Group motility as a mechanism of self-defence in bacteria
群体运动作为细菌的一种自卫机制
基本信息
- 批准号:1788986
- 负责人:
- 金额:--
- 依托单位:
- 依托单位国家:英国
- 项目类别:Studentship
- 财政年份:2016
- 资助国家:英国
- 起止时间:2016 至 无数据
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Programme overview:This MRC-funded doctoral training partnership (DTP) brings together cutting-edge molecular and analytical sciences with innovative computational approaches in data analysis to enable students to address hypothesis-led biomedical research questions. This is a 4-year programme whose first year involves a series of taught modules and two laboratory-based research projects that lead to an MSc in Interdisciplinary Biomedical Research. The first two terms consist of a selection of taught modules that allow students to gain a solid grounding in multidisciplinary science. Students also attend a series of masterclasses led by academic and industry experts in areas of molecular, cellular and tissue dynamics, microbiology and infection, applied biomedical technologies and artificial intelligence and data science. During the third and summer terms students conduct two eleven-week research projects in labs of their choice. Project:Antibiotic resistance is the ability of bacteria to resist the effects of medication used to treat them. One of the least understood mechanisms by which bacteria gain resistance is physical adaptation. An example of such adaptation is produced when bacteria move as swarms instead of as individuals under certain conditions of surface wetness and stiffness. These swarms consist in flagella-driven bacteria which expand over the surface at fast speed and invade larger regions than the swimming counterparts in the presence of antibiotics.Understanding how swarming motility is triggered and the physical mechanism of defense will provide us with methods to cease the swarming formation and to overcome these physical barriers which confer the resistance. Swarming starts with the expression of a specific phenotype at individual cell level which leads to a group phenomenon. The increase in resistance to antibiotic is hence supposed to be originated by this interplay between both scales. Thus, to address this problem, we will take an interdisciplinary approach combining molecular microbiology, cellular biophysics, and computational simulations.A dual-scale set up which combines data acquisition at both, colony and single-cell level scale will be developed and completed during the first stages of the project. Then, swarming dynamics will be studied in both scales when bacteria are exposed to different environmental conditions (sort and concentration of antibiotic, temperature, etc.). In parallel, a mathematical model will be developed to find out the physical mechanisms underlying the increase in resistance due to swarming motility. Finally, studies will focus on the response at chemical stress at single cell level which will determine swarmers' history of antibiotic exposure.
项目概述:这个由MRC资助的博士培训伙伴关系(DTP)将尖端的分子和分析科学与数据分析中的创新计算方法结合在一起,使学生能够解决以假设为主导的生物医学研究问题。这是一个为期4年的计划,其第一年涉及一系列教学模块和两个基于实验室的研究项目,导致跨学科生物医学研究硕士学位。前两个学期包括一系列教学模块,让学生在多学科科学中获得坚实的基础。学生还参加了一系列由学术和行业专家领导的大师班,这些专家在分子,细胞和组织动力学,微生物学和感染,应用生物医学技术以及人工智能和数据科学领域。在第三和夏季学期,学生在他们选择的实验室进行两个为期11周的研究项目。项目:抗生素耐药性是细菌抵抗用于治疗它们的药物作用的能力。细菌获得耐药性的机制之一是物理适应。这种适应的一个例子是,当细菌在一定的表面湿度和硬度条件下以群体而不是个体的方式移动时。这些菌群由鞭毛驱动的细菌组成,它们在抗生素存在的情况下以快速的速度在表面扩张,侵入比游泳对应物更大的区域。了解如何触发群集运动和防御的物理机制将为我们提供停止群集形成的方法,并克服这些赋予抵抗力的物理障碍。群集开始于在单个细胞水平上表达特定表型,这导致群体现象。因此,抗生素耐药性的增加被认为是由这两个尺度之间的相互作用引起的。因此,为了解决这一问题,我们将采取分子微生物学、细胞生物物理学和计算模拟相结合的跨学科方法。在项目的第一阶段,将开发并完成集落和单细胞水平的双尺度数据采集装置。然后,当细菌暴露于不同的环境条件(抗生素的种类和浓度、温度等)时,将在两个尺度上研究群集动力学。同时,将开发一个数学模型,以找出由于群集运动而增加阻力的物理机制。最后,研究将重点关注单细胞水平上化学应激的反应,这将确定蜂群的抗生素暴露史。
项目成果
期刊论文数量(0)
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科研奖励数量(0)
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专利数量(0)
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其他文献
吉治仁志 他: "トランスジェニックマウスによるTIMP-1の線維化促進機序"最新医学. 55. 1781-1787 (2000)
Hitoshi Yoshiji 等:“转基因小鼠中 TIMP-1 的促纤维化机制”现代医学 55. 1781-1787 (2000)。
- DOI:
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- 影响因子:0
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LiDAR Implementations for Autonomous Vehicle Applications
- DOI:
- 发表时间:
2021 - 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
吉治仁志 他: "イラスト医学&サイエンスシリーズ血管の分子医学"羊土社(渋谷正史編). 125 (2000)
Hitoshi Yoshiji 等人:“血管医学与科学系列分子医学图解”Yodosha(涉谷正志编辑)125(2000)。
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Effect of manidipine hydrochloride,a calcium antagonist,on isoproterenol-induced left ventricular hypertrophy: "Yoshiyama,M.,Takeuchi,K.,Kim,S.,Hanatani,A.,Omura,T.,Toda,I.,Akioka,K.,Teragaki,M.,Iwao,H.and Yoshikawa,J." Jpn Circ J. 62(1). 47-52 (1998)
钙拮抗剂盐酸马尼地平对异丙肾上腺素引起的左心室肥厚的影响:“Yoshiyama,M.,Takeuchi,K.,Kim,S.,Hanatani,A.,Omura,T.,Toda,I.,Akioka,
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