ABSTRACT
Objective:To investigate the efficacy of two-way needle suture technique (TNST) in the minimally invasive repair of acute closed Achilles tendon rupture.Methods:From June 2019 to June 2021, 26 patients with acute closed Achilles tendon rupture were treated at Zhengzhou Orthopedic Hospital. They were 20 males and 6 females, with a mean age of 28 (23, 31) years. The rupture end was (4.2±1.3) cm away from the calcaneal insertion, and the interval from injury to operation 4.3 (2.0, 5.0) d. Preoperative MRI examinations revealed in all the patients closed Achilles tendon rupture which was to be repaired by TNST. The operation time, incision length, incidence of complications, ankle dorsiflexion and plantar flexion were recorded. The Arner-Lindholm scoring was used to evaluate the clinical efficacy.Results:The operation time was (20.0±5.0) min and the incision length (2.5±0.4) cm. Postoperatively, all incisions healed by the first stage, with no complications like incision infection, skin edge necrosis, deep vein thrombosis at lower limbs, injury to the sural nerve, or re-rupture of the Achilles tendon. All patients were followed up for (12.0±6.0) months. At the last follow-up, the patients walked normally, their incisions healed well, the continuity of the Achilles tendon was good by palpation, their heel lift was strong, and all their activities were restored to the levels before rupture of the Achilles tendon. The ankle dorsiflexion was 22.6°±3.7° and the plantar flexion 25.3°±3.7°, According to the Arner-Lindholm evaluation, the clinical efficacy was rated as excellent in 25 cases and as good in 1 case, giving an excellent and good rate of 100% (26/26).Conclusion:In the minimally invasive repair of acute closed Achilles tendon rupture, TNST shows the advantages of limited surgical invasion, a low incidence of postoperative complications, and reliable curative effects.
ABSTRACT
<p><b>BACKGROUND AND OBJECTIVE</b>It has been reported that defective expression of TGFBR3 was found in non-small cell lung cancer (NSCLC). However, its molecular mechanisms remain unclear. The aim of this study is to investigate expression of TGFBR3 in NSCLC cell lines and normal human bronchial epithelial cell (HBEpiC), and to explore potential molecular mechanisms underlying inactivation of TGFBR3 gene.</p><p><b>METHODS</b>Western blot was performed to determine the expression of TGFBR3 in HBEpiC and NSCLC cell lines. Automatic image analysis was carried out to estimate relative expression of TGFBR3 protein. We screened for mutation of the promoter region of TGFBR3 gene using DNA direct sequencing. Bisulfite-sodium modification sequencing was used to detect the methylation status of TGFBR3 promoter.</p><p><b>RESULTS</b>TGFBR3 protein level was abnormally reduced in NSCLC cell lines as compared with HBEpiC. There was significant difference in TGFBR3 expression between the highly metastatic cell line 95D and non-metastatic cell lines, including LTEP-alpha-2, A549 and NCI-H460. No mutation and methylation was found in upstream sites -165 to -75 of the proximal promoter of TGFBR3 in HBEpiC and NSCLC cell lines. Hypermethylation was shown in upstream sites -314 to -199 of the distal promoter of TGFBR3 in HBEpiC and NSCLC cell lines.</p><p><b>CONCLUSION</b>Reduced expression of TGFBR3 was observed in NSCLC cell lines, especially in 95D, suggesting that TGFBR3 might play an important role in development and progression of NSCLC and correlate with NSCLC invasion and migration. The methylation event occurring at TGFBR3 promoter is not a major cause for reduction of TGFBR3 expression.</p>