Xian-Liang Zhou

Peking Union Medical College Hospital, Peping, Beijing, China

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Publications (18)37.26 Total impact

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    ABSTRACT: The prognostic significance of myocardial bridging in hypertrophic cardiomyopathy (HCM) remains controversial. This investigation sought to evaluate the impact of myocardial bridging on prognosis of patients with HCM. A total of 298 adult patients (73% male, mean age, 53 ± 12 years) with HCM were retrospectively enrolled at Fuwai Hospital from 1999 to 2011. Myocardial bridging was evaluated by coronary angiography. Follow-up data were collected by telephone interviews and mailed questionnaires. Thirty-four (11%, 34/298) patients were determined with myocardial bridging and the middle of left anterior descending artery was the most frequently involved segment (77%, 26/34). Patients with myocardial bridging were younger than those without bridging (48 ± 9 versus 54 ± 12 years, P = 0.001). During the follow-up of 4.2 ± 2.3 years (range, 0.7-12.2 years), the presence of myocardial bridging was not evidently associated with increased risk for all-cause death (P = 0.54), cardiovascular death (P = 0.60), sudden cardiac death (P = 0.53) and deterioration of heart failure (P = 0.84). Myocardial bridging was a relatively common morphological component of HCM but not a predictor for adverse clinical outcomes.
    The American Journal of the Medical Sciences 11/2013; · 1.33 Impact Factor
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    ABSTRACT: To evaluate the role of D-dimer and C reactive protein (CRP) in predicting inhospital death in acute aortic dissection (AD). A single-centre prospective study. University hospital in China. 114 patients with acute AD. Admission D-dimer and CRP concentrations were assayed. To observe the association of D-dimer and CRP with inhospital death. Increased levels of plasma D-dimer (9.84±3.53 vs 4.28±1.99, P < 0.001), CRP (14.08±2.81 vs 11.18±1.85, P < 0.001) and aortic diameter (45.2±9.5 vs 40.3±6.0, p = 0.007) were found in dead patients compared with those survived. Moreover, plasma D-dimer concentrations in type A were higher than that in type B (6.51±4.11 vs 4.87±2.29, p = 0.013). Plasma D-dimer concentrations had positive correlations with CRP levels (r=0.527, P < 0.001) and aortic diameter (r=0.227, p = 0.015), and had negative correlations with the type of AD (r=-0.232, p = 0.013) and the time from onset (r=-0.264, p = 0.005). The type of AD, D-dimer and CRP levels and the type of AD were strongly associated with inhospital mortality. The OR and 95% CI were 3.272, 1.638 to 6.535; 2.322, 1.134 to 4.757; and 0.126, 0.019 to 0.853, respectively. Furthermore, the sensitivity and specificity of D-dimer ≥5.67 μg/mL in predicting inhospital death in acute AD were 90.3% and 75.9% (95% CI 0.85 to 0.96), respectively. Moreover, the sensitivity and specificity of CRP levels ≥11.21 mg/L were 100% and 54.2%, respectively (95% CI 0.74 to 0.89). D-dimer ≥5.67 μg/mL, CRP ≥11.21 mg/L and type A acute AD were important risk factors and independently associated with acute AD inhospital death.
    Heart (British Cardiac Society) 06/2013; · 5.01 Impact Factor
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    ABSTRACT: BACKGROUND: The association between fish consumption and heart failure (HF) incidence is inconsistent. METHODS: We performed a systematic search of Pubmed and Embase (from 1953 to June 2012) using key words related to fish and HF. Studies with at least three categories of fish consumption reporting both relative risk (RR) and corresponding 95% confidence interval (CI) for HF incidence were included. The pooled RR and 95%CI were calculated using a fixed or random-effects model. The generalized least squares regression model was used to quantify the dose-response relationship between fish consumption and HF incidence. RESULTS: Five prospective cohort studies including 4750 HF events of 170 231 participants with an average of 9.7-year follow-up were selected and identified. Compared with those who never ate fish, individuals with higher fish consumption had a lower HF incidence. The pooled RRs for HF incidence was 0.99 (95%CI, 0.91 to 1.08) for fish consumption 1 to 3 times per month, 0.91 (95%CI, 0.84 to 0.99) for once a week, 0.87 (95%CI, 0.81 to 0.95) for 2 to 4 times per week, and 0.86 (95%CI, 0.84 to 0.99) for 5 or more times per week. An increment of 20 g of daily fish intake was related to a 6% lower risk of HF (RR: 0.94, 95%CI, 0.90 to 0.97; P for trend = 0.001). CONCLUSIONS: This meta-analysis suggests that there is a dose-dependent inverse relationship between fish consumption and HF incidence. Fish intake once or more times a week could reduce HF incidence.
    Chinese medical journal 03/2013; 126(5):942-948. · 0.90 Impact Factor
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    ABSTRACT: OBJECTIVE: Increased platelet activity predicts adverse cardiovascular events. The objective was to assess the effects of long-chain omega-3 polyunsaturated fatty acid (n-3 PUFA)-supplementation on platelet aggregation. METHODS AND RESULTS: We conducted a meta-analysis of randomized controlled trials identified using PubMed, Embase and the Cochrane Library. Fifteen studies were included. In comparison to placebo using the random-effect model, n-3 PUFA-supplementation significantly reduced adenosine diphosphate-induced platelet aggregation (standard mean difference [SMD] = -1.23 with 95% confidence interval [CI] -2.24 to -0.23, p = 0.02) and platelet aggregation units, determined using the VerifyNow(®) rapid platelet-function assay system (SMD = -6.78 with 95% CI -12.58 to -0.98, p = 0.02). There was a trend toward decreased collagen-induced (SMD = -0.70 with 95% CI -0.72 to 0.33, p = 0.18) and arachidonic acid-induced platelet aggregation (SMD = -0.43 with 95% CI -2.26 to 1.40, p = 0.64) compared with controls; however, statistical significance was not reached. CONCLUSIONS: Our meta-analysis demonstrates that n-3 PUFA-supplementation is associated with a significant reduction in platelet aggregation when the participants were at poor health status, but not in healthy persons. High-risk patients with cardiovascular disease and even diabetics may potentially benefit from n-3 PUFAs therapy. However, n-3 PUFAs may not be effective in primary prevention. Larger trials need to be carried out to confirm the present findings.
    Atherosclerosis 11/2012; · 3.71 Impact Factor
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    ABSTRACT: Liddle's syndrome is a rare autosomal-dominant monogenic form of salt-sensitive hypertension. This study aimed to screen the gene mutation in β and γ subunits of the epithelial sodium channel (ENaC) of a Chinese family with Liddle's syndrome, an autosomal dominant form of hypertension. DNA samples from the proband with early-onset, treatment-resistant hypertension and suppressed plasma renin activity were initially screened for mutations in the C-terminal exons of the ENaC β or γ subunit genes, using amplification by polymerase chain reaction and direct DNA sequencing. We also screened the C-terminus of SCNN1B and SCNN1G in family members, and screened for the mutation in 150 controls. Genetic analysis of the β ENaC gene revealed a missense mutation of CCC to TCC at codon 616 in the proband, her mother and her grandmother. One hundred and fifty randomly selected controls had not the mutation, indicating that this is not a common genetic polymorphism. There was no mutation of the γ ENaC gene in any of the individuals examined. Through direct DNA sequencing analysis, we established the diagnosis of Liddle's syndrome for the proband and her families, and provided tailored therapies to this abnormality. These results provide further evidence that Pro616Ser is a critical amino acid that has a key role in the inhibition of sodium channel activity.
    Chinese medical journal 04/2012; 125(8):1401-4. · 0.90 Impact Factor
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    ABSTRACT: The role of inflammation in aortic dissection (AD) has not fully been investigated. We evaluated the potential relationships between interleukin-6 (IL-6), C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), and matrix metalloproteinase-9 (MMP-9) and AD. Plasma concentrations of IL-6, TNF-α, MMP-9 and CRP were determined in 64 acute AD patients, 42 patients with chronic AD, 98 patients with hypertension alone, and 96 healthy subjects. IL-6 concentrations were higher in acute AD than that in hypertension and healthy controls (10.98±2.38 vs. 3.79±1.56 and 3.32±1.60 pg/ml, P<0.05, respectively). Increased CRP concentrations were found in acute AD compared with chronic AD and hypertension as well as healthy subjects (13.48±3.74 vs. 4.12±2.99, 1.62±0.65 and 1.12±0.35 mg/l, P<0.001, respectively). Higher MMP-9 concentrations were detected in acute AD, chronic AD and hypertension compared with healthy controls (37.75±9.38, 55.78±6.41 and 31.03±7.94 vs. 21.24±7.28 ng/ml, P<0.05, P<0.001 and P<0.05, respectively), and in the dead compared to the survived (107.29±9.38 vs. 86.80±7.93 ng/ml, P<0.001) among acute AD patients. In acute AD, the time after onset had positive correlation with TNF-α (r=0.497, P=0.000), and negative correlation with CRP (r=-0.424, P=0.000). Plasma CRP levels decreased significantly when the onset time increased (P=0.013). Moreover, in the patients with acute AD who underwent surgery and stenting, plasma MMP-9 concentrations increased immediately after surgical treatment and stenting, and reached the peak values at 24h, then decreased at 1 week (P<0.001). Our findings confirmed and extended previous studies that increased plasma inflammatory markers were significantly associated with AD.
    Clinica chimica acta; international journal of clinical chemistry 01/2012; 413(1-2):198-202. · 2.54 Impact Factor
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    Lin Zhang, Ling-Gen Gao, Ming Zhang, Xian-Liang Zhou
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    ABSTRACT: 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. 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. 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. 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.
    Molecular vision 01/2012; 18:55-63. · 1.99 Impact Factor
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    ABSTRACT: A few recent studies have reported that inflammation is associated with the prognosis of acute aortic dissection (AD). There is, however, no systemic investigation regarding the role of plasma C-reactive protein (CRP) and white blood cell (WBC) levels in predicting in-hospital clinical events of acute type A AD. The levels of high-sensitivity CRP and WBC counts were systemically determined after admission in 36 patients with acute type A AD. The variations of plasma CRP and WBC levels in different time windows (admission, 1, 2, 3, 4, 6, 8 days) in patients with acute type A AD were analyzed between patients with events and without events. During hospitalization, five patients died, and increased levels of CRP and WBC were found in patients died with acute type A AD compared with patients survived (P < 0.01, respectively). Medical treatment may significantly decrease inflammatory response in survived patients with acute type A AD. Additionally, patients with complication of pleural effusion showed higher CRP and WBC levels (P = 0.046, P = 0.018, respectively). Lower WBC levels were found in survived patients treated medically (P = 0.001). Moreover, mean CRP and WBC levels had positive correlations with aortic diameter (r = 0.364, P = 0.000; r = 0.333, P = 0.000, respectively) and age (r = 0.270, P = 0.000, respectively), while negative correlations with the time from onset of symptoms to hospital admission (r = -0.229, P = 0.000, r = -0.200, P = 0.002, respectively). Univariate analysis showed that age ≥ 65 years, CRP ≥ 12.05 mg/L, WBC ≥ 12.16 × 10(9)/L, aortic diameter ≥ 48 mm, pleural effusion and diastolic blood pressure ≥ 105 mmHg were associated with hospital mortality. While CRP ≥ 12.05 mg/L, WBC ≥ 12.16 × 10(9)/L, aortic diameter ≥ 48 mm were strongly associated with hospital mortality in multiple Logistic regression analysis. The results suggested that CRP and WBC were preferred markers for predicting the clinical events in patients with acute type A AD, especially death during hospitalization. Therefore, further study enrolling larger cohort, prospective study would be warranted.
    Chinese medical journal 09/2011; 124(17):2678-82. · 0.90 Impact Factor
  • Dan Wen, Xian-Liang Zhou, Jian-Jun Li, Ru-Tai Hui
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    ABSTRACT: Aortic dissection (AD) is a severe cardiovascular disease with high mortality and morbidity, which is characterized by acute onset and rapid progress. Mechanically, it has been considered that circulating blood flows into the media of the aorta through the rupture of the intima forming true and false lumens. Generally, its pathologic process is considered as follows: initially, inflammatory reaction, inflammatory cells infiltration in aortic wall, and then apoptosis of vascular smooth muscle cells, degenerating of aortic media, elastin fracture, and degradation. At last, the ingredients of the aorta are destroyed and lead to aortic dilatation, aneurysm formation, dissection and rupture. Currently, several biomarkers in peripheral blood including C-reactive protein (CRP), matrix metalloproteinases (MMPs), soluble elastin fragments (sELAF), D-dimer, smooth muscle myosin heavy chain, calponin, N-terminal pro-brain natriuretic peptide (NT-proBNP), big endothelin-1 (Big ET-1), genetic markers and so on, have been demonstrated to play a major role in evaluation of AD, for example, making early diagnosis and classifying of AD. Additionally, those markers may also guide our treatment therapies and predict the prognosis. The aims of this review mainly focus on the clinical implications of the biomarkers in AD.
    Clinica chimica acta; international journal of clinical chemistry 04/2011; 412(9-10):688-95. · 2.54 Impact Factor
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    ABSTRACT: Marfan syndrome is a systemic disorder of connective tissue, caused by mutations in the FBN1, TGFBR1 or TGFBR2 genes. This syndrome is characterized by involvement of three major systems, skeletal, ocular, and cardiovascular. The continuing improvements in molecular biology and increasing availability of molecular diagnosis in clinical practice allow recognition of Marfan syndrome in patients with incomplete phenotypes. Additionally, molecular analyses could also be used for preimplantation genetic diagnosis. The identification of a mutation allows for early diagnosis, prognosis, genetic counseling, preventive management of carriers and reassurance for unaffected relatives. The importance of knowing in advance the location of the putative family mutation is highlighted by its straightforward application to prenatal and postnatal screening.
    Chinese medical journal 03/2011; 124(6):930-4. · 0.90 Impact Factor
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    ABSTRACT: To evaluate the clinical features in Chinese patients with apical hypertrophic cardiomyopathy (AHCM) and typical hypertrophic cardiomyopathy (HCM). This retrospective analysis included 160 patients hospitalized in Fuwai hospital. Patients were divided into three groups: apical hypertrophic cardiomyopathy (AHCM, n = 41) group, non-obstructive typical hypertrophic cardiomyopathy group [NOHCM, LVOT < 30 mm Hg (1 mm Hg = 0.133 kPa) at rest, n = 52] and obstructive typical hypertrophic cardiomyopathy (OHCM, LVOT ≥ 30 mm Hg at rest, n = 67). Clinical features, diagnosis, therapy, and plasma levels of biomarkers of these three groups were analyzed. (1) The age at disease onset was older in AHCM group than in OHCM group [(49.9 ± 13.6) years vs. (41.4 ± 14.6) years, P < 0.01]. Exertional dyspnea appeared more often in HCM patients than in AHCM patients, NT-proBNP level was significantly lower in AHCM patients than in OHCM patients (P = 0.001). Plasma CK-MB, LDH, TnI and MYO levels were similar among the three groups. (2) Thirty-three AHCM patients were first hospitalized for suspected coronary heart disease (CHD) and CHD was excluded in 18 cases (43.9%). (3) The frequency of giant negative T waves (depth ≥ 10 mm) on ECG was 43.9%, 13.5% and 4.4% (P < 0.01) in AHCM, NOHCM and OHCM respectively. Half of AHCM patients showed left ventricular high voltage on ECG. (4) Cardiac magnetic resonance imaging is superior to echocardiography on correctly diagnosing AHCM. AHCM patients differ from typical OHCM patients in clinical characteristics. There were significant differences on echocardiography and electrocardiography features among three groups. Cardiac magnetic resonance imaging and giant negative T waves on ECG are helpful for the diagnosis of AHCM.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 03/2011; 39(3):228-32.
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    ABSTRACT: To investigate the association of orthostatic hypertension and hypotension with hypertensive target organ damage in middle and old-aged hypertensive patients. This cross-section study was conducted in 4711 hypertensive patients aged 40-75 years old in 7 communities of Xinyang County, Henan Province by a multistage cluster sampling method. All patients received a standardized questionnaire, physical and biochemical examinations, echocardiography, ankle-brachial blood pressure index and orthostatic blood pressure measurement. Orthostatic hypertension was defined as an elevation of systolic blood pressure by 20 mm Hg or more while orthostatic hypotension as a drop of blood pressure by 20/10 mm Hg or more. When an upright posture was assumed. Others not belonging to these two conditions were classified into orthostatic normotension. The prevalence of orthostatic hypertension and hypotension was 16.3% and 23.8% in hypertensive patients. Peripheral artery disease was significantly more frequent in hypertensives with orthostatic hypertension (10.1%) or hypotension (10.7%) than those with orthostatic normotensives (7.4%) (both P<0.05). Patients with orthostatic hypotension had more common left ventricular hypertrophy (53.0% vs 43.2%, P<0.001) and a decreased estimated glomerular filtration rate (38.6% vs 34.4%, P<0.05) than did those with orthostatic normotension. After controlling for age, gender, body mass index and other confounders, orthostatic hypertension was positively associated with peripheral arterial disease (OR 1.39, 95%CI 1.05-1.84) while orthostatic hypotension was significantly associated with peripheral arterial disease (OR 1.45, 95%CI 1.13-1.86) and left ventricular hypertrophy (OR 1.46, 95%CI 1.11-1.84). But no independent association was found between orthostatic hypertension or hypotension and a decreased estimated glomerular filtration rate in hypertensive patients. The adjusted odds ratios (OR) for left ventricular hypertrophy, as predicted by the quintiles of orthostatic systolic blood pressure changes, showed a J-shaped relationship in hypertensive women, and so did peripheral artery disease in untreated hypertensive patients. Hypertensive patients with orthostatic hypertension or hypotension may have an elevated risk of developing target organ damage.
    Zhonghua yi xue za zhi 01/2011; 91(4):220-4.
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    ABSTRACT: Mutations in the fibrillin-1 gene have been identified in patients with Marfan syndrome (MFS). This study aimed to identify the molecular defects in the fibrillin-1 gene in a Chinese family with Marfan syndrome, accompanied by aortic aneurysms/dissection. Two patients and one non-carrier in the family underwent complete physical, ophthalmic, and cardiovascular examinations. Genomic DNA was extracted from leukocytes of venous blood of these individuals in the family as well as 50 healthy normal controls. Polymerase chain reaction amplification and direct sequencing of all 65 coding exons of fibrillin-1 gene were analyzed. We found a novel mutation (c.8547T > G, p.Tyr2849X) in exon 65 of fibrillin-1 gene in a Chinese proband with Marfan syndrome, accompanied by aortic aneurysms/dissection. Sudden death at a young age of affected members was seen due to aortic aneurysms/dissection. By evaluating genotype-phenotype correlations of patients with mutations in the 3' end of fibrillin-1 gene (exons 64 and 65), we also found that the presence of nonsense mutations occurring in exons 64 and 65 appeared to be an indicator of early-onset aortic risk and sudden death. These results expand the mutation spectrum of fibrillin-1 gene and help in the study of the molecular pathogenesis of Marfan syndrome, indicating that mutations occurring in the 3' end of fibrillin-1 gene may play an independent functional role in the pathogenesis of Marfan syndrome.
    Chinese medical journal 10/2010; 123(20):2874-8. · 0.90 Impact Factor
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    Chinese medical journal 09/2010; 123(17):2471-4. · 0.90 Impact Factor
  • Ling-Gen Gao, Fang Luo, Ru-Tai Hui, Xian-Liang Zhou
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    ABSTRACT: Marfan syndrome (MFS) is a connective tissue disorder with autosomal dominant inheritance. Advances in medicine and surgery have increased the average lifespan of classically affected patients. Serious visual and/or musculoskeletal impairment often has detrimental effects on day-to-day activities and quality of life. MFS patients suffer from many problems at younger ages and with higher frequencies than the general population because of the degenerative nature of the genetic condition. In classical MFS, changes are caused by mutations in the fibrillin-1 gene (FBN1). Mutations in the fibrillin-2 gene were discovered in individuals with a phenotypically related disorder, congenital contractural arachnodactyly. Some of the clinical manifestations of MFS cannot be explained by mechanical properties alone. Recently, mutations in the genes required for transforming growth factor-beta signaling (TGFBR1 and TGFBR2) have been found in several disorders with varying degrees of overlap with classical MFS, including Loeys–Dietz syndrome and familial thoracic aortic aneurysms and dissections. MFS is a disorder that is variable in its phenotypic expression. Specific information about mutations in the large FBN1 gene will give rise to more information about the phenotype–genotype correlations. Possible molecular mechanisms for the pathogenesis of MFS will be discussed which may assist healthcare professionals to control environmental factors that provoke individual complications in MFS.
    Ageing research reviews 01/2010; · 5.62 Impact Factor
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    ABSTRACT: To investigate the prevalence of hyperuricemia and its associated risk factors in treated and untreated hypertensive patients in Chinese rural area. This cross-section study was performed in 5235 hypertensive patients aged 40 - 75 years old at Xinyang, Henan by using a multistage cluster sampling method. All patients underwent an investigation composed of a standardized questionnaire, physical and biochemical examination. Hyperuricemia was defined as serum uric acid levels > or = 420 micromol/L in men or > or = 360 micromol/L in women. The overall prevalence of hyperuricemia was 14.1%, and it was higher in men than in women (21.5% vs 10.2%, P < 0.01). With an increase of body mass index (BMI), the prevalence of hyperuricemia and serum uric acid level increased significantly in both sexes [BMI < 25, > or = 30: 14.4%, 30.4%, (328 +/- 83) micromol/L, (383 +/- 86) micromol/L in males; and 7.2%, 17.0%, (251 +/- 70) micromol/L, (293 +/- 75) micromol/L in females, respectively, all P < 0.01]. So did that with increase of age only in female patients (40 - 49 years vs > or = 70 years: 5.8% - 18.0%, respectively, P < 0.01). Antihypertensive treatment, lipid disorder, smoking and alcohol consumption also significantly increased the incidence of hyperuricemia and the serum uric acid level (all P < 0.01). However, no significant differences were found among patients with I, II, and III blood pressure levels (all P > 0.05). After adjustment for age and other conventional risk factors by using multiple logistic regression analysis, hyperuricemia was significantly associated with BMI, alcohol consumption and diuretics in males as well as BMI, lipid disorder, age, smoking, and antihypertensive treatment in females. Hyperuricemia is relatively less common in rural hypertensive patients. The associated risk factors of hyperuricemia and elevated serum uric acids include sex, age, BMI, antihypertensive medicines, lipid disorder, smoking and alcohol consumption. The effect of these factors is different between sexes.
    Zhonghua yi xue za zhi 10/2009; 89(38):2667-70.
  • Fang Luo, Xian-Liang Zhou, Jian-Jun Li, Ru-Tai Hui
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    ABSTRACT: Aortic dissection is an age-dependent life-threatening cardiovascular disease with high mortality rates. Recent research has shown that inflammation plays an important role in aortic dissection. Inflammatory cells, such as lymphocytes and macrophages, not only increase the expression of proteases and cell adhesion molecules but also release reactive oxygen species. These cells also contribute to apoptosis of smooth muscle cells in the aortic artery, and finally lead to medial degradation. This process has been considered to be the principal mechanism for aortic dissection. Furthermore, changes in systemic inflammatory biomarkers are associated with acute-phase reactions and complications in aortic dissection. These biomarkers are also used to predict the prognosis of aortic dissection and to distinguish acute aortic dissection from other chest pain diseases. In addition, elevated inflammatory cell activity in aortic wall, identified by positron emission tomography/computed tomography, is associated with serious clinical symptoms and leads to a poor clinical outcome in aortic dissection. Such observations may provide us with new sights into the mechanism of aortic dissection. In this review, we discuss the role of inflammation in the development and progression of aortic dissection. Understanding this inflammatory process may provide us with new strategies for pharmacological treatment of aortic dissection.
    Ageing research reviews 09/2008; 8(1):31-5. · 5.62 Impact Factor
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    ABSTRACT: The self-assembled electrode with the homocysteine monolayer (Hcy/Au) has been characterized by infrared spectroscopy and ac impedance spectroscopy in electrolyte. The Hcy/Au electrode is demonstrated to promote the electrochemical response of epinephrine (E) by cyclic voltammetry. A pair of well-defined redox waves was obtained and the calculated standard rate constant (k(s)) is 2.1x10(-2) cms(-1) at the self-assembled electrode. The reduction peak of E can be used to determine the concentration of E in presence of ascorbic acid (AA) owing to the Hcy/Au also promoting the electrochemical oxidation of AA.
    Talanta 05/2002; 56(6):1081-8. · 3.50 Impact Factor