PubMed · 543648
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
A F Borges. 1979. W-plasty.. https://doi.org/10.1097/00000637-197908000-00012
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Explore the source record for details and available documents.
OBJECTIVE: To ascertain if avoiding the vestibular portion of alar reductions during rhinoplasty could improve the cosmetic result of the postoperative nasal sill. DESIGN: Blind, randomized review of base-view photographs (40 patients) 1 year after rhinoplasty. SETTING: A surgical clinic, accredited by the Accreditation Association of Ambulatory Health Care. PARTICIPANTS: A consecutive sample of 40 patients (2 groups) who underwent alar reduction as a part of their rhinoplasty and whose 1-year postoperative photographs were reviewed by 2 facial plastic surgeons and 3 plastic surgeons. MAIN OUTCOME MEASURES: Midway through a 2-year period, the method of alar reduction was changed to include only the cutaneous portion of the nostril. Twenty-two patients had cutaneous-vestibular excisions; 18 patients had cutaneous-only excisions. The surgeon participants reviewed randomized photographs taken 1 year postoperatively and were asked to rate the alar sill for the degree of scarring and notching. RESULTS: Tabulation of the surgeons' ratings revealed significantly less perception of notching and scarring in the alar reduction group with the cutaneous-only excisions. CONCLUSION: Modification of alar reduction to avoid crossing the nostril rim appears to improve the aesthetic result.
Fibronectin and tenascin are matrix proteins known to be present in early experimental wound healing. As only limited data are available regarding early matrix changes in human myocardial infarction, the presence of tenascin and fibronectin was studied in human myocardial infarctions of different post-infarction times (6 h to 17 years), using immunohistochemistry. In normal myocardium, fibronectin immunostaining was found in the subendothelial space in vessels. Tenascin was not present in normal myocardium. While fibronectin was demonstrated in the ischaemic cardiomyocytes within 1 day, tenascin was found 4-6 days post-infarction and was located at the margin of the area of infarction. Tenascin expression then shifted from the margin to the centre of the area of infarction, where it could be found 2-3 weeks post-infarction. More than 4 weeks post-infarction, the scar tissue consisted of collagen fibres, with sparse (myo)fibroblasts. By that time, both tenascin and fibronectin expression had disappeared. Another interesting observation in this study was the presence of tenascin, but not fibronectin, surrounding vacuolated glycogen-rich cells, or so-called hibernating cardiomyocytes.