Ectopic expression of microRNA (miRNA) in rheumatoid arthritis (RA) fibroblast-like synoviocyte (RA FLS) is associated with the development of rheumatoid arthritis. The present study aimed to evaluate the effects of miRNA-140-5p (miR-140) on the properties of RA FLSs. It was found that miR-140 expression was decreased in 33 RA patients and extracted RA FLS samples, when compared to the corresponding healthy controls. Abnormally increased miR-140 expression in RA FLSs attenuated cell proliferation and increased cell apoptosis. Additionally, reduced pro-inflammatory cytokine production was observed in RA FLSs transfected with a miR-140 precursor. Furthermore, the 3'-UTR of the signal transducer and activator of transcription (STAT) 3 gene was identified as a target of miR-140. Notably, restoration of STAT3 expression rescued the regulatory effect of miR-140 on the proliferation, apoptosis and inflammatory cytokine production of RA FLSs. Therefore, the current findings indicated that miR-140 is a crucial modulator of both proliferation and apoptosis, shedding light on the etiology behind RA FLS viability, which is modulated by an interplay between miR-140 and STAT3 in the context of RA.

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Objective To investigate the association between sleep disturbances and behavioral problems as well as quality of life (QOL) in Chinese children with epilepsy. Methods Caregivers of 167 epileptic children aged 3 to 12 years completed the Child Sleep Habits Questionnaire (CSHQ), the Strengths and Difficulties Questionnaire (SDQ), and the Pediatric Quality of Life Inventory (PedsQL™, 4.0 Core). Results The prevalence of sleep disturbances (CSHQ total score >41) in epileptic children was 73.7% [95% CI (66.9%.80.4%)]. Epileptic children with sleep disturbances demonstrated more behavioral problems and lower QOL compared to those without sleep disturbances. Sleep disturbances such as sleep anxiety and daytime sleepiness were associated with more behavioral problems and lower QOL ( p <0.05). Linear regression analyses showed that higher disturbance in sleep duration domain were associated with more behavioral problems, while higher sleep disordered breathing domains was associated with lower QOL ( p <0.05). The interaction between sleep disturbances and behavioral problems in predicting QOL was not significant. The sensitivity analysis using 48 as an alternative cutoff for CSHQ total score obtained consistent results. Conclusion Sleep disturbances occur frequently among Chinese children with epilepsy, and are associated with more behavioral problems and lower QOL. The sleep disturbance-QOL association is unlikely contingent on behavioral problems. This study highlights the necessity of evaluating and treating sleep disturbances multidimensionally among children with epilepsy to promote their whole health and wellbeing.

NOX may play an important role in the integration of the redox signal in the oxidative molecular regulation mechanism in PKU.

Phenylketonuria (PKU) is the most frequent inherited disorder of amino acid metabolism. In our previous work, we investigated the role of NADPH oxidase (NOX) in a Pahenu2-BTBR PKU mouse model, and an in vitro cell culture model of PKU. In the current study, we evaluated various oxidative stress parameters, namely total antioxidant capacity (T-AOC), glutathione (GSH) and maleic dialdehyde (MDA) in the plasma of 40 PKU children, for further investigating the oxidative molecular regulation mechanism of NOX in PKU. It was observed that T-AOC and GSH markedly decreased in PKU as compared with the control group (P<0.01), and seemed to correlate negatively with Phe level. However, there was no statistical difference in MDA level among the three groups. And 8-isoprostane in the blood samples of PKU2 groups was slightly higher than control group (P<0.05). Additionally, mRNA levels of subunits of NOX included p47(phox) and p67(phox) significantly increased in PKU group (P<0.01). These results reflected that NOX is the important source of reactive oxygen species and is involved in the oxidative molecular regulation mechanism in PKU, which shows a new perspective toward understanding the biological underpinnings of PKU.