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作 者:黄深[1] 唐家荣[1] 张存泰[1] 孙莉萍[1] 郭丽芬[1] 孙萌[1]
机构地区:[1]430030武汉,华中科技大学同济医学院附属同济医院心内科
出 处:《中华心血管病杂志》2008年第7期602-607,共6页Chinese Journal of Cardiology
摘 要:目的运用膜片钳技术检测急性冠状动脉综合征(ACS)患者的CD4^+CD28^nullT淋巴细胞Kv1.3钾通道的数量是否增加,探讨CD4^+CD28^nullT淋巴细胞上Kv1.3钾通道的表达。方法选择17例ACS患者,11例年龄、性别匹配的正常体检者作为对照。运用荧光染色标记及膜片钳技术检测单个T淋巴细胞(CD4^+CD28砌。T淋巴细胞和CD4^+CD28^+T淋巴细胞)上Kv1.3钾通道的数量,比较Kv1.3通道在两种细胞上的差别。结果ACS患者的CD4^+CD28^null T淋巴细胞比例为(6.97±2.05)%,明显高于对照组的(1.38±0.84)%(P〈0.05)。ACS患者的CD4^+CD28^null T淋巴细胞数量与hsCRP浓度呈正相关(r=0.52,P〈0.05)。ACS患者CD4^+CD28^nullT淋巴细胞Kv1.3通道的电导、密度、数量明显高于对照组CD4^+CD28^nullT淋巴细胞(P〈0.01)。而两组CD4^+CD28^+T淋巴细胞间Kv1.3通道的电导、密度、数量差异无统计学意义(P〉0.05)。结论ACS患者CD4^+CD28^nullT淋巴细胞明显增多。ACS患者CD4^+CD28“T淋巴细胞上Kvl.3钾通道数量比自身和对照的CD4^+CD28^+T淋巴细胞明显增多,CD4^+CD28^nullT淋巴细胞的功能可能与Kv1.3钾通道增多相关。Objective The purpose of our study is to observe the voltage-gated potassium channel Kv1.3 expression on T cells from the peripheral blood of ACS patients by the patch clamp technique. Methods Kv1.3 potassium channels expression from 17 patients with ACS and 11 healthy agematched normal controls was detected in single cell ( CD4^± CD28^null T cells and CD4^± CD28^null T cells) by fluorescence microscopy and patch clamp. Results The percent of CD4^± CD28^null T cells are higher in the ACS(6. 97% ± 2. 05% ) than that in the controls ( 1.38% ± 0. 84%, P 〈 0.05 ). The concentration of hsCRP is directly correlated with the number of the CD4^+ CD28^nullT cells in the ACS ( r = 0. 52, P 〈 0.05 ), The conductance[ (6. 89 ± 1. 17)nS vs. (3.36±0.66)nS], dens[(1.95 ±0.80) n/μm^2 vs. (1.13 ± 0.57) n/Ixm2 ] and numbers[ (574. 5 ± 97.6) n/cell vs. (280. 3 ± 55. 3) n/cell] of the Kv1.3 channels on the CD4^±CD28^nullT cells are significantly higher than those on the CD4^±CD28^null T cells ( all P 〈0.01 ) in ACS patients, but were similar on CD4^±CD28^null T ceils between ACS patients and controls. Conclusion The CD4^± CD28^null T cells in the ACS and the numbers of Kv1.3 channels on the CD4^± CD28^nullT cells from the ACS patients are significantly upregulated and might contribute to the pathogenesis of ACS.
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