恶性肿瘤患者1497例医院感染因素分析

目的分析恶性肿瘤患者医院感染的主要因素,为有效防治提供依据。方法采用回顾性调查分析法,以桂林医学院第二附属医院2016年1月-2017年12月发生医院感染的恶性肿瘤患者1 497例为研究对象,对其恶性肿瘤类型、感染部位、分离的病原菌及药敏情况、年龄、住院时间、住院次数、肿瘤分期、有无侵入性操作等进行统计,分析医院感染的主要因素。结果 1 497例恶性肿瘤患者发生医院感染102例,感染率为6.81%。分离出病原菌45株,其中革兰阴性菌33株(73.33%),革兰阳性菌5株(11.11%),真菌7株(15.56%)。年龄、住院次数、住院时间、肿瘤分期和有无侵入性操作是恶性肿瘤患者发生医院感染的危险因素。结论恶性肿瘤患者医院感染发生率高,其中肺癌患者医院感染率居首位,感染部位以下呼吸道感染最多,以革兰阴性菌为主;年龄大、住院次数多、住院时间长、肿瘤分期晚及进行侵入性操作是恶性肿瘤患者发生医院感染的主要因素,因此,医、护、药师等应采用适当措施降低恶性肿瘤患者医院感染的发生率。     

miR-188-5p promotes oxaliplatin resistance by targeting RASA1 in colon cancer cells

The efficacy of chemotherapy for colon cancer is limited due to the development of chemoresistance. MicroRNA (miR)-188-5p is downregulated in various types of cancer. The aim of the present study was to explore the molecular role of miR-188 in oxaliplatin (OXA) resistance. An OXA-resistant colon cancer cell line, SW480/OXA, was used to examine the effects of miR-188-5p on the sensitivity of colon cancer cells to OXA. The target of miR-188-5p was identified using a luciferase assay. Cell cycle distribution was also assessed using flow cytometry. The measurement of p21 protein expression, Hoechst 33342 staining and Annexin V/propidium iodide staining was used to evaluate apoptosis. The expression of miR-188-5p significantly increased in SW480/OXA compared with wild-type SW480 cells. The luciferase assay demonstrated that miR-188-5p inhibited Ras GTPase-activating protein 1 (RASA1; also known as p120/RasGAP) luciferase activity by binding to the 3′-untranslated region of RASA1 mRNA, suggesting that miR-188-5p could target RASA1. In addition, miR-188-5p downregulation or RASA1 overexpression promoted the chemosensitivity of SW480/OXA, as evidenced by increased apoptosis and G₁/S cell cycle arrest. Moreover, RASA1 silencing abrogated the increase in cell apoptosis induced by the miR-188-5p inhibitor. The findings of the present study suggested that miR-188-5p could enhance colon cancer cell chemosensitivity by promoting the expression of RASA1.     

混合痔患者术后急性期的疼痛体验

目的:深入了解混合痔患者术后急性期疼痛体验,为采取有针对性的干预措施来缓解疼痛提供参考.方法:采用质性研究中的现象学方法,目的性抽样选取9例混合痔术后疼痛患者进行半结构式深度访谈,应用Colaizzi 7步分析法进行资料分析.结果:混合痔患者术后急性期疼痛体验可归纳为5个主题:①深度疼痛体验;②对疼痛的持续负面思考;③...     

异槲皮苷调控PTP1B改善胰岛素抵抗的网络药理学研究及体外实验验证

目的 采用网络药理学法及分子对接技术探析异槲皮苷改善胰岛素抵抗的分子机制,并通过体外实验研究异槲皮苷对胰岛素抵抗的干预作用及机制。方法 利用PubChem、PharmMapper、GEO、CTD、GeneCards、OMIM等多个数据库筛选异槲皮苷活性成分及胰岛素抵抗相关靶点;采用Cytoscape软件将异槲皮苷治疗胰岛素抵抗的潜在靶点构建蛋白质相互作用（PPI）网络,并根据度值筛选核心靶点。利用基因本体（GO）与京都基因与基因组百科全书（KEGG）富集分析寻找与靶点蛋白相关的生物学通路,采用AutoDock Tools软件模拟分子对接,预测异槲皮苷与关键靶点的结合度。体外实验采用异槲皮苷干预蛋白酪氨酸磷酸酶1B（PTP1B）质粒转染HepG2细胞,检测不同浓度异槲皮苷干预后PTP1B的活性;构建PTP1B质粒转染HepG2胰岛素抵抗细胞模型,给予异槲皮苷（40μmol/L）干预,葡萄糖氧化酶法、qRT-PCR、Western Blotting法检测PTP1B等相关因子的表达。结果 网络药理学筛选得到异槲皮苷改善胰岛素抵抗的交集靶点21个,富集到GO条目2 761个,主要涉及胰岛素受体信号通路、糖原生物合成过程的调控等,富集到KEGG通路89条,涉及包括胰岛素信号通路、胰岛素抵抗、磷脂酰肌醇-3-羟激酶（PI3K）-蛋白激酶B（Akt）信号通路、磷酸腺苷活化的蛋白激酶（AMPK）信号通路等。分子对接结果显示,异槲皮苷与靶点PTP1B、磷酸肌醇依赖性蛋白激酶1（PDPK1）、胰岛素受体（INSR）、糖原合酶激酶3β（GSK3β）、AKT2均有一定的结合活性。体外实验结果显示,异槲皮苷能有效抑制PTP1B活性,降低PTP1B过表达HepG2胰岛素抵抗细胞中PTP1B、GSK3β的表达,升高胰岛素受体底物1（IRS-1）、葡萄糖转运蛋白-1（GLUT-1）等因子的表达,改善细胞胰岛素抵抗。结论 异槲皮苷可能通过抑制PTP1B调控PI3K/Akt信号通路因子活性改善胰岛素抵抗。     

经食管实时三维超声心动图评价左心耳形态结构及功能的研究进展

由于左心耳解剖结构较为特殊,其功能及形态的评价对于临床房颤、血栓等疾病的诊断以及治疗具有重要意义。本文对经食管实时三维超声心动图应用于左心耳形态结构、功能评价中的价值进行阐述,分析当前临床超声技术发展现状。     

Contributors to impaired bone health in type 2 diabetes

Type 2 diabetes (T2D) is associated with numerous complications, including increased risk of fragility fractures, despite seemingly protective factors [e.g., normal bone mineral density and increased body mass index(BMI)]. However, fracture risk in T2D is underestimated by current fracture risk calculators. Importantly, post-fracture mortality is worse in T2D following any fracture, highlighting the importance of identifying high-risk patients that may benefit from targeted management. Several diabetes-related factors are associated with increased fracture risk, including exogenous insulin therapy, vascular complications, and poor glycaemic control, although detailed comprehensive studies to identify the independent contributions of these factors are lacking. The underlying pathophysiological mechanisms are complex and multifactorial, with different factors contributing during the course of T2D disease. These include obesity, hyperinsulinaemia, hyperglycaemia, accumulation of advanced glycation end products, and vascular supply affecting bone-cell function and survival and bone-matrix composition. This review summarises the current understanding of the contributors to impaired bone health in T2D, and proposes an updated approach to managing these patients.     

Drosophila as a diet discovery tool for treating amino acid disorders

Amino acid disorders (AADs) are a large group of rare inherited conditions that collectively impact one in 6500 live births, often resulting in rapid neurological decline and death during infancy. For several AADs, including phenylketonuria, dietary modification prevents physiological deterioration and ameliorates symptoms. Despite this remarkable potential for treatment success, dietary therapy for most AADs remains largely unexplored. Although animal models have provided novel insights into AAD mechanisms, few have been used for therapeutic diet discovery. Here, we find that of all the animal models, Drosophila is particularly well suited for nutrigenomic disease modelling, having amino acid pathways conserved with humans, exceptional genetic tractability, and the unique availability of a synthetic customisable diet.