Airborne fine particulate matter with an aerodynamic diameter equal to or smaller than 2.5 μm (abbreviated as PM 2.5 ) increases the risk of nasal lesions, but the underlying molecular mechanism has not been fully elucidated. In the atmosphere, the composition of PM 2.5 collected varies in physical and chemical properties, which affects its damage to human health. Thus, we constructed artificial PM 2.5 particles based on actual PM 2.5 and investigated the in vivo effects of artificial PM 2.5 exposure on the oxidative stress, inflammatory response, and nasal mucosa morphology of rats. The results showed that artificial PM 2.5 is comparable in composition ratio, size, and morphology to actual PM 2.5 . This in vivo study indicated that artificial PM 2.5 exposure reduces total superoxide dismutase and glutathione peroxidase activities, elevates malondialdehyde content in the nasal mucosa, and induces increased levels of pro-inflammatory mediators, including interleukin-1, interleukin-6 and tumor necrosis factor-α. Our data shows that artificial PM 2.5 particles could be used for experimental study of PM 2.5 toxicology, ensuring that the physical and chemical properties of experimental PM 2.5 are relatively constant and allowing for repeatability of this research. Oxidative damage and inflammatory response may be the toxic mechanisms that cause nasal lesions after exposure to artificial PM 2.5 .

Background Cisplatin is a commonly used chemotherapeutic drug in clinics, and long‐term application will lead to hearing impairment. LLY‐283, an inhibitor of PRMT5, has not been reported in deafness. Our study aimed to explore the mechanism of LLY‐283 in hearing impairment. Materials and Methods First, we performed RNA‐seq (cisplatin in the experimental group and DMSO in the control group) to obtain the biological processes mainly involved in differentially expressed genes (DEGs). CCK‐8 and LDH experiments were used to observe the effect of LLY‐283 on cisplatin‐induced auditory cell injury. ROS experiment was used to monitor the impact of LLY‐283 on oxidative damage of auditory cells. Effect of LLY‐283 on apoptosis of auditory cells detected by TUNEL experiment. PCR and Western blotting were used to detect the expression of genes and proteins related to auditory cell apoptosis in LLY‐283 cells. Meanwhile, we explored the effect of LLY‐283 on the expression of PRMT5 in cisplatin‐induced hearing impaired cells at RNA and protein levels. Results Biological process analysis showed that DEGs were mainly enriched in the apoptotic process involved in morphogenesis (‐Log10 P = 3.71). CCK‐8 and LDH experiments confirmed that LLY‐283 could save cisplatin‐induced auditory cell injury. ROS experiments confirmed that LLY‐283 could rescue cisplatin‐induced oxidative damage to auditory cells. TUNEL experiments confirmed that LLY‐283 could protect cisplatin‐induced apoptosis of auditory cells. Meanwhile, LLY‐283 could inhibit the expression of PRMT5 in auditory cells induced by cisplatin. Conclusion LLY‐283 can rescue cisplatin‐induced auditory cell apoptosis injury. LLY‐283 can inhibit the increase in PRMT5 expression induced by cisplatin.

Objectives This large-scale case-control study aimed to explore the trace elements (Zn & Cu) and risk factors associated with tinnitus severity (mild and moderate-to-severe tinnitus).Methods The serum levels of Zn & Cu of participants were measured by inductively coupled plasma mass spectrometry (ICP-MS). The potential risk factors were analyzed by simple and multiple logistic regression analysis.

Background The incidence of oropharyngeal squamous cell carcinomas (OPSCC) has increased in recent decades, and human papillomavirus (HPV) infection is the main cause of OPSCC. The data regarding causes of death (CODs) are vitally important in informing follow-up strategies and revising treatment strategies to deal with any possible preventable treatment-related COD. However, limited studies have assessed the competing COD by HPV status in patients with OPSCC. Objective We aimed to analyze the distribution of the competing COD according to HPV status in OPSCC. Methods We retrospectively included stage I-IVB patients with OPSCC from the Surveillance, Epidemiology, and End Results database between 2010 and 2015. The association between HPV status and head and neck cancer–specific mortality (HNCSM), second primary cancer mortality (SPCM), and noncancer-caused mortality (NCCM) were analyzed. The chi-square test, Kaplan-Meier analysis, and Fine and Gray model were used for statistical analysis. Results We included 5852 patients in this study and 73.2% (n=4283) of them had HPV-related tumors. A total of 1537 (26.3%) patients died, including 789 (51.3%), 333 (21.7%), and 415 (27%) patients who died from head and neck cancer, second cancer, and noncancer causes, respectively. The 5-year HNCSM, SPCM, NCCM, and overall mortality were 14.7%, 6.5%, 7.7%, and 26.4%, respectively. Those with HPV-positive disease had a lower cumulative incidence of HNCSM (subdistribution hazard ratio [sHR] 0.362, 95% CI 0.315-0.417; P<.001), SPCM (sHR 0.400, 95% CI 0.321-0.496; P<.001), and NCCM (sHR 0.460, 95% CI 0.378-0.560; P<.001) than those with HPV-negative disease. The 5-year risk of HNCSM was 26.9% and 10.7% in those with HPV-negative and HPV-positive disease, respectively (P<.001). The 5-year risk of SPCM was 12.4% and 4.6% in those with HPV-negative and HPV-positive disease, respectively (P<.001). The 5-year risk of NCCM of death was 13.7% and 5.8% in those with HPV-negative and HPV-positive disease, respectively (P<.001). Using the Fine and Gray competing-risks model, our results show that those with HPV-negative tumors had a significantly higher risk of HNCSM (P<.001), SPCM (P<.001), and NCCM (P<.001) than those with HPV-negative tumors. Conclusions HPV-positive OPSCC has a lower NCSM, SPCM, and NCCM as compared to those with HPV-negative OPSCC. HPV positivity is a favorable prognostic factor in the context of overcoming cancer as well as in terms of reducing the risk of other CODs in OPSCC. Our finding supports the need to tailor patient follow-up based on the HPV status of patients with OPSCC.