Laparoscopic simultaneous inguinal hernia repair and appendectomy in children: A multicenter study.

BACKGROUND: Inguinal hernias (IHs) are sometimes encountered incidentally in children during laparoscopic appendectomy. This study aims to evaluate the efficacy and outcomes of laparoscopic simultaneous inguinal hernia repair and appendectomy in children. METHODS: A multicentric study was performed in patients with AA and concurrent IH who received laparoscopic simultaneous inguinal hernia repair and appendectomy (study group), compared with patients who underwent two-stage laparoscopic procedures (control group) between September 2012 and January 2020. Intraoperative data, postoperative complications, and clinical outcomes were prospectively collected and retrospectively analyzed. RESULTS: 189 patients with AA and concurrent IH (117 children in the study group, and 72 children in the control group) were enrolled. No significant differences in preoperative characteristics were identified between the two groups. Patients in the study group had a shorter total operative time and hospital stay than those in the control group (43.2 ±â€¯8.1 vs 53.9 ±â€¯7.3 min, p < 0.001; 1.5 ±â€¯0.8 vs 2.2 ±â€¯0.9 days, p = 0.023). The study group incurred lower costs than the control group (9198.7 ±â€¯587.6 vs 14,392.5 ±â€¯628.6 RMB, p < 0.001). During follow-up (range 1.5-6.0 years), three children in the study group and two children in the control group experienced wound infection. One child in the study group had recurrent IH. CONCLUSIONS: Laparoscopic simultaneous procedures do not increase the incidence of wound infection or recurrent IH. Moreover, they avoid repeat anesthesia and hospitalization. Therefore, this approach is safe, feasible and cost-effective for children with AA and concurrent IH. LEVEL OF EVIDENCE: Level III.

MicroRNA-431 inhibits migration and invasion of hepatocellular carcinoma cells by targeting the ZEB1-mediated epithelial-mensenchymal transition.

MicroRNA-431 (miR-431) has been recognized as an oncogenic miRNA, being implicated in the initiation and development of human cancers. Recently, deregulation of miR-431 has been reported in several tumors. However, the clinical significance of miR-431 and its underlying role in human hepatocellular carcinoma (HCC) are poorly explored. Herein, we found that miR-431 expression was reduced in HCC tissues compared to noncancerous tissues. Otherwise, down-regulation of miR-431 was observed in aggressive tumor tissues. The levels of miR-431 expression in HCC cell lines were significantly lower than that in a nontransformed hepatic cell line. Clinical association analyses disclosed that a low level of miR-431 was prominently associated with poor prognostic features of HCC including venous infiltration, high Edmondson-Steiner grading and advanced tumor-node-metastasis (TNM) tumor stage. Our in vitro studies showed that up-regulation of miR-431 expression reduced cell invasion and migration in HCCLM3 cells. In contrast, down-regulation of miR-431 expression promoted SMMC-7721 cell invasion and migration. We found that up-regulation of miR-431 expression decreased zinc finger E-box binding homeobox 1 (ZEB1) expression and inhibited the epithelial-mesenchymal transition (EMT) with increased E-cadherin expression and decreased vimentin expression in HCCLM3 cells. Otherwise, down-regulation of miR-431 expression increased ZEB1 expression and promoted EMT in SMMC-7721 cells. Significantly, ZEB1 was identified as a target of miR-431 in HCC. ZEB1 knockdown abrogated the effect of miR-431 silencing on EMT and cell mobility in SMMC-7721 cells. In conclusion, miR-431 inhibits migration and invasion of HCC cells by suppressing ZEB1-mediated EMT.