Background and objectives Juvenile idiopathic arthritis (JIA), an autoimmune disease, has been proposed to be comorbid with obstructive sleep apnoea (OSA). We aimed at testing the hypothesis that patients with JIA may presented with high risk of OSA in a cohort study. Subjects and methods This is a cohort study including patients with JIA from 1999 to 2013 identified from a longitudinal health registry. A matched non-JIA control group was also included. The primary outcome variable was presence of OSA. A Cox proportional hazard model was developed to estimate the risk of OSA in patients with JIA. A cumulative probability model was adopted to assess the time-dependent effect of JIA on OSA development, implying a causal link of the association. Results A total of 2791 patients with JIA were included, and 11 164 individuals without JIA were selected as matched controls. A total of 95 included subjects had OSA: 31 in the JIA group and 64 in the control group. Patients with JIA were more likely to have OSA compared with controls (adjusted hazard ratio, aHR = 1.922, 95% confidence interval [CI] = 1.244–2.970). The incidence of developing OSA was particularly high among patients with JIA-associated deformity that presented at age 18–30 years (aHR = 1.993, 95% CI = 1.277–3.113) and males (aHR = 1.786, 95% CI = 1.097–2.906). The risk of developing OSA increased over 60 months (aHR = 2.523, 95% CI = 1.322–4.815) of follow-up after the JIA diagnosis. Conclusions Patients with JIA have a significantly increased risk of developing OSA compared with matched individuals without JIA.

Background: Metastasis is a severe problem in patients with oral squamous cell carcinoma (OSCC), which is the fifth most common cancer worldwide. Leukemia inhibitory factor (LIF) has been studied in different cancers, while the role of LIF in OSCC remains unclear. Methods: LIF expression was detected in 100 OSCC samples by immunohistochemistry. Effects of LIF on cell motility were evaluated in OSCC cell lines. High-throughput microarray analysis was also conducted. The correlation between LIF and the downstream effector was analyzed by real-time quantitative reverse transcription PCR. Results: Patients with OSCC who had lymph node metastasis or advanced cancer stages showed high LIF expression. OSCC patients with higher LIF expression, advanced stage, large tumor size, or lymph node metastasis had significantly shorter overall survival. LIF regulated cancer cell motilities through outside-in signaling. The inhibin beta A subunit (INHBA) gene was identified as a crucial downstream effector of LIF-promoted OSCC progression and restored migration and invasion abilities in LIF knockdown transfectants. Conclusion: LIF enhances regional lymphatic spread, thus leading to an advanced cancer stage. Regulation of LIF downstream molecules such as INHBA inhibits the invasion or migration ability of cancer cells. Thus, LIF can be a potential target in preventing cancer metastasis and spread.