ABSTRACT
Objective To investigate the alteration and significance of inflammatory factors in hypertension patients complicated with acute myocardial infarction(AMI).Methods Eighty seven AMI patients were grouped as normotensive group(n=43) or hypertensive group(n=44),25 healthy subjects served as control.Plasma level of IL-1?,IL-6,IL-8,TNF-? and IFN-? were determined at admission of hospitalization,24 h,48 h,5 d,7 d and 14 d after myocardial infarction using ELISA method.Results 1)Compared with the control group,the level of all inflammatory markers were elevated significantly in 2 weeks after myocardial infarction and showed a pattern of dynamic changes.2)Compared with normotensive group,IL-6 in hypertensive group was increased more significantly on 5th day(P=0.019) to 7th day(P=0.005)after AMI.Conclusion Inflammation was involved in the course of AMI since the early stage.Hypertension seems to exaggerated the inflammatory reaction after myocardial infarction.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the relation between the susceptibility to silicosis and the polymorphism of HLA-DRB1 *, DQB1 * genes in Chinese Hans.</p><p><b>METHODS</b>HLA-DRB1 * and DQB1 * gene polymorphism were tested in 48 silicosis patients and 100 normal controls by using polymerase chain reaction of sequence-specific primers (PCR-SSP).</p><p><b>RESULTS</b>The allele frequencies of DRB1 * 1401 and DQB1 * 05 in silicosis patients were significantly higher than those in normal controls (chi 2 = 5.61, P = 0.0066, RR = 17.40; chi 2 = 10.70, P = 0.0011, RR = 3.81, respectively), while the allele frequency of DRB1 * 09 was significantly lower in silicosis patients than that in controls (chi 2 = 5.70, P = 0.0187, RR = 0.21). There was a significant difference between the patient group and control group.</p><p><b>CONCLUSION</b>HLA-DRB1 * 1401 and DQB1 * 05 may be the susceptible genes and HLA-DRB1 * 09 the protection gene of silicosis, both susceptibility and protection may be related to HLA-DR gene locus. The joint action of allele genes may affect the pathogenesis of silicosis.</p>