ABSTRACT
Objective@#To investigate the effect of nicorandil on ventricular arrhythmia in patients with acute ST-segment elevation myocardial infarction (STEMI) treated with emergent percutaneous coronary intervention (PCI).@*Methods@#A total of 120 acute STEMI patients treated with emergent PCI in our hospital from January 2015 to June 2016 were randomly divided into control group and experiment group (n=60 each). Patients in both groups received conventional therapy.Patients in experiment group took 10 mg nicorandil orally before PCI and received oral nicorandil treatment (15 mg/d, three times daily) for 3 days.QT disperse(QTd), correct QTd(QTcd) and the occurrence rate of ventricular arrhythmia were compared between two groups.@*Results@#QTd at 6, 24, 48 and 72 hours((70.6±4.4), (67.2±5.3), (55.7±8.5), (48.2±8.2) ms, respectively) after PCI was significantly lower in the experiment group than those of control group ((77.1±7.1), (71.3±6.5), (65.1±8.1), (57.2±5.4) ms, all P<0.05). The level of QTd was also significantly lower in the experiment group at 6, 24, 48 and 72 hours((77.5±7.7), (67.7±8.6), (61.2±7.5), (52.9±8.4) ms, respectively) after PCI comared to those of control group ((88.6±8.1), (79.2±7.8), (74.4±7.4), (69.6±8.6) ms, all P<0.05). There was no significant difference in the incidence of reperfusion arrhythmia during PCI procedure between the two groups.The prevalence of the ventricular premature beat in the experiment group (25/60, 41.7%) was significantly lower than in the control group(45/60, 75.0%) within 3 days after PCI(P<0.01), the prevalence of the no sustained ventricular tachycardia and ventricular fibrillation in the experiment group(6/60, 10.0%) was also significantly lower than in the control group (18/60, 30.0%, P<0.01) within 3 days after PCI.@*Conclusions@#Nicorandil use prior and post PCI could decrease the occurrence rate of ventricular arrhythmia in STEMI patients undergoing emergent PCI, and this effect might be related with reduced QTd and QTcd post medication.
ABSTRACT
Seven genes (fabD, fabG, fabH, fabA, fabZ, fabB and fabI) of E.coli fatty acid biosynthetic enzymes were cloned by PCR amplifying and appropriate expression vectors were constructed. Under induction assay expression of plasmid encoded proteins was carried out in strain BL21(DE3) and seven enzymes were purified using Ni-NTA agarose resin. In the absence of [2-14C] malonyl-CoA fatty acid synthetic reaction was reconstituted in vitro by adding seven enzymes and co-factors. And several model reactions were established for identification of special fatty acid biosynthetic enzymes. Meanwhile Clostridium acetobutylicium FabZ function was characterized by this method.
ABSTRACT
FabB(?-ketoacyl-acyl carrier protein synthase Ⅰ)and FabF(?-ketoacyl-acyl carrier protein synthase Ⅱ)are two key enzymes of fatty acid biosynthesis in E.coli.The Gram-positive pathogenic bacterium Enterococcus faecalis has a fatty acid composition very similar to that of E.coli.Bioinformatic analysis reveals that though E.faecalis has two fabF homologues,there is no recognizable fabB homologue in the genome of E.faecalis.Two fabF homologues(fabF1 and fabF2)were amplified by using E.faecalis V583 genomitic DNA as template,and two plasmids,pHW13(fabF1)and pHW14(fabF2),were constructed.The results of experiments in vivo and in vitro have shown that fabF1 gene could complement E.coli fabB mutation and FabF1 possessed ?-ketoacyl-acyl carrier protein synthase Ⅰ(FabB)activity,while fabF2 gene could complement E.coli fabF mutation and FabF2 had ?-ketoacyl-acyl carrier protein synthase Ⅱ(FabF)activity.Meanwhile the data also shown that FabF2 possessed partial function of ?-ketoacyl-acyl carrier protein synthase Ⅰ(FabB),and it could make E.coli fabB mutation synthesized low amount of unsaturated fatty acid.From these data it is clear that FabF species enzymes could have activity of ?-ketoacyl-acyl carrier protein synthase Ⅰ(FabB).