Ultrathin Supratrochlear Artery Cutaneous Branch Flaps for Large Defects Around Eyebrows.

BACKGROUND: The key point of repairing large defects around eyebrows is to keep the eyebrow undistorted. The limited skin elevates the application difficulty of conventional methods such as direct suture or local flap. Forehead pedicle flaps do well in tension control. However, most of them are too thick for defects because the frontalis muscle must be included. Recently, 1 stable supratrochlear artery cutaneous branch was found, which provides an opportunity to make an ultrathin forehead flap with a good blood supply. This study aims to investigate whether the supratrochlear artery cutaneous branch flap could perform good esthetic reconstruction for defects around the eyebrow. METHODS: The authors retrospectively included 15 patients whose defect around the eyebrows was repaired by the supratrochlear artery cutaneous branch flap from June 2017 to June 2020. The authors followed up about their flap color and texture, scar, abnormal sensation, any complication, recurrence, and patient satisfaction for at least 6 months online or face-to-face. RESULTS: All of the flaps survived, without distortion of the eyebrows or inner canthi. Similar flap color, texture, and thickness with the nearby skin were obtained, except 2 patients reported pigmentation. Donor and receptor scars were acceptable. There was no recurrence or other complications. All of the patients were satisfied with the surgery effect. CONCLUSIONS: The supratrochlear artery cutaneous branch flap is a valuable alternative method to repair large defects around the eyebrows. It can avoid facial distortion and achieve good esthetic outcomes in single-stage surgery.

Experimental study on the influence of different aperture connectors on nanofat.

BACKGROUND: Nanofat, as a derivative of adipose tissue, has gradually become a research hotspot in beauty and regenerative medicine. However, the nanofat preparation method has not yet been standardized; it remains unknown whether the aperture of the connector has any influence on the transplantation effect. METHODS: Adipose tissue was mechanically emulsified into nanofat tissue through different connector apertures (1.0, 1.5, and 2.0 mm). Cell survival and apoptosis were measured using the volume of oil droplets, glucose transportation test, flow cytometry, cell counting kit-8 (CCK-8), wound healing assay, transwell migration assay, and fluorescence staining. The expression of adiponectin, GluT4, and PPAR-γ in nanofat-derived stem cells (NFSCs) was detected using quantitative real-time polymerase chain reaction (qRT-PCR). RESULTS: The fineness of nanofat tissue texture decreased with an increase in the aperture connector. The amounts of glucose transferred in the three groups (1, 1.5, and 2 mm) were 4.7 ± 0.894, 6.1 ± 1.026, and 6.9 ± 0.868 mmol/L, respectively. Flow cytometric analysis showed that the proportion of NFSCs in the 2.0 mm group was the highest (91.267±1.210%). Cell proliferation and migration abilities were stronger in the 1.5 and 2.0 mm groups. The numbers of late apoptotic and dead cells in the 2.0 mm group were significantly fewer than those in the two other groups. Expression levels of lipid-related genes were as follows: adiponectin > GluT4 > PPAR-γ in each component. CONCLUSIONS: As nanofat is emulsified, the use of larger aperture connectors (2.0 mm) appeared to decrease the degree of adipocyte lysis and increase the biological activity of adipose tissue.

HIF-1α inhibits mitochondria-mediated apoptosis and improves the survival of human adipose-derived stem cells in ischemic microenvironments.

BACKGROUND: Human adipose mesenchymal stem cells (hADSCs) show poor survival after transplantation, limiting their clinical application. Tissue regeneration resulting from stem cell treatment may be caused by attenuation of hypoxia-inducible factor-1α (HIF-1α). In this study, we constructed hADSCs stably expressing HIF-1α and investigated the potential effects of HIF-1α expression in the ischemic microenvironment on mitochondrial apoptosis and survival of hADSCs, and studied the mechanisms involved. METHOD: Apoptosis was induced by an ischemic microenvironment in vitro. ADSCs with stable HIF-1α expression were established. Cell survival and apoptosis were observed by CCK-8 assay, western blotting, flow cytometry, and fluorescence staining. ADSCs were subcutaneously transplanted into nude mice in the location where a hypoxia ischemic microenvironment was simulated in vivo. After 1, 3, and 7 d, mitochondrial apoptotic proteins were evaluated by immunohistochemistry and immunofluorescence staining. RESULTS: Exogenous HIF-1α downregulated mitochondrial reactive oxygen species, cytochrome c, caspase-9, and caspase-3, but inhibited mitochondrial membrane potential depolarization and increased the Bcl-2/bax ratio. HIF-1α prevented apoptosis and promoted vascular endothelial growth factor (VEGF) secretion as demonstrated by enzyme-linked immunosorbent assay (ELISA), terminal deoxyribonucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining, and flow cytometry analysis. HIF-1α enhanced the survival of transplanted ADSCs in nude mice. CONCLUSION: We have shown that through inhibition of the mitochondria-mediated apoptotic pathway and promotion of VEGF secretion in hADSCs in an ischemic microenvironment, HIF-1α may potentially be applied in clinical therapy and as an alternative strategy for improving hADSC therapy.