[The In Vivo Intervention and Relative Mechanism of Genistein on the Inflammation and Thrombophilia in Lymphoma-Bearing Mice].

OBJECTIVE: To investigate the in vivo intervention and relative mechanism of Genistein (GEN) on tumor-associated inflammatory and tumor thrombophilia in lymphoma-bearing mice. METHODS: Forty female Balb/c mice aged 5-6 weeks were injected with murine-derived Pro B-cell lymphoma cell line 38B9 to establish a lymphoma mouse model, which was randomly divided into control group, tumor-bearing group, GEN drug intervention group and cyclophosphamide (CTX）drug intervention group. Histopathologic was used to evaluate the tumorigenesis. Tumor formation was observed, and tumor tissues were collected of HE and immunohistochemical staining. ELISA and flow cytometry were used to detect the expression of inflammatory factors and the changes of thrombus indices in plasma after intervention of GEN and Cyclophosphamide (CTX) respectively. Immunohistochemistry method was used to detect the expression of CD19 in tomor tissues of tummor bearing mice. RESULTS: After 14 days of tumor bearing, the mice were tumorigenic. The lymphoma cells were diffusely distributed in the tumor tissue and the expression of CD19 in the tumor tissue was positive. The inflammatory factors such as IL-6, NETs and CLEC-2, and thrombotic indices such as TF, FIB and D-D in lymphoma-bearing mice were significantly higher than those before tumor-injection and lower than those after drug-intervention (all P<0.05). The levels of CLEC-2 and D-D in GEN group were significantly lower than those in CTX group (P<0.05). CONCLUSION: Tumor-associated inflammation and thrombophilia exist in lymphoma-bearing mice. GEN shows better anti-inflammatory and anti-thrombotic effects compared with CTX by interfering with tumor inflammatory factors.

[Association between familial febrile convulsions and HCN2 gene].

OBJECTIVE: To investigate the possible association of familial febrile convulsions with HCN2 gene. METHODS: PCR was conducted on the DNA of peripheral blood white cells from 60 children with familial febrile convulsion (FC) of Han nationality population in northern China aged 1.5 +/- 1.0 (8 months to 5 years old), to amplify the exons of HCN2 gene. The PCR products underwent sequencing to identify the possible mutations. 101 normal children from the same area were used as controls. RESULTS: No mutation was found in the exons of HCN2 gene, however, 14 single nucleotide polymorphisms (SNPs) were found among which there were 8 newly identified SNPs. Using 9 SNPs as markers, association study was conducted between the FC group and control group. There were no significant differences in allele frequencies and genotype frequencies of the 9 SNPs between the FC group and control group. CONCLUSION: HCN2 may not be a susceptibility gene for FC in Chinese population.