Knockdown of ubiquitin­specific peptidase 39 inhibits the malignant progression of human renal cell carcinoma.

Ubiquitin specific peptidase 39 (USP39) serves important roles in mRNA processing and is involved in tumorigenesis of multiple solid malignancies. However, the influence and underlying mechanism of USP39 on human renal cell carcinomas (RCC) remain to be elucidated. The current study investigated the functional roles of USP39 in human RCC cell lines. siRNA­mediated RNA interference was used to downregulate USP39 in RCC cells. CCK­8, wound healing and invasion assays were performed to assess the proliferative ability and metastatic potential. The cell cycle distribution and apoptosis were evaluated by flow cytometry. The activity of signaling pathways and the expression of cell cycle­related proteins were detected by western blot analysis. The siRNA­directed RNA interference targeting USP39 could effectively downregulate the expression level of USP39 in two RCC cell lines. Depletion of USP39 by siRNA significantly suppressed cell growth and decreased invasive capacity of RCC cells. Silencing of USP39 induced cell apoptosis and cell cycle arrest at G2/M phase. Additionally, the expression levels of apoptotic and G2/M phase­related proteins were notably decreased following depletion of USP39. Mechanistically, downregulation of USP39 blocked the activation of Akt and extracellular signal regulated kinase signaling pathways in RCC cells. These findings indicate that USP39 may serve as an oncogenic factor in RCC and could be a potential therapeutic candidate for human RCCs.

[Early and mid-term results of endovascular aneurysm repair for infrarenal abdominal aortic aneurysm].

OBJECTIVE: Endovascular aneurysm repair (EVAR) of abdominal aortic aneurysms (AAA) has become a viable alternative to open surgical repair in the last decade. We report here our experience on the mid-term results of EVAR and analysis of the outcomes associated with endograft AAA repair. METHODS: Between Nov 2002 and Mar 2007, 26 patients with AAA were enrolled in a single institution. Indications for EVAR included unfavorable condition of body (eg. Heart, lung, or renal dysfunction, etc) for open surgery and maximum diameter of AAA > 5.0 cm. Customized stent-grafts were Talent TM, Zenith and some of products made in China. All of the patients were followed up with ultrasonography or computed tomography angiography every 3 months first year after EVAR and every year after. RESULTS: The mean (SD) follow-up was 38.8 ± 12.7 months (median, 35.0 months; range, 24 to 64 months), and no patients were lost to follow-up. All cause mortality was 15.4% (4/26), with all deaths occurring within the first 2 postoperative year; 30-day mortality was 4.1%. No patient died during the operation. Completion angiography demonstrated successful sealing in 25 of 26 patients. There was no stent occlusion of renal artery. The mid term complication were observed including 2 type I endoleak after 3 months of the operation, 2 sustained type II endoleak caused by lumber artery, 1 aneurysm of left femoral artery after 16 months of operation, 1 proximal neck dilation after 12 month of operation. The aneurysm sac size didn't increase significantly during follow time, except one of the type I endoleak. CONCLUSIONS: The mid-term results of EVAR support the continued use in patients with contraindications for traditional open surgery of AAA. Close surveillance is mandatory for endoleak, especially for type I endoleak. Some proximal neck dilation can be caused by the stent-graft expansion, injury, and aortic pathological changes. Endoleak of type II can not lead to enlargement of aneurysm sac probably.

Phosphatidylcholine-specific phospholipase C activity and level increase evidently in thromboangitis obliterans.

Thromboangitis obliterans (TAO) is considered to be an inflammatory disease. Previous research has demonstrated that phosphatidylcholine-specific phospholipase C (PC-PLC) plays critical roles in various inflammatory responses. However, the connection between PC-PLC and TAO is undetermined. Therefore, we sought to investigate whether PC-PLC was implicated in TAO. In our study, there were two groups: TAO group and control group. The PC-PLC activity of serum of two groups (16 TAO patients and 11 controls) was detected by PC-PLC activity assay. The level and distribution of PC-PLC in posterior tibial arteries in seven TAO patients and four controls were detected by immunofluorescence staining method. PC-PLC activity increased greatly in serum of TAO patients. Immunofluorescence analysis also revealed an upregulation of PC-PLC in the vascular endothelium of TAO patients. Our data suggest that PC-PLC activity and level increase obviously in TAO patients. Our study may provide new clues for seeking pathogenesis of TAO. Furthermore, it may bring new insights into clinical diagnosis and treatment of TAO.