COMPARATIVE PROTEOMIC INVESTIGATION OF ARDS AND SYSTEMIC INFLAMMATORY INJURY
ARDS 和全身炎症损伤的比较蛋白质组学研究
基本信息
- 批准号:7724167
- 负责人:
- 金额:$ 0.26万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2008
- 资助国家:美国
- 起止时间:2008-06-01 至 2009-05-31
- 项目状态:已结题
- 来源:
- 关键词:Adult Respiratory Distress SyndromeAlveolarAnimalsBlood ProteinsBlood capillariesCellsClinicalClinical ResearchComputer Retrieval of Information on Scientific Projects DatabaseControl AnimalDiseaseEvaluationFundingGrantInflammatoryInflammatory ResponseInjuryInstitutionIntensive CareInvestigationIschemiaKupffer CellsLiquid substanceLiverLungMechanical ventilationMedicineMorbidity - disease ratePatientsPhysiological reperfusionPneumoniaProteomeProteomicsPulmonary EdemaPulmonary aspiration of gastric contentsRattusReactionReperfusion InjuryReperfusion TherapyResearchResearch PersonnelResourcesSamplingSepsisSourceTidal VolumeTraumaUnited States National Institutes of HealthVentilator-induced lung injuryalveolar type II cellcapillarycomparativeimprovedmortality
项目摘要
This subproject is one of many research subprojects utilizing the
resources provided by a Center grant funded by NIH/NCRR. The subproject and
investigator (PI) may have received primary funding from another NIH source,
and thus could be represented in other CRISP entries. The institution listed is
for the Center, which is not necessarily the institution for the investigator.
The acute respiratory distress syndrome (ARDS) is one of the most important causes for morbidity and mortality in intensive care medicine. It can be the sequel of diseases like sepsis, aspiration of gastric contents, pneumonia or trauma. It is characterized by an inflammatory reaction that leads to a breakdown of the alveolar-capillary barrier, resulting in an influx of fluid and proteins from the blood into the alveolar space. The exact mechanism of the inflammatory reaction is still incompletely understood. Numerous clinical and experimental trials have been made in order to improve the understanding and evaluate possible treatment options. It has been shown in clinical studies that the mode of mechanical ventilation, namely the tidal volume that is used, impacts survival of patients with this disease.
The focus of our studies was on three different aspects:
- The evaluation of pulmonary edema fluid samples of patients with ARDS compared to control samples
- Induction of ventilator induced lung injury in rats and comparison of the proteome of alveolar type II cells from these animals with cells from not ventilated control animals
- Induction of liver damage in rats by ischemia-reperfusion and evaluation of the proteome of the pulmonary alveolar type II cells to investigate the influence of a systemic inflammatory response on the proteome of these cells
- In an additional project in cooperation with the UCSF liver center, proteomic changes in inflammatory cells were investigated. This was done using isolated Kupffer cells from rats with ischemia-reperfusion injury.
这个子项目是许多研究子项目中的一个
由NIH/NCRR资助的中心赠款提供的资源。子项目和
研究者(PI)可能从另一个NIH来源获得了主要资金,
因此可以在其他CRISP条目中表示。所列机构为
研究中心,而研究中心不一定是研究者所在的机构。
急性呼吸窘迫综合征(ARDS)是重症监护医学中发病和死亡的重要原因之一。它可能是败血症、胃内容物吸入、肺炎或创伤等疾病的后遗症。它的特征是炎症反应,导致肺泡-毛细血管屏障的破坏,导致液体和蛋白质从血液流入肺泡腔。炎症反应的确切机制仍不完全清楚。已经进行了许多临床和实验性试验,以提高对可能的治疗方案的理解和评估。临床研究表明,机械通气的模式,即所使用的潮气量,会影响患有这种疾病的患者的生存。
我们研究的重点是三个不同的方面:
- 急性呼吸窘迫综合征患者肺水肿液标本与对照组比较
- 大鼠呼吸机肺损伤的诱导及其与非通气对照组肺泡II型细胞蛋白质组的比较
- 通过缺血-再灌注诱导大鼠肝损伤和评估肺泡II型细胞的蛋白质组以研究全身炎症反应对这些细胞蛋白质组的影响
- 在与UCSF肝脏中心合作的另一个项目中,研究了炎症细胞中的蛋白质组学变化。这是使用分离的枯否细胞从大鼠缺血再灌注损伤。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
数据更新时间:{{ journalArticles.updateTime }}
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
数据更新时间:{{ journalArticles.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ monograph.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ sciAawards.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ conferencePapers.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ patent.updateTime }}
MICHAEL A. MATTHAY其他文献
MICHAEL A. MATTHAY的其他文献
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
{{ truncateString('MICHAEL A. MATTHAY', 18)}}的其他基金
Prevention and Early Treatment of Acute Lung Injury
急性肺损伤的预防和早期治疗
- 批准号:
8705240 - 财政年份:2014
- 资助金额:
$ 0.26万 - 项目类别:
Allogeneic Human Mesenchymal Stem Cells for the Treatment of Acute Lung Injury
同种异体人间充质干细胞治疗急性肺损伤
- 批准号:
8144663 - 财政年份:2011
- 资助金额:
$ 0.26万 - 项目类别:
Allogeneic Human Mesenchymal Stem Cells for the Treatment of Acute Lung Injury
同种异体人间充质干细胞治疗急性肺损伤
- 批准号:
8693006 - 财政年份:2011
- 资助金额:
$ 0.26万 - 项目类别:
Allogeneic Human Mesenchymal Stem Cells for the Treatment of Acute Lung Injury
同种异体人间充质干细胞治疗急性肺损伤
- 批准号:
8326060 - 财政年份:2011
- 资助金额:
$ 0.26万 - 项目类别:
COMPARATIVE PROTEOMIC INVESTIGATION OF ARDS AND SYSTEMIC INFLAMMATORY INJURY
ARDS 和全身炎症损伤的比较蛋白质组学研究
- 批准号:
8169730 - 财政年份:2010
- 资助金额:
$ 0.26万 - 项目类别:
COMPARATIVE PROTEOMIC INVESTIGATION OF ARDS AND SYSTEMIC INFLAMMATORY INJURY
ARDS 和全身炎症损伤的比较蛋白质组学研究
- 批准号:
7957366 - 财政年份:2009
- 资助金额:
$ 0.26万 - 项目类别:
COMPARATIVE PROTEOMIC INVESTIGATION OF ARDS AND SYSTEMIC INFLAMMATORY INJURY
ARDS 和全身炎症损伤的比较蛋白质组学研究
- 批准号:
7601816 - 财政年份:2007
- 资助金额:
$ 0.26万 - 项目类别:
COMPARATIVE PROTEOMIC INVESTIGATION OF ARDS AND SYSTEMIC INFLAMMATORY INJURY
ARDS 和全身炎症损伤的比较蛋白质组学研究
- 批准号:
7369046 - 财政年份:2006
- 资助金额:
$ 0.26万 - 项目类别:
相似海外基金
Gain-of-function toxicity in alpha-1 antitrypsin deficient type 2 alveolar epithelial cells
α-1 抗胰蛋白酶缺陷型 2 型肺泡上皮细胞的功能获得毒性
- 批准号:
10751760 - 财政年份:2024
- 资助金额:
$ 0.26万 - 项目类别:
The role of alveolar macrophages and regulatory pathways in post-transplant lung inflammation.
肺泡巨噬细胞和调节途径在移植后肺部炎症中的作用。
- 批准号:
23K08315 - 财政年份:2023
- 资助金额:
$ 0.26万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Mechanical signaling through the nuclear membrane in lung alveolar health
通过核膜的机械信号传导影响肺泡健康
- 批准号:
10677169 - 财政年份:2023
- 资助金额:
$ 0.26万 - 项目类别:
Mechanistic studies of the genetic contribution of desmoplakin to pulmonary fibrosis in alveolar type 2 cells
桥粒斑蛋白对肺泡2型细胞肺纤维化的遗传贡献机制研究
- 批准号:
10736228 - 财政年份:2023
- 资助金额:
$ 0.26万 - 项目类别:
Pilot Studies of PAX3-FOXO1 Fusions Proteins in Alveolar Rhabdomyosarcoma
PAX3-FOXO1 融合蛋白在肺泡横纹肌肉瘤中的初步研究
- 批准号:
10726763 - 财政年份:2023
- 资助金额:
$ 0.26万 - 项目类别:
Novel alveolar mechanisms of hypoxemia in hepatopulmonary syndrome
肝肺综合征低氧血症的新肺泡机制
- 批准号:
10718446 - 财政年份:2023
- 资助金额:
$ 0.26万 - 项目类别:
Utilizing induced pluripotent stem cells to study the role of alveolar type 2 cell dysfunction in pulmonary fibrosis
利用诱导多能干细胞研究肺泡2型细胞功能障碍在肺纤维化中的作用
- 批准号:
10591174 - 财政年份:2023
- 资助金额:
$ 0.26万 - 项目类别:
Injury of blood brain and alveolar-endothelial barriers caused by alcohol and electronic cigarettes via purinergic receptor signaling
酒精和电子烟通过嘌呤受体信号传导引起血脑和肺泡内皮屏障损伤
- 批准号:
10638221 - 财政年份:2023
- 资助金额:
$ 0.26万 - 项目类别:
Alveolar Epithelial Cell Dysfunction Induced By Flavored E-Cigarette Aerosols
加味电子烟气雾剂引起的肺泡上皮细胞功能障碍
- 批准号:
10770080 - 财政年份:2023
- 资助金额:
$ 0.26万 - 项目类别:
Delineating the role of let-7 microRNA on lung AT2 cell homeostasis, alveolar regeneration, and interstitial lung disease
描述let-7 microRNA对肺AT2细胞稳态、肺泡再生和间质性肺疾病的作用
- 批准号:
10634881 - 财政年份:2023
- 资助金额:
$ 0.26万 - 项目类别: