Objective To investigate the expression changes of victims suffering from sudden cardiac death(SCD), eurological calcium adhesion proteins (N-Cadherin) and Bax and explore their significance in forensic medicine. Methods Separately select 33 samples of myocardial tissue suffering from sudden cardiac death and 29 samples of myocardial tissue from the cases which were diagnosed not dying of heart disease as SCD and controls. Histological methods were used to examine the morphologic changes in myocardial tissue, examining the expression changes of N-Cadherin and Bax and analyzing them in a statistic way. Results N-Cadherin was weakly positively expressed in myocardial tissue of group SCD and the cells shew disordered arrangement, which is obviously lower than the controls. The cells exhibited obvious features ordered arrangement in control group. The positive expression of Bax was detected in myocardial tissue of group SCD, which is obviously higher than the controls. Conclusion The expression changes observation of N-Cadherin and Bax will make a difference to the sudden cardiac death.

Objective:To exploring the regulatory effect of miR-29a on the transforming growth factor-β1 (TGF-β1) /Smad homolog 3 (Smad3) pathway during the process of rare earth neodymium oxide (Nd 2O 3) induced pulmonary fibrosis in mice. Methods:In March 2021, 72 SPF grade C57/BL6J male mice were selected and randomly divided into a control group, Nd 2O 3 group, Nd 2O 3+miR-29a agomir group, and Nd 2O 3+NC agomir group, with 18 mice in each group. The Nd 2O 3 group, Nd 2O 3+miR-29a agomir group, and Nd 2O 3+NC agomir group were treated with non exposed tracheal instillation, with a dust concentration of 250 mg/ml and a dust volume of 0.1 ml. The control group was given the same volume of physiological saline. After exposure to Nd 2O 3, 0.1 ml (5 nmol) of miR-29a agomir was injected into the tail vein of mice in the Nd 2O 3+miR-29a agomir group every 3 days, while 0.1 ml of NC agomir was injected into the tail vein of mice in the Nd 2O 3+NC agomir group. On the 7 th, 14 th, and 28 th days after dust exposure, 6 mice were killed in each group, and the lung tissue of the mice was taken out. HE staining was used to observe the pathological status of the mouse lung tissue; ELISA method was used to detect the levels of TGF-β1 and connective tissue growth factor (CTGF) in lung tissue; Use qRT-PCR detection method to detect the expression level of TGF-β1 mRNA; Using immunofluorescence assay to detect the expression level of Smad3 in mouse lung tissue; Use bioinformatics websites such as TargetScan7 and miRDB to predict the target gene of miR-29a. When the metrological date were satisfied with normal distribution, Mean±SD was used for comparison between groups, t test was used for two indepent samples, and LSD method was used when the variance was homogeneity in pairwise comparison. Results:HE staining showed that the Nd 2O 3 group of mice showed obvious infiltration of inflammatory cells and structural disorder of alveoli in the early stage of lung tissue. At 28 days, the collagen fibers in the mouse lung tissue increased and the lung tissue showed fibrotic honeycomb like changes. The degree of pulmonary fibrosis in the Nd 2O 3+miR-29a agomir group of mice was significantly reduced; The content of TGF-β1 and CTGF in the lung tissue of mice in the Nd 2O 3+miR-29a agomir group was lower than that in the Nd 2O 3+NC agomir group ( P<0.05) ; The relative expression level of TGF-β1 in the lung tissue of mice in the Nd 2O 3+miR-29a agomir group was lower than that in the Nd 2O 3+NC agomir group ( P<0.05) ; The expression level of Smad3 in the nucleus of the Nd 2O 3+miR-29a agomir group was lower than that of the Nd 2O 3+NC agomir group ( P<0.05). The prediction results of bioinformatics websites have found 152 downstream target genes related to miR-29a, among which FBN1, MAP2K6, KPNB1, COL1A2, SNIP1, LAMC1, and SP1 genes may be related to the regulatory effect of miR-29a on TGF-β1/Smad3 signaling pathway. Conclusion:miR-29a may affect lung fibrosis induced by rare earth Nd 2O 3 exposure in mice by regulating TGF-β1/Smad3 signaling pathway. Overexpression of miR-29a may inhibit TGF-β1/Smad3 signaling pathway and reduce the degree of pulmonary fibrosis in mice.

Objective:To exploring the regulatory effect of miR-29a on the transforming growth factor-β1 (TGF-β1) /Smad homolog 3 (Smad3) pathway during the process of rare earth neodymium oxide (Nd 2O 3) induced pulmonary fibrosis in mice. Methods:In March 2021, 72 SPF grade C57/BL6J male mice were selected and randomly divided into a control group, Nd 2O 3 group, Nd 2O 3+miR-29a agomir group, and Nd 2O 3+NC agomir group, with 18 mice in each group. The Nd 2O 3 group, Nd 2O 3+miR-29a agomir group, and Nd 2O 3+NC agomir group were treated with non exposed tracheal instillation, with a dust concentration of 250 mg/ml and a dust volume of 0.1 ml. The control group was given the same volume of physiological saline. After exposure to Nd 2O 3, 0.1 ml (5 nmol) of miR-29a agomir was injected into the tail vein of mice in the Nd 2O 3+miR-29a agomir group every 3 days, while 0.1 ml of NC agomir was injected into the tail vein of mice in the Nd 2O 3+NC agomir group. On the 7 th, 14 th, and 28 th days after dust exposure, 6 mice were killed in each group, and the lung tissue of the mice was taken out. HE staining was used to observe the pathological status of the mouse lung tissue; ELISA method was used to detect the levels of TGF-β1 and connective tissue growth factor (CTGF) in lung tissue; Use qRT-PCR detection method to detect the expression level of TGF-β1 mRNA; Using immunofluorescence assay to detect the expression level of Smad3 in mouse lung tissue; Use bioinformatics websites such as TargetScan7 and miRDB to predict the target gene of miR-29a. When the metrological date were satisfied with normal distribution, Mean±SD was used for comparison between groups, t test was used for two indepent samples, and LSD method was used when the variance was homogeneity in pairwise comparison. Results:HE staining showed that the Nd 2O 3 group of mice showed obvious infiltration of inflammatory cells and structural disorder of alveoli in the early stage of lung tissue. At 28 days, the collagen fibers in the mouse lung tissue increased and the lung tissue showed fibrotic honeycomb like changes. The degree of pulmonary fibrosis in the Nd 2O 3+miR-29a agomir group of mice was significantly reduced; The content of TGF-β1 and CTGF in the lung tissue of mice in the Nd 2O 3+miR-29a agomir group was lower than that in the Nd 2O 3+NC agomir group ( P<0.05) ; The relative expression level of TGF-β1 in the lung tissue of mice in the Nd 2O 3+miR-29a agomir group was lower than that in the Nd 2O 3+NC agomir group ( P<0.05) ; The expression level of Smad3 in the nucleus of the Nd 2O 3+miR-29a agomir group was lower than that of the Nd 2O 3+NC agomir group ( P<0.05). The prediction results of bioinformatics websites have found 152 downstream target genes related to miR-29a, among which FBN1, MAP2K6, KPNB1, COL1A2, SNIP1, LAMC1, and SP1 genes may be related to the regulatory effect of miR-29a on TGF-β1/Smad3 signaling pathway. Conclusion:miR-29a may affect lung fibrosis induced by rare earth Nd 2O 3 exposure in mice by regulating TGF-β1/Smad3 signaling pathway. Overexpression of miR-29a may inhibit TGF-β1/Smad3 signaling pathway and reduce the degree of pulmonary fibrosis in mice.