Objective To investigate the relationship between serum vitamin B12 level and arsenic methylation and the risk of arsenic poisoning in the arsenic exposed population.Methods Three villages in Midu County,Dali City,Yunnan Province were investigated.Cross-sectional study was used to select 103 subjects.The population was divided into three groups according to drinking water arsenic exposure situation and whether arsenic poisoning patients:28 cases of control group (not exposed to high arsenic),30 cases of arsenic patient group and 45 cases of non patient group.Instant peripheral blood samples and urine samples were collected.The content of arsenic in urine was determined by hydride generation cold trap and atomic absorption spectrophotometry.The levels of vitamin B12 in serum were determined by chemiluminescence immunoassay.The urine arsenic and serum vitamin B12 contents in different groups were compared,the arsenic poisoning prevalence rate in people with different levels of serum vitamin B12 was investigated,and the correlation between serum vitamin B12 level and the metabolism of arsenic methylation was analyzed.Results The level of urinary inorganic arsenic (iAs),monomethylated arsenic (MMA) and dimethylated arsenic (DMA),total arsenic (tAs) were significantly different between groups (F =13.032,20.778,21.978,22.155,all P ＜ 0.05).The levels of urine arsenic in patients with arsenic exposure [(94.56 ± 107.62),(75.76 ± 54.31),(270.19 ± 185.10),(444.02 ± 323.28) μg/g Cr] and non patient with arsenic exposure [(40.05 ± 47.47),(45.11 ± 46.06),(183.91± 151.45),(270.84 ± 231.45) μg/g Cr] were significantly higher than those in control group [(7.58 ± 4.82),(4.27 ± 2.01),(26.89 ± 11.45),(38.91 ± 13.34) μg/g Cr,all P ＜ 0.05].The serum levels of vitamin B12 were significantly different between groups (F =6.650,P ＜ 0.05),patients exposed to arsenic [(366.05 ± 120.03) ng/L] was significantly lower than the control group [(533.70 ± 180.12) ng/L,P ＜ 0.05].There were significant differences in the detection rate of arsenic poisoning among different levels of serum vitamin B12 (x2=8.13,P ＜ 0.05),the lower dose of vitamin B12,the more serious the incidence of arsenic poisoning.The content of vitamin B12 was negatively correlated with MMA％ (r =-0.21,P ＜ 0.05),and positively correlated with SMR (r =0.21,P ＜ 0.05).Conclusion Low levels of vitamin B12 in serum may increase the risk of arsenic poisoning.

Objective To investigate the influence of low-dose,long-term arsenite exposure on keratinocyte (HaCat) cell apoptosis and the expression of Bcl-2 and Bax proteins.Methods HaCat cells were exposed to different concentrations of NaAsO2[0(control group),0.05,0.10 μmol/L] for 15 weeks.A total of 10 000 cells in each group were measured to detect the level of apoptosis by flow cytometry.The protein expressions of Bcl-2 and Bax were determined by Western blotting method.Results The cell apoptosis rate was significantly different between groups (F =17.19,P ＜ 0.05).Compared with that of the control [(1.42 ± 0.13)％],the apoptosis rates of the 0.05 and 0.10 μmol/L groups [(1.23 ± 0.08)％ and (1.04 ± 0.06)％] decreased significantly (all P ＜ 0.05); the 0.10 μmol/L group was significantly lower than that of the 0.05 μmol/L group(P ＜ 0.05).The protein expressions of Bcl-2 and Bax were significantly different between groups (F=107.38,346.45,all P＜ 0.05).The protein expression of Bcl-2 of the 0.05 and 0.10 μmol/L groups were (143.89 ± 7.74)％ and (199.96 ± 12.18)％,respectively,which were significantly higher than that of the control group[(100.00 ± 1.45)％,all P ＜ 0.05] ; the 0.10 μmol/L group was significantly higher than that of the 0.05 μmol/L group (P ＜ 0.05).The protein expression of Bax of the 0.05 and 0.10 μmol/L groups were (70.78 ± 1.53)％ and (54.80 ± 1.34)％,respectively,which were markedly lower than that of the control group[(100.00 ± 3.09)％,all P ＜ 0.05]; the 0.10 μmoL/L group was significantly lower than that of the 0.05 μmol/L group(P ＜ 0.05).Conclusion Decreased level of apoptosis induced by low level and long-term arsenic exposure may be associated with increased expression of Bcl-2 protein and decreased expression of Bax protein.

【Objective】 To genetically analyze the D^el sample from a blood donor in Jiangyin and make clear the molecular basis of the serological phenotype. 【Methods】 The EDTA anticoagulant blood were collected: buffy coat were used for nucleic acid extract and cDNA analysis; red blood cells for serological test. Tube method and microcolumn gel were used for serological test. Genotyping kit were used for exon analysis. Gene mutation was analyzed using the sequence analyzer. 【Results】 Serological analysis demonstrated the sample′s RhD phenotype was D^el. The phenotype of RhCE was CCEe. Real-time fluorescence quota PCR result demonstrated the existence of all exones. Weak D15 and RHD^* DEL1 [RHD(1227G>A)], which had a high frequency of occurrence in China, were excluded according to real-time fluorescence quota PCR result. Sequence analyzing result verified RHD(28C>T) SNP mutation in cDNA. The genotype of this sample was RHD^*01 W. 61[RHD(28C>T)]. 【Conclusion】 A weak D61 was found among blood donors in our city, Jiangyin.