Evaluationthe right heart function has vital clinical value, especially in patients after surgical repair of tetralogy of Fallot(TOF).As an important tool used to assess the structure and function of heart, echocardiography has been used to evaluatethe right heart function of TOF after the surgery. This article reviews the current research on echocardiography techniques and right heart function in patients after surgical repair of Tetralogy of Fallot．
ObjectiveTo systematically review the efficacy and safety of non-myeloablative stem cell transplantation (NST) for the treatment of multiple myeloma (MM) after first autologous stem cell transplantation. MethodsSuch databases as The Cochrane Library (Issue 5, 2013), PubMed, EMbase, CBM, CNKI, VIP and WanFang Data were electronically searched to collect studies investigated the efficacy and safety of NST and non-NST for the treatment of MM after first autologous stem cell transplantation from the date of their establishment to June 13th 2013. Two reviewers independently screened studies according to the inclusion and exclusion criteria, extracted data and evaluated the methodological quality of the included studies. Then meta-analysis was performed using RevMan 5.1 software. ResultsSeven studies involving 1 961 participants were included, of which 626 cases were in the NST group and 1 335 cases were in the non-NST group. The results of meta-analysis showed that no significant difference was found between both groups in the overall survival rate (HR=1.06, 95%CI 0.78 to 1.44, P=0.69) and progress-free survival rate (HR=0.92, 95%CI 0.76 to 1.11, P=0.39). However, there were significant differences in the complete remission rate (RR=1.29, 95%CI 1.13 to 1.48, P=0.000 2) and treatment-related mortality rate (RR=3.40, 95%CI 2.27 to 5.07, P < 0.000 01). ConclusionThe efficacy of NST is not superior to non-NST for patients with MM which has received first autologous stem cell transplantation. It is not sufficient to recommend NST as the first-line treatment of MM based on the currently available evidence.
ObjectiveTo investigate the effect of PI3K/Akt/mTOR signaling pathway on liver injury induced by severe acute pancreatitis (SAP). MethodsForty healthy adult male Sprague-Dawley (SD) rats were randomly divided into 4 groups: Sham operation group (SO group), SAP group, PI3K inhibitor LY294002 group (LY294002 group), and mTOR kinase inhibitor rapamycin group (rapamycin group). The rat model with SAP was made by injection with 5% sodium deoxycholate through retrogradely bilio pancreatic duct. Serum levels of amylase (AMY), alanine aminotransferase (ALT), and aspartate transaminase (AST) were detected through the inferior vena at 6 h after modeling. Pathologic change of the liver was observed under the light microscope. TUNEL analysis was used to detect apoptotic index (AI) of the heptocyte. Expressions of Akt, phosphated-Akt (p-Akt), mTOR, phosphated-mTOR (p-mTOR) protein were evaluated by Western blot. Results①Compared with the SO group, the serum levels of AMY, ALT, AST, and the hepatocyte AI were significantly increased among the other three groups (P < 0.05). Compared with the SAP group, the serum levels of AMY, ALT, AST, and the hepatocyte AI were significantly decreased in the LY294002 group and rapamycin group (P < 0.05).②Compared with the SO group, the damages of the liver tissues were aggravated among the other three groups. The pathologies of the liver tissues were ameliorated in the LY294002 group and rapamycin group as compared with the SAP group.③Compared with the SO group, the levels of p-Akt/Akt, p-mTOR/mTOR were significantly increased among the other three groups (P < 0.05). Compared with the SAP group, the levels of p-Akt/Akt, p-mTOR/mTOR were significantly decreased in the LY294002 group (P < 0.05), but in the rapamycin group, only the p-mTOR/mTOR level was significantly decreased (P < 0.05). ConclusionThe activation of PI3K/Akt/mTOR signaling pathway might be one of the reasons for the liver injury induced by SAP and blocking this signaling pathway might be a potential target of preventing progress of SAP and alleviating liver injury induced by SAP.