A New Method for Stabilizing the Columellar Strut Used in Rhinoplasty: The Trans-Septal Columellar Stabilizing Suture.

PURPOSE: Minimal deformity or instability after columellar strut graft (CSG) placement can be solved by placing a suture between the columella strut and the caudal septum, such as a medial crura anchor suture or a projection control suture. However, this is very tedious. MATERIALS AND METHODS: A trans-septal columellar stabilizing suture (TCSS) was developed for the management of final tip projection and location and increasing stability after CSG placement. RESULTS: Tip projection and rotation could be carefully controlled by changing the position of the TCSS. In addition, the TCSS provided increasing stability for the columellar strut. It was not necessary to remove any prior suture or the graft. CONCLUSION: TCSS usefully controls the final positions and shapes of the tip and columella and provides stability to the columellar strut after CSG. Furthermore, the TCSS is a straightforward and time-saving procedure.

Extracorporeal shockwave therapy enhances peripheral nerve remyelination and gait function in a crush model.

BACKGROUND: Conservative treatment, such as electrical stimulation and steroid injection, have been employed in an attempt to improve symptoms after peripheral nerve injury, without significant success. Although non-invasive and safe extracorporeal shockwave therapy (ESWT) can be a practical alternative, the therapeutic effects of ESWT on peripheral nerve remyelination has not been established. OBJECTIVES: To investigate the effects of ESWT on peripheral nerve remyelination and gait function for 5 weeks in a sciatic nerve crush model. MATERIAL AND METHODS: In total, we divided 97 rats into 5 groups: group 1 - a healthy negative control group; group 2 - 3 weeks after sciatic nerve crush and 3 sessions of ESWT; group 3 - 5 weeks after crush injury with 3 sessions of ESWT; group 4 - 3 weeks after crush injury with no ESWT; and group 5 - 5 weeks after crush injury with no ESWT. The focused ESWT was applied to the unilateral sciatic nerve injury site. One session consisted of 1,500 stimuli, and the session were performed at intervals of 1 week. RESULTS: The degree of myelination and expression of myelin basic protein at the distal part of the injured sciatic nerve tended to increase in the ESWT groups compared with the no-ESWT groups 3 and 5 weeks after crush injury. Regarding the functional gait recovery, the print width and area of the injured leg in the ESWT groups was significantly larger than that in the no-ESWT groups 3 and 5 weeks after crush injury. CONCLUSIONS: The ESWT may enhance peripheral nerve remyelination and gait function in a nerve crush model. Long-term follow-up after ESWT and investigation of molecular mechanisms will be needed to confirm these therapeutic effects.

TLR4-mediated autophagic impairment contributes to neuropathic pain in chronic constriction injury mice.

Neuropathic pain is a complex, chronic pain state characterized by hyperalgesia, allodynia, and spontaneous pain. Accumulating evidence has indicated that the microglial Toll-like receptor 4 (TLR4) and autophagy are implicated in neurodegenerative diseases, but their relationship and role in neuropathic pain remain unclear. In this study, we examined TLR4 and its association with autophagic activity using a chronic constriction injury (CCI)-induced neuropathic pain model in wild-type (WT) and TLR4-knockout (KO) mice. The mice were assigned into four groups: WT-Contralateral (Contra), WT-Ipsilateral (Ipsi), TLR4 KO-Contra, and TLR4 KO-Ipsi. Behavioral and mechanical allodynia tests and biochemical analysis of spinal cord tissue were conducted following CCI to the sciatic nerve. Compared with the Contra group, mechanical allodynia in both the WT- and TLR4 KO-Ipsi groups was significantly increased, and a marked decrease of allodynia was observed in the TLR4 KO-Ipsi group. Although glial cells were upregulated in the WT-Ipsi group, no significant change was observed in the TLR4 KO groups. Moreover, protein expression and immunoreactive cell regulation of autophagy (Beclin 1, p62) were significantly increased in the neurons, but not microglia, of WT-Ipsi group compared with the WT-Contra group. The level of PINK1, a marker for mitophagy was increased in the neurons of WT, but not in TLR4 KO mice. Together, these results show that TLR4-mediated p62 autophagic impairment plays an important role in the occurrence and development of neuropathic pain. And what is more, microglial TLR4-mediated microglial activation might be indirectly coupled to neuronal autophage.

Peroneal Flap: Clinical Application and Cadaveric Study.

BACKGROUND: The goal of this study was to investigate the anatomy of the peroneal artery and its perforators, and to report the clinical results of reconstruction with peroneal artery perforator flaps. METHODS: The authors dissected 4 cadaver legs and investigated the distribution, course, origin, number, type, and length of the perforators. Peroneal artery perforator flap surgery was performed on 29 patients. RESULTS: We identified 19 perforators in 4 legs. The mean number of perforators was 4.8 per leg, and the mean length was 4.8 cm. Five perforators were found proximally, 9 medially, and 5 distally. We found 12 true septocutaneous perforators and 7 musculocutaneous perforators. Four emerged from the posterior tibia artery, and 15 were from the peroneal artery. The peroneal artery perforator flap was used in 29 patients. Retrograde island peroneal flaps were used in 8 cases, anterograde island peroneal flaps in 5 cases, and free peroneal flaps in 16 cases. The mean age was 59.9 years, and the defect size ranged from 2.0 cm×4.5 cm to 8.0 cm×8.0 cm. All the flaps survived. Five flaps developed partial skin necrosis. In 2 cases, a split-thickness skin graft was performed, and the other 3 cases were treated without any additional procedures. CONCLUSIONS: The peroneal artery perforator flap is a good alternative for the reconstruction of soft tissue defects, with a constant and reliable vascular pedicle, thin and pliable skin, and the possibility of creating a composite tissue flap.

Effect of Botulinum Toxin Type A on TGF-ß/Smad Pathway Signaling: Implications for Silicone-Induced Capsule Formation.

BACKGROUND: One of the most serious complications of breast surgery using implants is capsular contracture. Several preventive treatments have been introduced; however, the mechanism of capsule formation has not been resolved completely. The authors previously identified negative effects of botulinum toxin type A on capsule formation, expression of transforming growth factor (TGF)-ß1, and differentiation of fibroblasts into myofibroblasts. Thus, the authors investigated how to prevent capsule formation by using botulinum toxin type A, particularly by means of TGF-ß1 signaling, in human fibroblasts. METHODS: In vitro, cultured human fibroblasts were treated with TGF-ß1 and/or botulinum toxin type A. Expression of collagen, matrix metalloproteinase, and Smad was examined by Western blotting. The activation of matrix metalloproteinase was observed by gelatin zymography. In vivo, the effect of botulinum toxin type A on the phosphorylation of Smad2 in silicone-induced capsule formation was evaluated by immunocytochemistry. RESULTS: In vitro, the phosphorylation of Smad2 was inhibited by botulinum toxin type A treatment. The expression levels of collagen types 1 and 3 were inhibited by botulinum toxin type A treatment, whereas those of matrix metalloproteinase-2 and matrix metalloproteinase-9 were enhanced. Gelatin zymography experiments confirmed enhanced matrix metalloproteinase-2 activity in collagen degradation. In vivo, botulinum toxin type A treatment reduced capsule thickness and Smad2 phosphorylation in silicone-induced capsules. CONCLUSION: This study suggests that botulinum toxin type A plays an important role in the inhibition of capsule formation through the TGF-ß/Smad signaling pathway. CLINICAL QUESTION/LEVEL OF EVIDENCE: Therapeutic, V.