MR ANGIOGRAPHY OF FASD MOUSE MODEL

FASD小鼠模型的MR血管造影

• 批准号: 8363218
• 负责人: KATHLEEN K SULIK
• 金额: $ 1.84万
• 依托单位: DUKE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-07-01 至 2012-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8363218
• 关键词: Angiography; Apoptotic; Autopsy; Carotid Arteries; Carotid Body; Cell Death; Cessation of life; Child; Development; Embryo; Epidemiologic Studies; Ethanol; Fetal Alcohol Exposure; Fetal Alcohol Spectrum Disorder; Funding; Grant; Head and neck structure; Hypoxia; Laboratories; Microscopy; Mus; National Center for Research Resources; Principal Investigator; Research; Research Infrastructure; Resources; Source; Sudden infant death syndrome; Testing; United States National Institutes of Health; alcohol exposure; cost; mouse model; research study; respiratory; response

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Autopsies of children who have died of sudden infant death syndrome (SIDS) have identified deficits of the carotid body and the carotid arteries as one of the potential causative factors in their deaths. Likewise, epidemiological studies have identified prenatal ethanol exposure as another component involved in a certain subset of cases of SIDS. Finally, experiments from our laboratory have demonstrated ethanol-induced apoptotic cell death in regions of the developing mouse embryo that are crucial to the proper development of both the carotid body and carotid arteries. The experiments proposed here will test the hypotheses that early gestional ethanol exposure will result in hypoplasia of the carotid body, deficits in the normal respiratory response to hypoxia and abnormal vasculature of the head and neck, particularly the carotid arteries and their proximal branches.

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