产ESBLs肺炎克雷伯菌ESBLs基因与可移动遗传元件相关性分析

目的 了解产超广谱β-内酰胺酶(extended spectrum beta-lactamases, ESBLs)肺炎克雷伯菌(Klebsiella pneumoniae, Kpn)ESBLs基因与可移动遗传元件(mobile genetic elements, MGEs)标记基因的携带情况及其相关性。方法 收集从住院患者标本中分离出的产与非产ESBLs Kpn非重复菌株各100株，采用PCR检测细菌中4种ESBLs基因与8种MGEs标记基因，并作指标聚类分析。结果 产ESBLs Kpn中，ESBLs基因阳性率高达100%；MGEs标记基因以IS26、ISEcp1、traA、trbC和intI1基因为主，阳性率高于非产ESBLs Kpn(P<0.05)；ESBLs基因与MGEs标记基因的同时检出率明显高于非产ESBLs Kpn (P<0.05)；基因blaSHV-12、blaOXA-1与MGEs基因tnpU、tnp513、merA、intI1相关联，基因blaTEM-1、blaCTX-M-125与MGEs基因ISEcp1、IS26、traA相关联。产与非产ESBLs Kpn均没有只检出MGEs标记基因的菌株。结论 产ESBLs Kpn ESBLs基因和MGEs标记基因携带率高，两者存在相关性，可能是产ESBLs Kpn出现多重耐药的重要原因；MGEs标记基因在Kpn中可能不是单独存在的。     

不同产地冻干地黄中5种重金属及有害元素的含量测定

摘 要 目的： 用火焰原子吸收分光光度计和原子双道荧光光度计分别对不同产地冻干地黄中的Pb、Cd、Cu、As和Hg 5种重金属和有害元素进行检测。方法: 采用硝酸-高氯酸对样品进行消化后,采用原子吸收分光光度法测定Pb、Cd和Cu含量,采用原子荧光光度法测定As和Hg的含量。 结果: 各元素线性关系良好,相关系数均大于0.997 4,平均回收率为97.88%～100.90%,RSD为0.019%～4.20%（n=6）,同时发现10批样品中的4批样品部分重金属和有害元素超过《中国药典》限量标准。 结论:该方法准确度高,操作简便,快捷,适用于冻干地黄中重金属和有害元素的测定。     

Effects of iron manipulation on trace elements level in a model of colitis in rats

AIM: Trace elements (TE) metabolism is altered in inflammatory bowel diseases. TE (zinc and copper) are constituents of antioxidant enzymes. Iron is involved in the pathogenesis of chronic inflammation. The aim was to evaluate zinc and copper status and the effects of iron manipulation in experimental colitis. METHODS: Twenty-four male Sprague-Dawley rats were divided into four groups: standard diet, iron-deprived diet, iron-supplemented diet, and sham-treated controls. Macroscopic damage was scored. DNA adducts were measured in the colon. Liver and colonic concentration of TE were measured. RESULTS: Macroscopic damage was reduced in iron-deprived groups and increased in iron-supplemented rats. Damage to the DNA was reduced in iron-deprived groups and increased in iron-supplemented groups. Liver and colonic iron concentrations were reduced in iron-deprived and increased in iron-supplemented rats. Liver zinc concentration was reduced after supplementation whereas colonic levels were similar in controls and treated rats. Liver copper concentration was reduced in all the colitic groups except in the iron-supplemented group whereas colonic concentration was increased in iron-deprived rats. CONCLUSION: Iron deprivation diminishes the severity of DNBS colitis while supplementation worsens colitis. Zinc and copper status are modified by iron manipulation.     

Calculation of pulsatile flow and particle paths in an aneurysm-model

Summary The velocity field and the wall shear stress have been calculated numerically by the finite element method to the time-dependent Navier-Stokes equations for pulsatile flow in a model of an aneurysm. The results show a complex flow field with two eddies growing and disappearing during the cardiac cycle. Downstream at the outlet vessel high wall shear stress occurs, which may lead to a downstream-growing of the aneurysm.With the knowledge of a sufficiently accurate flow field, the calculation of several particle paths has been carried out. Starting points and starting time are varied. The paths demonstrate the time-dependent development, shift and disappearance of vortices during the pulsatile cycle and provide hints on zones of stasis. These are significant factors in thrombogenesis.Supported by the Fonds zur Förderung der wissenschaftlichen Forschung, project number P4671     

Overexpressed growth hormone (GH) synergistically promotes carcinogen‐initiated liver tumour growth by promoting cellular proliferation in emerging hepatocellular neoplasms in female and male GH‐transgenic mice

Abstract: Background/Aims: Growth hormone (GH), when overexpressed in male and female GH‐transgenic mice, is known to induce liver tumours within 1 year. This study aimed to gain a clearer understanding of the interaction between GH and tumour cells in vivo. Methods/Results: The carcinogen diethylnitrosomine (DEN) was administered to neo‐natal transgenic and non‐transgenic mice maintained in a “hepatocarcinogenesis resistant” genetic background (C57BL/6J). Macroscopic, microscopic and liver weight/body weight ratio analyses revealed that carcinogen‐induced hepatocarcinogenesis was dramatically accelerated in young GH‐transgenic mice compared to non‐transgenic counterparts. Image analysis of microscopic hepatocellular neoplasms showed rapidly increasing tumour burdens, and neoplastic foci size over time in young adult GH‐transgenic mice. The magnitude of enhanced tumour growth was equivalent in both male and female transgenic mice, whereas much lower and sexually dimorphic tumour growth rates (males>females) were observed in non‐transgenic mice treated with DEN. BrdU labelling experiments demonstrated that rapid tumour growth in carcinogen‐treated GH‐transgenic mice was due to the promotion of cell proliferation in emerging lesions. Tumour cell proliferation in young GH‐transgenic mice was 2.6‐ and 4‐fold higher, respectively, than that observed in similar age male and female non‐transgenic mice. Interestingly, both GH‐transgenic and non‐transgenic mice displayed progressively slower tumour growth rates in older animals. Conclusion: Overall, GH synergistically promotes carcinogen‐induced hepatocarcinogenesis in both sexes of GH‐transgenic mice by stimulating tumour cell proliferation.