Summary:Recent advances in 3-dimensional (3D) surface imaging technologies allow for digital quantification of complex breast tissue. We performed 11 unilateral breast reconstructions with deep inferior epigastric artery perforator (DIEP) flaps (5 immediate, 6 delayed) using 3D surface imaging for easier surgery planning and 3D-printed molds for shaping the breast neoparenchyma. A single- or double-pedicle flap was preoperatively planned according to the estimated tissue volume required and estimated total flap volume. The DIEP flap was then intraoperatively shaped with a 3D-printed mold that was based on a horizontally inverted shape of the contralateral breast. Cosmetic outcomes were assessed as satisfactory, as confirmed by the postoperative 3D measurements of bilateral breasts. We believe that DIEP flap reconstruction assisted with 3D surface imaging and a 3D-printed mold is a simple and quick method for rebuilding a symmetric breast.
BackgroundOxidative stress has been suggested as a mechanism underlying skin aging, as it triggers apoptosis in various cell types, including fibroblasts, which play important roles in the preservation of healthy, youthful skin. Catechins, which are antioxidants contained in green tea, exert various actions such as anti-inflammatory, anti-bacterial, and anti-cancer actions. In this study, we investigated the effect of (+)-catechin on apoptosis induced by oxidative stress in fibroblasts.MethodsFibroblasts (NIH3T3) under oxidative stress induced by hydrogen peroxide (0.1 mM) were treated with either vehicle or (+)-catechin (0–100 μM). The effect of (+)-catechin on cell viability, apoptosis, phosphorylation of c-Jun terminal kinases (JNK) and p38, and activation of caspase-3 in fibroblasts under oxidative stress were evaluated.ResultsHydrogen peroxide induced apoptotic cell death in fibroblasts, accompanied by induction of phosphorylation of JNK and p38 and activation of caspase-3. Pretreatment of the fibroblasts with (+)-catechin inhibited hydrogen peroxide-induced apoptosis and reduced phosphorylation of JNK and p38 and activation of caspase-3.Conclusion(+)-Catechin protects against oxidative stress-induced cell death in fibroblasts, possibly by inhibiting phosphorylation of p38 and JNK. These results suggest that (+)-catechin has potential as a therapeutic agent for the prevention of skin aging.
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