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Little is known about the influence of metabolic syndrome (MetS) on coronary artery calcification (CAC) in China. In this article, we aimed to explore the distribution of CAC in populations with and without MetS, and estimate the influence of MetS and its components on CAC in a community-based population of Beijing.A total of 1647 local residents of Beijing, age 40-77 years, were recruited for a cardiovascular risk factors survey and were determined fasting plasma glucose (FPG), blood lipids, and 64 multi-detector computed tomography (64-MDCT) coronary artery calcium score (CACS) measurement (Agatston scoring). The distribution of CAC was described, and the influence of MetS components on CAC was evaluated.In this population, the prevalence and extent of CAC increased with increasing age and both were higher in MetS subjects compared to nonMetS subjects (all P0.05), with the exception of those older than 65 years old. The risk of CAC increased with increasing numbers of MetS components, and the odds ratios for predicting positive CAC in subjects with 1, 2, 3, and = 4 MetS components were 1.60, 1.84, 2.12, and 3.12, respectively (all P0.05). Elevated blood pressure, elevated FPG, elevated triglycerides, and overweight increased the risk of CAC, yielding odds ratios of 2.64, 1.67, 1.32, and 1.37, respectively (all P0.05).In the Beijing community-based population, MetS increases the risk of CAC. The risk of CAC increases with increasing numbers of MetS components. Not only the number, but also the variety of risk factors for MetS is correlated with the risk of CAC. Elevated blood pressure, hyperglycemia, hypertriglyceridemia and overweight increase the risk of CAC.

To investigate the influence of uric acid on coronary artery calcification in the natural population in Beijing.From April to July 2012, 903 subjects from the natural population(aged 37-76 years for men, aged 42-76 years for women)in Xishan community, Beijing, were selected to accept a survey on the risk factors of cardiovascular. Blood tests and CT coronary artery calcium scans were carried out.At the 1 Quartile(1 Q), 2 to 3 Quartile(2-3 Q)and 4 Quartile(4 Q)of uric acid levels, the prevalence rates of coronary artery calcium were 37.2% , 45.5% , 60.6% (P0.001) and the coronary artery calcium scores were (109.7±333.1)AU, (133.9±356.9)AU, (200.8±459.4) AU (P0.001)respectively. Data from the univariate logistic regression analysis showed that with the increase of uric acid, the prevalence rates of coronary artery calcium also increased(OR2-3Q = 1.41, 95% CI:1.02-1.95, P = 0.040; OR4Q = 2.60, 95% CI:1.78-3.80, P0.001). However, the relationship between uric acid and coronary artery calcium disappeared when using the multivariate logistic regression analysis(OR2-3Q = 0.92, 95% CI: 0.60-1.43, P = 0.713;OR4Q = 1.38, 95% CI:0.80-2.39, P = 0.247).Uric acid did not seem to be an independent risk factor for coronary artery calcium, although the prevalence and extent of coronary artery calcium increased along with the increasing trend of uric acid.

To investigate the clinical manifestations of patients with pulmonary artery hypertension (PAH) associated with hereditary hemorrhagic telangiectasia (HHT).This retrospective analysis summarized the clinical features of 6 patients with PAH associated with HHT hospitalized at department of cardiology in Cardiovascular Institute and Fuwai Hospital between January 2006 and May 2009.The mean age of the 6 patients (3 male) was 34 years (8 - 67 years). Recurrent epistaxis were present in all patients, there were 4 patients with severe PAH and 2 patients with moderate PAH. All of the six patients with PAH associated with HHT were misdiagnosed at the first hospital visit. Clinical symptoms were significantly improved in 4 patients and remained unchanged in 2 patients combined hepatic venous malformation post medical therapy.Misdiagnosis for patients with PAH associated with HHT is a common phenomenon in daily clinical practice. Patients could benefit from the corresponding medical therapy after the establishment of the correct diagnosis.

To determine the optimal contrast injection protocol for 64-MDCT coronary angiography.One hundred and fifty consecutive patients scheduled to undergo retrospectively electrocardiographically gated 64-MDCT. Each 30 patients were assigned to use a different contrast protocol: group 1: uniphasic protocol (contrast injection without saline flush); group 2: biphasic protocol (contrast injection with saline flush); group 3A, 3B and 3C: triphasic protocol (contrast media+different saline diluted contrast media+saline flush). Image quality scores and artifacts were compared and evaluated on both transaxial and three-dimensional coronary artery images among each contrast protocol.Among the triphasic protocol groups, group 3A (30%:70% contrast media-saline mixture was used in second phase) used the least contrast media and had the least frequency of streak artifacts, but there were no significant differences in coronary artery attenuation, image quality, visualization right and left heart structures. Among the uniphasic protocol group (group 1), biphasic protocol group (group 2) and triphasic protocol subgroup (group 3A), there were no significant differences in image quality scores of coronary artery (P=0.18); uniphasic protocol group had the highest frequency of streak artifacts (20 cases) (P0.05) and had the most amount contrast media (67.0+/-5.3 ml); biphasic protocol group had the least amount of contrast media (59.9+/-4.9 ml) (P0.05) and had the highest attenuation of left main coronary artery and right coronary artery (P0.01), but had the least amount of clear visualization right heart structure (6 cases); triphasic protocol group (group 3A) had the most amount of clear visualization right heart structures (29 cases) were the most among the three groups (P0.05).Biphasic protocol are superior to the traditional uniphasic protocols for using the least total contrast media, having the least Streak artifacts and without image quality degradation. However, it is also important to visualize the right atrium and ventricle, so triphasic protocol (30%:70% contrast media-saline mixture was used in second phase) should be used for 64-MDCT coronary CT angiography.

The key role of an inhibitory receptor, Programmed Death-1, has been evaluated in 273 patients with autoimmune myasthenia gravis. At the genetic level, SNP's genotyping showed no significant association to the disease. Gene expressions in patients were not different from that in controls. Interestingly, at the cell-surface protein level, there were significant elevated levels of PD-1 on T cells and its ligand PD-L1 on monocytes in the patients compared to controls. However, we could not demonstrate any secreted soluble forms of PD-1 among the patients and controls. Thus, our study shows PD-1 might have a natural regulatory property behind MG.

To study the genetic pathogenesis of myasthenia gravis (MG) caused by cytotoxic T lymphocyte associated antigen-4 (CTLA-4) gene polymorphisms and regulation function of transcription factor.ELISA assay was used to determine the expression level of serum sCTLA-4 in MG. Four single nucleotide polymorphisms (SNPs) of CTLA-4 at exon 1 +49, promoter -318, -1661, -1772 were analyzed by restriction fragment length polymorphism (RFLP). Transcription factor nuclear factor 1(NF-1) and c/EBPbeta binding site were confirmed by chromatin immunoprecipitation(CHIP) assay.It was found that the frequencies of the GG+49 genotype and G+49 allele are higher in MG patients with thymoma than those in patients of thymic hyperplasia and normal thymus subgroups. T/C-318 is not correlated with MG. The frequency of CT-1772 genotype is significantly higher in MG patients, especially in MG patients with thymoma, when compared with that in healthy controls. Meanwhile, the frequency of the G-1661 allele and GG-1661 genotype is lower in MG patients. Linkage disequilibrium (LD) between each SNPs in promoter -1772, -1661, -318 and coding sequence 1 (CDS 1) +49 is apparent. sCTLA-4 levels in patients' sera are correlated with the haplotype and genotype. T/C-1772 and A/G-1661 SNPs change the sequence of transcription factor NF-1 and c/EBPbeta binding sites. DNA variants lose site-specific binding activity of transcription factor regulated by lectin ConA and PHA.There are strong positive linkages among four SNPs. C/T-1772 and A/G-1661 polymorphisms can result in inefficient transcription of CTLA-4 gene. TC-1772 mutation also affects gene splicing. These SNPs may constitute a factor of susceptibility to disease.