BackgroundPulmonary brosis is the sequela of many pulmonary diseases, such as pneumoconiosis and idiopathic pulmonary brosis. The principal characteristics of pulmonary brosis comprise myo broblast proliferation, alveolar damage and deposition of extracellular matrix components, which causes abnormal lung structure remodeling and an irreversible decline in lung function; however, the detailed mechanisms remain unclear. The current study focused on the role of ZC3H4, a new member of the zinc nger protein family, in SiO 2 -induced pulmonary brosis. MethodsThe expression of ZC3H4 and broblast activation markers (COL1A1, COL3A1 and ACTA1) was measured by western blotting and immuno uorescence staining after SiO 2 exposure (50 µg/cm 2 ). The functional change in broblasts was studied with a scratch assay and a 3D migration assay. The CRISPR/Cas9 system was used to explore the regulatory mechanisms of ZC3H4 in pulmonary broblast cells. ResultsThe expression levels of ZC3H4 and sigmar1 (a key regulator of ER stress) were increased in pulmonary broblast cells and were associated with broblast activation, as indicated by the increase in COL1A1, COL3A1 and ACTA1, as well as the migration ability. The SiO 2 -enhanced broblast activation was attenuated by speci c knockdown of ZC3H4 and inhibition of ER stress, demonstrating that ZC3H4 activated broblasts via the sigmar1/ER stress pathway. Interestingly, an ER stress blockade also inhibited ZC3H4 expression, indicating the positive feedback regulatory mechanism of ER stress on ZC3H4. ConclusionsOur results demonstrate that ZC3H4 and sigmar1 might act as novel therapeutic targets for silicosis, providing a reference for further pulmonary brosis research.

It is significant to use recycled waste plastic bags in concrete to solve the issue of the disposal of leftover polyethylene in the environment. This research incorporated the plastic bags’ polyethylene into concrete and evaluated the mechanical properties of concrete, to reduce cracking to some extent and increase the tensile & flexural strengths and deformation capacity. Six mixtures were used with varying percentages of waste plastic bags (i.e., 0%, 0.3%, 0.6%, 0.9%, 1.2%, and 1.5%). The sorptivity test was conducted following ASTM C1585 and the volume of permeable voids test was according to the ASTM C642 requirements. The pullout strength of the steel rebar in a concrete cylinder was also determined. With waste polyethylene, it was noted that the flexural strength increased, pull-out bond strength declined and initial sorptivity increased. This decline in the volume of permeable voids was due to the heterogeneity of the mixture which leads to the low density of the mixture due to waste plastic bags. Experiments proved that substituting plastic bags for fine aggregates in concrete, increases flexural and split tensile strengths while decreasing compressive and pullout strength.

Abstract Background Pulmonary fibrosis is the sequela of many pulmonary diseases, such as pneumoconiosis and idiopathic pulmonary fibrosis. The principal characteristics of pulmonary fibrosis comprise myofibroblast proliferation, alveolar damage and deposition of extracellular matrix components, which causes abnormal lung structure remodeling and an irreversible decline in lung function; however, the detailed mechanisms remain unclear. The current study focused on the role of ZC3H4, a new member of the zinc finger protein family, in SiO2-induced pulmonary fibrosis. Methods The expression of ZC3H4 and fibroblast activation markers (COL1A1, COL3A1 and ACTA1) was measured by western blotting and immunofluorescence staining after SiO2 exposure (50 µg/cm2). The functional change in fibroblasts was studied with a scratch assay and a 3D migration assay. The CRISPR/Cas9 system was used to explore the regulatory mechanisms of ZC3H4 in pulmonary fibroblast cells. Results The expression levels of ZC3H4 and sigmar1 (a key regulator of ER stress) were increased in pulmonary fibroblast cells and were associated with fibroblast activation, as indicated by the increase in COL1A1, COL3A1 and ACTA1, as well as the migration ability. The SiO2-enhanced fibroblast activation was attenuated by specific knockdown of ZC3H4 and inhibition of ER stress, demonstrating that ZC3H4 activated fibroblasts via the sigmar1/ER stress pathway. Interestingly, an ER stress blockade also inhibited ZC3H4 expression, indicating the positive feedback regulatory mechanism of ER stress on ZC3H4. Conclusions Our results demonstrate that ZC3H4 and sigmar1 might act as novel therapeutic targets for silicosis, providing a reference for further pulmonary fibrosis research.