This paper is aimed to construct a 3D model of arterial vessels system of digital rat. Firstly, the special injection medium was perfused into the arterial blood vessels of Sprague-Dawley rat; the quality of perfusion through the digital radiography system was evaluated at the same time. Then we used the sectional anatomy imaging system and achieved the digital rat atlas of sectional anatomy (sectional anatomy images were captured at 100 microm intervals, with the resolution of 4,917 x 3,446 x 24 bit and in a total of 1,464 slices). Finally, the 3D model of arterial vessels system of digital rat was constructed by segmentation, and the visualization programs were developed on Visual C+ + and Visualization ToolKit (VTK). By use of this model, the 3D microstructure of arterial system of digital rat can be obtained accurately. Remarkably, it will benefit the study of the blood vessels system on laboratory rat.
Animals ; Arteries ; anatomy & histology ; Image Processing, Computer-Assisted ; methods ; Imaging, Three-Dimensional ; methods ; Male ; Models, Anatomic ; Models, Animal ; Rats ; Rats, Sprague-Dawley

Objective To explore the mechanism by which puerarin alleviates the cardiotoxicity induced by doxorubicin in myocardial cells. Methods Cells in the logarithmic growth phase were divided into normal control group,model group,low-(20 mmol·L-1),medium-(40 mmol·L-1) and high-(80 mmol·L-1) dose puerarin groups,and positive control group(captopril,1 mmol·L-1). Except for the normal control group,the other groups were co-incubated with 5 mmol·L-1 doxorubicin. Cell viability was assessed using CCK-8 and lactate dehydrogenase (LDH) assays. ROS levels were detected using a ROS probe. Autophagy flux was detected by transfection with HBAD-mcherry-EGFP-LC3 adenovirus. Western Blot was used to measure the protein expression levels of Beclin-1,LC3,p62,p-AMPKα,and AMPKα. Lysosomal function was assessed using a lysosomal probe. Immunofluorescence was used to detect the relative intensity and co-localization of ASMase and LAMP1. Molecular docking analysis was performed to predict the binding capacity of PUE with ASMase. Differential gene expression was analyzed by gene set enrichment analysis. Results Compared to the normal control group,the model group showed reduced cell viability (P<0.01),increased release levels of LDH and ROS (P<0.05,P<0.01),increased number of autophagosomes (P<0.01),and decreased number of autophagic lysosomes (P<0.05). Beclin-1 protein expression and LC3-II/LC3-I ratio decreased(P<0.01),but p62 protein expression increased(P<0.01). Fluorescence intensity of lysosome decreased(P<0.01),whereas fluorescence intensity of ASMase increased(P<0.01). Immunofluorescence co-localization of ASMase and LAMP1 increased (P<0.01),the ratio of p-AMPKα/AMPKα decreased(P<0.05). Compared to the model group,the high-dose puerarin group showed a rebound in cell viability (P<0.05). The medium-and high-dose puerarin groups showed a decreasing trend in LDH level (P<0.05),and all puerarin groups showed a decreasing trend in ROS level (P<0.01). The number of autophagosomes in high-dose puerarin group reduced (P<0.01). The number of autophagic lysosomes in all puerarin groups increased (P<0.05,P<0.01). The high-dose puerarin group showed increased expression of Beclin-1 (P<0.05) and LC3-II/LC3-I ratio,and decreased p62 expression (P<0.01). All puerarin groups showed increased lysosomal fluorescence intensity (P<0.05,P<0.01). The medium-and high-dose puerarin groups showed a decrease in ASMase fluorescence intensity(P<0.05),a reduction in the immunofluorescence co-localization of ASMase with LAMP1 (P<0.01),and an increase in the p-AMPKα/AMPKα ratio (P<0.01). Molecular docking analysis discovered puerarin showed a binding energy of-8.6 kcal·mol-1 with ASMase. Gene enrichment analysis indicated that the differentially expressed genes in the doxorubicin cardiotoxicity model were related to apoptosis,autophagy,and lysosomal function. Conclusion Puerarin can alleviate doxorubicin-induced cardiotoxicity in myocardial cells and protect myocardial cells by regulating autophagy through AMPK/ASMase,as well as restoring autophagic flux.

OBJECTIVE: To explore the effect of occupational high temperature exposure on type 2 diabetes( T2 DM) in male steel workers. METHODS: A cluster random sampling method was used to select 684 male steel workers,who exposed to occupational high temperature in a steel enterprise in Tangshan City,as the high temperature group,and 1 153 male steel workers without occupational high temperature exposure as the control group. The high temperature level of workers in these two groups was measured. The cumulative exposure( CE) of high temperature was calculated,and occupational health exam was performed. The multivariate logistic regression analysis and restricted cubic splines were used to analyze the relationship between high temperature CE and T2 DM. RESULTS: The prevalence of T2 DM in high-temperature group was higher than that in the control group( 13. 0% vs 7. 9%,P < 0. 05). The multivariate logistic regression analysis results showed that the risk of T2 DM in the high temperature group was higher than that in the control group after adjusting for age,body mass index,smoking,drinking,physical exercise and parents with diabetes( P < 0. 05). The 95% confidence interval was 1. 65( 1. 17-2. 33). Restricted cubic spline analysis showed that the high temperature CE was correlated with the prevalence of T2 DM in workers( P < 0. 01) and showed a linear correlation( nonlinearity test,P > 0. 05). CONCLUSION: Occupational high temperature exposure is associated with the occurrence of T2 DM in male steel workers. The male steel workers with high temperature CE show high prevalence of T2 DM risk.