Relationship between platelet endothelial cell adhesion molecule 1 and leiomodin 1 gene polymorphisms and carotid plaque vulnerability / 中国脑血管病杂志

Objective To investigate the relationship between platelet endothelial cell adhesion molecule I (PEC AMI )/leiomodin 1 ( LMOD1 ) gene polymorphism loci and the risk of carotid plaque vulnerability in patients with ischemic stroke. Methods Ischemic stroke patients with carotid plaque admitted to Beijing Tiantan Hospital from May 2014 to October 2017 were enrolled prospectively. The demographic data and relevant clinical information were collected Carotid artery high-resolution magnetic resonance imaging (MRI) was used to distinguish vulnerable and stable plaques. The patients were enrolled in vulnerable plaque group and stable plaque group in turn. Real-time polymerase chain reaction was used. The TaqMan probe was use to conduct genotyping and statistical analysis of the PECAM1 ,LMOD1 gene polymorphism loci rsl 867624 and rs2820315 in the vulnerable plaque group and the stable plaque group. Binary logistic regression analysis was used to investigate the risk factors affecting the vulnerability of carotid atherosclerotic plaques. Results A total of 270 ischemic stroke patients with carotid plaque were enrolled, including 189 with vulnerable plaques and 81 with stable plaques. The polymorphism analysis of the PECAM1 gene locus rsl867624 in the two groups showed that the allele T was a vulnerable plaque risk gene,and its gene frequency in the vulnerable plaque group and the stable plaque group was 87. 3% (330/378) and 79. 6% (129/162;OR, 1.759,95% CI 1.080 -2.864 respectively,P = 0. 022). Analysis of the LM0D1 gene SNP locus rs2820315 showed that allele C was a risk gene for vulnerable plaques,and its gene frequency in the vulnerable plaque group and the stable plaque group was 87.6% (331/378) and 80.9% respectively (13I/I62;0tf, I. 667,95% CI 1. 014 -2. 738, P =0. 042). Logistic regression analysis showed that age (OR, 1.069,95% CI 1.022-1. 118, P = 0.004 ),PECAM1 gene rsl867624 locus T/T genotype (OR, 2.202,95% CI 1. 035 -4. 688 tP =0. 041) ,and LMODl gene rs2820315 locus C/C genotype ( OR,2. 199,95% CI 1. 005 -4. 809 , P =0.048) were the risk factors for the formation of vulnerable plaques. Conclusion The single nucleotide polymorphism locus rsl867624 of PECAM1 gene and single nucleotide polymorphism locus rs2820315 of LMODl gene were associated with carotid plaque vulnerability.

Study on the optimal dose of remifentanil combined with dexmedetomidine for awake tracheal intubation / 中国生化药物杂志

Objective To investigate the optimal dose of remifentanil combined with dexmedetomidine for awake tracheal intubation.Methods 60 cases with difficult airway general anesthesia surgery from March 2014 to August 2016 in Jinhua People's Hospital were selected and divided into group R1,R2,R3,20 cases in each group.0.6μg/kg dexmedetomidine 10 minutes micro pump intravenously,Simultaneous target-controlled infusion effect of the chamber concentration of remifentanil.2.0ng/mL remifentanil in group R1,2.3ng/mL remifentanil in group R2,2.5ng/mL remifentanil in group R3.All patients underwent full surface anesthesia with 2％lidocaine under visual soft mirror guidance.The heart rate(HR),mean arterial pressure(MAP)and Ramsay sedation score at before anesthesia(T0),at the end of the administration(T1),intubation(T2),immediately after intubation(T3),tracheal catheter placement reaction score and record tracheal intubation during respiratory depression,cardiovascular adverse events,postoperative follow-up of tracheal intubation process satisfaction.Results MAP,HR and RR at T2,T3 in group R1 were significantly higher than those in group R2 and R3,the difference was statistically significant(P<0.05).The incidence of hypertension in the group R3 was significantly lower than that in group R1,while the incidence of respiratory depression and tachycardia was significantly higher than that in group R1,the difference was statistically significant(P<0.05),RSS score and satisfaction scores in group R3 were significantly higher than those in group R1,the reaction score in group R3 was significantly lower than the group R1,the difference was statistically significant(P<0.05).Within group comparison,the mean arterial pressure and heart rate and respiratory rate at T2 and T3 in group R1 was significantly higher than those at T1,heart rate was significantly faster than T1,the respiratory rate was significantly faster than T1,the difference was statistically significant(P<0.05),T2 and T3 in group R3 were significantly slower than those at T0,the difference was statistically significant(P<0.05).Conclusion Remifentanil combined with dexmedetomidine can be safely and effectively used for awake intubation under glidescope guiding in difficult airway patients.In the full airway surface anesthesia,dexmedetomidine micropump 0.6μg/kg simultaneous target transfusion effect of the concentration of remifentanil 2.3ng/mL is a more reasonable medication.

The study on apoptosis induced by disodium cantharidinate and vitamin B6 in glioblastoma cells U87 / 实用肿瘤学杂志

Objective The purpose of this study is to investigate the apoptosis mechanisms of glioblasto-ma cell line U87 induced by sodium cantharidinate ( SCA) in vitro.Methods Growth inhibition of U87 by 0.625μg/mL,1.25μg/mL,2.5μg/mL,5μg/mL SCA at 24 h,48 h,72 h were analyzed by MTT assay respec-tively.Morphological changes of U 87 nuclear were detected by fluorescence microscope .U87 cell apoptosis and cell cycle arrest were detected after SCA treatment for 24 h and 48 h by flow cytometry.The changes of apoptosis-related genes Bcl -2,Bax,Caspase-3 expression were analyzed after 24 h of SCA treatment by RT -PCR as-say.Results MTT assay showed that growth inhibition of U 87 cell induced by SCA was accompanied with the in-creased drug concentration ,Hoechst33258 staining showed the morphology of apoptotic U 87 cells nucleui ,chromo-some condensation ,nuclear condensation ,some nuclear fragmentation and formation of apoptotic bodies .Flow cy-tometry showed that SCA could induce cell cycle arrest at the G 2/M phase,and could induce apoptosis of U87.RT-PCR results showed that after 24 h of SCA treatment caspase -3,bax expression of U87 was significantly higher than the control group(P0.05).Conclusion Our results demonstrate that SCA can inhibit U87 pro-liferation and induce apoptosis of U 87 .