Objective:To investigate the effect of modified alar reduction with external incision to correct alar hypertrophy.Methods:From January 2017 to January 2019, 16 patients(1 male and 15 females, aged 21 to 39 with alar hypertrophy were treated in the plastic surgery department of the Second Affiliated Hospital of Nanchang University. Modified alar reduction with external incision were applied. In order to rotate the free alar lobules, the incision was extended in nasal lobules to the vestibular floor and remove part of the vestibular tissue of the alar lobules during the operation. Then the free alar was moved into the nostril to make the alar junction shift inward and upward, and reposition the alar junction to correct the alar hypertrophy and the wide nasal base. Photos of patients in frontal, side, and basal view before operation, 1 month, 6 months after operation. Intercanthal distance (ICD)、interinter-alar width (IW)、nasal base width (BW) were measured. The ratios of IW, BW and ICD before operation, 1 month, and 6 months after operation, and the narrowing rate of IW and BW at 1 month and 6 months after operation were summarized. The incision scar was evaluated with reference to the Vancouver Scar Scale. Normally distributed variables were compared using an paired t test. Nonparametric continuous variables were compared using Wilcoxon rank sum test. When P<0.05, the difference is considered statistically significant. Results:Sixteen patients were followed up for 6 to 12 months, averaged of 8 months. The IW/ICD of 16 patients at preoperation, after operation 1 month and 6 months were 1.160±0.080, 1.049±0.047 (0.110±0.049 decrease than before operation) and 1.038±0.047 (0.120±0.049 decrease than before operation). The differences were statistically significant ( P<0.05). The IW constriction rates were 9.3% at 1 month after operation and 10.2% at 6 months after operation. BW/ICD at preoperation, after operation 1 month and 6 months were 1.035±0.047, 0.960±0.039(0.072±0.019 smaller than preoperation), and 0.950±0.034(0.079±0.020 smaller than preoperation). Compared with preoperative data, the difference was statistically significant ( P<0.05). The BW reduction rates were 7.0% at 1 month after operation and 7.6% at 6 months after operation. The Vancouver Scar Scale score was 3(2.25, 3) at 1 month after operation, 1(0.25, 1) at 3 months after operation and 1(0, 1) at 6 months after operation. The differences were statistically significant ( P<0.05). There was a statistically significant difference between 3 months after surgery and 1 month after surgery ( Z=-3.472, P=0.001). There was no statistically significant difference between 6 months after surgery and 3 months after surgery ( Z=-1.414, P=0.157). All patients had no significant postoperative complications such as incision infection, asymmetry of nasal alae, obstruction of nasal ventilation, etc. Postoperative alar and nasal base profiles were significantly improved. Conclusions:Modified alar reduction with external incision can effectively treat alar hypertrophy without obvious postoperative complications. It is a good operation to correct alar hypertrophy.

Lipoma is the most common superficial benign tumor in clinical practice. Generally, lipoma is small in size. Giant lipoma is not common, and giant lipoma in tendon sheath is rare. We reports a case of axillary subcutaneous lipoma and giant lipoma in the tendon sheath. The preoperative diagnosis was a surface lipoma for the lack of clinical experience. Only color Doppler ultrasound is performed in the outpatient clinic. The preoperative examination was not sufficient, so the difficulties of the surgery was increased. We share the process for the clinician.

Objective:To investigate the effect of modified alar reduction with external incision to correct alar hypertrophy.Methods:From January 2017 to January 2019, 16 patients(1 male and 15 females, aged 21 to 39 with alar hypertrophy were treated in the plastic surgery department of the Second Affiliated Hospital of Nanchang University. Modified alar reduction with external incision were applied. In order to rotate the free alar lobules, the incision was extended in nasal lobules to the vestibular floor and remove part of the vestibular tissue of the alar lobules during the operation. Then the free alar was moved into the nostril to make the alar junction shift inward and upward, and reposition the alar junction to correct the alar hypertrophy and the wide nasal base. Photos of patients in frontal, side, and basal view before operation, 1 month, 6 months after operation. Intercanthal distance (ICD)、interinter-alar width (IW)、nasal base width (BW) were measured. The ratios of IW, BW and ICD before operation, 1 month, and 6 months after operation, and the narrowing rate of IW and BW at 1 month and 6 months after operation were summarized. The incision scar was evaluated with reference to the Vancouver Scar Scale. Normally distributed variables were compared using an paired t test. Nonparametric continuous variables were compared using Wilcoxon rank sum test. When P<0.05, the difference is considered statistically significant. Results:Sixteen patients were followed up for 6 to 12 months, averaged of 8 months. The IW/ICD of 16 patients at preoperation, after operation 1 month and 6 months were 1.160±0.080, 1.049±0.047 (0.110±0.049 decrease than before operation) and 1.038±0.047 (0.120±0.049 decrease than before operation). The differences were statistically significant ( P<0.05). The IW constriction rates were 9.3% at 1 month after operation and 10.2% at 6 months after operation. BW/ICD at preoperation, after operation 1 month and 6 months were 1.035±0.047, 0.960±0.039(0.072±0.019 smaller than preoperation), and 0.950±0.034(0.079±0.020 smaller than preoperation). Compared with preoperative data, the difference was statistically significant ( P<0.05). The BW reduction rates were 7.0% at 1 month after operation and 7.6% at 6 months after operation. The Vancouver Scar Scale score was 3(2.25, 3) at 1 month after operation, 1(0.25, 1) at 3 months after operation and 1(0, 1) at 6 months after operation. The differences were statistically significant ( P<0.05). There was a statistically significant difference between 3 months after surgery and 1 month after surgery ( Z=-3.472, P=0.001). There was no statistically significant difference between 6 months after surgery and 3 months after surgery ( Z=-1.414, P=0.157). All patients had no significant postoperative complications such as incision infection, asymmetry of nasal alae, obstruction of nasal ventilation, etc. Postoperative alar and nasal base profiles were significantly improved. Conclusions:Modified alar reduction with external incision can effectively treat alar hypertrophy without obvious postoperative complications. It is a good operation to correct alar hypertrophy.

Lipoma is the most common superficial benign tumor in clinical practice. Generally, lipoma is small in size. Giant lipoma is not common, and giant lipoma in tendon sheath is rare. We reports a case of axillary subcutaneous lipoma and giant lipoma in the tendon sheath. The preoperative diagnosis was a surface lipoma for the lack of clinical experience. Only color Doppler ultrasound is performed in the outpatient clinic. The preoperative examination was not sufficient, so the difficulties of the surgery was increased. We share the process for the clinician.

Objective:This study aims to explore the potential effects of adipose-derived stem cell-extracellular vesicles(ASC-EVs) on TGFβ-Smad signaling pathway during myofibroblast trans-differentiation in vitro. Methods:ASCs were isolated from liposuction and flow cytometry was used to detect the surface protein markers. ASC-EVs were isolated from the supernatant of the third to fifth generation ASCs, and the microscopic morphology was observed by transmission electron microscope. The particle size distribution was detected by nano-particle tracking analyzer NanoSight and the membrane surface marker proteins CD63, Alix and TSG101 were detected by flow cytometry. The uptake of EVs by dermal fibroblasts co-cultured with PKH67 fluorescence labeled ASC-EVs was observed by confocal microscope. Dermal fibroblasts were continuously induced by TGFβ1 for five days, and ASC-EVs at the dose of 50 and 100 μg/ml were added. The expression of α-SMA and Smad-2/3/4 were detected by immunofluorescence staining, RT-PCR and Western Blot.Results:The results of flow cytometry showed that the surface markers CD73, CD49d, CD90 and CD105 of the third generation ASCs, were positive, and CD34 and CD45 were negative. Under transmission electron microscope, ASC-EVs was a round membranous vesicle with clear edge and surrounded by bilayer phospholipid membrane. The particle size of more than 95% of the ASC-EVs was distributed between 30 nm to 261 nm, with an average of (166.0±86.1)nm. The specific marker proteins of extracellular vesicle, CD63, Alix and TSG101 were highly expressed. Under confocal microscope, ASC-EVs with green fluorescence were uptake by dermal fibroblasts and distributed in the cytoplasm, and part of ASC-EVs was distributed around the nucleus.TGF-β1 induced a significant increase in the expression of α-SMA in dermal fibroblasts, and the addition of 50 or 100 μg/ml ASC-EVs reduced the expression of α-SMA genes and proteins, but did not show a dose-dependent manner. The gene and protein expression changes of Smad-2/3/4 were consistent with α-SMA. In addition, ASC-EVs could significantly reduced the content of type Ⅰ collagen in the supernatant, but had no significant effect on the secretion of type Ⅲ collagen.Conclusions:The mechanism of ASC-EVs inhibiting scar hyperplasia may be closely related to the suppression of TGF-β-Smad signaling pathway in dermal fibroblasts, inhibition of myofibroblast trans-differentiation and reduction of type Ⅰ collagen secretion.

Objective:This study aims to explore the potential effects of adipose-derived stem cell-extracellular vesicles(ASC-EVs) on TGFβ-Smad signaling pathway during myofibroblast trans-differentiation in vitro. Methods:ASCs were isolated from liposuction and flow cytometry was used to detect the surface protein markers. ASC-EVs were isolated from the supernatant of the third to fifth generation ASCs, and the microscopic morphology was observed by transmission electron microscope. The particle size distribution was detected by nano-particle tracking analyzer NanoSight and the membrane surface marker proteins CD63, Alix and TSG101 were detected by flow cytometry. The uptake of EVs by dermal fibroblasts co-cultured with PKH67 fluorescence labeled ASC-EVs was observed by confocal microscope. Dermal fibroblasts were continuously induced by TGFβ1 for five days, and ASC-EVs at the dose of 50 and 100 μg/ml were added. The expression of α-SMA and Smad-2/3/4 were detected by immunofluorescence staining, RT-PCR and Western Blot.Results:The results of flow cytometry showed that the surface markers CD73, CD49d, CD90 and CD105 of the third generation ASCs, were positive, and CD34 and CD45 were negative. Under transmission electron microscope, ASC-EVs was a round membranous vesicle with clear edge and surrounded by bilayer phospholipid membrane. The particle size of more than 95% of the ASC-EVs was distributed between 30 nm to 261 nm, with an average of (166.0±86.1)nm. The specific marker proteins of extracellular vesicle, CD63, Alix and TSG101 were highly expressed. Under confocal microscope, ASC-EVs with green fluorescence were uptake by dermal fibroblasts and distributed in the cytoplasm, and part of ASC-EVs was distributed around the nucleus.TGF-β1 induced a significant increase in the expression of α-SMA in dermal fibroblasts, and the addition of 50 or 100 μg/ml ASC-EVs reduced the expression of α-SMA genes and proteins, but did not show a dose-dependent manner. The gene and protein expression changes of Smad-2/3/4 were consistent with α-SMA. In addition, ASC-EVs could significantly reduced the content of type Ⅰ collagen in the supernatant, but had no significant effect on the secretion of type Ⅲ collagen.Conclusions:The mechanism of ASC-EVs inhibiting scar hyperplasia may be closely related to the suppression of TGF-β-Smad signaling pathway in dermal fibroblasts, inhibition of myofibroblast trans-differentiation and reduction of type Ⅰ collagen secretion.