ABSTRACT
Objective: To analyze the clinical and imaging characteristics of stage Ⅰ occupational cement pneumoconiosis patients. Methods: In October 2021, the data of patients with occupational cement pneumoconiosis diagnosed by the Third Hospital of Peking University from 2014 to 2020 were collected, and the data of the patients' initial exposure age, dust exposure duration, diagnosis age, incubation period, chest X-ray findings, lung function and other data were analyzed retrospectively. Spearman grade correlation was used for correlation analysis of grade count data. The influencing factors of lung function were analyzed by binary logistic regression. Results: A total of 107 patients were enrolled in the study. There were 80 male patients and 27 female patients. The inital exposure age was (26.2±7.7) years, the diagnosis age was (59.4±7.9) years, the dust exposure duration was (17.9±8.0) years, and the incubation period was (33.1±10.3) years. The initial dust exposure age and the dust exposure duration in female patients were less than those in men, and the incubation period was longer than that in men (P<0.05). The imaging analysis showed the small opacities as"pp"accounted for 54.2%. 82 patients (76.6%) had small opacities distributed in two lung areas. The lung areas distribution of small opacities in female patients was less than that in male patients (2.04±0.19 vs 2.41±0.69, P<0.001). There were 57 cases of normal pulmonary function, 41 cases of mild abnormality and 9 cases of moderate abnormality. The number of lung regions with small opacities on X-ray was the risk factor for abnormal lung function in cement pneumoconiosis patients (OR=2.491, 95%CI=1.197-5.183, P=0.015) . Conclusion: The patients with occupational cement pneumoconiosis had long dust exposure duration and incubation period, light imaging changes and pulmonary function damage. The abnormal lung function was related to the range of pulmonary involvement.
Subject(s)
Humans , Female , Male , Adolescent , Young Adult , Adult , Middle Aged , Aged , Retrospective Studies , Pneumoconiosis , Dust , Hospitals , Image Processing, Computer-AssistedABSTRACT
OBJECTIVE: To investigate the induction and activation of heparinase by extracellular histones in acute respiratory distress syndrome(ARDS) induced by chlorine in mice.METHODS: The specific pathogen free adult male C57 BL/6 mice were randomly divided into control group, chlorine injured group, histone injured group, anti-histone antibody group and heparinase inhibitor group, with six mice in each group.The mice in the control group and histone injured group were exposed to clean air, and the mice in the other three groups were exposed to chlorine gas at a dose of 580.0 mg/m~3 for 30 minutes by systemic dynamic inhalation.Mice in the histone injured group were injected with 50 mg/kg body weight calf thymus histone by tail vein.One hour before exposure, mice in the anti-histone antibody group were pretreated with 20 mg/kg body weight anti-histone H4 antibody by tail vein injection, and mice in the heparinase inhibitor group were injected with 2 mg/kg body weight OGT2115(heparinase inhibitor). The other three groups were given equal volume of 0.9% sodium chloride solution by tail vein injection. After 24 hours of exposure, arterial blood was collected for blood gas analysis and the lung tissue was collected for histopathological examination. The protein level of heparinase in lung tissue were detected using enzyme-linked immunosorbent assay, and the activity of heparinase were detected by measuring the product of heparan degradation. The protein expression of pro-heparinase and active heparinase were detected by Western blotting.RESULTS: The dyspnea developed of mice in the chlorine injured group and histone injured group, diffuse inflammation occurred in lung tissue, the oxygenation index in arterial blood decreased(all P<0.05), and the protein level and activity of heparinase in lung tissue, as well as the relative expression of pro-heparinase and active heparinase were increased compared with the control group(all P<0.05). The dyspnea, hypoxemia and acute lung injury of mice in the anti-histone antibody group were alleviated, and the protein level of heparinase in lung tissue, as well as the relative expression levels of pro-heparinase and active heparinase were decreased(all P<0.05), compared with chlorine injury group and histone injury group.The dyspnea, hypoxemia and acute lung injury were alleviated in the heparinase inhibitor group, and the activity of heparinase and the relative expression of pro-heparinase in the lung tissue were decreased compared with the chlorine injury group(all P<0.05). CONCLUSION: During the occurrence and development of chlorine-induced ARDS in mice, extracellular histones aggravate lung injury by inducing the expression and activation of heparinase. Acute lung injury can be alleviated by inhibiting the expression and activation of heparinase.