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摘要: 目的分析严重肝病患者全血、腹水合并细菌感染的致病菌菌种分布特点及药敏试验结果,为合理选用抗菌药物提供依据。方法采用BACTEC 9120细菌培养仪及PHNIX100全自动细菌鉴定仪对血液和腹水进行培养鉴定及药敏试验。结果两类标本共检出255株阳性标本,血培养187株,腹水68株。其中G-菌占多数,占59.6%,主要是:大肠埃希菌,肺炎克雷伯氏菌。分离出的G-菌对喹诺酮类、氨基糖甙类、第二、三、四代头孢菌素敏感率大都在50%以上,亚胺培南敏感率在80%以上。G+菌占40.4%,主要是:表皮葡萄球菌。G+菌对大多数常用抗菌药物严重耐药情况;对庆大霉素、第四代喹诺酮类、吗啉恶酮、奎奴普丁/达福普丁敏感率稍高,对万古霉素敏感率最高。结论随着细菌的种类及耐药性不断发生改变,应根据药敏试验结果合理使用抗生素。Abstract: Objective To analyze the distribution of pathogenic bacterial strains and their results of drug susceptibility assay in severe liver disease patients with blood and/or ascites infection, and thus provide basis for rational use of antibacterial drugs.Methods Collected blood and/or ascites samples were cultured, identified and tested for drug susceptibility on BACTEC 9120 Automated Blood Culture System and PHNIX 100 Automated Microbiology System.Results Altogether 255 strains of pathogens (187strains from blood culture and 68 form ascites culture) were identified, among which the gram-negative bacteria were most common, accounting for up to 59.6%.The strains of the gram-negative bacteria were mainly: Escherichia coli and Klebsiella pneumoniae.For all the isolated gram-negative strains, the susceptibility rates to quinolones, aminoglycosides, complex antibiotics、second and third-generation of cephalosporins were found to be above 50, and it was above 80% to imipenem, .of the 255 isolated strains, 103 strains were gram-positive (40.4%) , with a predominance being Staphylococcus epidermidis.The isolated gram-positive strains responded poor to most of the commonly used antibacterial agents and slightly higher to gentamicin 、linezolidfourth-generation of quinolones、quinupristin/ dalfopristin, and highest to vancomycin..Conclusion With the continuously altering of strains and drug resistance of the bacteria, rational use of antibiotics should be dependent on the drug susceptibility tests.
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Key words:
- severe liver /
- bacterium /
- susceptibility test /
- antibiotics
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【据Journal of Hepatology 2020年10月报道】题:肝细胞特异性NRF2激活可改善脂肪性肝炎的纤维化和癌变(作者Mohs A等)
慢性肝病中的炎症诱导氧化应激,因此可能导致肝损伤、纤维化和癌变的进展。KEAP1/NRF2轴是细胞氧化还原平衡的主要调节器。该研究探讨了KEAP1/NRF2系统是否参与了人类和小鼠肝病的进展。
在一个特征明确的非酒精性脂肪性肝病患者队列(n=63)中,通过肝RNA测序研究了氧化应激的临床相关性,并与组织学和临床参数进行相关分析。为了进行功能分析,将肝细胞特异性NEMO敲除(NEMO△hepa)小鼠与肝细胞特异性KEAP1敲除(KEAP1△hepa)小鼠杂交。
对人肝脏切片的免疫组织化学分析显示,慢性肝病患者的氧化应激增加,NRF2高表达。儿童非酒精性脂肪性肝病队列中肝脏样本的RNA测序显示,NRF2活化的显著增加与炎症分级相关,但与脂肪变性的分级无关,这在第二个成人非酒精性脂肪性肝病队列中得到证实。在小鼠中,微阵列分析显示KEAP1缺失诱导NRF2靶基因参与谷胱甘肽代谢和外源性应激(如Nqo1)。此外,在删除KEAP1后,NEMO△hepa肝脏中最重要的抗氧化剂之一谷胱甘肽(GSH)的缺乏得到了挽救。与NEMO△hepa肝相比,NEMO△hepa /KEAP1△hepa肝显示出细胞凋亡减少以及参与细胞周期调节和DNA复制的基因显著下调。因此,与NEMO△hepa相比,NEMO△hepa /KEAP1△hepa肝脏表现为纤维生成减少,肿瘤发生率降低,肿瘤数量减少,肿瘤大小减小。
非酒精性脂肪性肝炎患者的NRF2活化与炎症分级相关,但与脂肪变性无关。小鼠功能分析表明,在慢性肝病中,激活的NRF2通过改善纤维化、肝细胞癌变的发生和发展,而起到保护作用。
KEAP1/NRF2轴是细胞氧化还原平衡的主要调节系统。两个不同人群队列的非酒精性脂肪性肝炎患者中,NRF2的活性与炎症分级相关。在小鼠中,由于KEAP1缺失导致的NRF2激活可改善肝细胞的纤维化、肝细胞癌变的发生和进展。
摘译自MOHS A, OTTO T, SCHNEIDER KM, et al. Hepatocyte-specific NRF2 activation controls fibrogenesis and carcinogenesis in steatohepatitis[J]. J Hepatol, 2021, 74(3): 638-648.
(吉林大学第一医院感染病中心肝病科 李丽 华瑞 报道)
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其他类型引用(1)
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