Obstructive Sleep Apnea and WTC dust: Does Chronic Intermittent Hypoxia exacerbate WTC dust induced lung injury

阻塞性睡眠呼吸暂停和世贸中心粉尘:慢性间歇性缺氧是否会加剧世贸中心粉尘引起的肺损伤

基本信息

  • 批准号:
    10459204
  • 负责人:
  • 金额:
    $ 50万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2021
  • 资助国家:
    美国
  • 起止时间:
    2021-07-01 至 2024-06-30
  • 项目状态:
    已结题

项目摘要

Project Summary Collapse of the World Trade Center (WTC) twin towers led to a large dust cloud of particles that consisted of a mixture of highly alkaline fibers that were either inhaled or swallowed and were deposited in the conducting airways of WTC responders, recovery workers and local residents. This led to both physical and chemical irritation and resulted in upper and lower airway injury resulting in chronic sinusitis, obstructive sleep apnea (OSA), bronchial wall thickening, airways obstruction and airway hyperreactivity, as well as a sarcoid like granulomatous inflammation of the lungs. Potential mechanisms of lung injury include upregulation of genes and proteins related to inflammation and oxidative stress. Additionally, metabolomic analysis suggests that oxidative stress mediates lung function decline. Since abnormal pulmonary structure and function can appear many years after the initial dust exposure, it is likely that additional oxidative stress may precipitate or worsen lung injury. Previous studies, including our own, (WTCSNORE) have shown a prevalence of 75% obstructive sleep apnea (OSA) in WTC subjects. We hypothesize that the presence of OSA in WTC responders represents a two- hit model that alters the metabolomic profile of the lung and mitochondrial function in lung macrophages resulting in exacerbated lung injury. To test this hypothesis, we will perform a longitudinal analysis of the effects of CIH following WTC dust exposure on oxidative stress markers, macrophage phenotype, mitochondrial function and physiological function of the lung in a mouse model of WTC dust exposure and identify the changing serum metabolomic profile associated with CIH. These studies will allow for the investigation of the fundamental role that macrophages play in mediating the two-hit process that results in lung injury in WTC exposed individuals. Furthermore, examination of serum biomarkers and their correlation to established processes in the animal model, will allow for the identification of novel biomarkers that can be used in future studies to track the progress of disease in WTC exposed individuals. These studies will help us achieve our long-term goal of defining the mechanisms underlying OSA worsening of the toxicity of WTC dust exposure. To test our hypothesis, in aim 1 we will analyze time related effects of CIH on WTC. In aim 2 we will perform a longitudinal analysis of the metabolomic profile in the serum and the lung of mice exposed to WTC dust and CIH. These studies have a significant clinical impact on the WTC responder population. They will provide. metabolomic profiles that will act as biomarkers of early lung injury in individuals with OSA. In addition, if OSA exacerbates lung injury, treatment of OSA may help in the prevention of WTC dust related respiratory illnesses.
项目总结

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 }}

Andrew J Gow其他文献

70 - A Cell Specific Role of INOS in Acute Lung Injury; Recruitment and Activation of Macrophages
  • DOI:
    10.1016/j.freeradbiomed.2015.10.109
  • 发表时间:
    2015-10-01
  • 期刊:
  • 影响因子:
  • 作者:
    Thea Golden;Andrew J Gow
  • 通讯作者:
    Andrew J Gow

Andrew J Gow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('Andrew J Gow', 18)}}的其他基金

2023 Nitric Oxide GRC and GRS
2023 一氧化氮 GRC 和 GRS
  • 批准号:
    10608028
  • 财政年份:
    2023
  • 资助金额:
    $ 50万
  • 项目类别:
Obstructive Sleep Apnea and WTC dust: Does Chronic Intermittent Hypoxia exacerbate WTC dust induced lung injury
阻塞性睡眠呼吸暂停和世贸中心粉尘:慢性间歇性缺氧是否会加剧世贸中心粉尘引起的肺损伤
  • 批准号:
    10314852
  • 财政年份:
    2021
  • 资助金额:
    $ 50万
  • 项目类别:
NO-Modified Biomolecules and Pulmonary Signaling
NO 修饰的生物分子和肺部信号传导
  • 批准号:
    8707538
  • 财政年份:
    2008
  • 资助金额:
    $ 50万
  • 项目类别:
NO-Modified Biomolecules and Pulmonary Signaling
NO 修饰的生物分子和肺部信号传导
  • 批准号:
    7526781
  • 财政年份:
    2008
  • 资助金额:
    $ 50万
  • 项目类别:
NO-Modified Biomolecules and Pulmonary Signaling
NO 修饰的生物分子和肺部信号传导
  • 批准号:
    8289980
  • 财政年份:
    2008
  • 资助金额:
    $ 50万
  • 项目类别:
NO-Modified Biomolecules and Pulmonary Signaling
NO 修饰的生物分子和肺部信号传导
  • 批准号:
    8581605
  • 财政年份:
    2008
  • 资助金额:
    $ 50万
  • 项目类别:
NO-Modified Biomolecules and Pulmonary Signaling
NO 修饰的生物分子和肺部信号传导
  • 批准号:
    7883563
  • 财政年份:
    2008
  • 资助金额:
    $ 50万
  • 项目类别:
NO-Modified Biomolecules and Pulmonary Signaling
NO 修饰的生物分子和肺部信号传导
  • 批准号:
    8098350
  • 财政年份:
    2008
  • 资助金额:
    $ 50万
  • 项目类别:
NO-Modified Biomolecules and Pulmonary Signaling
NO 修饰的生物分子和肺部信号传导
  • 批准号:
    7657295
  • 财政年份:
    2008
  • 资助金额:
    $ 50万
  • 项目类别:
Surfactant Proteins and NO in Inflammatory Disease
炎症性疾病中的表面活性蛋白和 NO
  • 批准号:
    6673989
  • 财政年份:
    2003
  • 资助金额:
    $ 50万
  • 项目类别:

相似海外基金

I-Corps: Neurostimulation Platform for Effective Treatment of Palatal Collapse in Obstructive Sleep Apnea
I-Corps:有效治疗阻塞性睡眠呼吸暂停中腭塌陷的神经刺激平台
  • 批准号:
    2346870
  • 财政年份:
    2024
  • 资助金额:
    $ 50万
  • 项目类别:
    Standard Grant
SBIR Phase I: Non-invasive Closed Loop Neuromodulation to Treat Obstructive Sleep Apnea
SBIR 第一阶段:无创闭环神经调节治疗阻塞性睡眠呼吸暂停
  • 批准号:
    2304265
  • 财政年份:
    2023
  • 资助金额:
    $ 50万
  • 项目类别:
    Standard Grant
Upper airway collapsibility, loop gain and arousal threshold: an integrative therapeutic approach to obstructive sleep apnea
上气道塌陷、循环增益和唤醒阈值:阻塞性睡眠呼吸暂停的综合治疗方法
  • 批准号:
    10859275
  • 财政年份:
    2023
  • 资助金额:
    $ 50万
  • 项目类别:
Screening for Obstructive Sleep Apnea Syndrome by Oral Function and the Investigation of the Effectiveness of Muscle Function Training
口腔功能筛查阻塞性睡眠呼吸暂停综合征及肌肉功能训练效果研究
  • 批准号:
    23K09512
  • 财政年份:
    2023
  • 资助金额:
    $ 50万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Developing a P4 Medicine Approach to Obstructive Sleep Apnea
开发治疗阻塞性睡眠呼吸暂停的 P4 医学方法
  • 批准号:
    10555805
  • 财政年份:
    2023
  • 资助金额:
    $ 50万
  • 项目类别:
Fair risk profiles and predictive models for outcomes of obstructive sleep apnea through electronic medical record data
通过电子病历数据对阻塞性睡眠呼吸暂停结果进行公平的风险概况和预测模型
  • 批准号:
    10678108
  • 财政年份:
    2023
  • 资助金额:
    $ 50万
  • 项目类别:
Positive Airway Pressure For The Treatment Of The Obstructive Sleep Apnea Syndrome In Children With Down Syndrome
气道正压通气治疗唐氏综合症儿童阻塞性睡眠呼吸暂停综合症
  • 批准号:
    10911685
  • 财政年份:
    2023
  • 资助金额:
    $ 50万
  • 项目类别:
A new method to discover patients with obstructive sleep apnea using artificial intelligence and 2D and 3D images in addition to several complications
一种利用人工智能、2D 和 3D 图像发现阻塞性睡眠呼吸暂停患者的新方法,此外还存在多种并发症
  • 批准号:
    23K07638
  • 财政年份:
    2023
  • 资助金额:
    $ 50万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
MicroRNAs as Biomarkers for Obstructive Sleep Apnea
MicroRNA 作为阻塞性睡眠呼吸暂停的生物标志物
  • 批准号:
    10555810
  • 财政年份:
    2023
  • 资助金额:
    $ 50万
  • 项目类别:
A Personalized Surgical Approach for the Treatment of Children with Obstructive Sleep Apnea and Small Tonsils
治疗患有阻塞性睡眠呼吸暂停和小扁桃体的儿童的个性化手术方法
  • 批准号:
    10634395
  • 财政年份:
    2023
  • 资助金额:
    $ 50万
  • 项目类别:
{{ showInfoDetail.title }}

作者:{{ showInfoDetail.author }}

知道了