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Wang Z.,Capital Medical University | Liu Y.,Capital Medical University | Liu J.,Capital Medical University | Liu K.,Capital Medical University | And 3 more authors.
Journal of Atherosclerosis and Thrombosis | Year: 2011

Aim: Hyperplasia suppressor gene/mitofusion-2 (HSG/Mfn2) is a hyperplasia suppressor gene and an essential component of mitochondrial fusion machinery; however, the association between the single nucleotide polymorphism (SNP) of HSG/Mfn2 and hypertension is unclear. Methods: In this study, 542 normotensive subjects (NT group) and 539 hypertensive patients (EH group) were screened for an association study between HSG/Mfn2 and hypertension. Results: The results showed that the genotype distribution and allelic frequency of rs873457, rs2336384, rs1474868, rs4846085 and rs2236055 were significantly different (P<0.05 for all) between EH and NT groups, although those of rs4240897 and rs873458 were not. When comparing the dominant model, significant differences still existed (P<0.05 for all). The allelic frequency of rs4240897 was also slightly different between EH and NT groups (P = 0.047). When subgrouped by sex, the genotype distribution and allelic frequency of all the SNPs (except rs873458) were significantly different in male (P<0.05 for all) but not in female groups. For all the SNPs, only the allelic frequency of rs4240897 was obviously different in female NT and EH groups (P<0.01). Logistic regression showed that body mass index and rs873457 were closely associated with BP after adjusting for age. The frequency of the C-G-A-A-A-C-C haplotype was significantly higher in essential hypertensive patients versus control individuals, both in the entire population, in male or female groups (P<0.01 for all). As for other haplotypes, most were only significantly different in the entire population and male subjects. Conclusion: The genetic variations of HSG/Mfn2 may be associated with hypertension in male Chinese. Source


To explore the 15-years change in fasting TG level and the accumulative incidence of type 2 diabetes mellitus (T2DM) from 1992 to 2007, and to assess the association between the change in TG level and the accumulative onset risk of T2DM. A total of 11 387 subjects aged 35 - 64 years were recruited from 6 provinces in China in the baseline survey in 1992, and were followed-up for cardiovascular disease till 2007. In 2007, 9184 subjects were successfully followed-up and 5966 subjects entered into the second examination. Totally 5408 participants, who were free of diabetes at baseline and had complete information for both check ups, were included in this analysis. Fasting TG levels were categorized into three groups: < 1.70 mmol/L, 1.70 - 2.25 mmol/L and ≥ 2.26 mmol/L. The association between 15-years change in TG level and the accumulative onset risk of T2DM was assessed by logistic regression analysis. In 1992, the mean level of TG was 1.49 mmol/L in male and 1.26 mmol/L in female. During the 15 years, TG levels increased by 0.25 mmol/L and 0.53 mmol/L in male and female, respectively. The prevalence of elevated TG (< 1.70 mmol/L) increased from 23.4% in 1992 to 39.0% in 2007. The 15-year accumulative incidence of diabetes was 13.9% in male and 11.8% in female. The incidence rates were 10.5%, 16.2% and 26.6% for TG levels of < 1.70 mmol/L, 1.70 - 2.25 mmol/L and ≥ 2.26 mmol/L, respectively. Multivariate logistic regression analysis showed that the baseline TG level was significantly associated with the onset risk of diabetes after adjustment for other cardiovascular risk factors. At any given baseline TG level, the onset risk of diabetes increased with the TG levels in the second examination in 2007. After adjusting other risk factors, participants with the highest categories of both baseline and follow-up TG levels had 2.1 folds higher accumulative onset risk of diabetes (RR = 3.39, 95%CI 2.49 - 4.61) than those with the lowest categories of both baseline and follow-up TG levels. Baseline TG level is independently associated with diabetes onset risk, and the change of TG level in a 15-year interval predicts the onset risk of diabetes beyond the baseline TG level. Source


Lu Y.H.,Beijing Institute of Heart
Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases | Year: 2011

The purpose of the present study aimed to evaluate the left ventricular systolic function and diastolic filling characteristics in pulmonary thromboembolism (PTE). A total of 102 patients with PTE, including acute or acute on chronic PTE, were consecutively recruited from January of 2006 to December of 2010. The patients [53 males and 49 females; age (64 ± 14) years, range 23 - 85 years] all underwent Doppler echocardiographic assessment before thrombolytic therapy or within 24 h of hospital admission to the emergency intensive care unit of Beijing Anzhen hospital. Fifty-one age- and gender-matched healthy controls [29 males and 22 females; age (61 ± 9) years, range 31-79 years] were recruited from the Health Center. One hundred and sixty age- and gender-matched coronary artery disease (CAD) patients [90 males and 70 females, age (61 ± 11) years, range 29 - 81 years] with positive coronary artery angiography were also included as controls during the period of January of 2009 through December of 2010. Trans-thoracic Doppler echocardiography was used to assess the trans-mitral filling pattern and left ventricular systolic function in all the subjects. The trans-mitral blood flow peak of early (E) wave less than that of the auricular (A) wave, or the ratio of E/A greater than 2, were defined as abnormal left ventricular diastolic filling. Left ventricular ejection fraction (LVEF) greater than 50% was defined as preserved systolic function. The prevalence of abnormal left ventricular diastolic filling and systolic dysfunction were compared with Chi-square test between the PTE patients and the 2 control groups. Tricuspid regurgitation was identified in 72.5% (74/102) of the 102 PTE patients, abnormal left ventricular diastolic filling was detected in 77.5% (79/102) of the PTE patients, and 95.1% (97/102) of the PTE patients had preserved left ventricular systolic function with LVEF of > 50%. Further analysis revealed that the abnormal left ventricular diastolic filling was more frequent in PTE patients with CAD and/or hypertension than in other PTE patients (χ(2) = 5.280, P < 0.05), 85.2% (52/61) and 65.9% (27/41), respectively. Overall, the prevalence of abnormal left ventricular diastolic filling in PTE patients (77.5%, 79/102) was significantly higher than that in healthy controls (25.5%, 13/51, χ(2) = 38.300, P < 0.001), and the fraction of left ventricular systolic dysfunction was significantly lower (4.9%, 5/102) than that in CAD patients (29.4%, 47/160, χ(2) = 23.450, P < 0.001). In the PTE patients with neither CAD nor hypertension, the abnormal left ventricular diastolic filling was still more frequent (65.9%, 27/41) than in healthy controls (25.5%, 13/51, χ(2) = 15.070, P < 0.001), but there was no significant difference when compared with that in CAD patients (73.8%, 118/160, χ(2) = 1.013, P > 0.05). The results strongly suggest that abnormal left ventricular diastolic filling constitutes a common and a major form of left ventricular dysfunction in PTE patients. It indicates that enhanced alertness to and early identification of abnormal left ventricular diastolic filling may play an important role in improving prognosis for PTE. Source


Xin Y.,Beijing Institute of Heart
Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology | Year: 2013

This study was aimed to evaluate an effective and stable method for obtaining mesenchymal stem cells (MSC) and endothelial progenitor cells (EPC) from the rabbit bone marrow and to investigate the biological characteristics of MSC and EPC. Mononuclear cells were obtained from rabbit bone marrow using density gradient method, and were differentially adhered to the cell culture plate enclosed with fibronectin. Then, MSC and EPC were amplified with EGB-2MV medium. Trypan blue method was used to test the passage survival rate. Growth curve, MTT and DNA cycle were used to evaluate the proliferation ability of MSC and EPC. MSC were identified with induced differentiation into the osteoblasts and adipocytes, and their immune phenotype was detected by flow cytometry (FCM). EPC were characterized by the special digestion of Dil-ac-LDL, FITC-UEA-I, and the conjunction with CD133, VEGFR2/KDR and CD34, their purity was also calculated. The results indicated that the colony was obviously formed when the mononuclear cells were cultured for 24 hours and, 80% of the cells became long spindle and integrated at d 8. Cells, which were adhered for twice, were cultured with EGM-2MV medium, began to extend at d 3, and became strip-shaped and integrated for about 80% at d 8. Passage survival rates were more than 90% for both cells, and after passage 2 the growth curve was like "S". Optical density was changed obviously when the cells were cultured for 3 - 5 d, but there were no significant difference of cell cycles between MSC and EPC, which G0-G1 was (93.32 ± 1.65)% and (93.05 ± 1.95)% respectively. Positive rates were (99.7 ± 1.12)%, (99.1 ± 2.33)%, (4.8 ± 0.38)%, (6.8 ± 0.49)% and (0.4 ± 0.08)% for CD90, CD44, CD14, CD45 and CD79a respectively. MSC were identified by induced differentiation into osteoblasts and adipocytes. Positive rates of the EPC, which were adhered for twice and passaged 2, were (82.1 ± 3.4)% for fluorescent staining of Dil-ac-LDL and FITC-UEA-I, and (74.2 ± 3.2)%, (64.7 ± 4.3)% and (43.5 ± 1.5)% for CD133, VEGFR2/KDR and CD34 respectively. It is concluded that high-purity MSC can be obtained with density gradient and differential adhesion method, and high-proliferation EPC can be cultured with EGM-2MV medium in cell plates enclosed with fibronectin, so they may become the optimal seed cells for tissue engineering study. Source


Zhang L.,Peking Union Medical College | Gao L.-G.,Chinese Peoples Liberation Army | Zhang M.,Beijing Institute of Heart | Zhou X.-L.,Peking Union Medical College
Molecular Vision | Year: 2012

Purpose: Transforming growth factor beta receptor II (TGFBR2) gene mutations are associated with Marfan syndrome; however, the relationship between the mutations and clinical phenotypes are not clear. Methods: Genomic DNA from peripheral blood leukocytes of a Chinese proband with Marfan syndrome, five of the proband's relatives, and 100 unrelated Chinese control subjects were isolated and screened for fibrillin-1 (FBN1) and TGFBR2 gene mutations by direct sequencing, and a genotype-phenotype study was performed following a review of the literature on TGFBR2 mutations in the search area. Also, the structure of TGFBR2 protein before and after gene mutation was analyzed. Results: The results identified a novel missense TGFBR2 mutation p.V453E (c.1358T>A) in the proband and two relatives that was located in the F-helix in the kinase domain of TGFBR2. No such genetic change was observed in the unrelated controls. No FBN1 mutation was detected in any of the subjects. Genotype-phenotype analyses indicated that F-helix mutations are related to type 2 Marfan syndrome and Loeys-Dietz syndrome, and these mutations can lead to severe cardiovascular (93.8%) and skeletal (81.3%) lesions and minor ocular lesions (25%). Losartan treatment can slow-down the progression of aortic lesions. Conclusions: The findings extend the mutation spectrum of Marfan syndrome, and that mutations at the F-helix in the kinase domain of TGFBR2 may be associated with the development of severe cardiovascular and skeletal lesions and minor ocular lesions. These findings have implications for genetic testing, diagnosis, and treatment in individuals with transforming growth factor beta (TGF-β) signaling-related disorders. © 2012 Molecular Vision. Source

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