ABSTRACT
Objective:To explore the value of social support rating scale using in patients with vasovagal syncope (VVS) .Methods:Social support rating scale (SSRS) established by XIAO Shui-yuan was used .A total of 200 VVS patients were collected from inpatients and outpatients and they received social support status investigation ,another 100 normal people were collected from our physical examination center were regarded as control (normal control group) .Results:Compared with normal control group ,there were significant reductions in scores of each item and total score of social support [ (37.22 ± 9.15) scores vs .(33.50 ± 8.64) scores] in VVS group ,P<0.05 or <0.01 ;compared with male patients ,there were significant rise in scores of subjective support [ (17.63 ± 6.72) scores vs . (18.62 ± 7.56) scores] ,utilization of support [ (7.51 ± 2.26) scores vs .(8.92 ± 2.82) scores] and total social sup-port [(34.32 ± 10.61) scores vs .(36.79 ± 7.86) scores] ,and significant reduction in objective support score [(9.28 ± 4.15) scores vs .(8.37 ± 3.49) scores] in female patients , P<0.05 or <0.01;compared with middle-aged and aged group ,there were significant rise in scores of subjective support [ (17.08 ± 6.34) scores vs .(19.51 ± 6.73) scores] and total social support [(33.18 ± 10.74) scores vs .(36.87 ± 8.73) scores] ,and significant reduction in uti-lization of support score [ (8.47 ± 2.60) scores vs .(7.53 ± 1.95) scores] in young group ,P<0.05 or <0.01. Con-clusion:Social support assessment is help to perform individualized diagnosis and therapy for patients with vasovagal syncope ,and help to improve their quality of life .
ABSTRACT
To investige the relationship between expression levels of interferon regulatory factors [IRF] in patients with coronary artery disease. Prospective case-control study. Department of cardiology, Puren Hospital, Wuhan University of Science and Technology, Wuhan, China [PRC]. Between October 2010 and July 2011, 106 patients [aged 37-71 years] were enrolled. Patients were assigned to four groups: acute myocardial infarction [AMI] [n = 28], stable angina [SA] [n = 26], unstable angina [UA] [n= 26], and control group [without CAD, n=26]. Blood samples were drawn from all the patients via the antecubital vein following a 12 h fasting period [HDL-C], low density lipoprotein cholesterol [LDL-C] and high sensitivity C-reactive protein [hs-CRP] were measured. The mRNA and protein expression levels of IRF-1, IRF-2, IRF-4 and IRF-8 in each patient were measured using PCR and western blotting. Serum levels of IL-12 and IFN-gamma were detected by ELISA. Within both the AMI and UA groups, IL-12 and IFN-gamma were significantly increased compared with SA and control patients. Both the mRNA and protein expression levels of IRF-1, IRF-2 and IRF-8 in the AMI and UA groups were significantly higher than those in the SA and control groups. There was no significant difference between the SA and control groups. The increase in expression levels of IRF-1, IRF-2 and IRF-8 may be associated with atherosclerotic plaque formation and rupture, which are seen in AMI and UA
ABSTRACT
This study examined the relationship between PDGF-induced proliferation of vascular smooth muscle cells (VSMCs) and Nur77 expression and the effect of atorvastatin on VSMC proliferation and Nur77 in PDGF-treated VSMCs. Rat VSMCs were isolated and cultured. After incubation with atorvastatin or Nur77 siRNA, the cells were stimulated with PDGF and detected for BrdU incorporation to measure the proliferation of the VSMCs. Quantitative PCR and Western blotting were used to determine the Nur77 protein and the CREB phosphorylation level, to observe their relations with PDGF-induced VSMC proliferation. Our results showed that PDGF increased the BrdU incorporation in VSMCs, suggesting that it induced the proliferation of the cells. The VSMC proliferation was associated with increased Nur77 expression and elevated CREB phosphorylation. Atorvastatin inhibited the PDGF-induced VSMC proliferation, suppressed Nur77 expression. After silencing of Nur77 gene, the PDGF-induced VSMC proliferation was decreased. It was concluded that PDGF-induced VSMC proliferation was related to the Nur77 expression and CREB phosphorylation. Atorvastatin reduced the Nur77 expression and, at the same time, inhibited the VSMC proliferation.