RÉSUMÉ
Objective:To explore influence of tirofiban on plasma level of growth differentiation factor-15(GDF-15) and serum level of platelet activating factor(PAF)in patients with acute myocardial infarction(AMI)undergoing percutaneous coronary intervention(PCI).Methods:A total of 110 AMI patients undergoing emergency PCI from Jan 2015 to Dec 2016 were selected.According to random number table,they were randomly and equally divided in-to routine treatment group(received dual antiplatelet therapy etc.)and tirofiban group(received tirofiban based on routine treatment group).TIMI blood flow grade and cardiac function after PCI,plasma GDF-15 and serum PAF levels before and after treatment,and incidence of adverse events were compared between two groups.Results:Compared with routine treatment group on 7d after PCI,there were significant reductions in serum PAF level [(10.2 ± 1.7)μg/L vs.(8.3 ± 1.4)μg/L]and plasma GDF-15 level[(2.6 ± 0.8)μg/L vs.(1.5 ± 0.6)μg/L]in tirofiban group,P=0.001 both.Compared with routine treatment group on six months after PCI,there was signifi-cant rise in left ventricular ejection fraction[(52.8 ± 6.6)% vs.(57.5 ± 7.3)%],and significant reductions in left ventricular end-systolic dimension[(45.4 ± 7.1)mm vs.(40.2 ± 6.9)mm],left ventricular end-diastolic dimension [(57.0 ± 7.2)mm vs.(52.4 ± 7.6)mm]and incidence rate of adverse events(14.5% vs.1.8%)in tirofiban group,P<0.05 or <0.01. Conclusion:Compared with routine treatment,tirofiban can more significantly reduce plasma GDF-15 and serum PAF levels,improve cardiac function in AMI patients after PCI,and it′s safe,which is worth extending.
RÉSUMÉ
<p><b>OBJECTIVE</b>To study the mutation of FRMD7 gene in a Chinese family with congenital idiopathic nystagmus.</p><p><b>METHODS</b>Forty-six individuals in the Chinese family with congenital idiopathic nystagmus, including 16 patients, 19 normal siblings and 11 spouses, were investigated under informed consent. Genomic DNA of all 46 members was isolated by standard protocol. The X-linked inherited pattern was ascertained by investigating the history of the family members and the clinical feature of each individual. The genome scan on X chromosome was performed after PCR amplification for microsatellite markers. LOD scores were calculated with Linkage 5.1. Direct DNA sequence analysis was carried out to find the gene mutation responsible for the disease.</p><p><b>RESULTS</b>A maximum LOD score of 8.55 (theta=0) was obtained with polymorphic marker DXS1047. Haplotype construction of the family defined the disease interval between DXS8059 and DXS8033. Direct DNA sequence analysis revealed a heterozygous mutation of G990T in exon 9 of the FRMD7 gene in all patients, which was not present in unaffected family members.</p><p><b>CONCLUSION</b>Congenital nystagmus is a clinically and genetically heterogeneous ocular movement disease. The mutation of G990T of the FRMD7 gene is the underlying molecular pathogenesis for this family with congenital nystagmus.</p>