Penetrating atherosclerotic ulcer is an ulcerating atherosclerotic lesion that penetrates the elastic lamina and is associated with hematoma formation within the media of the aortic wall. This pathologic condition is distinct from classic aortic dissection and aortic rupture; however, care should be taken in making the diagnosis, particularly if the disease is discovered incidentally. At computed tomography (CT), penetrating atherosclerotic ulcer manifests as focal involvement with adjacent subintimal hematoma and is often associated with aortic wall thickening or enhancement. Magnetic resonance imaging is superior to conventional CT in differentiating acute intramural hematoma from atherosclerotic plaque and chronic intraluminal thrombus and allows unenhanced multiplanar imaging. Spiral CT involves shorter examination times and allows high-quality two- and three-dimensional image reconstruction. CT angiography can demonstrate complex spatial relationships, mural abnormalities, and extraluminal pathologic conditions. Transesophageal echocardiography has been reported to be highly sensitive and specific in the differentiation of aortic disease, and intravascular ultrasonography may also be useful in this setting. Although rupture or other life-threatening complications are rare, patients with penetrating atherosclerotic ulcer must be followed up, particularly during the 1st month after onset. Surgical treatment may become necessary in cases involving evidence of intramural hematoma expansion, signs of impending rupture, inability to control pain, or blood pressure changes.
The location of ulcerlike projections is the principal predictor of progression, and careful follow-up study is needed for patients with an ulcerlike projection located from the ascending aorta to the aortic arch.
We have found that the imprinted H19 gene can be expressed either biallelically or monoallelically in the developing human placentae. H19 biallelic expression is confined to the placenta until 10 weeks of gestation, after which it becomes exclusively maternal, and does not affect allele-specificity or levels of IGF2 expression. The promoter region of H19 is hypomethylated at all stages of placental development, while the 3' portion shows progressive methylation of the paternal allele with gestation. Our observations demonstrate that the establishment of functional H19 imprinting occurs during the early development of the placenta and provide an opportunity to understand the mechanism by which the H19 primary imprint is manifested in somatic cells.
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