Objective To investigate the change of AQP1 and AQP2 before and after the release of obstruction and explore the relationship between reabsorption dysfunction of renal tubule and the change of AQPs. Methods The model of unilateral ureter obstruction (UUO) was established by surgery. Western blot and immunohistochemistry were used to study the expression of AQPs before and after obstruction. Results In UUO model, both AQPs began to down-regulate one day after obstruction, the expression of both AQPs became lower one day after the release of obstruction. And they started to up-regulate 7 day after the release of obstruction. AQP2 became normal since 14 days after the release of obstruction, and AQP1 became normal since 21 days after the release of obstruction. Conclusion The expression of AQP1 and AQP2 were descended in hydronephrosis. The dysfunction of renal tubule and the osmotic-dependent polyuria after the release of obstruction in UUO were caused by the down - regulation of AQPs.

Common iliac artery ureteral fistula is a rare but potentially life-threatening disease which is difficult to diagnose clinically. This paper reports a case of common iliac artery ureteral fistula. The patient was admitted to our hospital due to ureterostomy bleeding for one day. He underwent radical cystectomy and bilateral ureterostomy for bladder cancer 4 years ago, and also underwent radiotherapy and bilateral ureteral stents indwelling after the operation. Angiography revealed a left common iliac artery pseudoaneurysm, and a left common iliac artery ureteral fistula was considered. The left common iliac artery stent-graft was implanted. The patient recovered well after the operation, and there was no obvious hematuria during follow-up period of 6 months.

Objective:To investigate the effect and mechanism of lactoferrin (LF) on biological behaviors of brain glioma cells.Methods:The effect of LF at different concentrations (0, 100, 200 and 300 μg/mL) on the proliferative ability of human glioma cell line U87MG was analyzed by MTT assay to screen the optimal drug concentration. U87MG cells were divided into blank control group and LF (200 μg/mL) treatment group. Edu staining, Transwell assay, Mito-Tracker staining and DCFH-DA staining were used to detect the cell proliferation, migration, mitochondrial activity and reactive oxygen level. Autophagy marker protein microtubule associated protein 1 light chain 3B (LC3B) expression was detected by immunofluorescent chemical staining; contents of superoxide dismutase (SOD) and malonaldehyde (MDA) were detected by colorimetric chemical sensors; expressions of genes related to epithel-to-mesenchymal transformation (E-cadherin, fibronectin, N-cadherin, vimentin and Snail) were detected by reverse transcription (RT)-PCR; expressions of apoptosis-related proteins (Bax and Bcl-2) were detected by Western blotting.Results:Compared with blank control group, the LF treatment group had significantly decreased proportions of Edu positive cells and Mito-Tracker positive cells, number of cell migration and SOD content, and statistically increased proportion of DCFH-DA positive cells, MDA content and LC3B immunofluorescent staining intensity in cytoplasm ( P<0.05). Compared with blank control group, the LF treatment group had significantly decreased E-cadherin mRNA expression and Bcl-2 protein expression, and statistically increased fibronectin, N-cadherin, vimentin and Snail mRNA expressions and Bax protein expression ( P<0.05). Conclusion:LF can effectively inhibit the proliferation, migration, invasion and other biological behaviors of glioma cells, whose mechanism is closely related to mitochondrial activity.

BACKGROUND: MicroRNA-20a (miR-20a) is dysregulated in many types of malignancies, including human hepatocellular carcinoma (HCC), but its expression level and functional significance in HCC are still disputed. We aimed to study the role of miR-20a-5p in HCC and its downstream molecular mechanisms. METHODS: We used real-time polymerase chain reaction to detect the expression of miR-20a-5p and runt-related transcription factor 3 ( RUNX3 ) in HCC and paraneoplastic tissue, transfected Huh7 and highly metastatic human hepatocellular carcinoma (MHCC97H) cells. A live cell workstation was used to observe the proliferation and migration of transfected cells. The invasiveness of transfected cells was verified by Transwell assay. Cell apoptosis was detected by flow cytometry. The expression levels of proteins after transfection were measured using simple western immunoblot measurements. Gene expression profiles between HCC and normal samples were obtained from The Cancer Genome Atlas. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment results were processed by the database for annotation, visualization and integrated discovery. Potential target genes of miR-20a-5p were predicted to further investigate how miR-20a-5p regulates epithelial-mesenchymal transition (EMT) in HCC. RESULTS: MiR-20a-5p was significantly highly expressed in HCC tissues, and overexpression of miR-20a-5p significantly promoted HCC cell proliferation, migration, and invasion and inhibited apoptosis in vitro. The protein expression of E-cadherin was decreased and that of vimentin was increased after overexpression of miR-20a-5p in HCC cells. We discovered the intersection of genes from miRDB, miR TarBase, and TargetScan, obtained 397 target genes and finally focused on RUNX3. RUNX3 was not only reduced in HCC specimens but also drastically reduced in HCC cells overexpressing miR-20a-5p. RUNX3 expression decreased with elevated miR-20a-5p, which activated downstream EMT signaling and promoted cell proliferation, migration, and invasion. CONCLUSIONS Since RUNX3 is involved in EMT in HCC, as proven by previous research, our findings provide further evidence for a novel regulatory pathway comprising the miR-20a/RUNX3/EMT axis that upregulates EMT signaling and enhances the migration of HCC cells.
Humans ; Carcinoma, Hepatocellular/pathology* ; Epithelial-Mesenchymal Transition/genetics* ; Liver Neoplasms/pathology* ; Gene Expression Regulation, Neoplastic/genetics* ; MicroRNAs/metabolism* ; Cell Movement/genetics* ; Cell Line, Tumor ; Cell Proliferation/genetics* ; Core Binding Factor Alpha 3 Subunit/metabolism*