论文部分内容阅读
为探讨 Ｌｐ（ａ）、ａｐｏ（ａ）与脑梗塞病因学的关系，阐明ａｐｏ（ａ）基因表型对脑梗塞的调控作用，检测了 ９０ 例经 Ｃ Ｔ 确诊的脑梗塞患者血清 Ｌｐ（ａ）含量，并分离出 １３ 种 ａｐｏ（ａ）表型，与对照（以年龄、性别配比）比较。结果表明，高 Ｌｐ（ａ）者（≥３０ｍ ｇ／ｄｌ）患脑梗塞的危险性为正常者（＜ ３０ｍ ｇ／ｄｌ）的 ３５６ 倍（ Ｐ＜ ０．０１），ａｐｏ（ａ）分子量与 Ｌｐ（ａ）水平呈高度负相关，ｒ＝ － ０．４８１，说明 ａｐｏ（ａ）大小决定了约 ４８％ 的 Ｌｐ（ａ）水平。ａｐｏ（ａ）等位基因 Ｌｐ Ｂ、 Ｌｐ Ｓ１、 Ｌｐ Ｓ２ 可能是易发脑梗塞者的基因标志。
To investigate the relationship between Lp (a), apo (a) and etiology of cerebral infarction and to elucidate the regulatory effect of apo (a) gene phenotype on cerebral infarction and to detect the serum Lp (a ), And 13 kinds of apo (a) phenotypes were isolated and compared with the control (by age and gender). The results showed that the risk of cerebral infarction in high Lp (a) patients (≥30m g / dl) was 3.56 times higher than those in normal subjects (<30m g / dl) (P <0.01) Was negatively correlated with Lp (a) level, r = - 0.481, indicating that apo (a) size determines about 48% of Lp (a) levels. Apo (a) alleles Lp B, Lp S1, Lp S2 may be susceptible to cerebral infarction genetic markers.