Poststroke sudden sensorineural hearing loss (SSNHL) can hinder communication between patients and healthcare professionals, thereby restricting participation in rehabilitation programs and limiting improvements in physical performance. However, the relationship between stroke and SSNHL remains unclear. This study employed a nationwide population-based dataset to investigate the relationship between stroke and SSNHL. The Taiwan Longitudinal Health Insurance Database was used to compile data from 11,115 stroke patients and a comparison cohort of 33,345 matched nonstroke enrollees. Each patient was followed for 5 years to identify new-onset SSNHL. Stratified Cox proportional-hazard regression analysis was used to examine the association of stroke with subsequent SSNHL. Among the 44,460 patients, 66 patients (55,378 person-years) from the stroke cohort and 105 patients (166,586 person-years) from the comparison cohort were diagnosed with SSNHL. The incidence of SSNHL was approximately twice as high among stroke patients than among nonstroke patients (1.19 and 0.63/1000 person-years, respectively). Stroke patients had a 71% increased risk of SSNHL, compared with nonstroke patients (adjusted hazard ratio [HR] 1.71, 95% confidence interval [CI] 1.24–2.36). We also observed a remarkable increase in risk of SSNHL in stroke patients within 1-year of follow-up (adjusted HR 5.65, 95% CI 3.07–10.41) or under steroid therapy during hospitalization (adjusted HR 5.14, 95% CI 2.08–12.75). Patients with stroke had a higher risk of subsequent SSNHL compared with patients without stroke. In particular, stroke patients within 1-year follow-up and those undergoing steroid therapy during hospitalization should be treated with the utmost caution, considering that the risk of SSNHL increases by more than 5-fold.

Purpose: Sleep apnea (SA)-induced chronic intermittent hypoxia increases oxidative stress and inflammation, which may contribute to the pathophysiology of Parkinson’s disease (PD). This study evaluated the risk of PD following SA diagnosis. Patients and methods: This was a 3-year nationwide population-based matched cohort study using claims data from the National Health Insurance Research Database (NHIRD), Taiwan. We analyzed 1,944 patients diagnosed as having SA between 1997 and 2005 and a matched cohort of 9,720 non-SA patients from the NHIRD. Patients with a history of PD were excluded. Each patient was followed up for 3 years to evaluate subsequent PD development. Results: Of the 11,664 patients, 17 (0.9%) and 38 (0.4%) from the SA and matched non-SA cohorts, respectively, were subsequently diagnosed as having PD during follow-up. After adjustments for potential confounders, the SA cohort had a 1.85-fold higher risk of PD than the non-SA cohort (95% confidence interval [CI] =1.02–3.35; P=0.042). After age and sex stratification, PD development was independently associated with SA only in men (adjusted hazard ratio [HR], 2.26; 95% CI =1.11–4.63; P<0.05) and in patients aged ≥60 years (adjusted HR, 1.93; 95% CI =1.01–3.71; P<0.05). Conclusion: Our study suggests that patients with SA are at an increased longitudinal risk of PD. Furthermore, age and male sex are independently associated with the risk of PD.

Atopic Dermatitis (AD) is a chronic and relapsing skin disease. The medications for treating AD are still limited, most of them are topical corticosteroid creams or antibiotics. The current study attempted to discover potential AD treatments by integrating a gene network and genomic analytic approaches. Herein, the Single Nucleotide Polymorphism (SNPs) associated with AD were extracted from the GWAS catalog. We identified 70 AD-associated loci, and then 94 AD risk genes were found by extending to proximal SNPs based on r² > 0.8 in Asian populations using HaploReg v4.1. Next, we prioritized the AD risk genes using in silico pipelines of bioinformatic analysis based on six functional annotations to identify biological AD risk genes. Finally, we expanded them according to the molecular interactions using the STRING database to find the drug target genes. Our analysis showed 27 biological AD risk genes, and they were mapped to 76 drug target genes. According to DrugBank and Therapeutic Target Database, 25 drug target genes overlapping with 53 drugs were identified. Importantly, dupilumab, which is approved for AD, was successfully identified in this bioinformatic analysis. Furthermore, ten drugs were found to be potentially useful for AD with clinical or preclinical evidence. In particular, we identified filgotinub and fedratinib, targeting gene JAK1, as potential drugs for AD. Furthermore, four monoclonal antibody drugs (lebrikizumab, tralokinumab, tocilizumab, and canakinumab) were successfully identified as promising for AD repurposing. In sum, the results showed the feasibility of gene networking and genomic information as a potential drug discovery resource.

Asthma is a common and heterogeneous disease characterized by chronic airway inflammation. Currently, the two main types of asthma medicines are inhaled corticosteroids and long-acting β2-adrenoceptor agonists (LABAs). In addition, biological drugs provide another therapeutic option, especially for patients with severe asthma. However, these drugs were less effective in preventing severe asthma exacerbation, and other drug options are still limited. Herein, we extracted asthma-associated single nucleotide polymorphisms (SNPs) from the genome-wide association studies (GWAS) and phenome-wide association studies (PheWAS) catalog and prioritized candidate genes through five functional annotations. Genes enriched in more than two categories were defined as “biological asthma risk genes.” Then, DrugBank was used to match target genes with FDA-approved medications and identify candidate drugs for asthma. We discovered 139 biological asthma risk genes and identified 64 drugs targeting 22 of these genes. Seven of them were approved for asthma, including reslizumab, mepolizumab, theophylline, dyphylline, aminophylline, oxtriphylline, and enprofylline. We also found 17 drugs with clinical or preclinical evidence in treating asthma. In addition, eleven of the 40 candidate drugs were further identified as promising asthma therapy. Noteworthy, IL6R is considered a target for asthma drug repurposing based on its high target scores. Through in silico drug repurposing approach, we identified sarilumab and satralizumab as the most promising drug for asthma treatment.

Nephrolithiasis is a common disease affecting almost all populations, with an increasing prevalence over the past decades. Previous studies revealed several functional polymorphisms associated with the pathogenesis of nephrolithiasis. However, data on Asian populations are limited. In this study, three candidate polymorphisms were selected from previous studies to investigate the correlations with nephrolithiasis in a Taiwanese population. In total, 454 nephrolithiasis patients were recruited from Kaohsiung Medical University Hospital, with SNP frequency for 1513 subjects of general population from the Taiwan Biobank (TWB) as a genotypic reference. Results revealed that subjects with minor TT genotype at rs1256328 (alkaline phosphatase, liver/bone/kidney (ALPL)) have higher susceptibility to nephrolithiasis (odds ratio (OR) = 2.03, p = 0.0013). In addition, subjects carrying the minor AA genotype at rs12654812 (regulator of G protein signaling 14 (RGS14)) have higher susceptibility to nephrolithiasis (OR = 1.91, p = 0.0017). Among nephrolithiasis patients, subjects with GG at rs7627468 (calcium-sensing receptor (CASR)) have lower pH level in urine (p = 0.0088). Importantly, rs7627468 is associated with the expressions of IQCB1 and EAF2. rs12654812 could influence the expression of RGS14 itself, MXD3, and FGFR4. In summary, this study successfully validated the genetic roles of rs1256328 and rs12654812 in human nephrolithiasis.

Chronic rhinosinusitis (CRS) is defined as a state of inflammation that persists in the paranasal sinuses for 12 weeks or more.¹ Chronic rhinosinusitis is among the most prevalent chronic disease entities affecting the adult population,² with an estimated annual prevalence of 4.9% to 16%.^3,4 Inflammation of the sinonasal mucosa can cause obstruction of the sinus ostia as well as the opening of the eustachian tube, with subsequent impairment of middle ear pressure regulation.^5,6 Sinusitis has been detected in 78% of patients with repetitive and intractable otitis media with effusion.⁷ Evidence has shown that patients with CRS frequently develop middle ear disorders due to anatomic and functional connections.⁵ Existing evidence suggests that improvements or the resolution of middle ear disorders often follow the successful treatment of sinusitis.^8,9