LncRNA PCAT6 promotes occurrence and development of ovarian cancer by inhibiting PTEN.

OBJECTIVE: The purpose of this study was to explore the expression and function of long non-coding RNA (lncRNA) PCAT6 in ovarian cancer. PATIENTS AND METHODS: Quantitative Real-Time-Polymerase Chain Reaction (qRT-PCR) was used to detect the expression of lncRNA PCAT6 in 42 pairs of ovarian cancer tissues and adjacent normal tissues. Then, the relationship between PCAT6 expression and pathological indicators of ovarian cancer was analyzed. Subsequently, the transfection efficiency of PCAT6 in ovarian cancer cells was verified, and the PCAT6 knockdown model was constructed using lentiviruses in SKOV3 and CAOV3 ovarian cancer cell lines. In addition, Cell Counting Kit-8 (CCK-8) test, wound healing assay and transwell invasion and migration experiments were performed to estimate the effect of PCAT6 on the biological function of ovarian cancer cells, to further explore the possible potential mechanisms. RESULTS: QRT-PCR results showed that the expression level of PCAT6 in ovarian cancer was higher than that in the adjacent normal tissues. The incidence of distant metastasis and lymph node metastasis in patients with high expression of PCAT6 was higher than those with low PCAT6 expression. Compared with the NC group, the proliferation, metastasis and invasion ability of ovarian cancer cells in si-PCAT6 group decreased significantly. QRT-PCR results demonstrated that the PTEN expression was increased after the knockdown of PCAT6. In addition, the recovery experiment also revealed that PCAT6 and PTEN have a mutual regulation, which can jointly regulate the development of ovarian cancer. CONCLUSIONS: LncRNA PCAT6 was up-regulated in ovarian cancer tissues and was closely related to distant metastasis or lymph node metastasis. Additionally, lncRNA PCAT6 might promote the proliferation, migration and invasion of ovarian tumor cells by inhibiting PTEN.

Management of bleeding in vascular surgery.

Management of acute coagulopathy and blood loss during major vascular procedures poses a significant haemostatic challenge to anaesthetists. The acute coagulopathy is multifactorial in origin with tissue injury and hypotension as the precipitating factors, followed by dilution, hypothermia, acidemia, hyperfibrinolysis and systemic inflammatory response, all acting as a self-perpetuating spiral of events. The problem is confounded by the high prevalence of antithrombotic agent use in these patients and intraoperative heparin administration. Trials specifically examining bleeding management in vascular surgery are lacking, and much of the literature and guidelines are derived from studies on patients with trauma. In general, it is recommended to adopt permissive hypotension with a restrictive fluid strategy, using a combination of crystalloid and colloid solutions up to one litre during the initial resuscitation, after which blood products should be administered. A restrictive transfusion trigger for red cells remains the mainstay of treatment except for the high-risk patients, where the trigger should be individualized. Transfusion of blood components should be initiated by clinical evidence of coagulopathy such as diffuse microvascular bleeding, and then guided by either laboratory or point-of-care coagulation testing. Prophylactic antifibrinolytic use is recommended for all surgery where excessive bleeding is anticipated. Fibrinogen and prothrombin complex concentrates administration are recommended during massive transfusion, whereas rFVIIa should be reserved until all means have failed. While debates over the ideal resuscitative strategy continue, the approach to vascular haemostasis should be scientific, rational, and structured. As far as possible, therapy should be monitored and goal directed.