Ag-HA膜的结晶状况对其抗菌性能的影响

以离子束增强沉积(IBAD)镀膜方法,在Ti6AL4V骨植入材料上镀羟基磷灰石(HA)膜.将镀HA的Ti6AL4V在室温下置入100ppm的AgNO3溶液中浸泡48小时,银离子通过离子交换过程进入HA膜.含银的HA(Ag-HA)膜具有抗大肠杆菌和金黄色葡萄球菌的能力.经研究发现,晶态Ag-HA膜抗菌性能颇佳,与此相反,在非晶态的磷酸钙上细菌生长良好.结晶状况对其抗菌性能有重要影响.结晶较好的HA膜有利于Ag+与晶态HA中的Ca2+进行离子交换而进入HA膜,在一定条件下Ag+从晶格中释放出来,起到抗菌作用.     

人工模拟体液中离子注氮工业纯钛腐蚀行为

采用电化学技术研究了人工模拟体液中离子注氮对人体医用金属材料工业纯钛的耐蚀性的影响 .腐蚀电位和阳极极化曲线表明 ,离子注氮明显提高了材料的耐蚀性 .X射线衍射与AES分析发现材料表面形成钛的氮化物膜层 ,其机械隔离与化学效应抑制了腐蚀     

注银碳基生物医学材料的抗菌机理研究

选用革兰氏阴性菌-大肠杆菌,采用平板菌落计数法对注银碳基生物医学材料样品直接接触和间接接触的抗菌效果进行对比.研究结果表明:注银后材料表面形成的富银层是材料抗菌性的主要原因.对注银剂量相同的样品,直接接触比其滤液的抗菌效果好,说明注银碳基材料的抗菌性是溶出的银离子和材料表面未溶出的络合状银离子共同作用的结果,且以银离子溶出杀菌为主.通过紫外光谱法探究银离子和细菌染色体DNA的相互作用机制,发现银离子与DNA之间存在静电和碱基作用,导致DNA分子天然构象遭到破坏,起到抗菌作用.     

不锈钢及以其为基底的TiN膜注银的抗菌性的XRD分析

择优取向为(111)的TiN涂层，沉积表面光滑、硬度高、耐磨性好、结合强度高、耐腐性能强，因此，被用于矫形外科及骨植入材料．银离子有很好的抗菌性，所以生长含银的TiN膜可将这些优良的机械和生物性能相结合．本文研究银离子注入不锈钢及以不锈钢为基底的TiN膜的微观结构对其抗菌机理的影响．XRD分析的结果表明Ag 注入没有影响TiN(111)择尤取向．银在不锈钢和TiN膜上的晶面择优取向为(200)，(111)．这有可能是银注入这两种材料不同抗菌性的原因．     

人工模拟体液中施子注氮工业纯钛腐蚀行为

采用电化学技术研究了人工模拟体液中离子注氮对人体医用金属材料工业纯钛的耐蚀性的影响。腐蚀电位和阳极极化曲线表明,离子注氮明显提高了材料的耐蚀性。Ｘ射线衍射与ＡＥＳ分析发现材料表面形成钛的氮化物膜层,其机械隔离与化学效应抑制了腐蚀。     

溶胶—凝胶法制备不锈钢基Ag-SiO2抗菌膜及其结构性能表征

采用溶胶--凝胶法和浸渍提拉法在不锈钢板上制备了含银的二氧化硅薄膜.利用X射线衍射仪（XRD）分析了膜层的组成,通过测试接触角研究了薄膜的亲水性,测试了薄膜对质量分数10%的FeCl₃溶液的耐腐蚀性能,并对覆膜不锈钢的抗菌性和附着性进行了测定.结果表明:采用溶胶—凝胶法可在不锈钢基板上制得含银的SiO₂抗菌膜,经过10min氧化处理和5次提拉,并经热处理后,抗菌膜与不锈钢结合牢固,亲水性和耐蚀性提高,对金黄色葡萄球菌抑菌率达到100%.     

超疏水材料表面的空气膜与自清洁作用对细菌黏附行为的影响

超疏水材料因其特殊的润湿性被广泛用作抑菌材料，许多研究认为超疏水材料与细菌溶液间的空气膜是其抑菌的关键因素，但鲜有研究能直接证明空气对细菌黏附的影响.本文应用电化学阳极氧化法和分子自组装方法，在钛箔表面制备了超亲水的二氧化钛纳米孔柱阵列(NPA)和超疏水的NPA.通过超声去除超疏水NPA固-液界面的空气膜，对比研究细菌在超疏水样品有无超声情况下的黏附，其中细菌黏附应用荧光显微镜进行表征.结果表明，超疏水NPA相对于超亲水NPA表现出明显的抗菌效果；肉眼可见的空气膜在局部区域内，可明显阻碍细菌的黏附，从而影响细菌在超疏水材料表面的分布；但从黏附细菌的整体数量对比，超疏水NPA固-液界面的空气膜对细菌的黏附数量并没有显著影响.此外，超疏水材料表面黏附的细菌易在常规的实验漂洗过程中脱离材料，这提示了在考察超疏水材料的抑菌性能时，需要考虑材料的自清洁作用对其抑菌性能表征的干扰.     

钛合金表面羟基磷灰石膜及组织相容性

在乙酸钙、磷酸二氢钙为主成分的弱酸性电解液中,以乙二胺四乙酸(EDTA)和柠檬酸作为络合剂,采用微弧氧化的方法,在钛合金表面成功地直接制备出含有羟基磷灰石(HA)的陶瓷层.随着电解液Ca/P的增加,膜层中HA含量升高,膜层表面孔洞分布更均匀,表面变粗糙.动物种植试验表明,陶瓷层覆盖植入体产生的炎症反应较弱,新的肌肉组织能够在膜层表面生长.     

羟基磷灰石/碳纳米管复合生物材料的制备与表征

为了赋予碳纳米管(CNTs)表面良好的生物性能,拓展CNTs在硬组织生物材料及组织工程支架材料中的应用,采用化学共沉淀和水热后处理法宏量制备了羟基磷灰石(HA)/多壁碳纳米管(MWCNTs)复合材料,通过调节制备过程中浓硝酸纯化的MWCNTs加入量,考察不同MWCNTs含量的HA/MWCNTs复合材料的结合形式.扫描电子显微镜(SEM)和透射电镜(TEM)表征结果表明,当ω(MWCNTs)＝15%时,MWCNTs表面均匀地包覆了一层由纳米HA晶粒紧密相连的膜层,在此情况下MWCNTs与纳米HA形成最佳结合状态.体外细胞培养实验表明,制备的HA/MWCNTs复合材料具有良好的生物相容性.     

钛合金/HA涂层新型医用复合材料的制备及研究现状

钛合金/HA涂层材料是一种新型的生物医用复合材料,HA涂层与钛合金基体间的结合强度是影响该材料长期应用效果的重要因素;对其生物相容性的研究,是该复合材料能广泛应用于临床的关键.对此从制备技术、涂层与基体间的结合强度和材料的生物相容性三方面研究了该材料的现状.并指出对医用钛合金/HA涂层复合材料的研究,不仅应从制备工艺出发,探索出能制备涂层与基体间具有足够结合强度、符合临床应用、具有长期应用价值植入材料的制备技术,而且还应加强植入物生物相容性的基础理论研究,确切理解材料表面性能影响生物相容性的原理.通过合适的工艺参数提高钛合金/HA复合材料的生物相容性与生物活性,为该材料在临床中的广泛应用打下坚实的基础.     

Gene expression in Pseudomonas aeruginosa biofilms.

Bacteria often adopt a sessile biofilm lifestyle that is resistant to antimicrobial treatment. Opportunistic pathogenic bacteria like Pseudomonas aeruginosa can develop persistent infections. To gain insights into the differences between free-living P. aeruginosa cells and those in biofilms, and into the mechanisms underlying the resistance of biofilms to antibiotics, we used DNA microarrays. Here we show that, despite the striking differences in lifestyles, only about 1% of genes showed differential expression in the two growth modes; about 0.5% of genes were activated and about 0.5% were repressed in biofilms. Some of the regulated genes are known to affect antibiotic sensitivity of free-living P. aeruginosa. Exposure of biofilms to high levels of the antibiotic tobramycin caused differential expression of 20 genes. We propose that this response is critical for the development of biofilm resistance to tobramycin. Our results show that gene expression in biofilm cells is similar to that in free-living cells but there are a small number of significant differences. Our identification of biofilm-regulated genes points to mechanisms of biofilm resistance to antibiotics.     

A component of innate immunity prevents bacterial biofilm development

Antimicrobial factors form one arm of the innate immune system, which protects mucosal surfaces from bacterial infection. These factors can rapidly kill bacteria deposited on mucosal surfaces and prevent acute invasive infections. In many chronic infections, however, bacteria live in biofilms, which are distinct, matrix-encased communities specialized for surface persistence. The transition from a free-living, independent existence to a biofilm lifestyle can be devastating, because biofilms notoriously resist killing by host defence mechanisms and antibiotics. We hypothesized that the innate immune system possesses specific activity to protect against biofilm infections. Here we show that lactoferrin, a ubiquitous and abundant constituent of human external secretions, blocks biofilm development by the opportunistic pathogen Pseudomonas aeruginosa. This occurs at lactoferrin concentrations below those that kill or prevent growth. By chelating iron, lactoferrin stimulates twitching, a specialized form of surface motility, causing the bacteria to wander across the surface instead of forming cell clusters and biofilms. These findings reveal a specific anti-biofilm defence mechanism acting at a critical juncture in biofilm development, the time bacteria stop roaming as individuals and aggregate into durable communities.     

Aminoglycoside antibiotics induce bacterial biofilm formation

Biofilms are adherent aggregates of bacterial cells that form on biotic and abiotic surfaces, including human tissues. Biofilms resist antibiotic treatment and contribute to bacterial persistence in chronic infections. Hence, the elucidation of the mechanisms by which biofilms are formed may assist in the treatment of chronic infections, such as Pseudomonas aeruginosa in the airways of patients with cystic fibrosis. Here we show that subinhibitory concentrations of aminoglycoside antibiotics induce biofilm formation in P. aeruginosa and Escherichia coli. In P. aeruginosa, a gene, which we designated aminoglycoside response regulator (arr), was essential for this induction and contributed to biofilm-specific aminoglycoside resistance. The arr gene is predicted to encode an inner-membrane phosphodiesterase whose substrate is cyclic di-guanosine monophosphate (c-di-GMP)-a bacterial second messenger that regulates cell surface adhesiveness. We found that membranes from arr mutants had diminished c-di-GMP phosphodiesterase activity, and P. aeruginosa cells with a mutation changing a predicted catalytic residue of Arr were defective in their biofilm response to tobramycin. Furthermore, tobramycin-inducible biofilm formation was inhibited by exogenous GTP, which is known to inhibit c-di-GMP phosphodiesterase activity. Our results demonstrate that biofilm formation can be a specific, defensive reaction to the presence of antibiotics, and indicate that the molecular basis of this response includes alterations in the level of c-di-GMP.     

Pseudomonas biofilm formation and antibiotic resistance are linked to phenotypic variation

Colonization of the lungs of cystic fibrosis (CF) patients by the opportunistic bacterial pathogen Pseudomonas aeruginosa is the principal cause of mortality in CF populations. Pseudomonas aeruginosa infections generally persist despite the use of long-term antibiotic therapy. This has been explained by postulating that P. aeruginosa forms an antibiotic-resistant biofilm consisting of bacterial communities embedded in an exopolysaccharide matrix. Alternatively, it has been proposed that resistant P. aeruginosa variants may be selected in the CF respiratory tract by antimicrobial therapy itself. Here we report that both explanations are correct, and are interrelated. We found that antibiotic-resistant phenotypic variants of P. aeruginosa with enhanced ability to form biofilms arise at high frequency both in vitro and in the lungs of CF patients. We also identified a regulatory protein (PvrR) that controls the conversion between antibiotic-resistant and antibiotic-susceptible forms. Compounds that affect PvrR function could have an important role in the treatment of CF infections.     

没食子鞣质及其有效提取物对牙菌斑生物膜形态结构和活性的作用

研究药物没食子鞣质及其有效提取物对牙菌斑生物膜形态结构和活力的影响,了解常态生物膜形成过程中生物膜活力的变化,以及药物作用下生物膜形态结构和活力的变化,探讨药物对牙菌斑生物膜的作用机制.采用倒置荧光显微镜结合特异荧光染料标记常态牙菌斑生物膜生长过程中死菌和活菌变化,及药物处理后牙菌斑生物膜中死菌和活菌的构成,观察常态牙菌斑生物膜形竺过程中生物膜结构及活力的变化以及药物作用下生物膜形态结构和活力的变化;研究和评估常态牙菌斑生物膜的形态结构和细菌活力及实验药物对牙菌斑生物膜结构和细菌活性的影响.结果显示,从早期细菌定植粘附到形成成熟生物膜结构的各个过程中都存在一定数量的死菌.24 h常态生物膜结构中活菌面积占主导地位,有少量的死菌存在,细菌互相紧密粘附在一起,生物膜结构清晰,其间有各管道结构.0.05%洗必泰24 h细菌生物膜作用后,细菌总量明显下降,残存滞留的细菌基本为死菌.0.023%的氟化钠(NaF)作用细菌生物膜后,生物膜结构发生了明显的变化,细菌总量明显减少,但是存在的细菌以活菌为主.经过4mg/mL的没食子鞣质及其有效提取物作用后,生物膜中各管道结构模糊不清,细菌变得散开,生物膜细菌总量减少,与24 h常态生物膜比,有显著差异(P<0.05),生物膜结构密度下降,其中有大量的死菌和部分活菌存在.实验组活菌百分比与阴性对照组活菌百分比相比有显著差异(P<0.05).由此得出结论,实验药物对牙菌斑生物膜的作用一方面是对生物膜中细菌的杀灭,另一方面是改变牙菌斑孝竺膜的形态结构,降低生物膜密度及调整生物膜内部死活菌的比例.     

Natural conjugative plasmids induce bacterial biofilm development

Horizontal gene transfer is a principal source of evolution leading to change in the ecological character of bacterial species. Bacterial conjugation, which promotes the horizontal transfer of genetic material between donor and recipient cells by physical contact, is a phenomenon of fundamental evolutionary consequence. Although conjugation has been studied primarily in liquid, most natural bacterial populations are found associated with environmental surfaces in complex multispecies communities called biofilms. Biofilms are ideally suited to the exchange of genetic material of various origins, and it has been shown that bacterial conjugation occurs within biofilms. Here I investigate the direct contribution of conjugative plasmids themselves to the capacity of the bacterial host to form a biofilm. Natural conjugative plasmids expressed factors that induced planktonic bacteria to form or enter biofilm communities, which favour the infectious transfer of the plasmid. This general connection between conjugation and biofilms suggests that medically relevant plasmid-bearing strains are more likely to form a biofilm. This may influence both the chances of biofilm-related infection risks and of conjugational spread of virulence factors.     

三价砷存在条件下毒砂表面微结构对热氧化硫杆菌附着性的影响

Understanding bacterial adsorption and the evolution of biofilms on arsenopyrite with different surface structures is of great significance to clarifying the mechanism of microbe–mineral interfacial interactions and the production of acidic mine drainage impacting the environment. In this study, the attachment of Sulfobacillus thermosulfidooxidans cells and subsequent biofilm formation on arsenopyrite with different surface structures in the presence of dissolved As(Ⅲ) was studied. Arsenopyrite slices with a specific surface were obtained by electrochemical corrosion at 0.26 V. The scanning electronic microscopy-energy dispersion spectra analyses indicated that the arsenopyrite surface deficient in sulfur and iron obtained by electrochemical treatment was not favorable for the initial adsorption of bacteria, and the addition of As(Ⅲ) inhibited the adsorption of microbial cells. Epifluorescence microscopy showed that the number of cells attaching to the arsenopyrite surface increased with time; however, biofilm formation was delayed significantly when As(Ⅲ) was added.     

细菌生物膜的自然属性与致病性

细菌生物膜是相对于单个分散游离状态的细菌而言的另一种独特的生存形式,其最具特征性的表型决定了这种群聚性细菌集团对人体内环境和对自然界有着广泛的适应性.     

生物膜和生物膜形成菌的研究

细菌生物膜是一个复杂的微生物群落,生物膜巾除了水和细菌以外,还含有细菌分泌的胞外聚合物、吸附的营养物质、代谢产物及DNA等细菌裂解产物.介绍细菌生物膜的形成过程,并综述了近年来医学领域以几种成膜力强的条件致病菌为研究对象,从基因水平上证实了细菌细胞表面结构鞭毛、纤毛、胞外聚合物和群体感应信号分子等细胞因子对生物膜形成的影响.     

Caenorhabditis elegans: plague bacteria biofilm blocks food intake

Bubonic plague is transmitted to mammals, including humans, by the bites of fleas whose digestive tracts are blocked by a mass of the bacterium Yersinia pestis. In these fleas, the plague-causing bacteria are surrounded by an extracellular matrix of unknown composition, and the blockage depends on a group of bacterial genes known as the hmsHFRS operon. Here we show that Y. pestis creates an hmsHFRS-dependent extracellular biofilm to inhibit feeding by the nematode Caenorhabditis elegans. Our results suggest that feeding obstruction in fleas is a biofilm-mediated process and that biofilms may be a bacterial defence against predation by invertebrates.