Cystic Duct Exploration in Laparoscopic Cholecystectomy.

BACKGROUND: Bile duct injury (BDI) is a severe complication following cholecystectomy and is therefore a particularly concerning surgical predicament for hepatobiliary surgeons. Owing to very high medical compensation awarded to patients suffering from BDI, surgeons need to exercise caution during surgery to avoid BDI. Herein, we explored a novel method to identify cystic duct during laparoscopic cholecystectomy (LC), expanding the applicability of this surgical approach. METHODS: Patients receiving LC between April 2021 and October 2022 at the Gaoyou People's Hospital were included in this retrospective clinical study and divided into two groups according to whether the cystic duct was incised (one group with LC alone, while another with laparoscopic cholecystectomy and cystic duct exploration [LCCDE]). Clinical and baseline characteristics of patients were collected, and the preoperative and postoperative biochemical parameters were compared. The surgical outcomes of LCCDE were observed. RESULTS: A total of 114 patients had undergone LC, while 162 patients had received LCCDE as treatment. There were no significant differences in age, gender, common bile duct diameter, preoperative and postoperative biochemical parameters between the two groups. No significant difference in the mean operation time between the LC and LCCDE groups was noted (p = 0.409). In the LCCDE group, white secretions in the cystic duct were observed in 92 patients (56.8%). CONCLUSIONS: The presence of intraoperative white secretions in the cystic duct may further confirm the presence of cystic duct, thereby enabling earlier detection of BDI. Importantly, LCCDE, as the new surgical method explored in this study, does not extend the operation time.

LINC01296 promotes proliferation of cutaneous malignant melanoma by regulating miR-324-3p/MAPK1 axis.

OBJECTIVE: To investigate the functions and potential molecular mechanism of LINC01296 regarding the progression of cutaneous malignant melanoma (CMM) by the regulation of miR-324-3p/MAPK1 axis. METHODS: The candidate differential lncRNAs of CMM were selected from GEPIA database, and quantitative real-time PCR (qRT-PCR) was utilized to assess the expression level of LINC01296 in human CMM tissues and cell lines. Cell proliferation assay, Colony formation assay, Ethynyl-2'-deoxyuridine (EDU) assay in vitro and tumorigenicity assays in nude mice in vivo were performed to examine the functions of LINC01296. Bioinformatics analysis, luciferase reporter assay and rescue experiments were also gained an insight into the underlying mechanisms of LINC01296 in CMM cell lines by miR-324-3p/MAPK1 axis. RESULTS: In this study, the up-regulation of LINC01296 was found in CMM tissues and cell lines. Functionally, the over-expression of LINC01296 promoted the proliferation in CMM cell lines. In addition, immunochemistry analysis confirmed that the levels of MAPK1 and Ki-67 in sh-LINC01296-xenografted tumors was weaker than that in sh-NC-xenografted tumors. Then, bioinformatics analysis confirmed that LINC01296 interacted with miR-324-3p. Further investigations showed that MAPK1, which collected from the potential related genes of LINC01296, was the conjugated mRNA of miR-324-3p by luciferase reporter assay. Finally, the rescue experiments suggested the positive regulatory association among LINC01296 and MAPK1, which showed that MAPK1 could reverse the promoting-effect of LINC01296 in CMM cells in vitro. CONCLUSIONS: Therefore, our findings provided insight into the mechanisms of LINC01296 via miR-324-3p/MAPK1 axis in CMM, and revealed an alternative target for the diagnosis and treatment of CMM.

Overexpression of miR-574-3p suppresses proliferation and induces apoptosis of chronic myeloid leukemia cells via targeting IL6/JAK/STAT3 pathway.

The present study aimed to elucidate the potential roles and regulatory mechanism of microRNA (miR)-574-3p in the development of chronic myeloid leukemia (CML). The expression of miR-574-3p in peripheral blood obtained from patients with CML was examined. Subsequently, miR-574-3p was overexpressed and suppressed in CML K562 cells to further investigate the effects of miR-574-3p on cell proliferation, and apoptosis. Furthermore, a luciferase reporter assay was performed to investigate whether interleukin-6 (IL-6) was a target of miR-574-3p. In addition, the regulatory association between miR-574-3p and the IL-6/Janus kinase (JNK)/signal transducer and activator of transcription-3 (STAT3) signaling pathway was explored. The expression of miR-574-3p in the peripheral blood obtained from patients with CML was significantly lower compared with that in healthy controls. Overexpression of miR-574-3p significantly inhibited the proliferation and induced the apoptosis of K562 cells, whereas suppression of miR-574-3p exhibited opposite effects. In addition, IL-6 was identified to be a direct target of miR-574-3p. Overexpression of IL-6 significantly promoted the proliferation and inhibited the apoptosis of K562 cells. Furthermore, overexpression of miR-574-3p inhibited the activation of the JAK/STAT3 signaling pathway, which was rescued by overexpression of IL-6. The results of the current study indicate that miR-574-3p overexpression may serve an important role in inhibiting proliferation and inducing apoptosis of K562 cells via suppression of IL-6/JAK/STAT3 signaling pathway activation. miR-574-3p may serve as a potential therapeutic target for CML.