Association of ambient air pollution and Air Quality Index with risk of sudden sensorineural hearing loss: a cross-sectional study.

OBJECTIVES: To explore the associations of air pollutants and Air Quality Index (AQI) with risk of sudden sensorineural hearing loss (SSNHL) DESIGN: Cross-sectional study SETTING: Medical record data and local population data collected between 2014 and 2022 in Changshu, China were retrospectively reviewed. PARTICIPANTS: Adults aged 18 years and above who were diagnosed with SSNHL in Changshu No. 1 People's Hospital or Changshu No. 2 People's Hospital from the spring of 2014 to the fall of 2022 were included in the study. OUTCOME MEASURE: SSNHL was diagnosed by clinicians using the Chinese diagnostic criteria for SSNHL. RESULTS: Compared with those exposed to the lowest tertile of carbon monoxide (CO), the prevalence ratio for those exposed to middle and high tertiles of CO were 1.113 (95% CI 1.022 to 1.213) and 1.230 (95% CI 1.105 to 1.369), respectively. The risk of SSNHL was increased by 30.6% (95% CI 9.9% to 55.4%) per doubling increment of CO. No categorical association was found between ozone (O3) exposure and risk of SSNHL, however, an increased risk of 22.2% (0.8%-48.2%) was identified for each doubling of O3. No association was identified between other pollutants and AQI and risk of SSNHL. CONCLUSIONS: In this study, CO and O3 were associated with an increased risk of SSNHL in Changshu, China. Further studies are warranted to confirm our findings.

In Vitro and In Vivo Analyses Reveal Tumor-Derived Exosome miR-558 Promotes Angiogenesis in Tongue Squamous Cell Carcinoma by Targeting Heparinase.

This study aimed to investigate the role of miR-558 in tumor angiogenesis by targeting heparinase (HPSE) in tongue squamous cell carcinoma (TSCC)-derived exosomes. In the present study, the role of exosome miR-558 in angiogenesis in vitro and in vivo was investigated by cell proliferation, migration, tube formation, subcutaneous tumor formation in mice, and in vivo Matrigel plug assay. The target genes of miR-558 were detected by means of dual luciferase assay. It was found that TSCC cells secrete miR-558 into the extracellular environment, with exosome as the carrier. Human umbilical vein endothelial cells (HUVEC) ingested exosomes, which not only increased the expression level of miR-558, but also enhanced their proliferation, migration, and tube formation functions. In vivo Matrigel plug assay demonstrated that TSCC cell-derived exosome miR-558 promoted neovascularization in vivo. Compared with negative control cells, TSCC cells overexpressing miR-558 formed subcutaneous tumors in nude mice, with larger volume, heavier mass, and more vascularization. Dual luciferase assay confirmed that HPSE was the direct target gene regulated by miR-558. HPSE promoted the proliferation, migration, and tube formation of HUVECs, and the knockout of HPSE could downregulate the pro-angiogenic effect of miR-558. In summary, miR-558 in TSCC exosomes promotes the proliferation, migration, and tube formation of HUVECs by targeting HPSE, and enhancing tumor angiogenesis.

Decoding gene expression signatures in mice trigeminal ganglion across trigeminal neuropathic pain stages via high-throughput sequencing.

Trigeminal neuropathic pain (TNP) arises due to peripheral nerve injury, the mechanisms underlying which are little known. The altered gene expression profile in sensory ganglia is critical for neuropathic pain generation and maintenance. We, therefore, assessed the transcriptome of the trigeminal ganglion (TG) from mice at different periods of pain progression. Trigeminal neuropathic pain was established by partial infraorbital nerve transection (pIONT). High-throughput RNA sequencing was applied to detect the mRNA profiles of TG collected at 3 and 10 days after modeling. Injured TG displayed dramatically altered mRNA expression profiles compared to Sham. Different gene expression profiles were obtained at 3 and 10 days after pIONT. Moreover, 314 genes were significantly upregulated, and 81 were significantly downregulated at both 3 and 10 days post-pIONT. Meanwhile, enrichment analysis of these persistent differentially expressed genes (DEGs) showed that the MAPK pathway was the most significantly enriched pathway for upregulated DEGs, validated by immunostaining. In addition, TG cell populations defined by single-nuclei RNA sequencing displayed cellular localization of DEGs at a single-cell resolution. Protein-protein interaction (PPI) and sub-PPI network analyses constructed networks and identified the top 10 hub genes for DEGs at different time points. The present data provide novel information on the gene expression signatures of TG during the development and maintenance phases of TNP, and the identified hub genes and pathways may serve as potential targets for treatment.