Objective To investigate the value of cytokinesis-block micronuclei(CBMN)assay in estimation of the biological doses of the victims of radiation accident.Methods Samples of peripheral blood were collected from the 5 victims(Subjects 1-5)at 16 h after the radiation accident of Taiyuan,Shanxi Province.And the peripheral blood samples and bone marrow sample were collected from the victim No.1 at 23 and 24 h after the radiation.Eight days after the accident Subject 1 underwent allogeneic peripheral blood hematopoietic stem cell transplantation.At difierent time points in the period of 1 year after the accident.peripheral blood samples were collected from these 5 victims.CBMN assay was conducted on the peripheral blood lymphocytes on the samples,and the biological doses were estimated based on the micronuclei(MN)frequencies.The nuclear division index(NDI)obtained from in vitro irradiation experiment using high dose of 60Coγ-rays was used to estimate the exposed doses for Subject 1. Dynamic arialysis of the MN frequency for the 5 victims was performed in the period of 1 year after the accident.Results The MN frequency of Subject 1 surpassed the value corresponding to the upper limit of the MN dose.effective curve.The dose range estimated bv the combination of the CBMN and NDI (CBMN+NDl)assay was 10-20 Gy for Subject 1.The doses estimated by MN frequency for Subjects 2,3,4,and 5 were 3.6,2.9,2.3,and 2.9 Gy,respectively.The estimated doses were in accordance with those estimated by physicat method.chromosome aberration analysis.and clinical symptoms.Prominent decrease of the MN frequency was observed at 26 d after the accident(18 d after the transplantation)for Subject 1(u=3.295,P<0.05).Gradual decrease of MN frequency was observed after the accident for Subjects 2,3,4,and 5.The MN frequencies 1 month after the accident of Subjects 3,4,and 5 were all significantly lower than those 16 h later(u=6.874,4.526,and 7.811,P<0.05).Conclusions Quick and accurate.CBMN assay reinforces and verifies the result of chromosome aberration analysis.The new index CBMN+NDI assay is of reference valne for estimating higher dose of irradiation.

Objective To evaluate the molluscicidal effect of niclosamide ethanolamine salt powder?granula(PG)against Oncomelania hupensis. Methods The molluscicidal experiment was carried out by the dusting method with niclosamide etha?nolamine salt 4%PG. The experiments were respectively done in the laboratory and the tidal flats wetlands. At the same time , the niclosamide ethanolamine salt 4%dustable powder(DP)was as the control group. The single blind method was used for the quality control. The corrected mortality and the median lethal concentration(LC50)were compared between PG and DP in the molluscicidal experiment of the laboratory. The corrected mortality and the reduced rate of snails’density were compared be?tween PG and DP in the tidal flats wetlands. Results The mortality rates of the snails were 96.67%and 100%respectively on 1 d after dusting 4.0 g/m2 of 4% PG and 2.0 g/m2 of 4% DP in the laboratory. The results showed that the mortality rates of the snails were higher with 4%DP than 4%PG in each dosage(t1 d=3.60,P<0.01). The LC50(s) of 1d,3 d,7 d after dusting the molluscicide also showed that the molluscicidal effects of DP were better than PG. The corrected mortality rates were 91.71%, 92.91%,90.57%,85.33%and 71.09%,90.11%,90.13%,85.26%on 3 d,7 d,15 d,30 d after dusting with 4%PG and 4%DP,respectively,in the fields. Statistics showed that the mortality rates of snails were higher on 3 d,7 d after dusting with PG than DP(c23 d=731.57,c27 d=25.90,P<0.01),but there were no significant differences between PG and DP on 15d,30d af?ter dusting(c215 d=0.53,c230 d=0.01,P>0.05). Conclusions 4%PG has both the adsorption of powder and the penetrability of the granules. The molluscicidal effects of 4%PG and 4%DP are almost the same. However,the drift of the powder was still not effectively controlled. This problem need to be further studied.

Background and objectives:Hepatic steatosis and inflammation are key characteristics of non-alcoholic fatty liver disease(NAFLD).However,whether and how hepatic steatosis and liver inflammation are differentially regulated remains to be elucidated.Considering that disruption of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3(Pfkfb3/iPfk2)dissociates fat deposition and inflammation,the present study examined a role for Pfkfb3/iPfk2 in hematopoietic cells in regulating hepatic steatosis and inflammation in mice. Methods:Pfkfb3-disrupted(Pfkfb3+-)mice and wild-type(WT)littermates were fed a high-fat diet(HFD)and examined for NAFLD phenotype.Also,bone marrow cells isolated from Pfkfb3+/-mice and WT mice were differentiated into macrophages for analysis of macrophage activation status and for bone marrow transplantation(BMT)to generate chimeric(WT/BMT-Pfkfb3+/-)mice in which Pfkfb3 was disrupted only in hematopoietic cells and control chimeric(WT/BMT-WT)mice.The latter were also fed an HFD and examined for NAFLD phenotype.In vitro,hepatocytes were co-cultured with bone marrow-derived macrophages and examined for hepatocyte fat deposition and proinflammatory responses.Results:After the feeding period,HFD-fed Pfkfb3+/-mice displayed increased severity of liver inflam-mation in the absence of hepatic steatosis compared with HFD-fed WT mice.When inflammatory activation was analyzed,Pfkfb3+/-macrophages revealed increased proinflammatory activation and decreased anti-proinflammatory activation.When NAFLD phenotype was analyzed in the chimeric mice,WT/BMT-Pfkfb3+/-mice displayed increases in the severity of HFD-induced hepatic steatosis and inflammation compared with WT/BMT-WT mice.At the cellular level,hepatocytes co-cultured with Pfkfb3+/-macrophages revealed increased fat deposition and proinflammatory responses compared with hepatocytes co-cultured with WT macrophages. Conclusions:Pfkfb3 disruption only in hematopoietic cells exacerbates HFD-induced hepatic steatosis and inflammation whereas the Pfkfb3/iPfk2 in nonhematopoietic cells appeared to be needed for HFD feeding to induce hepatic steatosis.As such,the Pfkfb3/iPfk2 plays a unique role in regulating NAFLD pathophysiology.