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Background: The objective of the study is to determine the safety and efficiency of the modified laparoscopic percutaneous extraperitoneal closure (LPEC) to treat pediatric patients with inguinal hernia or hydrocele. Methods: From January 2014 to July 2018, the patients with inguinal hernia or hydrocele who were operated on using modified LPEC were included. We modified LPEC with a sledge-shaped needle and reinforcement flag. By means of medial umbilical fold, the reinforcement surgery should be performed on the patients with huge internal rings (diameter >1.5 cm). Operative time, complication rate, incidence of reinforcement, and contralateral patent processus vaginalis were described between inguinal hernia and hydrocele. Results: In this study, 764 patients with inguinal hernia and 435 patients with hydrocele were successfully performed by the modified LPEC. The 383 (50.1%) patients with inguinal hernia and 266 (61.1%) patients with hydrocele were identified with a contralateral patency of internal ring and underwent simultaneous prophylactic surgery. During surgical procedures, the medial umbilical fold reinforcement (inguinal hernia/hydrocele = 50/1) was performed on 51 patients. Hernia recurrence occurred in 2 cases. All patients had a good cosmetic appearance without additional dissection. Conclusion: Modified LPEC using a sledge-shaped needle and applying the medial umbilical fold reinforcement is a safe and effective surgical procedure. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC) is one of the most common fatal cancers worldwide, and the identification of novel treatment targets and prognostic biomarkers is urgently needed because of its unsatisfactory prognosis. Regulator of G-protein signaling 19 (RGS19) is a multifunctional protein that regulates the progression of various cancers. However, the specific function of RGS19 in HCC remains unclear. The expression of RGS19 was determined in clinical HCC samples. Functional and molecular biology experiments involving RGS19 were performed to explore the potential mechanisms of RGS19 in HCC. The results showed that the expression of RGS19 is upregulated in HCC tissues and is significantly associated with poor prognosis in HCC patients. RGS19 promotes the proliferation and metastasis of HCC cells in vitro and in vivo. Mechanistically, RGS19, via its RGS domain, stabilizes the MYH9 protein by directly inhibiting the interaction of MYH9 with STUB1, which has been identified as an E3 ligase of MYH9. Moreover, RGS19 activates β-catenin/c-Myc signaling via MYH9, and RGS19 is also a transcriptional target gene of c-Myc. A positive feedback loop formed by RGS19, MYH9, and the β-catenin/c-Myc axis was found in HCC. In conclusion, our research revealed that competition between RGS19 and STUB1 is a critical mechanism of MYH9 regulation and that the RGS19/MYH9/β-catenin/c-Myc feedback loop may represent a promising strategy for HCC therapy., (© 2024. The Author(s).)

N6-Methyladenosine (m 6 A) plays key roles in the regulation of biological functions and cellular mechanisms for ischaemia reperfusion (IR) injury in different organs. However, little is known about the underlying mechanisms of m 6 A-modified mRNAs in hepatic IR injury. In mouse models, liver samples were subjected to methylated RNA immunoprecipitation with high-throughput sequencing (MeRIP-seq) and RNA sequencing (RNA-seq). In total, 16917 m 6 A peaks associated with 4098 genes were detected in the sham group, whereas 21,557 m 6 A peaks associated with 5322 genes were detected in the IR group. There were 909 differentially expressed m 6 A peaks, 863 differentially methylated transcripts and 516 differentially m 6 A modification genes determined in both groups. The distribution of m 6 A peaks was especially enriched in the coding sequence and 3'UTR. Furthermore, we identified a relationship between differentially m 6 A methylated genes (fold change≥1.5/≤ 0.667, p value≤0.05) and differentially expressed genes (fold change≥1.5 and p value≤0.05) to obtain three overlapping predicted target genes (Fnip2, Phldb2, and Pcf11). Our study revealed a transcriptome-wide map of m 6 A mRNAs in hepatic IR injury and might provide a theoretical basis for future research in terms of molecular mechanisms.