The postoperative choledochoscopy in the management of the residual hepatolithiasis involving the caudate lobe: A retrospective study.

ABSTRACT: To reveal the role of the postoperative choledochoscopy in treating the residual calculi in the caudate lobe (CL) of the liver.We recruited 66 patients with T-tube/percutaneous transhepatic cholangioscopy tract who still had residual gallstones in the CL at least 6 weeks after the operation. Imaging examinations determined the gallstones' locations in the patients, and all of them underwent the postoperative choledochoscopic examination through the T-tube/percutaneous transhepatic cholangioscopy tract for therapeutic intervention.Among the 66 patients, the residual gallstones were mostly located in the Spiegel lobe (48/66, 72.7%), and the residual gallstones that located in the origin of the CL bile branches were successfully determined in the 57 patients (57/66, 86.4%), the remaining 9 patients were unclear because the proximal ducts were severely narrow or even atresia. The mean frequency of the postoperative choledochoscopy was 3.6 (range, 1-10) times. There were 9 patients with complications, and no mortality occurred. In the origin-proved 57 patients, 6 patients failed to remove the gallstones altogether, and the final residual gallstone clearance rate was 77.3% (51/66). There was no significant difference between the Spiegel lobe and the other parts of the CL in determining the bile duct's origins, gallstone clearance rate, and complications. However, the frequency of choledochoscopy in the other parts of the CL was more than in the Spiegel lobe.The postoperative choledochoscopy, an essential method for treating the residual gallstones in the CL, commands high efficiency for calculi extraction and fewer complications. The main reasons for failing to remove the residual gallstones are that the bile duct's origins could not be determined, and the distal bile ducts are atretic in the CL.

miR-202 Suppresses Hepatocellular Carcinoma Progression via Downregulating BCL2 Expression.

miRNAs play an important role in progression of hepatocellular carcinoma (HCC). In this work, we assessed the function of miR-202 in human HCC and identified BCL2 as its target. We found miR-202 expression was found significantly downregulated, while BCL2 expression was markedly upregulated in HCC tissues and cell lines (HepG2, Hep3B, and HCCLM3). Both miR-202 and BCL2 were closely correlated with major vascular invasion and advanced TNM stage as well as overall survival of HCC patients. Overexpression of miR-202 significantly inhibited cell proliferation, induced apoptosis and cell cycle arrest at the G0/G1 phase, and prevented tumor formation in a xenograft nude mouse model. Further, miR-202 dramatically inhibited migration, invasion, and epithelialmesenchymal transition. miR-202 bound to the 3-untranslated region (3-UTR) of BCL2 mRNA and downregulated the expression level of BCL2 protein. Exogenous BCL2 overexpression weakened the inhibitory effects of miR-202, while inhibition of BCL2 enhanced the inhibitory effects of miR-202. In conclusion, miR-202 serves as a tumor suppressor in HCC progression by downregulating BCL2 expression, indicating miR-202 might be a potential target for HCC.

miR-146b level and variants is associated with endometriosis related macrophages phenotype and plays a pivotal role in the endometriotic pain symptom.

OBJECTIVE: The aim of this study was to explore the effect of miR-146b expression and variants on endometriosis and its associated pain symptom. MATERIALS AND METHODS: Genotyping and expression of miR-146b was performed on 74 endometriosis patients and 23 healthy controls. ESCs were subsequently co-cultured with peripheral blood (PB)-derived monocytes (PBMC)-driven macrophages. After overexpression and inhibition of miR-146b, cytokine production from the macrophages were determined by enzyme-linked immunosorbent assay (ELISA). Western blot were done to measure the regulation of IRF5 by miR-146b. RESULTS: We found that miR-146b expression was increased in PF supernatant and PF CD14 + monocytes/Macrophages of endometriosis patients, with endometriosis patients with pain (EPWP) showing higher miR-146b expression compared with the endometriosis patients without pain (EPNP). CT/CC genotype of miR-146b rs1536309 was associated with the risk of pain symptom of endometriosis. For the function studies, we found that miR-146b was involved in the negative regulation of inflammation through attenuating IRF5 expression. Macrophages from patients who carries CT/CC genotype of miR-146b rs1536309 showed decreasing miR-146b expression and enhancement of the ability of pro-inflammation. CONCLUSIONS: Our findings suggest an important role of miR-146b level and variants in endometriosis that helps to regulate the process of endometriosis and its associated pain.

T-box Transcription Factor Tbx3 Contributes to Human Hepatocellular Carcinoma Cell Migration and Invasion by Repressing E-Cadherin Expression.

Tbx3, a member of the T-box family of transcription factors, contributes directly to tumor formation, migration, and invasion. However, the role of Tbx3 in the metastasis of HCC remains unclear. In the present study, Tbx3 expression was detected in HCC tissues and cells by Western blot, and Tbx3 expression was regulated by use of siRNAs or lentivirus-mediated vectors. Here we found that Tbx3 protein expression increased in HCC tissues and cell lines. Tbx3 expression was positively associated with multiple tumor nodes, venous infiltration, and advanced TNM tumor stage. Survival analysis demonstrated that Tbx3 expression was an independent prognostic factor for HCC patients. In vitro assays further validated that Tbx3 indeed prompted HCC cell migration and invasion. In addition, Tbx3 expression was negatively related with E-cadherin expression in HCC tissues. Mechanically, Tbx3 inhibited the expression of E-cadherin, and then facilitated epithelial-mesenchymal transition (EMT) of HCC cells. Furthermore, the effect of Tbx3 knockdown on HCC cells was attenuated by E-cadherin knockdown. In conclusion, Tbx3 may be a novel prognostic factor, and it contributes to HCC cell migration, invasion, and EMT by repressing E-cadherin expression. Thus, Tbx3 may be recommended as a therapeutic target for HCC patients.

[Antitumor effect of DHA compound in vitro and in vivo and its mechanism].

OBJECTIVE: To study the anticancer effect in vitro and in vivo and mechanism of DHA compound. METHODS: Cervical cancer cell line HeLa cells, glioma cell line U251 cells and mouse hepatoma H(22) tumor were used in this study. Transmission electron microscopy and fluorescence microscopy were used to observe the morphological changes of cell apoptosis. Western blot was used to detect the expression of caspase-3. RT-PCR was used to determine the effect on Bcl-2 and Bax mRNA transcription in U251. RESULTS: Antitumor effect was observed in vivo and in vitro. Typical morphological changes were seen in cancer cells. The level of caspase-3 was significantly increased and the content of Bcl-2 mRNA was decreased significantly, while the content of Bax mRNA was significantly increased in the U251 cells after treatment with DHA compound. CONCLUSION: DHA compound can inhibit the growth of some types of tumors and the increase of caspase-3 and Bax mRNA and decrease of Bcl-2 mRNA may be involved in its mechanism of action.