ABSTRACT
Objective: To analyze the relationship between monocyte to high-density lipoprotein cholesterol (HDL-C) ratio (MHR) in patients with ST-segment elevation myocardial infarction(STEMI) in order to explore the predictive value of MHR in thrombus burden level in STEMI patients. Methods: A total of 357 STEMI patients treated in our hospital from 2015-01 to 2016-12 were enrolled. Thrombus burden was confirmed by angiography and the patients were divided into 2 groups: Low thrombus burden group, n=156 and High thrombus burden group, n=201. MHR was compared between 2 groups; the predictive value of MHR in thrombus burden level was studied by multivariate Logistic regression analysis and ROC curve assessment. Results: MHR was higher in High thrombus burden group than that in Low thrombus burden group [M (Q1, Q3) 25.4 (13.5, 44.6) vs 16.0 (9.2, 22.1)], P<0.001; multivariate Logistic regression analysis indicated that MHR was the independent predictor for high thrombus burden occurrence (OR=1.067, 95％ CI 1.031-1.105), P<0.001; the area under ROC curve for MHR was 0.688 in STEMI patients. Conclusion: MHR was the independent predictor for high thrombus burden occurrence in STEMI patients.
ABSTRACT
The clinical data of one patient with autoimmune polyendocrinopathy syndrome type I were collected. PCR-DNA direct bidirectional sequencing was applied for mutation screening of 14 exons in autoimmune regulator (AIRE) gene in the patient and her parents. A total of 50 unrelated healthy controls were selected and tested. The bioinformatic methods were used to predict the possible impact of the mutations on the structure and function of the AIRE protein. The results of sequencing showed that heterozygous mutation c.622G>T (p.G208W) in exon 5 of the AIRE gene was detected in the patient and was a novel mutation, which had not been reported in the HGMD database and latest articles. This mutation was not detected in the 50 unrelated normal controls. The novel mutation of c.622G>T (p.G208W) in AIRE gene might play an important role in the pathogenesis of this case of autoimmune polyendocrinopathy syndrome type I.