Predictors of vulnerable atherosclerotic plaques induced by cholesterol and balloon injury in rabbits / 中华心血管病杂志

<p><b>OBJECTIVE</b>To detect the optimal predictors of vulnerable atherosclerotic plaques.</p><p><b>METHODS</b>Forty New Zealand white rabbits underwent balloon-induced abdominal aortic wall injury and were fed a high cholesterol and saturated fat diet containing 1% cholesterol for 8 weeks. Rabbits were then randomly divided into two groups: group A (n = 20, the aortic segments rich in plaques were incubated transluminally with recombinant adenovirus carrying p53) and group B [n = 20, incubated transluminally with β galactosidase (LacZ) genes]. Two weeks later, rabbits underwent pharmacological triggering with injection of Chinese Russell's viper venom (CRVV) and histamine. Before pharmacologically triggering, concentrations of hs-CRP, sVCAM-1 and sICAM-1 were measured by means of Enzyme-linked-immunosorbent assay (ELISA). Fibrinogen was analyzed by nephelometer. Ultrasound imaging, accuracy densitometry (AD) examination and intravascular ultrasound (IVUS) were performed to analyze the in vivo features of vulnerable plaques. Logistic regression was used to detect the predictors for vulnerable plaques.</p><p><b>RESULTS</b>The ratio of plaque rupture after pharmacological triggering was significantly higher in group A (89.5%, 17/19) than in group B (22.2%, 4/18). Serum hs-CRP level was significantly higher in plaque rupture group than in non-rupture group before pharmacological triggering (P < 0.05). In the meantime, parameters derived from ultrasound imaging [intima-media thickness (IMT) and peak velocity (VP), values of accuracy densitometry], measurements of IVUS [external elastic membrance area (EEMA), plaque area (PA), plaque burden (PB), eccentric index (EI) and remodeling index (RI)] were significantly larger in plaque rupture group than in non-rupture group. Logistic regression showed that EI (OR = 26.917), PA (OR = 19.301), sVCAM-1 (OR = 1.339) and AII-c% (OR = 0.458) were independent predictors for plaque rupture (all P < 0.05).</p><p><b>CONCLUSION</b>The major predictors of vulnerable plaques were eccentric index (EI) and plaque area (PA), sVCAM-1 and AII-c% in this model.</p>

Roles of monocyte chemoattractant protein-1, RANTES and Fractalkine on promoting vulnerability of atherosclerotic plaques / 中华心血管病杂志

<p><b>OBJECTIVE</b>To elucidate the roles of monocyte chemotactic factors (MCP-1, RANTES and Fractalkine) on the vulnerability of atherosclerotic plaques in patients with stable (SAP) and unstable angina pectoris (UAP).</p><p><b>METHODS</b>Patients with SAP (n = 50) and UAP (n = 50) underwent coronary angiography (CAG) and intravenous ultrasound (IVUS) were included in the study. Monocyte chemotaxis was assayed by the transwell chamber. Concentrations of hs-CRP, MCP-1, RANTES and Fractalkine were measured by Enzyme-linked-immunosorbent assay (ELISA). mRNA expression of MCP-1, RANTES and Fractalkine in the monocytes was detected by RT-PCR.</p><p><b>RESULTS</b>IVUS evidenced soft lipid plaques in 48% UAP patients and in 16% SAP patients (P < 0.05). SAP patients had mainly fibrous and mixed plaques. Plaque burden and vascular remodeling index were significantly higher in UAP patients than in SAP patients (P < 0.01). The averaged number of migrated monocytes in the UAP patients were higher than that in patients with SAP (P < 0.01). Concentration of hs-CRP, MCP-1, RANTES and Fractalkine were significantly higher in UAP patients than those of SAP patients (P < 0.05 or P < 0.01). mRNA expression of MCP-1, RANTES and Fractalkine in patients with UAP was significantly higher than those of SAP patients (P < 0.05).</p><p><b>CONCLUSION</b>Upregulated monocyte chemotactic factors (MCP-1, RANTES and Fractalkine) might promote coronary plaque vulnerability in UAP patients.</p>

Study on the incidence of β-Thalassemia and genotypes among children under 7 year-olds in Nanning, Liuzhou and Baise areas, Guangxi province / 中华流行病学杂志

Objective To conduct research of β-Thalassemia incidence and genotypes on children below 7 years of age in Nanning, Liuzhou and Baise areas, Guangxi province. Methods A total of 2261 children aged below 7 in Nanning, Liuzhou and Baise areas were studied. Venous blood was detected by routine blood test, hemoglobin analysis and β-Thalassemia genotyping. Results Among 2261 samples, 125 showed high level of HbA2 and were diagnosed as β-Thalassemia (5.53%). Genotypes of the patients were classified as: 59 cases with β-globin gene eondon (CD) 41-42 mutation, 33 cases CD17 mutation, 18 cases with TA TA box nt-28 mutation, 7 with IVS-Ⅱ-654 mutation, 3 with CD43 mutation, 3 with HbE mutation, one with CD71-72 and TATA box nt-29 mutation, respectively. The genotyping frequencies of β-Thalassemia were as follows: 47.20% for CD41-42 mutation, 26.40% for CD17 mutation, 14.40% for TATAbox nt-28 mutation, 5.60% for IVS-Ⅱ -654 mutation, 2.40% for CD43 mutation, 2.40% for HbE mutation, 0.80% for CD71-72 mutation and TATAbox nt-29 mutation respectively. Conclusion This study on children in the area with high incidence of β-Thalassemia reflected the incidence and characteristics of genotypes in this area. Our data also provided evidence for the development of a program on genetic counseling and prevention for thalassemia.

Isolation, Identification and Bioactivity Assays of Endophytic Bacteria Associated with Taxus chinensis / 微生物学通报

Two endophytic-bacteria isolates of G18 and F19 were isolated from the stem of Taxus chinensis. The G18 and F19 were respectively classified into Psudomonas sp. and Stenotrophomonas sp. based on biological characteristics and 16S rDNA sequence analysis. The bioactivity analysis showed that the fermented broths of the G18 and F19 exhibited antagonistic activities against three pathogenic bacteria, and had good antagonistic effectiveness to Verticillium dahliae and Colletotrichum gloeosporioides, respectively. The G18 can degrade salicylic acid, and the F19 can do dichlorvos.

Atrial electrical, contractile and structural remodeling induced by short-term atrial tachycardia in a canine model / 中华心血管病杂志

<p><b>OBJECTIVE</b>To evaluate atrial remodeling induced by short term pacing in a canine model.</p><p><b>METHODS</b>Transvenous lead was inserted into the right atrial appendage of anesthetized mongrel dogs and paced for 5 hours at 450 bpm (n=12). Effective refractory period (ERP) and P-wave duration were measured before and post pacing and left ventricular pressure was monitored during the procedure. Echocardiography was performed to observe the presence or absence of spontaneous echo contrast and to assess the effect of rapid atrial pacing on atrial function. All measurements were obtained in sinus rhythm. Histology of the myocardium in left atrial trabeculae and appendages was examined by electron microscopy.</p><p><b>RESULTS</b>Compared to pre-pacing status, ERP was significantly reduced [(87.27 +/- 16.35) ms vs. (113.27 +/- 11.99) ms, P<0.01] at a cycle length of 300 ms, P-wave duration significantly increased [(56.09 +/- 8.62) ms vs. (52.09 +/- 7.63) ms, P<0.01], the peak velocity of atrial contraction significantly decreased [(48.92 +/- 10.80) cm/s vs. (59.25 +/- 9.37) cm/s, P<0.05] while heart rates and left ventricular pressure were not affected post five hours rapid atrial pacing. Pacing also induced significantly cellular ultrastructures changes including myofibrils loss, glycogen accumulation, mitochondria loss and swelling.</p><p><b>CONCLUSION</b>Short term pacing resulted in atrial electrical, contractile and structural remodeling.</p>

The role of atherosclerotic plaque stability and inflammation in the pathogenesis of acute coronary syndrome / 中华心血管病杂志

<p><b>OBJECTIVE</b>To elucidate the effect of inflammation and coronary atherosclerotic plaque destabilization in the pathogenesis of acute coronary syndromes (ACS).</p><p><b>METHODS</b>Twenty-eight patients with ACS and 13 patients with stable angina pectoris (SA) were examined by intravascular ultrasound (IVUS). Coronary plaque morphology and areas in culprit lesions were analyzed. The serum levels of hs-CRP, MMP-9, TIMP-1, sCD40L were also measured.</p><p><b>RESULTS</b>Soft plaques were dominant in culprit lesions of ACS patients (71.4%, 20/28), and hard plaques were dominant in culprit lesions of SA patients [76.9% (10/13), P = 0.004]. At the culprit site, plaque area, plaque burden and remodeling index were all significantly larger in culprit lesions of ACS patients than those of SA patients (all P < 0.05). Positive remodeling was more frequent in ACS patients than in SA patients, whereas negative remodeling was more frequent in SA patients (P < 0.05). The serum levels of hs-CRP, MMP-9, sCD40L were higher in ACS group compared with SA group (P < 0.05, respectively). Moreover, hs-CRP level was positively correlated with MMP-9 (r = 0.671, P = 0.000) and sCD40L (r = 0.494, P = 0.008), respectively, in ACS patients. There was no difference in TIMP-1 between two groups (P = 0.234).</p><p><b>CONCLUSIONS</b>These results suggest that structurally vulnerable plaques are essential element in the pathogenesis of ACS and inflammation might play an important role in plaque vulnerability.</p>

Establishing an animal model of unstable atherosclerotic plaques / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Atherosclerotic plaque rupture and coronary thrombosis are the main causes of acute coronary syndromes. However, there is no animal model of unstable atherosclerotic plaques. The presence of the p53 gene in advanced atherosclerotic plaques and the sensitivity to p53-induced apoptosis of smooth muscle cells isolated from these plaques prompted us to build an animal model of unstable atherosclerotic plaques using p53 gene transfer.</p><p><b>METHODS</b>Sixty-four New Zealand white rabbits were randomly divided into two groups: group A (n=54) and group B (n=10). Rabbits in group A underwent balloon-induced abdominal aortic wall injury and were then given a diet of 1% cholesterol, while rabbits in group B were given a diet of 1% cholesterol without the induction of aortic wall injury. At the end of the eighth week, rabbits in group A were randomly divided into two subgroups: group A1 (n=27) and group A2 (n=27). Recombinant adenovirus carrying p53 or beta-galactosidase (LacZ) genes were injected through a catheter into the aortic segments rich in plaques in groups A1 and A2, respectively. Two weeks later, 10 rabbits each from groups A1 and A2 were killed to observe the occurrence of spontaneous plaque ruptures, and the remaining rabbits in groups A1, A2, and B all underwent pharmacological triggering with an injection of Chinese Russell's viper venom (CRVV) and histamine.</p><p><b>RESULTS</b>The over expression of p53 in group A1 [(32.4 +/- 10.2)% vs (15.8 +/- 3.6)% in group A2 and (16.2 +/- 6.7)% in group B, P < 0.001, respectively] resulted in a marked increase in cellular apoptosis [(2.5 +/- 0.8)% vs (1.0 +/- 0.3)% in group A2 and (0.9 +/- 0.4)% in group B, P < 0.01, respectively], an accumulation of inflammatory cells within the plaques, and a significant decrease in vascular smooth muscle cells (VSMCs) and in the thickness of the fibrous caps. Although spontaneous plaque rupture was rare in group A1, plaque ruptures and thrombosis occurred in 12 rabbits with a total of 20 lesions after pharmacological triggering. By contrast, pharmacological triggering led to plaque rupture and thrombosis in only 5 rabbits for a total of 7 lesions in group A2 and in none of the rabbits in group B.</p><p><b>CONCLUSION</b>After transfection with human wild-type p53 gene and pharmacological triggering, plaque rupture and thrombosis occur in most atherosclerotic lesions in rabbits, thus offering a reliable model for the further study of unstable atherosclerotic plaques.</p>