Na+ TRANSPORT INHIBITION BY RESPIRATORY SYNCYTIAL VIRUS
呼吸道合胞病毒对 Na 转运的抑制
基本信息
- 批准号:7110384
- 负责人:
- 金额:$ 12.01万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2003
- 资助国家:美国
- 起止时间:2003-09-30 至 2008-07-31
- 项目状态:已结题
- 来源:
- 关键词:A549AlveolarAmilorideAnatomyAnimal ModelAnimalsApoptosisBiochemicalBronchiolitisCell physiologyCell surfaceCellsChildClinicalCytopathologyDevelopmentDoctor of PhilosophyElectrophysiology (science)EnsureEnvironmentEpithelialEpithelial CellsHumanHypoxemiaIn Situ HybridizationIn VitroInbred BALB C MiceInfectionIon ChannelIon TransportIonsKnowledgeLaboratory Animal MedicineLaboratory AnimalsLiquid substanceLower respiratory tract structureLungMarinesMeasurementMeasuresMediatingMentorsMiningMusNecrosisNorthern BlottingNosePatch-Clamp TechniquesPathogenesisPathologyPathway interactionsPhysiologyPropertyProtein SubunitsProteinsResearchRespiratory Syncytial Virus InfectionsRespiratory Tract DiseasesRespiratory physiologyRespiratory syncytial virusReverse Transcriptase Polymerase Chain ReactionRibavirinRoleScientistSeminalStructure of respiratory epitheliumTechniquesTestingTracheaTrainingUbiquitinUniversitiesUpper respiratory tractViralViral PathogenesisVirusWestern Blottingalveolar epitheliumcomparativeepithelial Na+ channelin vitro Modelin vivomonolayermulticatalytic endopeptidase complexpatch clampprotein expressionrespiratoryrespiratory virusstoichiometryveterinary science
项目摘要
CANDIDATE: I graduated from the University of Bristol in 1992, with Honours in Anatomical Science and Veterinary Science. At UAB I received training in laboratory animal medicine, laboratory animal pathology, and viral pathogenesis in animal models (Ph.D. February 2000; mentor Dr. Patricia Fultz). Subsequently, I elected to join Dr. Matalon's research group, where I might build on my knowledge of viral pathogenesis by cross-mining in electrophysiology, and apply these techniques to study the pathogenesis of human respiratory viral pneumonitides.
RESEARCH: Respiratory syncytial virus (RSV) is commonest cause of lower respiratory tract disease in children worldwide. Pathogenesis of RSV-induced bronchiolitis is poorly understood, and effects of RSV infection on ion transport (a seminal function of respiratory epithelial cells) have not been investigated. I hypothesize that RSV infection of respiratory epithelial cells reduces their Na ? transport capacity. Preliminary studies have demonstrated that this hypothesis is correct, both in vitro and in RSV-infeeted BALB/c mice. My aims for years 01-
03 are to: (1) quantify alterations in Na + transport across airway and alveolar epithelia in vivo and ex vivo, after infection of BALB/c mice with RSV; (2) define changes in Na + currents and amiloride-sensitive channel activity after RSV infection of murine epithelial cells in vitro; and (3) correlate alterations in Na + transport induced by RSV in vitro and in vivo with alterations in ENaC expression by marine respiratory epithelia. My plan for years 04-05 is to determine the role of the ubiquitin/proteasome pathway in mediating reduced Na+ transport after RSV infection of respiratory epithelia, and to identify the role of the RSV small hydrophobic (SH) gene product in modulation of Na + transport. I will use a combined electrophysiologic and biochemical
approach to investigate effects of RSV on Na + transport at all levels, from the single cell to the whole animal, and to correlate these effects to Na + channel expression and degradation. My project will emphasize cross-training in diverse techniques, including short-circuit measurements across monolayers, radioisotopic ion flux studies, whole cell and single channel patch-clamp, and measurement of alveolar fluid clearance and nasal potential difference in mice.
ENVIRONMENT: This SERCA, with Dr. Matalon (lung physiology) as mentor and Dr. Sullender (respiratory syncytial virus) as co-mentor, will provide the training and setting I require for my maturation into an independent scientist focused on comparative pathophysiologic effects of respiratory viruses on normal epithelial cell function.
我1992年毕业于布里斯托尔大学,获得了解剖学和兽医学的荣誉学位。在UAB,我接受了实验动物医学、实验动物病理学和动物模型病毒发病机制的培训(2000年2月博士学位,导师Patricia Fultz博士)。随后,我选择加入Matalon博士的研究小组,在那里我可以通过交叉挖掘电生理学对病毒发病机制的了解,并将这些技术应用于研究人类呼吸道病毒性肺炎的发病机制。
项目成果
期刊论文数量(3)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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IAN CHRISTOPHER DAVIS其他文献
IAN CHRISTOPHER DAVIS的其他文献
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{{ truncateString('IAN CHRISTOPHER DAVIS', 18)}}的其他基金
Role of ATII cell senescence in influenza pathogenesis in aging
ATII细胞衰老在流感发病机制中的作用
- 批准号:
10741215 - 财政年份:2023
- 资助金额:
$ 12.01万 - 项目类别:
Role of alterations in the ATII cell lipidome in influenza pathogenesis
ATII 细胞脂质组变化在流感发病机制中的作用
- 批准号:
9917813 - 财政年份:2017
- 资助金额:
$ 12.01万 - 项目类别:
Role of alterations in the ATII cell lipidome in influenza pathogenesis
ATII 细胞脂质组变化在流感发病机制中的作用
- 批准号:
9298233 - 财政年份:2017
- 资助金额:
$ 12.01万 - 项目类别:
The role of adenosine in the pathogenesis of influenza
腺苷在流感发病机制中的作用
- 批准号:
8080241 - 财政年份:2010
- 资助金额:
$ 12.01万 - 项目类别:
The role of adenosine in the pathogenesis of influenza
腺苷在流感发病机制中的作用
- 批准号:
8298185 - 财政年份:2010
- 资助金额:
$ 12.01万 - 项目类别:
The role of adenosine in the pathogenesis of influenza
腺苷在流感发病机制中的作用
- 批准号:
8078108 - 财政年份:2010
- 资助金额:
$ 12.01万 - 项目类别:
The role of adenosine in the pathogenesis of influenza
腺苷在流感发病机制中的作用
- 批准号:
8689136 - 财政年份:2010
- 资助金额:
$ 12.01万 - 项目类别:
The role of adenosine in the pathogenesis of influenza
腺苷在流感发病机制中的作用
- 批准号:
8509777 - 财政年份:2010
- 资助金额:
$ 12.01万 - 项目类别:
Na+ TRANSPORT INHIBITION BY RESPIRATORY SYNCYTIAL VIRUS
呼吸道合胞病毒对 Na 转运的抑制
- 批准号:
6931548 - 财政年份:2003
- 资助金额:
$ 12.01万 - 项目类别:
Na+ TRANSPORT INHIBITION BY RESPIRATORY SYNCYTIAL VIRUS
呼吸道合胞病毒对 Na 转运的抑制
- 批准号:
6802676 - 财政年份:2003
- 资助金额:
$ 12.01万 - 项目类别:
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