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Coronary heart disease (CHD) is a kind of cardiovascular diseases originated from atherosclerosis (AS), and chronic inflammation is one of the pathological characteristics. The peripheral blood leukocytes, especially mononuclear cells, play an important role in the AS processes. Recently, in a series of Epigenome-Wide Association Studies (EWAS), multiple DNA differential methylation sites in peripheral blood cells were found to be statistically associated with CHD, which suggested that these DNA differential methylation sites might serve as new risk factors for CHD. The recognition of the variant of DNA methylation as a common epigenetic nucleic acid modification in the occurrence and development of CHD, is ongoing. DNA methylation has the potential to become warning biomarkers, which might provide new ideas and evidences for mechanistic studies of CHD.
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Obesity-related hypertension is a common hypertension as well as a common chronic disease with wide distribution and great harm to human health. In recent years, this disease has become one of the hot issues of public health due to the significant increase in prevalence. The pathogenesis and pathway of obesity-related hypertension are not yet clear, and the research on its pathogenesis has received extensive attention. Studies have shown that they are regulated in most biological processes, including differentiation, proliferation, migration, and apoptosis. The miR-200 family is a group of miRNAs, which have been suggested to play a crucial role in obesity-related hypertension and glucolipid metabolism dysfunction in recent years. This paper reviews relevant research results, suggesting that the expression level of miR-200 family in obese patients with hypertension is higher than that in healthy people, which regulates the occurrence and development of hypertension through mediating oxidative stress response and GATA expression level. This review reveals the relationship between miR-200 family and obesity-related hypertension, which offers new clues to explore potential therapeutic targets for obesity-related hypertension.
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We reviewed the data of an 18-year-old male patient complained of weakness of limbs and hypokalemia for 6 months. CT scan revealed left adrenal adenoma. He was diagnosed as primary aldosteronism(PA). Laboratory tests showed hypokalemia and hyperaldosteronemia. After potassium supplement and blood pressure lowering treatment, laparoscopic resection of the left adrenal adenoma was performed, and severe hyperkalemia occured 2 hours after surgery(maximum serum potassium 7.02 mmol/L). After hyperrisotonic glucose+ insulin(10% glucose 200 ml+ 50% glucose 40 ml+ insulin 8U)+ cation exchange resin(Sodium Polystyrene Sulfonate 20 g) treatment, serum potassium returned to normal range within 12 hours. The plasma aldosterone, blood potassium and blood pressure returned to normal during the 5-month follow-up. According to the experience of this case report, after resection of aldosteronoma, the changes of serum electrolyte should be closely monitored, the occurrence of hyperkalemia should be vigilant.
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With the rapid development of modern economy, road traffic has become increasingly busy, and the accompanying environmental pollution problem is becoming increasingly prominent. Air pollutants emitted from automobile exhaust, including particulate matters, NOx, CO, and hydrocarbons (PAHs), can cause high risk of cardiovascular disease and premature death. This article summarizes the related epidemiological research progress on this topic from published literatures in recent years. We reviewed acute and chronic health damage to the cardiovascular system caused by traffic related air pollutants, including changes in heart rate variability and blood system indicators, potential association with coronary arteriosclerosis, coronary heart disease, and death of cardiovascular disease. The results show that traffic-related air pollutants can cause decrease in heart rate variability, increased blood pressure and changes in blood indicators, increase acute mortality from cardiovascular diseases. Long-term exposure to traffic-related air pollutants can induce increased risk of coronary atherosclerosis and coronary heart disease, and lead to increased mortality from cardiovascular diseases. In the future, more attention should be paid to traffic-related air pollution, and more researches are recommended to comprehensively evaluate the relationship between traffic-related air pollution and cardiovascular health damages, especially in early-stage. At the same time, active researches on the mechanism of cardiovascular toxicity of traffic-related air pollutants are needed, so as to promote the early prevention of cardiovascular diseases.
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Objective@#To explore the relationship between HCM pathogenic gene mutations and clinical phenotypes by analyzing the prenatal diagnosis and genetic characteristics of a pregnant woman from a family with hypertrophic cardiomyopathy (HCM). @*Methods@#The clinical data of the proband and her family members was collected. The DNA was extracted from the peripheral blood, amniotic fluid cells and cultured amniotic fluid cells of proband. Next generation sequencing (NGS) was utilized for screening pathogenetic loci of the proband. The suspected mutation sequences of HCM pathogenic candidate genes MYH7 and MYBPC3 were directly sequenced after PCR. Pathogenicity prediction of amniotic fluid cells was performed by using genetic data and bioinformatics software, such as Mutation taster, PolyPhen-2 and ANTHEPROT. @*Results@#The sequencing results showed that heterozygous mutations of MYH7 c.1988G＞A (p.Arg663His) and MYBPC3 c.151G＞A (p.Ala51Thr) were found in the proband. The phenotype of her father was normal, and no abnormal mutations were detectable. Her mother also showed normal phenotype but carried MYBPC3 c.151G＞A heterozygous mutation. Only MYH7 c.1988G＞A heterozygous mutation was found in the fetus and no abnormal variation of MYBPC3 was showed. The prediction of mutation effect and analysis of protein structure and function revealed that the two missense mutations could affect the hydrophobicity and antigenicity of the protein. The genetic data demonstrated MYH7 c.1988G＞A was defined as a pathogenic mutation. @*Conclusion@#MYH7 c.1988G＞A should be a newly generated pathogenic mutation in the proband, or caused by reproductive chimerism of her parents. MYBPC3 c.151G＞A mutation may promote the occurrence of HCM. Although the fetus only carries MYH7 c.1988G＞A, her phenotype may still display as HCM.
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Objective@#To investigate the expression and clinical significance of circDLGAP4 from peripheral blood in coronary heart disease (CAD). @*Methods@#The relative expression level of circDLGAP4 in peripheral blood leukocytes (PBLs) from 142 CAD patients and 169 healthy controls were detected by real-time PCR. Logistic regression, Spearman correlation and multivariate regression analysis were used to investigate the correlation of circDLGAP4 with CAD. THP-1 macrophages were treated with oxidized low density lipoprotein (ox-LDL) to construct an atherosclerotic foam cell model. The levels of circDLGAP4 mRNA were detected at different time points. @*Results@#The mRNA expression of circDLGAP4 in PBLs of CAD patients was significantly decreased compared with controls (P=0.019). With increased unit (2 -ΔCt ) of circDLGAP4 expression, the risk of CAD occurrence reduced by 41.6% (adjusted OR=0.584, 95% CI: 0.394-0.866, P=0.007). The expression of circDLGAP4 was negatively correlated with T2DM history (β=-0.182，P=0.030). The level of circDLGAP4 in ox-LDL-treated THP-1 macrophages was decreased in a time-dependent manner. @*Conclusion@#The expression of circDLGAP4 was significantly decreased in PBLs of CAD patients and THP-1 macrophages-derived foam cells, and might be a protective factor in the pathophysiology of CAD.
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Objective To investigate the expression and relationship of canonical transient receptor potential channel-3 (TRPC3) and brain-derived neurotrophic factor (BDNF) in the hippocampus of a rat model of Alzheimer's disease (AD). Methods SD rats were randomly divided into PBS, AD, and AD+BDNF experimental groups. AD models were generated by intracerebroventricular injection ofβ-amyloid protein (Aβ1-42). BDNF was injected via the lateral ventricle catheter after 14 days. The Morris water maze test was used to assess the spatial learning and memory ability of the rats. The expression of TRPC3 and BDNF mRNA and protein in the hippocampus were detected by RT-PCR and Western blotting, respectively. Results The Morris water maze test showed that the escape latencies of the fifth day in the AD group were longer than those in the PBS group (P ＜ 0. 05). The escape latencies in the AD+BDNF group were shorter than those in the AD group (P ＜ 0. 05). RT-PCR and Western blotting results showed that the expression of both TRPC3 and BDNF were reduced in the AD group compared with the PBS group (P ＜ 0. 05). TRPC3 expression was increased in the AD+BDNF group compared with the AD group (P ＜ 0. 05). Conclusion The expression of BDNF and TRPC3 is decreased in the hippocampus of AD rats. An exogenous BDNF injection appears to improve the spatial learning and memory of AD rats that are impaired by a Aβ1-42 injection, possibly via TRPC3 upregulation, and may play a protective role in neurons.
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Objective To identify the characteristics oral fungus in HIV-infected patients with HAART in Kunming.Methods Oral mucosal swab samples were collected from 99 patients with HIV infection with or without HAART.The fungi were isolated and cultured,and were identified by using API 20 C AUX yeast identification system.Results The positive rate of oral Candida in was significantly higher in HIV-infected patients without HAART (53.3％) than those with HAART (20.4％) (x2=11.669,P＜0.01).In 41 strains of isolated candida,C.albicans was the most prevalent (78.0％),followed by C parapsilosis (9.8％),C.glabrata (9.8％) and C tropicalis (2.4％).Conclusions HAART can decrease the positive rate of oral Candida in patients with HIV infection,but has little effect on asymptomatic HIV carrier.
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Objective To analyze Blimp1 expression difference in the latent and active of tuberculosis patients and the healthy , and assess possibility of as the new tuberculosis diagnostics molecules .Methods 60 patients with active TB (active tuberculosis group) ,50 participants with latent(latent tuberculosis group) ,and 50 healthy people(control group) were enrolled separately .Using fluorescence quantitative polymerase chain reaction were used to determin Blimp 1 mRNA expression in the peripheral blood mono-nuclear cells .Results Blimp1 mRNA expression level of the active tuberculosis group was 15 .35 times than the control group ,and 2 .21 times than the latent tuberculosis group ,the difference was statistically significant (P<0 .05) .Conclusion Blimp1 gene proba-bly plays a role in the immune response to tuberculosis .it provides new ideas for the laboratory diagnosis of tuberculosis and new clues for further exploring the pathogenesis mechanism of tuberculosis .
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To investigate the health impacts of crystalline silica mixed dust and other potential occupational hazards on workers in ceramic factories, a cohort study of 4851 workers registered in the employment records in 3 ceramic factories in Jingdezhen city of China between 1972 and 1974 was identified. The cohort mortality was traced throughout 2003 with an accumulation of 128970.2 person-years, revealed 1542 deaths. Standardized mortality ratios (SMRs) were calculated for the main causes of death by using Chinese national mortality rates as reference. The mortality from all causes in three ceramic factories was 12.0 per thousand and the cumulative mortality was 31.8%. Malignant neoplasm, cardiovascular diseases, respiratory diseases, infectious diseases were the first four illnesses that threaten workers' life, and they accounted for 73.2% of all deaths. The results of this study showed that the standardized mortality ratio for all subjects was 1.02, which is very close to that expected on the basis of the China national mortality rates. Statistically significant mortality excesses for respiratory disease (SMR=1.36), pneumoconiosis (SMR=37.34), infectious disease (SMR=5.70) and pulmonary tuberculosis (SMR=3.88) were observed. The mortality of 2938 dust-exposed workers was higher than that of 1913 non dust-exposed workers. Except for pneumoconiosis, the mortality from lung cancer, non-malignant respiratory diseases and pulmonary tuberculosis in dust-exposed workers were significantly increased as compared with that in non-exposed workers, and the relative risks (RRs) were 1.86 (1.16-2.99), 2.50 (1.84-3.40), 1.81 (1.34-2.45). The exposure-response relationships between cumulative dust exposure level and mortality from all causes, colorectal cancer, lung cancer, respiratory diseases, and pulmonary tuberculosis were also identified. The findings indicated that silica mixed dust in ceramic factories has harmful impact on the workers' health and life span in ceramic factory.