A retrospective analysis of pathological and clinical diagnoses: report of 240 pediatric autopsies.

Reduction of childhood mortality is a worldwide health priority. By investigating the most frequent causes of childhood death and analyzing the major causes of misdiagnosis, this study aims to quantify the value of autopsy and guide further research for improving health services. A total of 240 autopsied cases were recruited into the study. The major causes of death according to the system were respiratory diseases, followed by neoplasms and infectious diseases, while the top three causes of death according to diseases were lobular pneumonia, septicemia, and malignant histiocytosis. Agreement between pathologic and clinical diagnoses was shown in 169 autopsies (70.5%), and the other 71 cases (29.6%) had been misdiagnosed. This study demonstrated the value of the routine autopsy by documenting the high rate of disagreement between clinical and autopsy diagnoses. However, the role of routine autopsy for determining in-born errors of metabolism is limited.

[ERK signaling pathway mediated epithelial-mesenchymal transition induced by SiO2 in human bronchial epithelial cells].

OBJECTIVE: To determine the role of extracellular signal regulated kinase (ERK) signaling pathway in SiO2 induced epithelial-mesenchymal transition (EMT) in human bronchial epithelial cells (HBEC) in vitro. METHODS: HBEC were treated with SiO2 (0-300 µg/mL) for 72 h or pretreated with U0126 (0-30 µmol/L) for 1 h and then treated with 200 µg/mL SiO2 for 72 h. Western blot was used to detect the protein expression of E-cadherin and α-smooth muscle actin (α-SMA). The activity of ERK was examined by mitogen-activated protein kinase (MAPK) activity assay kit in HBEC exposing to SiO2 (200 µg/mL) for 0-8 h. RESULTS: The expression of E-cadherin decreased gradually in SiO2 -stimulated HBEC, and the effect was most significant at 300 µg/mL (P<0.01). The expression of α-SMA increased and the effect was most evident at 200 µg/mL (P<0.01). With SiO2 treatment, the activity of ERK was upregulated significantly. The phosphorylation of ERK increased at 30 min and decreased after 1 h. U0126 significantly inhibited SiO2 -induced expression changes in E-cadherin and α-SMA. At 30 µmol/L, the effect was most evident(P<0.01). CONCLUSION: ERK signaling pathway mediated EMT induced by SiO2 in HBEC.