄的构成类型与对照组相比,差异无统计学意义(P>0.05),但谵妄持续时间显著缩短(P<0.05)。结论镇静镇痛集束的应用可有效降低气管插管患者的谵妄持续时间,可能对改善预后起到积极作用。
Objective: To explore potential genes associated with the formation and rupture of intracranial aneurysms based on the Gene Expression Omnibus (GEO) database. Methods: A total of 133 mRNA microarrays were collected from the GEO database. Differential mRNA gene analysis was performed on the data of each group in the GEO2R platform, and the common differential genes were screened and the gene ontology enrichment analysis and the Kyoto Gene and Genomic Encyclopedia pathway enrichment analysis were completed. The screened differential genes were introduced into the String online database to obtain the interaction between the proteins encoded by the differential genes. Results: Forty-two common differential genes were screened, and the main biological processes involved included the transcriptional regulation of oxidative stress, the positive regulation of chemokine production, and the positive regulation of autophagy of giant cells by RNA polymerase II promoter. Molecular functions included protein binding, RNA polymerase II transcriptional co-repressor activity, transcriptional activator activity, and protein kinase C binding. The main signal pathways covered included hypoxia-inducible factor-1 signaling pathway, glucagon signaling pathway, and metabolic pathway signaling pathway. Conclusions: The formation and rupture of the intracranial aneurysm may be initially screened with amidoxime reduction component 1, tumor necrosis factor-α-inducible protein 6, haptoglobin, mast cell membrane-expressing protein 1, zipper containing kinase, phospholipase Cβ4 and blood and nervous system expression factor-1. In addition to the previously knownintracranial aneurysms mechanisms, cellular autophagy and hypoxia inducible factor-1 pathway may also be involved in the formation of intracranial aneurysms.
