PubMed · 8353340
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H G Borst. 1993. Modified elephant trunk procedure.. https://doi.org/10.1111/j.1540-8191.1993.tb00402.x
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The role of elastin in the aortic wall calcification and involved mechanisms were investigated. The major hypothesis of this work is that elastin is one of the major components to regulate calcification of bioprosthetic heart valve (BHV). The relationship between the elastin content and the calcification rate of the aortic wall was established using collagen-elastin matrices (CEM) made of varying ratios of collagen and elastin (90 and 10, 50 and 50, and 20 and 80). Biophysical characterization of CEM was performed by water content measurement and the tensile strength test. The conformational changes of the calcifiable matrix were evaluated as a function of elastin content using Fourier transform infrared (FTIR) spectroscopy. The calcium contents in CEM implanted in the rat subcutaneous model for 7 days were measured using atomic absorption (AA) spectroscopy. As the concentration of elastin in CEM increased from 10 to 80%, the total amount of calcium accumulated in CEM also increased. The calcium level in CEM containing the collagen and an elastin ratio of 20:80 was 20.16 +/- 0.70 microg/mg compared with 1.96 +/- 0.04 microg/mg in CEM containing the collagen and an elastin ratio of 90:10. The calcification rate of CEM pretreated with ethanol increased, as the elastin concentration in the CEM. However, the calcification rate of CEM pretreated with ethanol is significantly lower than that of the untreated control. The permeation rate of ethanol through CEM with the collagen and an elastin ratio of 20:80 (0.37 +/- 0.13 mmol/cm(2)/h) is significantly smaller than that through CEM with 90:10 (0.94 +/- 0.27 mmol/cm(2)/h). These results indicate that elastin has a significant role in tissue calcification and that elastin's resistance to ethanol penetration partially contributes less effectiveness of ethanol on aortic wall calcification.
BACKGROUND: Major vascular injuries (MVI) still occur in laparoscopic surgery. METHODS: We report our institution's experience of two MVI (aortic lesions) in a series of 3545 laparoscopies (July 1991-December 2000). We compared this experience with other series reporting MVI from Medline, Embase, Current Contents, and Best Evidence. RESULTS: There were no deaths, but we had 23 postoperative and eight intraoperative bleedings, including two hepatic vessel lesions during dissection and six vascular lesions (four minor vessels and two aortic) related to trocar insertion. Prevention and treatment options are also discussed. CONCLUSIONS: The incidence of MVI reported in the literature is 0.05%, but the true incidence is difficult to estimate because results are not always comparable and there is a possibility of underreporting. The mortality rates (8-17%) are high. No technique or instrumentation is completely safe; therefore, a high level of alertness must be maintained at all times and precautions must be adopted to avoid major complications.
The role of angiogenesis in the growth and metastasis of solid tumors is well established. However, the role of angiogenesis in hematologic malignancies was only recently appreciated. We show that HTLV-I-transformed T cells, but not HTLV-I-negative CD4(+) T cells, secrete biologically active forms of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) and, accordingly, induce angiogenesis in vitro. Furthermore, fresh ATL leukemic cells derived from patients with acute ATL produce VEGF and bFGF transcripts and proteins. The viral transactivator Tax activates the VEGF promoter, linking the induction of angiogenesis to viral gene expression. Angiogenesis is associated with the adhesion of HTLV-I-transformed cells to endothelial cells and gap junction-mediated heterocellular communication between the 2 cell types. Angiogenesis, cell adhesion, and communication likely contribute to the development of adult T-cell leukemia-lymphoma and represent potential therapeutic targets.