[An improved method of electrode placement for ECG monitoring in children].

OBJECTIVE: This study examines the impacts of an improved electrode placement on the electrocardiogram (ECG) results in order to determine a better electrode placement for ECG monitoring in children. METHODS: ECG was recorded using the traditional electrode placement and the modified electrode placement (with shortened electrode distance) respectively in 50 pediatric patients. The amplitudes of P wave and QRS wave on ECG by the two measurements were compared. Furthermore, the impacts of different body positions on the amplitudes of P wave and QRS wave were studied after applying the modified electrode placement. RESULTS: There were no significant differences in the amplitudes of P wave and QRS wave on ECG by the traditional electrode placement and the modified electrode placement (P>0.05). When modified electrode placement was utilized, the body position change did not lead to significant changes in the amplitudes of P wave and QRS wave (P>0.05). CONCLUSIONS: A satisfactory ECG can be obtained with the modified electrode placement independent of patient's body position, suggesting that the modified electrode placement can be used instead of the traditional placement in children.

[Neferine protects endothelial cells against damages induced by LPC and relationship with asymmetric dimethylarginine].

OBJECTIVE: To investigate the protective effect of neferine against damages of endothelial cells induced by lysophos-phatidylcholine (LPC) and the relationship with asymmetric dimethylarginine (ADMA). METHOD: The human umbilical vein endothelial cells (HUVEC-12) were treated with LPC (10 mg x L(-1)) for 24 h to establish the model of endothelial cells damages; HUVECs were prior exposed to neferine (0.1, 1.0 or 10.0 micromol x L(-1) ) for 1 h, and then exposed to LPC in the presence of the neferine for 24 h. At the end of the experiment, the cultured medium was collected for measuring the concentration of nitric oxide (NO), aleic dialdehyde (MDA) as well as ADMA and the cells were collected for measuring the level of intracellular reactive oxygen species (ROS). RESULT: Compared with control group, exposure of endothelial cells to LPC (10 mg x L(-1)) for 24 h significantly increased the concentration of MDA and ADMA in the medium and the level of intracellular ROS and coinstantaneously significantly decreased the concentration of NO in the medium. Neferine (0.1, 1.0 or 10.0 micromol x L(-1)) significantly inhibited the elevated concentration of MDA, ADMA as well as the level of intracellular ROS and coinstantaneously significantly attenuated the decreased level of NO induced by LPC. CONCLUSION: Neferine can protect the endothelial cells against damages induced by LPC and the protective effect is related to the decrease of the concentration of ADMA.

Expression and significance of inflammatory factors and bone formation mediators in carotid atherosclerotic plaque / 中南大学学报(医学版)

OBJECTIVE@#To compare protein levels of pro-inflammatory factors and bone formation mediators in the fibrous cap and shoulder region of non-calcified and calcified carotid endarterectomy (CEA) plaques.@*METHODS@#Twenty-two CEA plaques were classified as non-calcified and calcified groups (n=11 each) in accordance with the American Heart Association (AHA) consensus in 1995. To make frozen sections and H&E staining using plaque, the mean percent of carotid stenosis and calcification area was determined by quantitative histomorphometry. The protein levels of pro-inflammatory interleukin-8 (IL-8), monocyte chematactic protein-1 (MCP-1), bone formation mediators bone morphogenetic protein-6 (BMP-6), and osteocalcin in the fibrous cap and shoulder region of plaques were determined by western blot and were quantified using ImageJ software.@*RESULTS@#MCP-1 and IL-8 protein were 1.3 (P>0.05) and 1.5 (P0.05) and 2.1 (P<0.01) folds greater in the calcified plaques compared with those of the non-calcified plaques.@*CONCLUSION@#Inflammation is more likely to occur in non-calcified carotid plaques, and calcification in the plaques may be associated with bone formation, which indicates that decreased inflammation may be the beginning of calcification in carotid atherosclerotic plaques.

[Effect of the polymorphism of the angiotensin-converting enzyme gene on the drug treatment in patients with chronic heart failure].

OBJECTIVE: To investigate the effect of the insertion (I)/deletion (D) polymorphism of the angiotensin-converting enzyme (ACE) gene on the drug treatment in patients with chronic heart failure. METHODS: The genotype was determined by polymerase chain reaction (PCR) in 79 patients with chronic heart failure. Plasma Ang II levels that were assessed by radio-immunity assay (RIA), left ventricular end-diastolic diameters (LVDD) and left ventricular ejection fractions (EF) and that were studied with echocardiography were measured before and after the treatment. RESULTS: ACE gene DD polymorphism was associated with greater LVDDs [DD vs. ID (P <0.001), DD vs. II (P < 0.001)], higher plasma Ang II levels [DD vs. ID (P < 0.05), DD vs. II (P < 0.001)] and the greatest decreased magnitude of plasma Ang II levels after treatment [DD vs. ID (P < 0.05), DD vs. II (P < 0.001)]. CONCLUSION: In patients with chronic heart failure, ACE gene DD polymorphism might be a marker of a higher level of activation of the renin-angiotensin system (RAS). Patients with the DD allele would expect a greater beneficial effect on endocrine by the drug treatment including ACE inhibitor and beta-blocker.