Objective: To analyze the trend of disease burden of hearing loss attributable to occupational noise exposure in China from 1990 to 2021, so as to provide the evidence for optimizing noise prevention strategies and occupational health surveillance systems. Methods: Data on disability-adjusted life years (DALY) and age-standardized DALY rate (ASDR) for hearing loss attributable to occupational noise exposure in China from 1990 to 2021 were collected from the Global Burden of Disease 2021 database. The estimated annual percent change (EAPC) was used to analyze the trend in ASDR from 1990 to 2021. Results: From 1990 to 2021, the DALY for hearing loss attributable to occupational noise exposure in China increased from 1.279 7 million person-years to 2.683 9 million person-years, and the ASDR increased from 123.08/105 to 133.99 /105 (EAPC=0.324%, 95%CI: 0.296%-0.352%). From 1990 to 2021, the ASDR for hearing loss attributable to occupational noise exposure among males and females in China increased from 141.04/105 and 104.92/105 to 149.99/105 and 118.06/105, with EAPC values of 0.269% (95%CI: 0.231%-0.307%) and 0.413% (95%CI: 0.392%-0.433%). In 1990, the 60-65 years age group had relatively high DALY and ASDR, with 0.157 6 million person-years and 446.06/105, respectively. In 2021, the ≥70 years group had relatively high DALY of 0.434 7 million person-years, while the 60-<65 years group had relatively high ASDR of 510.64/105. Except for the 15-20 and 20-25 years groups, all other age groups showed an increasing trend in ASDR for hearing loss attributable to occupational noise exposure from 1990 to 2021. Among them, the ASDR increased faster in the 55-<60, 60-<65, 65-<70, and ≥70 years groups, with EAPC values of 0.364% (95%CI: 0.311%-0.417%), 0.459% (95%CI: 0.389%-0.529%), 0.564% (95%CI: 0.505%-0.623%), and 0.295% (95%CI: 0.212%-0.377%), respectively. Conclusions From 1990 to 2021, the disease burden of hearing loss attributable to occupational noise exposure in China showed an increasing trend. Males, the elderly had a higher disease burden, while the burden increased faster in females and middle-aged and elderly populations.

ObjectiveTo investigate the mechanism of protective effect of ethanol extracts of Hemsleya chinensis （HC-EE） on hydrochloric acid/ethanol （HCl/EtOH）-induced acute gastric ulcer in rats. MethodLipopolysaccharide （LPS）-induced RAW264.7 cells were used to evaluate inhibitory effect of HC-EE on the production of inflammatory mediators in vitro. A rat acute gastric ulcer model induced by HCl/EtOH （60% ethanol in 150 mmol·L^-1 HCl） was used to evaluate protective effect of HC-EE on acute gastric ulcer. Rats were divided into five groups， including normal group， model group， HC-EE low dose （HC-EE 30， 30 mg·kg^-1） group， HC-EE high dose （HC-EE 60， 60 mg·kg^-1） group and ranitidine （35 mg·kg^-1） group. For model and drug-treated groups， vehicle solvent or drugs were orally administered twice daily for 7 consecutive days before the rats were subjected to HCl/EtOH to induce acute gastric ulcer. After being anesthetized， ulcer surface of each rat was obtained and recorded using electronic imaging technology， and the ulcer inhibition rate was calculated by ImageJ 1.8.0. Hematoxylin-eosin （HE） and periodic acid-Schiff （PAS） staining were used to observe the pathological histological changes in rats. Content of nitric oxide （NO） in cell culture medium was measured by the Griess method. The levels of interleukin-1β （IL-1β）， tumor necrosis factor-α （TNF-α）， IL-6， vascular cell adhesion molecule-1 （VCAM-1） and prostaglandin E₂ （PGE₂） in rat serum （or cell culture medium） were determined by enzyme linked immunosorbent assay （ELISA）. The protein expressions of phosphorylation （p）-p38 mitogen activated protein kinase （MAPK）/p38 MAPK and p-nuclear transcription factor-κB （NF-κB） p65/NF-κB p65 in rat gastric tissue were detected by Western blot. ResultIn vitro assay showed HC-EE could significantly down-regulate the expressions of NO， TNF-α， IL-1β， IL-6 and VCAM-1 in LPS-induced cells （P<0.05， P<0.01）. In vivo experimental results showed that， compared with the normal group， gastric tissue of the model group was severely damaged， and the area of gastric ulcer was significantly enlarged， levels of TNF-α， IL-6 were significantly increased （P<0.01）， and the level of PGE₂ was significantly decreased （P<0.01）， the phosphorylation levels of of p38 MAPK， NF-κB p65 in gastric tissue were significantly increased （P<0.01）. Compared with the model group， HC-EE dose-dependently improved HCl/EtOH-induced gastric tissue injury and inflammatory cell infiltration， and it could increase ulcer inhibition rate， significantly decreased the release of TNF-α and IL-6 （P<0.01）， HC-EE 60 group could increase the content of PGE₂ （P<0.05）， and significantly inhibit the phosphorylation levels of p38 MAPK and NF-κB p65 （P<0.05， P<0.01）. ConclusionHC-EE can exert protective effect on HCl/EtOH-induced acute gastric ulcer in rats， and its mechanism may be related to the inhibition of expression of inflammatory mediators mediated by p38 MAPK/NF-κB signaling pathway.