Objective:To establish a simplified anatomical model with the selected rabbits widely distributed in China′s dry region as the reference species and compare the result of internal exposure dose coefficients based on the present mode and ERICA.Methods:A simplified anatomical model based on anatomy and geometry was established for rabbits. Combined with Monte Carlo program, the deposited energy of radionuclide particles in rabbit tissues/organs was obtained, and the internal and external exposure dose coefficient for rabbits was calculated following the empirical formula.Results:Simplified anatomy model-based dose coefficients were 129I 4.81 × 10 -6, 137Cs 4.34 × 10 -5, and 134Cs 3.81 × 10 -5(μGy·h -1)/(Bq·kg -1) for internal exposure and 129I 3.16 × 10 -7, 137Cs 2.39 × 10 -4 and 134Cs 6.22 × 10 -4(μGy·h -1)/(Bq· kg -1) for external exposure. respectively. ERICA-based dose coefficients were 129I 4.44 × 10 -5, 137Cs 1.94 × 10 -4 and 134Cs 2.34 × 10 -4(μGy·h -1)/(Bq·kg -1) for internal exposure and 129I 2.19 × 10 -6, 137Cs 2.52 × 10 -4 and 134Cs 6.95 × 10 -4(μGy·h -1)/(Bq·kg -1) for external exposure, respectively. Conclusions:The simplified anatomical model established is based on the measured data and focuses on the radiation doses to biological tissues/organs, and the calculated result based on the present model are closer to the actual situation, and can provide reference values for the reference biological evaluation of non-human species.

Objective:To investigate the relationship between NOD-like receptor protein 3 (NLRP3) gene promoter region-30 single nucleotide polymorphism (SNP) (rs3738448) G/T and dilated cardiomyopathy (DCM) and its related risk factors.Methods:A case-control study method was used to collect 137 patients and 140 healthy controls; polymerase chain reaction-restriction endonuclease fragment length polymorphism technology combined with sequence alignment after DNA sequencing was used for data statistics; After Hardy-Weinberg balance test, the χ 2 test was used for correlation analysis; logistic regression was used to analyze the correlation between multiple risk factors and the SNP site and the incidence of DCM; SNPinfo database was used to predict and analyze the transcription factors affected by the SNP. Results:A total of GG and GT genotypes were detected at this SNP locus, and their genotype distributions were in line with Hardy-Weinberg equilibrium ( P>0.05). At the same time, the difference between the DCM group and the control group was significant ( P<0.05). Multivariate logistic regression analysis indicated that mean arterial pressure, C-reactive protein and B-type brain natriuretic peptide were independent risk factors for the onset of DCM (all P<0.05). The incidence of DCM in -30(RS3738448)G/T genotype GT group was 2.243 times higher than that in GG group (95% CI: 1.043-4.827, P<0.05). Logistic regression analysis under dominant, recessive and additive genetic models showed that there was a correlation between the dominant inheritance of SNP and the occurrence of DCM ( OR=0.44, AIC=370.4, BIC=381.3, P<0.05). Conclusions:The -30 (rs3738448) G/T SNP in the promoter region of the NLRP3 gene is associated with the pathogenesis of DCM, and provides population genetic data for the study of polymorphisms in the promoter region of NLRP3 gene.