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- 저자 : Jaime Villalba-Caloca (검색결과 1 건)
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Experimental Tracheal Replacement: Angiogenesis and Null Apoptosis Promote Stenosis
J. Alfredo Santibáñez-Salgado,Avelina Sotres-Vega,Miguel O. Gaxiola-Gaxiola,,Jaime Villalba-Caloca,Karen Bobadilla Lozoya,Joaquín A. Zúñiga-Ramos 대한흉부외과학회 2021 Journal of Chest Surgery (J Chest Surg) Vol.54 No.3
Background: Tracheal replacement is a challenge for thoracic surgeons due to stenosis in the trachea-prosthesis anastomosis. We propose that stenosis occurs due to fibrosis as a result of an abnormal healing process, characterized by an increased expression of wound healing growth factors (vascular endothelial growth factor [VEGF], survivin, and CD31), which promote angiogenesis and decrease apoptosis. We analyzed the immunoreactivity of VEGF, survivin, CD31, and caspase-3 in the development of fibrotic stenosis in prosthetic tracheal replacement. Methods: Fourteen dogs were operated on: group I (n=7) received a 6-ring cervical tra- cheal segment autograft, while in group II (n=7), a 6-ring segment of the cervical trachea was resected and tracheal continuity was restored with a Dacron prosthesis. The follow-up was 3 months. Immunoreactivity studies for VEGF, survivin, CD31, and caspase-3 were per- formed. A statistical analysis was done using the Wilcoxon signed rank test. Results: Four animals in group I were euthanized on the 10th postoperative day due to autograft necrosis. Three animals completed the study without anastomotic stenosis. Moderate expression of VEGF (p=0.038), survivin (p=0.038), and CD31 (p=0.038) was found. All group II animals developed stenosis in the trachea-prosthesis anastomotic sites. Micros- copy showed abundant collagen and neovascularization vessels. Statistically significant immunoreactive expression of VEGF (p=0.015), survivin (p=0.017), and CD31 (p=0.011) was observed. No expression of caspase-3 was found. Conclusion: We found a strong correlation between fibrosis in trachea-prosthesis anas- tomoses and excessive angiogenesis, moderate to intense VEGF, CD31, and survivin ex- pression, and null apoptotic activity. These factors led to uncontrolled collagen production.
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