ABSTRACT
Objective To analyze the risk factors associated with acute type A aortic dissection,and to establish an effective predictive scoring model for early clinical intervention.Methods A retrospective review of 200 patients diagnosed as acute type A aortic dissection in the Department of Emergency,Guangdong Provincial People's Hospital between April 1,2012 and March 31,2017 was conducted as a modeling group.There were 160 males and 40 females with age of (53.30 ±13.19) years.According to the criteria of dissection rupture within 72 h after CTA examination,patients were divided into a rupture group (100 cases) and an unruptured group (100 cases).A prediction model of rupture risk was established based on the multivariate Logistic regression analysis of the risk factors of acute A-type aortic dissection in the early stage.After the establishment of the model,a prospective review of 80 patients diagnosed as acute type A aortic dissection in our hospital between April 1,2017 and May 31,2018 was conducted as a validation group.There were 57 males and 23 females with age of (54.00 ±13.68) years.In the validation group,there were 53 patients with rupture and 27 patients without rupture.Furthermore,this model was verified in the validation group.The scores were divided into low-risk rupture and high-risk rupture according to the best cut-off value of the receiver operating model curve of the modeling group.Results Logistic regression analysis showed that 10 factors were finally established the rupture risk prediction score model.The factors were as following:age ＞63 years (2 points),women (2 points),ventilator assisted ventilation (3 points),AST ＞80 U/L (2 points),no distortion of the inner membrane (2 points),diameter of the aortic sinus ＞41 mm (1 point),maximum diameter of the ascending aorta ＞48 mm (1 point),ratio of false lumen area to true lumen area ＞2.12 (2 points),Lac ＞1.9 mmol/ L (3 points),and WBC ＞14.2×109/L (1 point).The results of validation showed that the scoring model had a high predictive value (AUC =0.928,95％ CI:0.872-0.984,P ＜ 0.001) and goodness of fit (Hosmer-Lemeshow x2 =8.331,P =0.402).Moreover,the scoring model was further divided into low-risk (0-6 points) and high-risk (7-19 points),with sensitivity of 83.0％ and specificity of 86.0％.Conclusions The predictive model of dissection risk in the acute type A aortic dissection constructed within 72 h after CTA is helpful for the evaluation of the disease and early intervention,and has certain clinical application value.
ABSTRACT
BACKGROUND:In recent years,the incidence of skeletal muscle injury becomes higher and higher,but the skeletal muscle repair ability is limited;therefore,studies on the molecular mechanism of skeletal muscle repair play a positive role in the treatment of skeletal muscle injury.OBJECTIVE:To explore the role of microRNA in skeletal muscle regeneration.METHODS:C2C12 myoblasts were cyclic stretched in vitro by the Flexercell-5000 flexible device,and the appropriate stretch condition which could induce myogenesis was selected.The microRNA expression alteration during mechanical stretch-induced myoblast myogenesis was explored using high-throughout sequencing,and the differentially expressed microRNAs were further studied by the bioinformatics analysis.RESULTS AND CONCLUSION:10％ deformation,0.125 Hz cyclic mechanical stretch could promote myoblast proliferation and increase MyoD and Myogenin expressions in C2C12 myoblasts.MicroRNA expression profile alteration,including the downregulated miR-500-3p/1934-5p/31-3p/378a-5p/3473b/331-3p/5097 and upregulated miR-340-5p/449c-Sp/1941-3p,were all involved in the stretch-mediated myoblast myogenesis,and the MAPK signal pathway seemed to participate in this process.These results suggest that the low frequency of the cyclic mechanical stretch can upregulate the expression levels of myogenic regulatory factors through the alteration of MicroRNA expression,further inducing myogenesis,which the MAPK signal pathway may be involved in.
ABSTRACT
To investigate the mechanisms of serine/threonine kinase Pim-3 inhibition of fulminant hepatic apoptosis. Thirty-two rats were randomly divided into four groups (n = 8 each): normal controls (A); pretreatment with Ringer's solution (B), vector plasmid (C), or Pim-3 recombinant plasmid (D) by hydrodynamics-based procedure followed by intraperitoneal injections of lipopolysaccharide (LPS) and D-galactosamine (D-GalN) after one day. At 8 h after the LPS/D-GalN injections, liver tissues were collected from all groups of mice and analyzed for cell apoptosis by detecting caspase-3 activity (measured in relative fluorescence units, RFU). Changes in expression of relevant genes were determined by RT-PCR and Western blotting. Caspase-3 activity was induced in response to LPS/D-GalN injection. Pim-3-pretreated rats showed a lower level of caspase-3 activity than the Ringer's-pretreated or vector plasmid-pretreated rats [(141.7+/-13.7)RFU vs. (508.1+/-32.0) or (493.5+/-33.1) RFU; all P less than 0.01]. High expressions of the liver injury marker gene, iNOS, and the apoptosis-induced genes, p53 and Bax, were found after LPS/D-GalN challenge, and were suppressed by exogenous Pim-3 gene injection. In addition, exogenous Pim-3 gene injection induced high expression of the liver anti-apoptosis protein, Bcl-2, but had no effect on Bax protein expression. The Pim-3 gene can block fulminant hepatic apoptosis by affecting the expression of the iNOS liver injury gene and the p53, Bax and Bcl-2 apoptosis-related genes.
Subject(s)
Animals , Male , Rats , Apoptosis , Caspase 3 , Metabolism , Liver , Metabolism , Pathology , Liver Failure , Metabolism , Pathology , Protein Serine-Threonine Kinases , Genetics , Rats, WistarABSTRACT
<p><b>OBJECTIVE</b>To evaluate the value of ischemic preconditioning in clinical hepatectomy.</p><p><b>METHODS</b>A total of 48 unselected patients undergoing liver resection were analyzed by randomized controlled trial from December 2004 to June 2006. Forty-eight unselected patients were randomized into two groups: IP group (5 minutes of ischemia followed by 5 minutes of reperfusion) and control group (received Pringle's maneuver no and no IP was given). Postoperative days 1, 3 and 7, the liver function were checked. Perioperative mortality, morbidity and hospitalized days were compared.</p><p><b>RESULTS</b>In IP group, ischemic times were 5 - 80 min, mean 31 min, hospitalized days were 13 - 50 days, mean 20 days. In control group, ischemic times were 10 - 60 min, mean 27 min, hospitalized days were 10 - 33 days, mean 17 days. Forty-seven patients were satisfactory with postoperative recovery, except one patient died of chronic liver dysfunction after 3 months postoperatively. Postoperative days 1, 3 and 7, the ALT, AST, TBIL, ALB levels in two groups were not statistically significant (P > 0.05).</p><p><b>CONCLUSIONS</b>The clinical use of IP through 5 minutes of warm ischemia in this technique of hepatectomy does not protect the liver from hepatic injury induced by the IRI.</p>