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1.
Tianjin Medical Journal ; (12): 647-649, 2013.
Article in Chinese | WPRIM | ID: wpr-474936

ABSTRACT

Objective To investigate the effects of high density lipoprotein (HDL) on thrombin-activated platelet al-pha-granulemembrane protein (CD62P) and lysosome intact membrane protein (CD63) expressions in vitro. Methods The equivalent volume of washed platelets prepared by hand was preincubated with HDL (1 g/L) in 37℃water for 15 minutes, which was then stimulated with different concentrations of thrombin (0.5 U/mL, 1 U/mL and 10 U/mL) for 10 minutes in wa-ter of 37℃. Meanwhile another three groups of washed platelets were incubated with thrombin (0.5 U/mL, 1 U/mL and 10 U/mL) for 10 minutes, respectively. The CD62P and CD63 from each sample were analyzed by flow cytometry (FCM). Results The CD62P positive rates of HDL-preincubated groups were significantly lower than those of different concentrations of thrombin groups (0.5 U/mL,1 U/mL and 10 U/mL) in the absence of HDL (11.55%± 1.34% vs 18.14%± 1.50%, 17.19%± 0.17% vs 26.24%± 0.77% and 19.79%± 0.32% vs 80.38%± 5.66%,P < 0.01). Meanwhile, The CD63 positive rates of HDL-preincubated groups were also significantly lower than those of thrombin-treated (0.5 U/mL, 1 U/mL and 10 U/mL) groups without HDL, namely,2.92%±0.22%vs 8.09%±0.48%(P<0.001), 4.20%±0.98%vs 14.15%±1.39%(P<0.001) and 5.12%± 0.09% vs 24.48%± 1.71%(P < 0.01). Conclusion HDL inhibits the expression of CD62P and CD63 on throm-bin-stimulated platelets in vitro.

2.
Article in Chinese | WPRIM | ID: wpr-427720

ABSTRACT

ObjectiveTo investigate the expression and activity of p38 mitogen-activated protein kinase (p38 MAPK)in hippocampus CA1 and CA3 area of rats with conditioned fear.Methods 24 h after rat model of conditioned fear was established,rats were sacrificed,then expression of p38 MAPK and phosphorylated p38 MAPK (Thr180/Tyr182) in hippocampus CA1 and CA3 area of rats were detected by western blot.ResultsCompared with control group ( ratios of value of gray scale were 1.0 ± 0.1 and 1.0 ± 0.2,respectively),expression of p38 MAPK and phosphorylated p38 MAPK (Thr180/Tyr182) in hippocarpus CA1 area of rats with conditioned fear (9.4 ± 2.6 and 7.8 ± 2.1,respectively) were significantly increased ( n =9,P < 0.05 ).Compared with control group ( 2.1 ± 0.5 and 1.4 ± 0.5,respectively),expression of p38 MAPK and phosphorylated p38 MAPK (Thr180/Tyr182 ) in hippocampus CA3 area of rats with conditioned fear (6.2 ± 3.3 and 2.6 ± 0.6,respectively)were also significantly increased ( n =9,P < 0.05 ).Conclusionp38 MAPK may play important role in the formation of long term memory of conditioned fear.

3.
Article in Chinese | WPRIM | ID: wpr-407415

ABSTRACT

BACKGROUND: Ambulatory blood pressure monitoring can sensitively and objectively reflect blood pressure level, which is closely related to target organ damage and disease prognosis. In hypertension, vascular endothelial damage is the most common lesion to target organs. There is little known about how ambulatory pulse pressure correlates to large artery elasticity and vascular endothelial function. OBJECTIVE: To investigate changes of large artery elasticity and of vascular endothelial function in patients with primary hypertension using an automatic pulse wave velocity determinator and ultrasound techniques, and to analyze the correlation of ambulatory pulse pressure to large artery elasticity and vascular endothelial function.DESIGN: A non-randomized concurrent control clinical observation. SETTING: Diagnosis and Treatment Center for Coronary Heart Disease, the 305 Hospital of Chinese PLA. PARTICIPANTS: A total of 156 inpatients and/or outpatients, who were recently confirmed with primary hypertension, were recruited for this study between June 2005 and April 2007. Patients consisted of 114 males and 42 females. All patients averaged 56 ± 4 years of age (range: 40-75). Inclusive criteria: Corresponding to diagnostic standards for preventing and treating hypertension instituted in 2004 by Chinese scholars. Confirmed as primary hypertension within 1 month. Not receiving any blood pressure lowering, hypolipidemic or nitrate-like drug treatments. Written informed consents for laboratory measurements were obtained from all subjects. The study was approved by the hospital's Ethics Committee. METHODS: According to the mean pulse pressure over 24 hours, all patients were assigned into 3 groups: Group A (mean pulse pressure < 40 mm Hg, n=92), group B (40 mm Hg ≤ mean pulse pressure < 60 mm Hg, n=39) and group C (mean pulse pressure > 60 mm Hg, n=25). In each group, daytime pulse pressure and night-time pulse pressure, as well as 24-hour mean pulse pressure were measured using a non-invasive portable ambulatory blood pressure monitor (ABPM-04, Meditech Inc, USA). Carotid-femoral and carotid-radial arterial pulse wave velocities were measured using an automatic pulse wave velocity determinator to evaluate large artery dilation. Blood flow mediated and nitroglycerin-dependent dilatation of the brachial artery was determined using a high-resolution ultrasound technique to evaluate vascular endothelial function. MAIN OUTCOME MEASURES: Correlations of ambulatory pulse pressure to large artery dilation and arterial endothelial function. RESULTS: All 156 patients were included in the final analysis. Correlation of ambulatory pulse pressure to large artery dilation: Carotid-femoral arterial pulse wave velocity was significantly positively correlated to daytime pulse pressure, night-time pulse pressure and 24-hour mean pulse pressure, with coefficient of partial correlation being 0.310, 0.281 and 0.303, respectively, P < 0.01). There were no significant correlations of carotid-radial arterial pulse wave velocity to daytime pulse pressure, night-time pulse pressure or 24-hour pulse pressure (P > 0.05). Correlation of ambulatory pulse pressure to arterial endothelial function: There was a linear relationship between ambulatory pulse pressure and blood flow-mediated blood vessel dilatation values. Linear correlation analysis was performed, taking ambulatory pulse pressure as an independent variable, and endothelial-dependent dilatation as a dependent variable. Results demonstrated that blood flow-mediated blood vessel dilatation was significantly negatively correlated to daytime pulse pressure, night-time pulse pressure and 24- hour mean pulse pressure (r = -0.684, -0.597, -0.668, P < 0.01). There was no correlation of ambulatory pulse pressure to non-endothelial-dependent blood vessel dilatation. CONCLUSION: Ambulatory pulse pressure increase is closely related to large artery elasticity decrease and injury to endothelial function in patients with primary hypertension.

4.
Chinese Medical Journal ; (24): 1333-1335, 2003.
Article in English | WPRIM | ID: wpr-311687

ABSTRACT

<p><b>OBJECTIVE</b>To determine mutations of two common potassium channel subunit genes KCNQ1, KCNH2 causing long QT syndrome (LQTS) in the Chinese.</p><p><b>METHODS</b>Thirty-one Chinese LQTS pedigrees were characterized for mutations in the two LQTS genes, KCNQ1 and KCNH2, by sequencing.</p><p><b>RESULTS</b>Two novel KCNQ1 mutations, S277L in the S5 domain and G306V in the channel pore, and two novel KCNH2 mutations, L413P in the transmembrane domain S1 and L559H in the transmembrane domain S5 were identified. The triggering factors for cardiac events developed in these mutation carriers included physical exercise and excitation. Mutation L413P in KCNH2 was associated with the notched T wave on ECGs. Mutation L559H in KCNH2 was associated with the typical bifid T wave on ECGs. Mutation S277L in KCNQ1 was associated with a high-amplitude T wave and G306V was associated with a low-amplitude T wave. Two likely polymorphisms, IVS11 + 18C > T in KCNQ1 and L520V in KCNH2 were also identified in two LQTS patients.</p><p><b>CONCLUSIONS</b>The mutation rates for both KCNQ1 (6.4%) and KCNH2 (6.4%) are lower in the Chinese population than those from North America or Europe.</p>


Subject(s)
Female , Humans , Male , Asian People , Cation Transport Proteins , China , DNA-Binding Proteins , ERG1 Potassium Channel , Ether-A-Go-Go Potassium Channels , KCNQ Potassium Channels , KCNQ1 Potassium Channel , Long QT Syndrome , Genetics , Mutation , Potassium Channels , Genetics , Potassium Channels, Voltage-Gated , Trans-Activators , Transcriptional Regulator ERG
5.
Chinese Medical Journal ; (24): 509-512, 2002.
Article in English | WPRIM | ID: wpr-302265

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the relationship between the U wave on electrocardiogram and the midmyocardium in rabbit left ventricle free wall in vivo.</p><p><b>METHODS</b>The monophasic action potentials in the epicardium, midmyocardium, and endocardium of the left ventricle free wall were recorded simultaneously in 16 rabbits. The rabbits were then given an intravenous injection of Sotalol (1, 1.5 and 2.0 mg/kg) in 30 minutes intervals, and measurements were taken.</p><p><b>RESULTS</b>In the basic condition, there were no U wave on electrocardiogram. The U wave appeared after the intravenous Sotalol at 1.5 mg/kg, and the U wave became greater with increased dosage of intravenous Sotalol (2 mg/kg). The repolarization duration of the midmyocardium was prolonged longer than that of the epicardium and endocardium by Sotalol, and the repolarization duration of the epicardium coincided with the apex of the T wave, The repolarization duration of the midmyocardium coincided with the end point of the U wave.</p><p><b>CONCLUSION</b>The U wave may originate from the delayed repolarization of the midmyocardium.</p>


Subject(s)
Animals , Rabbits , Action Potentials , Anti-Arrhythmia Agents , Pharmacology , Dose-Response Relationship, Drug , Electrocardiography , Endocardium , Physiology , Heart Ventricles , Pericardium , Physiology , Sotalol , Pharmacology , Ventricular Function
6.
Article in Chinese | WPRIM | ID: wpr-411208

ABSTRACT

Objective To explore the relationship between flood ing and the prevalence of schistosomiasis in the river beach area. Met hods The subjects were investigated on the ways of exposure, frequency and duratio n of water conta cted from May to November in 1999, and eggs of Schistosoma were examined bef ore and after flooding. Results Exposure to infested water for human being s in the area comprised productive, living and recreational contacts including 11 kinds of activities, and 53.55% of the subjects contacted infested w ater. The number of person, frequency and duration of water contacted in floodin g strongly increased; the infection rate and density among population stron gly increased after flooding. There was significant difference between the infec tion rate in exposure group and that in non-exposure group. Conclusions It can be inferred that flooding has increased water contacted and i nfection, therefore, health education should be strengthened to avoid or dec rease water contact.

7.
Article in Chinese | WPRIM | ID: wpr-546173

ABSTRACT

Objective To explore the effect of IL-1? and IL-6 on MMP-3 gene expression in human coronary artery smooth muscle cells.Methods We used IL-1?(20 ?g/L) and IL-6(10 ?g/L) to stimulate human coronary artery smooth muscle cells,which were co-culture for 0,2,4,8,24,36 h.IL-1?(0,5,20,40 ?g/L) and IL-6(0,5,10,50 ?g/L) were used to stimulate human coronary artery smooth muscle cells,which were co-cultured for 6 h.Then we detected the gene expression by fluorescent quantitation PCR.Results In the same concentration of IL-1? and IL-6,gene expression was up-regulated at 2 h,at 8 h the expression reached the peak,then began to descend.In different concentration of IL-1? and IL-6,gene expression was up-regulated with the dose of IL-1? and IL-6(IL-1?: r=0.907,P=0.000;IL-6: r=0.919,P=0.000).There were significant differences in MMP-3 expression among different groups(IL-1?: F=24.047,P=0.000;IL-6: F=14.081,P=0.001).There were no significant differences in matrix metalloproteinase-3 between IL-1? 20 and 40 ?g/L groups(P=0.154) and between IL-6 5 ?g/L and 10 ?g/L(P=0.292).Conclusion It suggests that IL-1? and IL-6 can promote MMP-3 gene expression in human coronary artery smooth muscle cells,and it may be one of the mechanisms of inflammation effect in acute coronary syndrome.

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