REGULATION OF THE DUCTUS ARTERIOSIS

动脉导管的调节

基本信息

  • 批准号:
    7349767
  • 负责人:
  • 金额:
    $ 3.79万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2006
  • 资助国家:
    美国
  • 起止时间:
    2006-05-01 至 2007-04-30
  • 项目状态:
    已结题

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. In the premature infant, the ductus arteriosus frequently remains open for many days or weeks after delivery. As many as 70% of newborns delivered prior to 28 weeks gestation will require some form of therapy to close their patient ductus. If left unclosed, a persistent patent ductus arteriosus is associated with significant morbidity: bronchopulmonary dysplasia (with its prolonged need for mechanical ventilation) and necrotizing enterocolitis. Numerous studies have shown that early closure of the ductus arteriosus decreases the severity of bronchopulmonary dysplasia and decreases the incidence of necrotizing enterocolitis. Although inhibitors of prostaglandin synthesis, like indomethacin, induce ductus closure in 85% of preterm infants in whom they are used, ductus reopening occurs in 20-30% of treated infants. Recent studies demonstrate that the postnatal development of ductus wall hypoxia is an essential step in the anatomic remodeling (luminal endothelial proliferation, migration, and smooth muscle cell death) that leads to permanent closure. The studies proposed in this application will examine the mechanisms involved in early, spontaneous ductus closure in the full-term newborn and those involved in the delayed closure of the premature baboon model of persistent patent ductus arteriosus, which is the only model that mimics the long-term events surrounding ductus patency in the preterm human. They will examine the hypothesis that vasoactive factors that alter ductus tone (e.g., prostaglandins, nitric oxide) also interact with an deregulate the growth factors and death factors involved in anatomic remodeling. They will examine mechanisms to increase ductus wall hypoxia in the preterm newborn. They will use immunohistochemical, Western, and Northern techniques to study changes in mRNA and protein expression; they will use assays of cell migration, proliferation, and cell death in isolated vessels, endothelial and smooth muscle cells in culture. They will characterize changes in receptor populations and test their findings in vivo. These studies should increase our understanding of what initiates and sustains the process of ductus closure after birth and why it does not occur in the preterm infant.
该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者(PI)可能从另一个NIH来源获得主要资金,因此可以在其他CRISP条目中表示。所列机构为中心,不一定是研究者所在机构。在早产儿中,动脉导管在分娩后经常保持开放许多天或数周。在妊娠28周之前分娩的新生儿中,多达70%需要某种形式的治疗来关闭其患者导管。如果不关闭,持续性动脉导管未闭与显著的发病率相关:支气管肺发育不良(长期需要机械通气)和坏死性小肠结肠炎。大量研究表明,动脉导管早期关闭可降低支气管肺发育不良的严重程度,并降低坏死性小肠结肠炎的发生率。尽管前列腺素合成抑制剂(如消炎痛)可诱导85%使用该药物的早产儿的导管关闭,但20-30%接受治疗的婴儿会发生导管重新打开。最近的研究表明,导管壁缺氧的出生后发展是导致永久性关闭的解剖学重塑(管腔内皮细胞增殖、迁移和平滑肌细胞死亡)的重要步骤。本申请中提出的研究将检查足月新生儿中早期自发性导管闭合所涉及的机制,以及持续性动脉导管未闭的早产狒狒模型延迟闭合所涉及的机制,该模型是模拟早产儿中导管通畅周围长期事件的唯一模型。他们将研究改变导管张力的血管活性因子(例如,前列腺素、一氧化氮)还与解剖重塑中涉及的生长因子和死亡因子的失调相互作用。他们将研究早产新生儿导管壁缺氧增加的机制。他们将使用免疫组织化学,Western和北方技术来研究mRNA和蛋白质表达的变化;他们将使用细胞迁移,增殖和细胞死亡的测定在离体血管,内皮细胞和平滑肌细胞培养。他们将描述受体群体的变化,并在体内测试他们的发现。这些研究应该增加我们对出生后是什么启动和维持导管闭合过程以及为什么它不会发生在早产儿中的理解。

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 }}

RONALD I CLYMAN其他文献

RONALD I CLYMAN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('RONALD I CLYMAN', 18)}}的其他基金

Genes contributing to patent ductus arteriosus susceptibility in preterm newborns
导致早产儿动脉导管未闭易感性的基因
  • 批准号:
    8514057
  • 财政年份:
    2011
  • 资助金额:
    $ 3.79万
  • 项目类别:
Genes contributing to patent ductus arteriosus susceptibility in preterm newborns
导致早产儿动脉导管未闭易感性的基因
  • 批准号:
    8150874
  • 财政年份:
    2011
  • 资助金额:
    $ 3.79万
  • 项目类别:
Genes contributing to patent ductus arteriosus susceptibility in preterm newborns
导致早产儿动脉导管未闭易感性的基因
  • 批准号:
    8704991
  • 财政年份:
    2011
  • 资助金额:
    $ 3.79万
  • 项目类别:
Genes contributing to patent ductus arteriosus susceptibility in preterm newborns
导致早产儿动脉导管未闭易感性的基因
  • 批准号:
    8296493
  • 财政年份:
    2011
  • 资助金额:
    $ 3.79万
  • 项目类别:
CLOSURE OF THE PRIMATE DUCTUS ARTEROISUS
灵长类动物动脉导管闭合
  • 批准号:
    7716091
  • 财政年份:
    2008
  • 资助金额:
    $ 3.79万
  • 项目类别:
REGULATION OF THE DUCTUS ARTERIOSUS
动脉导管的调节
  • 批准号:
    7716048
  • 财政年份:
    2008
  • 资助金额:
    $ 3.79万
  • 项目类别:
REGULATION OF THE DUCTUS ARTERIOSUS
动脉导管的调节
  • 批准号:
    7562419
  • 财政年份:
    2007
  • 资助金额:
    $ 3.79万
  • 项目类别:
CLOSURE OF THE PRIMATE DUCTUS ARTEROISUS
灵长类动物动脉导管闭合
  • 批准号:
    7562473
  • 财政年份:
    2007
  • 资助金额:
    $ 3.79万
  • 项目类别:
REGULATION OF THE DUCTUS ARTERIOSIS
动脉导管的调节
  • 批准号:
    7165308
  • 财政年份:
    2005
  • 资助金额:
    $ 3.79万
  • 项目类别:
ASSOCIATION OF SERUM INDOMETHACIN LEVELS AND DUCTAL CLOSURE IN PREMATURE INFANTS
早产儿血清吲哚美辛水平与导管闭合的关系
  • 批准号:
    7204890
  • 财政年份:
    2005
  • 资助金额:
    $ 3.79万
  • 项目类别:

相似海外基金

Molecular identification of the oxygen sensor(s) in the fetal ductus arteriosus and pulmonary artery: an integrated multiomic comparison of mitochondria in vital fetal arteries with opposing oxygen responses
胎儿动脉导管和肺动脉中氧传感器的分子识别:对胎儿重要动脉中具有相反氧反应的线粒体进行综合多组学比较
  • 批准号:
    462691
  • 财政年份:
    2022
  • 资助金额:
    $ 3.79万
  • 项目类别:
    Operating Grants
Pharmacologic Contributors to Patent Ductus Arteriosus
动脉导管未闭的药理学贡献者
  • 批准号:
    10444540
  • 财政年份:
    2022
  • 资助金额:
    $ 3.79万
  • 项目类别:
1/2 percutaneous intervention versus observational trial of arterial ductus in lower gestational age infants (PIVOTAL)
1/2 经皮介入治疗与低胎龄儿动脉导管观察性试验 (PIVOTAL)
  • 批准号:
    10349765
  • 财政年份:
    2022
  • 资助金额:
    $ 3.79万
  • 项目类别:
1/2 percutaneous intervention versus observational trial of arterial ductus in lower gestational age infants (PIVOTAL)
1/2 经皮介入治疗与低胎龄儿动脉导管观察性试验 (PIVOTAL)
  • 批准号:
    10719307
  • 财政年份:
    2022
  • 资助金额:
    $ 3.79万
  • 项目类别:
2/2 Percutaneous Intervention Versus Observational Trial of Arterial ductus management in Low-weight infants (PIVOTAL) Data Coordinating Center
2/2 低体重婴儿动脉导管管理的经皮介入与观察试验 (PIVOTAL) 数据协调中心
  • 批准号:
    10594961
  • 财政年份:
    2022
  • 资助金额:
    $ 3.79万
  • 项目类别:
Pharmacologic Contributors to Patent Ductus Arteriosus
动脉导管未闭的药理学贡献者
  • 批准号:
    10653150
  • 财政年份:
    2022
  • 资助金额:
    $ 3.79万
  • 项目类别:
2/2 Percutaneous Intervention Versus Observational Trial of Arterial ductus management in Low-weight infants (PIVOTAL) Data Coordinating Center
2/2 低体重婴儿动脉导管管理的经皮介入与观察试验 (PIVOTAL) 数据协调中心
  • 批准号:
    10347461
  • 财政年份:
    2022
  • 资助金额:
    $ 3.79万
  • 项目类别:
DUCTUS ARTERIOSUS STENT TO IMPROVE CONGENITAL HEART DEFECT MORTALITY
动脉导管支架可改善先天性心脏缺陷死亡率
  • 批准号:
    10323573
  • 财政年份:
    2021
  • 资助金额:
    $ 3.79万
  • 项目类别:
DUCTUS ARTERIOSUS STENT TO IMPROVE CONGENITAL HEART DEFECT MORTALITY
动脉导管支架可改善先天性心脏缺陷死亡率
  • 批准号:
    10547086
  • 财政年份:
    2021
  • 资助金额:
    $ 3.79万
  • 项目类别:
DUCTUS ARTERIOSUS STENT TO IMPROVE CONGENITAL HEART DEFECT MORTALITY
动脉导管支架可改善先天性心脏缺陷死亡率
  • 批准号:
    10706595
  • 财政年份:
    2021
  • 资助金额:
    $ 3.79万
  • 项目类别:
{{ showInfoDetail.title }}

作者:{{ showInfoDetail.author }}

知道了