[Clinical analysis of 28 cases of calculous pyonephrosis undergoing B-ultrasound-guided renal puncture and drainage followed by secondary percutaneous nephrolithotomy].

Objective: To investigate the therapeutic effects of first phase renal puncture and drainage guided by B ultrasound and second phase percutaneous nephrolithotomy(PCNL) in the treatment of urinary calculi complicated with pyonephrosis. Methods: From January 2014 to April 2018, 28 patients with upper ureteral segment and kidney calculi complicated with pyonephrosis were collected. All patients received the pyonephrosis puncture under B ultrasound. After the inflammation was controlled and the clinical situation improved, the second phase was treated by PCNL. During the operation, routine in dwelling ureteral stent drainage and renal fistula wereperformed. The outcomes of the operation were observed. Results: A total of 28 cases were successfully punctured, the obstruction was relieved and the inflammation was controlled. Additionally, the second phase of PCNL surgery was successful, and there were no significant stone residues after PCNL. There were no complications such as severe systemic inflammatory response syndrome and severe hemorrhage. After 3 to 12 months of follow-up, renal function was restored to varying degrees, and there were no renal failure patients who needednephrectomy. Conclusions: Early diagnosis of urinary calculi complicated with pyonephrosis is the key to successful treatment. Active and effective B ultrasound-guided renal puncture and drainage, drainage of pus, and removal of urinary obstruction can improve the safety of the second phase of PCNL, and thus it attaches great importance to the treatment of pyonephrosis.

MiR-181a promotes cell proliferation and migration through targeting KLF15 in papillary thyroid cancer.

INTRODUCTION: Papillary thyroid cancer (PTC) is the predominant histological type of thyroid cancer, accounting for 80% of thyroid cancers. MiR-181a is a novel microRNA that is usually upregulated in multiple cancers. This study aims to explore the role and underlying mechanism of miR-181a in PTC. METHODS: CCK8 and Transwell assays were performed to evaluate cell viability and migration. The mRNA level of miR-181a and KLF15 was calculated by qRT-PCR. The protein level of E-Cadherin, N-Cadherin and GAPDH was evaluated by western blot. Dual luciferase assay was conducted to validate that miR-181a directly targeting the 3'-UTR of KLF15 mRNA in TPC-1 cells. RESULTS: We observed that miR-181a was overexpressed and KLF15 was low expressed in PTC tissues and cell lines. Upregulation of miR-181a or downregulation of KLF15 predicted poor outcomes in PTC patients. MiR-181a improved cell growth of PTC, migration and epithelial-mesenchymal transition (EMT) in TPC-1 cells. KLF15 was a target gene of miR-181a and its expression was mediated by miR-181a. KLF15 partially reversed the facilitating effect of miR-181a on cell proliferation and migration in TPC-1 cells. CONCLUSION: We discovered that miR-181a served as an oncogene downregulating KLF15, thereby inhibiting cell proliferation, migration and the EMT. These findings demonstrate that miR-181a plays a significant role in PTC progression and could be a therapeutic target for PTC.

MiR-181a promotes cell proliferation and migration through targeting KLF15 in papillary thyroid cancer

IntroductionPapillary thyroid cancer (PTC) is the predominant histological type of thyroid cancer, accounting for 80% of thyroid cancers. MiR-181a is a novel microRNA that is usually upregulated in multiple cancers. This study aims to explore the role and underlying mechanism of miR-181a in PTC.MethodsCCK8 and Transwell assays were performed to evaluate cell viability and migration. The mRNA level of miR-181a and KLF15 was calculated by qRT-PCR. The protein level of E-Cadherin, N-Cadherin and GAPDH was evaluated by western blot. Dual luciferase assay was conducted to validate that miR-181a directly targeting the 3′-UTR of KLF15 mRNA in TPC-1 cells.ResultsWe observed that miR-181a was overexpressed and KLF15 was low expressed in PTC tissues and cell lines. Upregulation of miR-181a or downregulation of KLF15 predicted poor outcomes in PTC patients. MiR-181a improved cell growth of PTC, migration and epithelial–mesenchymal transition (EMT) in TPC-1 cells. KLF15 was a target gene of miR-181a and its expression was mediated by miR-181a. KLF15 partially reversed the facilitating effect of miR-181a on cell proliferation and migration in TPC-1 cells.ConclusionWe discovered that miR-181a served as an oncogene downregulating KLF15, thereby inhibiting cell proliferation, migration and the EMT. These findings demonstrate that miR-181a plays a significant role in PTC progression and could be a therapeutic target for PTC.