3 research outputs found

    Stanford type B aortic dissection is more frequently associated with coronary artery atherosclerosis than type A

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    Abstract Background The relationship between aortic dissection and coronary artery disease is not clear. The purpose of this study was to clarify the difference in the rate of coronary artery atherosclerosis between Stanford type A and type B aortic dissection by reviewing our institutional database. Methods One hundred and forty-five patients (78 males, 67 females; mean age: 60 ± 12 years) admitted to our hospital with acute aortic dissection who underwent coronary angiography during hospitalization from 2000 through 2002 were enrolled in this study. The background characteristics, coronary risk factors, and coronary angiography findings (number of significant stenoses, stenoses according to Bogaty standards, extent index) of patients were compared between type A (Group A; n = 71) and type B dissection (Group B; N = 74). Results Significantly more patients had prior histories of complications from ischemic heart disease in Group B than in Group A (P = 0.04), with no significant differences in comparison to other risk factors observed except for hypertension. Significantly (p = 0.005) more stenoses were observed in Group B (1.54 ± 0.04) than in Group A (0.38 ± 0.1). A significantly higher (P < 0.05) index score indicating the severity of coronary atherosclerosis was observed in Group B (1.49 ± 0.09) than in Group A (0.72 ± 0.07). Conclusions Stanford type B acute aortic dissection was significantly more frequently associated with coronary artery atherosclerosis than type A

    Tie2 is tied at the cell-cell contacts and to extracellular matrix by Angiopoietin-1

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    Angiopoietin-1 (Ang1) binds to and activates Tie2 receptor tyrosine kinase. Ang1-Tie2 signal has been proposed to exhibit two opposite roles in the controlling blood vessels. One is vascular stabilization and the other is vascular angiogenesis. There has been no answer to the question as to how Tie2 induces two opposite responses to the same ligand. Our group and Dr. Alitalo's group have demonstrated that trans-associated Tie2 at cell-cell contacts and extracellular matrix (ECM)-anchored Tie2 play distinct roles in the endothelial cells. The complex formation depends on the presence or absence of cell-cell adhesion. Here, we review how Ang1-Tie2 signal regulates vascular maintenance and angiogenesis. We further point to the unanswered questions that must be clarified to extend our knowledge of vascular biology and to progress basic knowledge to the treatment of the diseases in which Ang1-Tie2-mediated signal is central
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