[The heat shock protein 70-2 gene +1267(A/G) polymorphism and susceptibility to ankylosing spondylitis in Chinese Han population].

Objective: To investigate the association between the heat shock protein 70-2 gene polymorphism and ankylosing spondylitis (AS).

Methods: The polymorphisms of HSP70-2 gene Pst I 1267 site were analysed in 176 Chinese Han AS patients and 127 healthy controls by PCR and restriction fragment length polymorphisms(RFLP) methods.

Results: In AS patients HSP70-2 genotypes AA, AG and GG were 46.

[Anti-apoptosis effect of VEGF on the human chronic myelocytic leukemia cell line K562].

To explore the effects of vascular endothelial growth factor (VEGF) on the mechanisms of CML pathogenesis, the effect of VEGF on K562 cell apoptosis induced by As(2)O(3) was analyzed through morphologic observation, DNA fragmentation agarose gel electrophoresis and DNA ploidy flow cytometry analysis, and the effect of VEGF on the expression of bcl-X(L), Bax and caspase-3 in K562 cells was determined by Western blot, meanwhile the expression difference between bcl-X(L) and Bax mRNA in above conditions was detected by RT-PCR. The results showed that after VEGF added, the apoptosis of K562 cells reduced, however, there was no significant changes in cell cycle distribution (P > 0.05).

[Relationship between heat shock protein 70-hom gene polymorphism and ankylosing spondylitis].

Objective: To investigate the association between heat shock protein 70-hom (HSP70-hom) gene polymorphism and ankylosing spondylitis(AS) in Chinese Han patients.

Methods: Genomic DNA from 98 Chinese AS patients and 70 ethnically matched controls were typed for HSP70-hom polymorphism by polymerase chain reaction-restriction fragment length polymorphism.

Results: The HSP70-hom genotypes in the AS patients consisted of homozygote AA (60.

[Inhibition of K562 cell proliferation by wild type p16 and p53 genes co-transfection].

The tumor suppressor gene p53 and p16, both of which play an important role in inhibition of tumorigenesis, are homozygously deleted in human myeloid leukemia cell line K562. To explore the inhibition of K562 cell proliferation by wild type p16 and p53 genes, both p16 and p53 genes were co-transfected into K562 cells mediated by liposome. The expression of the two genes was measured by immunocytochemical method, the cell cycle was analysed by flow cytometry, and the number of recovered viable cells was assessed after transfection.