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Objective: To explore the effect of simulated gas of thermobaric bomb charge explosion on cognitive function and the related mechanism of damage. Methods: In January 2022, thirty-two SPF rats were selected and randomly divided into control group, exposed group 1, 2 and 3 (the exposure time of the simulated gas of the explosion of the thermobaric bomb charge was 5 min, 10 min and 15 min, respectively) according to random number table method, with 8 rats in each group. The simulated gas of the explosion of the thermobaric bomb charge were CO 0.15%, CO(2) 3%, NO 0.1%, O(2) 15%, and the rest were N(2). After 30 days of exposure, water maze was used to detect the learning and memory function of rats. Golgi staining was used to observe the number distribution and morphological structure of hippocampal neurons in rats. Western blot was used to detect the expression of Tau-5, pSer262, pSer396, pThr181 and pThr231 proteins in rats. Repeated measure ANOVA was used to compare the design data of repeated measure, one-way ANOVA was used for multi-group mean comparison, and LSD method was used for pound-wise comparison. Results: There were significant differences in the results of repeated measurement ANOVA of the water maze localization navigation test ( F =80.98, P <0.001), and there was an interaction between the group and the training days ( F =2.16, P =0.022). There were significant differences in escape latency of rats at the 2nd, 3rd, 4th and 5th days among all groups ( P <0.05). The results of spatial exploration showed that the frequency of rats crossing the platform was significantly different among all groups ( F =4.49, P =0.011). The frequency of rats crossing the platform in exposed group 2 and exposed group 3 was lower than that in control group, and the frequency of rats crossing the platform in exposed group 3 was lower than that in exposed group 1 ( P <0.05). With the increase of exposure time, the number of hippocampal neurons decreased, and the dendrite spine density of neurons in CA1 region decreased ( P <0.05). Compared with the control group, there was no significant difference in the relative expression level of Tau-5 protein in all exposed groups ( P >0.05), but the expression level of pSer262 protein was significantly increased ( P <0.05). Compared with the control group, the protein expressions of pSer396, pThr181 and pThr231 in exposed group 2 and exposed group 3 were significantly increased ( P <0.05) . Conclusion: The simulated gas of the explosion of the thermobaric bomb charge may contribute to the development of cognitive dysfunction by damaging hippocampal neurons with aberrant phosphorylation of Tau proteins.

Objective: To explore the effect of nerve injury in rats by neurobehavioral experiments, in order to provide a model and idea for further clarification of the traumatic brain injury mechanism under explosion exposure. Methods: From May 2021 to August 2022, 160 SPF male rats were randomly divided into four groups, including control group, 60 kPa group (low intensity group), 90 kPa group (medium intensity group) and 120 kPa group (high intensity group). The blast induced traumatic brain injury (bTBI) model of rats was established by using the shock tube platform to simulate the shock wave parameters of the explosion overpressure of 60 kPa, 90 kPa and 120 kPa. Acute observation was carried out after 24 h and 7 d of explosive exposure, and chronic recovery observation was carried out after 28 d and 90 d. The time effect of shock wave brain injury in different situations was discussed by open field, light dark test, active avoidance test. Finally, the results of brain injury in rats were detected by pathological tissue staining. Results: After 24 h explosion exposure, compared with the control group, the rest time of rats in low and high intensity groups increased, the total movement distance decreased, and the number of visits to the camera obscura decreased, with statistical significance ( P <0.05). After 7 days of exposure, compared with the control group, the rest time of rats in high intensity group increased, and the number of visits to the obscura decreased, with statistical significance ( P <0.05). After 28 and 90 days of exposure, compared with the control group, there were no significant differences in rest time, total exercise distance and times of visiting the camera obscura in all intensity groups ( P >0.05). After 24 h of explosive exposure, compared with the control group, the cell morphology of rats in each intensity group was normal, and no inflammatory cell infiltration was observed. Conclusion: In the acute phase (24 h) of blast exposure, rats have no desire to explore the outside world, and shock wave exposure may damage the neurological function of rats.

Objective: To evaluated the potential developmental toxicity and teratogenicity of ammonium dinitroamide (ADN) by micromass test (MM Test) and embryonic stem cell test models. Methods: In September 2018, rat embryos were isolated and limb bud cells were collected. The limb bud cells were treated with different concentrations of ADN (0, 312.50, 625.00, 1250.00, 2500.00, 5000.00, 10000.00 μg/ml) . Half proliferation inhibitory concentration and half differentiation inhibitory concentration were calculated and the teratogenic effects were evaluated according to the criteria. For the embryonic stem cell test, the effects of different concentrations of ADN (0, 39.06, 78.13, 156.25, 312.50, 625.00, 1250.00, 2500.00 μg/ml) on the differentiation of mouse embryonic stem cells (mESCs) into myocardial cells and the cytotoxicity of mESCs and 3T3 cells were detected. The embryonic toxicity was evaluated according to the criteria. In this study, both 5-fluorouracil (5-FU) , a known strong embryonic toxic drug, and penicillin-G (P-G) , a non-embryonic toxic drug, were used to verify the effectiveness of the model, and the validated test model was applied to evaluate the embryonic toxicity of ADN. Results: In the MM Test, the inhibition rates of proliferation and differentiation of limb bud cells in ADN groups were higher than that in control group ( P <0.05) . And the half proliferation inhibitory concentration and half differentiation inhibitory concentration of ADN on limb bud cells were 7480.32 and 4526.09 μg/ml, respectively. ADN was determined to be non-teratogenic by standard. In the embryonic stem cell test, the inhibition rates of mESCs proliferation in ADN groups were higher than that in control group, and the inhibition rates of 3T3 cells in 156.25, 312.50, 625.00, 1250.00, 2500.00 μg/ml ADN groups were higher than that in control group ( P <0.05) . The half proliferation inhibitory concentration and half differentiation inhibitory concentration of ADN on mESCs were 1851.73 and 1796.39 μg/ml, respectively, and the half proliferation inhibitory concentration on 3T3 cells was 3334.35 μg/ml. ADN was determined to be non-embryotoxic by standard. Conclusion: After evaluation by MM Test and embryonic stem cell models, ADN has no embryo toxicity and is a non-teratogenic substance.

Objective: To investigate the current situation of exposure of solid particles in medical staff and the occurrence of related diseases, and to understand the distribution characteristics of occupational exposure and the influencing factors. Methods: In August 2016, the stratified cluster sampling method was adopted to select three tertiary general hospitals with different regions, different administrative levels and departments in Shandong Province. A face-to-face questionnaire survey was conducted on the basic situation of the staff of the hospital, the status of exposure to occupational hazards and the health effects. Two-class logistic regression analysis was used to analyze the relationship between medical staff's solid particle contact and occupational health effects. In August 2016, the stratified cluster sampling method was adopted to select three tertiary general hospitals with different regions, different administrative levels and departments in Shandong Province, which were in contact with the basic conditions and occupational hazards of the staff of the hospital. Current situation and health impacts were conducted face-to-face questionnaires. Two-class logistic regression analysis was used to analyze the relationship between medical staff's solid particle contact and occupational health effects. Results: The overall contact rate of solid particles of medical staff was 41.5% (1843/4 446) , and the solid particles with the highest contact rate were 28.2% (1254/4 446) of talc dust. There was a statistically significant difference in the contact rate of solid particles between medical staff of different occupations, current working age, education and hospital type (χ(2)=76.30, 41.26, 26.16, 188.97, P <0.05) . There were significant differences in the conditions and types of solid particles in different departments (χ(2)=740.23, P <0.05) . Compared with the control group, the incidence of allergic asthma, chronic tracheobronchitis and dermatitis was higher in the contact group medical staff ( P <0.05) . Contact with zirconia dust, talc dust, cotton dust is a risk factor for dermatitis in medical staff ( OR =2.09, 1.45, 1.34) ; exposure to zirconia dust and cotton dust is a risk factor for chronic tracheobronchitis in medical staff ( OR =2.38, 1.66) ; exposure to zirconia dust, gypsum dust is a risk factor for allergic asthma in medical staff ( OR =3.90, 1.52) . Conclusion: The contact rate of solid particles in medical staff is high, and there are many types of contact. Frequent contacted with solid particles is a dangerous cause of related diseases. The working environment of medical staff should be further monitored and be strengthen the targeted protective measures and regulatory systems for the exposure of medical personnel to solid particles.

Objective: To investigate the relationship between mRNA expression of manganese superoxide dismutase (MnSOD) and manganese neurotoxicity., Methods: Thirty-one patients with occupational chronic manganese poisoning (case group), as well as 31 controls exposed to the same condition (control group), were included in the study. Whole blood RNA was extracted, and the mRNA expression of MnSOD was measured by RT-PCR; the two groups were compared in terms of the mRNA expression of MnSOD. PC12 cells were treated with 0, 100, 200, 400, 600, 800, and 1000 ümol/L MnCl₂ for l, 2, 3, and 4 d; the cell viability was determined by MTT assay, and the mRNA expression of MnSOD was measured by RT-PCR., Results: The case group had significantly lower mRNA expression of MnSOD than the control group (0.390 ± 0.080 vs 0.582 ± 0.219, P < 0.05). MnCl2 had a toxic effect on PC12 cells; the concentration of MnCl₂ was positively correlated with the toxic effect but negatively correlated with the mRNA expression of MnSOD., Conclusion: MnSOD mRNA may be involved in the manganese-induced damage of nerve cells. It is hypothesized that high mRNA expression of MnSOD may play an inhibitory effect on manganese neurotoxicity.