title: [The association of apolipoprotein B gene polymorphism with cerebral infarction with positive family history and its effect on plasma lipid levels].
abstract: OBJECTIVE
  To explore the relationship between apolipoprotein B (apoB) gene G12669A polymorphism and cerebral infarction with family history, and to evaluate the effect of G12669A polymorphism on plasma lipid levels.
  
  
  METHODS
  Peripheral blood samples were collected from 147 members of 15 cerebral infarction families, including 47 cerebral infarction patients with positive family history (CIFH-P), 43 first-degree relatives (CIFH-I), 28 second-degree relatives (CIFH-II), and 29 third-degree relatives (CIFH-III), 83 sporadic cerebral infarction (SCI) patients, and 100 healthy controls. Polymerase chain reaction- restriction fragment length polymorphism was used to detect the apoB gene G12669A polymorphism. Oxidase method was used to detect the levels of triglyceride (TG), total cholesterol (TC), high-density lipoprotein (HDL), and low-density lipoprotein (LDL). The serum levels of lipoprotein (a) [LP (a)], apoB-100, and apoAI were determined by immune method.
  
  
  RESULTS
  (1) The frequencies of A allele in the CIFH-P, CIFH-I, CIFH-II, CIFH-III, and SCI groups patients and control group were 0.106, 0.081, 0.036, 0.034, 0.090, and 0.045 respectively, that of the CIFH-P group being significantly higher than that of the control group (P < 0.05), and those of the CIFH-I, CIFH-II, CIFH-III, and SCI groups not being significantly different from that of the control group. (2) In both CIFH-P and SCI groups, the TC and LDL-C levels of the patients with G/A gene type were significantly higher than those of the G/G gene type, while the HDL-C level of the patients with G/A gene type was significantly lower than that of the G/G gene type (all P < 0.05).
  
  
  CONCLUSIONS
  A allele in G12669A polymorphism may be one of the genetic factors influencing the susceptibility to CI in the individuals with a positive family history, and it may play its role through its influence on the blood lipid levels.
authors.affiliation: Department of Neurology, Xiangya Hospital, Central South University, Changsha 410008, China.
authors.forename: Bao-Qiong
authors.initials: BQ
authors.lastname: Liu
authors.forename: Le
authors.initials: L
authors.lastname: Zhang
authors.forename: Qi-Dong
authors.initials: QD
authors.lastname: Yang
authors.forename: Yun-Hai
authors.initials: YH
authors.lastname: Liu
authors.forename: Zhong-Yang
authors.initials: ZY
authors.lastname: Hu
authors.forename: Hong-Wei
authors.initials: HW
authors.lastname: Xu
authors.forename: Xiao-Ping
authors.initials: XP
authors.lastname: DU
authors.forename: Jian
authors.initials: J
authors.lastname: Xia
mesh_terms: D000368:Aged; D000483:Alleles; D001055:Apolipoproteins B / Q000235:genetics*; D001483:Base Sequence; D002544:Cerebral Infarction / Q000097:blood* / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008055:Lipids / Q000097:blood*; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D010375:Pedigree; D011110:Polymorphism, Genetic; D012307:Risk Factors
chemical_list: D001055:Apolipoproteins B; D008055:Lipids