How Does Leadership in Safety Management Affect Employees' Safety Performance? A Case Study from Mining Enterprises in China.

Leadership is a necessary element for ensuring workplace safety. Rather little is known about the role of leadership safety behaviours (LSBs) in the mining industry. Using regression analysis and structural equation modelling analysis, this study examined the cause-and-effect relationships between leadership safety behaviours and safety performance. Data were collected by questionnaires from 305 miners in China. Data were analysed using exploratory factor analysis and confirmatory factor analysis, which identified five main dimensions of LSBs: safety management commitment, safety communication with feedback, safety policy, safety incentives, and safety training; the analysis also identified three main dimensions of safety performance: employee's safety compliance, safety participation, and safety accidents. The results showed the overall effects of each LSB variable on safety compliance in descending order as: safety training (0.504), safety incentives (0.480), safety communication with feedback (0.377), safety management commitment (0.281), and safety policy (0.110). The overall effects of each LSB variable on safety participation in descending order were: safety training (0.706), safety incentives (0.496), safety management commitment (0.365), and safety policy (0.247). Furthermore, we found that safety management commitment and safety incentives increased employees' safety behaviours, but this influence was mediated by safety training, safety policy, and safety communication with feedback.

What Influences Miners' Safety Risk Perception?

The risks faced by the mining industry have always been prominent for every walk of life in China. As the direct cause of accidents, individual unsafe behaviors are closely related to their risk perception. So, it is important to explore the factors affecting miners' risk perception and analyze the influencing mechanisms between these factors and risk perception. The questionnaire survey method was used to collect the data of risk perception from nearly 400 respondents working in metal mines in China. Exploratory factor analysis and confirmatory factor analysis were used to analyze and process collected data. The impact of four factors affecting miners' risk perception was verified, namely: organizational safety atmosphere, organizational trust, knowledge level, and risk communication. Then, regression analysis, Pearson correlation analysis, and structural equation model analysis were used to examine the effect of the four influencing factors on miners' risk perception. The four influencing factors all have a positive impact on miners' risk perception; knowledge level has the largest explained variation of miners' risk perception, followed by risk communication. Organizational trust and organizational safety atmosphere have an indirect and positive impact on miners' risk perception intermediated by knowledge level and risk communication. The results offer four important aspects of mine safety management to help miners establish quick and accurate risk perception, thereby reducing unsafe behaviors and avoiding accidents.

[Compound porcine cerebroside and ganglioside relieves brain injury and promotes expression of cerebellin 4 in neonatal mice with intrauterine hypoxia].

Objective To study the effects of compound porcine cerebroside and ganglioside injection (CPCGI) on brain injury and expression of cerebellin 4 (CBLN4) in neonatal mice after intrauterine hypoxia. Methods A total of 15 healthy adult pregnant mice were randomly divided into 3 groups: control group with 3 mice, model group and CPCGI treatment group with 6 mice in each group. From the 14th day of pregnancy, the pregnant mice in the CPCGI treatment group and model group were put into the animal hypoxia box to produce the intrauterine hypoxia fetal mouse models. After the delivery of mother, the neonatal mice in the CPCGI treatment group and model group were given CPCGI (1 mL/kg) and PBS via abdominal cavity, respectively, while the control group received no treatment. At 40 days postpartum, the memory ability of mice was trained with a platform jumper test. After the platform test, the brain tissue of the mice was taken out. The expression of neurogenolase (NSE), interleukin-1 beta (IL-1ß), CBLN4 and synaptophsin (SYN) were detected by immunofluorescence staining. The relative expression of CBLN4 protein in the hippocampus of mice was detected by Western blot analysis. Results Compared with the control group, hypoxia caused a significant decrease in learning and memory ability of newborn mice, and CPCGI could significantly improve the memory of mice. After hypoxia, the expression of NSE, CBLN4 and SYN in the neonatal cerebellum significantly decreased, and the expression of IL-1ß significantly increased. The expression of NSE, CBLN4 and SYN in CPCGI treatment group was significantly higher than those in the model group, and the expression of IL-1ß was significantly lower than that in the model group. Conclusion CPCGI can reduce neuronal damage in neonatal mice after hypoxia, which may be related to the reduction of IL-1ß expression and the promotion of synaptic reconstruction.

[Sophoridine inhibits the proliferation of human gastric cancer MKN45 cells and promotes apoptosis].

The purpose of the study was to investigate the effect of sophoridine on the proliferation and apoptosis of human gastric cancer MKN45 cells and the possible mechanism. MKN45 cells were randomly divided into control and sophoridine (including 6 subgroups) groups. Cell proliferation was detected by methyl thiazolyl tetrazolium (MTT) colorimetric method. The protein expression of high mobility group-box 3 (HMGB3) was observed by immunocytochemical staining and Western blot. Hoechst 33342 staining method was used to observe the morphological changes of cells treated with sophoridine. Apoptosis was detected by flow cytometry. The results showed that the proliferation of cells was inhibited by 48-hour treatment of sophoridine in a dose-dependent manner. Compared with control group, sophoridine group showed decreased HMGB3 protein expression and increased apoptotic rate. These results suggest that sophoridine can inhibit the proliferation of MKN45 cells and promote their apoptosis, which may be related to down-regulation of HMGB3 protein expression.

[Effect of chondroitinase ABC on growth associate protein 43 and glial fibrillary acidic protein after spinal cord injury in rats].

OBJECTIVE: To investigate the effect of chondroitinase ABC (ChABC) on the expression of growth associated protein 43 (GAP-43) and glial fibrillary acidic protein (GFAP) after spinal cord injury (SCI) in rats. METHODS: A total of 150 adult female SD rats, weighing 250-300 g, were randomly divided into ChABC treatment group (group A), saline treatment group (group B), and sham operation group (group C) with 50 rats in each group. In groups A and B, the rats were made the SCI models and were treated by subarachnoid injection of ChABC and saline; in group C, the rats were not treated as a control. At 1, 3, 7, 14, and 21 days after operation, the Basso, Beattie, and Bresnahan (BBB) score system was used to evaluate the motion function, and immunofluorescent histochemical staining was used to observe the expressions of GAP-43 and GFAP. RESULTS: At different time points, the BBB scores of groups A and B were significantly lower than those of group C (P < 0.05); there was no significant difference in BBB score between groups A and B after 1, 3, and 7 days of operation (P > 0.05), but the BBB score of group A was significantly higher than that of group B after 14 and 21 days of operation (P < 0.01). At different time points, the GAP-43 and GFAP positive neurons of groups A and B were significantly higher than those of group C (P < 0.05). After 14 and 21 days of operation, the GAP-43 positive neurons of group A were more than those of group B (P < 0.01). After 7, 14, and 21 days of operation, the GFAP positive neurons of group A were significantly less than those of group B (P < 0.01). CONCLUSION: ChABC can degrade glial scar, improve the microenvironment of the injured region and enhance the expression of GAP-43, which promotes axonal growth and extension.