RESUMEN
Chronic hepatitis B virus (HBV) infection and aflatoxin B(1) (AFB(1)) exposure interact synergetically to induce hepatocellular carcinoma. One suggested mechanism for this interaction is the enhanced activation of AFB(1) in chronically HBV-infected individuals. Whereas no associations between chronic HBV infection and AFB(1)-albumin adducts were observed in several studies in adults, hepatitis B surface antigen (HbsAg)-positive children were found to have elevated adducts in Gambia. To assess the association between chronic HBV infection and AFB(1)-albumin adduct level in Taiwan, 200 junior high school adolescents from 20 townships were assayed for HBsAg and AFB(1)-albumin adducts. The mean AFB(1)-albumin adduct level was higher in HBsAg-positive compared with HBsAg-negative subjects. The association between HBsAg status and AFB(1)-albumin adducts remained after multivariate adjustment. This finding additionally supports the synergetic interaction between HBV and AFB(1), but the mechanism remains to be elucidated.
Asunto(s)
Aflatoxina B1/metabolismo , Albúminas/metabolismo , Aductos de ADN/sangre , Antígenos de Superficie de la Hepatitis B/sangre , Hepatitis B Crónica/sangre , Adolescente , Aflatoxina B1/orina , Femenino , Hepatitis B Crónica/epidemiología , Humanos , Modelos Lineales , Masculino , TaiwánRESUMEN
A series of unsteady-state reaeration tests were performed in a 500-L tank at 0.81-4.58 m3/h diffused-air flow rate and 288-302 K water temperature. Three different types of impurities: soybean oil, surfactant, and diatomaceous earth were doped to simulate the impurities in wastewaters and the effects of the impurities on the oxygen transfer rate were investigated. The ASCE and the two-zone oxygen mass-transfer models were used to analyze the unsteady-state reaeration data and the volumetric mass-transfer coefficients determined from the unsteady-state reaeration data were correlated as a function of the diffused-air flow rate, water temperature, and impurity concentration. The results showed that the alpha factors based on the ASCE model are less sensitive to the impurity concentration while the presence of the impurities significantly reduces the alpha factors in the gas bubble zone. The saturation DO concentration and volumetric oxygen mass-transfer rate can be predicted by the two-zone model along with the correlation obtained in this study.
Asunto(s)
Oxígeno/química , Contaminantes Químicos del Agua/metabolismo , Agua/química , Presión Atmosférica , Tierra de Diatomeas/química , Difusión , Cinética , Matemática , Modelos Químicos , Aceite de Soja/química , Tensoactivos/química , TemperaturaRESUMEN
The "NK-triggering-antigen regulator" (Nktar) gene is a locus identified in the C57BL/6 genome which regulates the ability of unlabeled activated Con A blasts to compete for recognition of labeled syngeneic Con A blasts by BALB/c NK cells. Linkage analysis on Con A blasts from (BALB/c x CByB6F1) N2 backcross progeny for (1) relative level of competitive inhibition of BALB/c NK lysis of syngeneic Con A blasts and (2) genotypes at polymorphic microsatellite markers distributed throughout the mouse genome mapped the Nktar gene locus to a 5-cM region of chromosome 10 containing the interferon-gamma receptor (Ifngr) gene locus. N2 Con A blasts exhibited an inverse relationship between (a) their cell surface density of IFN-gammaR molecules detected by FACS with monoclonal anti-CD119 and (b) their cold target inhibition of BALB/c NK self-reactivity. Con A blasts from Ifngr(-/-) knockout mice showed a relatively high level of inhibition of BALB/c NK self-lysis and a relatively low level of class I MHC, which were both reversed by transient transfection with the Ifngr gene. Sequencing studies showed that Balb/c Ifngr encodes a Gly(69) whereas C57BL/6 Ifngr encodes Glu(69) due to a difference at nucleotide 284. Sequencing studies of N2 progeny demonstrated 100% concordance between their Nktar inhibitory phenotype and their Ifngr genotype. These findings demonstrate that the Nktar and Ifngr loci are identical. They further indicate that polymorphisms related to the Ifngr locus and affecting expression of cell surface IFN-gammaR may underlie genetic differences in the availability of NK-triggering antigens (NKTAgs) to recognition by self-reactive BALB/c NK cells by differentially affecting the ability of IFN-gammaR molecules to mediate up-regulation of NKTAg-masking class I molecules.