Impact of background music on reading comprehension: influence of lyrics language and study habits.

Numerous studies have explored the effects of background music on reading comprehension, however, little is known about how native language (L1) lyrics and second language (L2) lyrics in background music influence reading comprehension performance for college students. The present study used a mixed experimental design to examine the effects of listening habits (between-participants variable: non-listeners or listeners), music type (between-participants variable: L1 (Mandarin) pop music, L2 (English) pop music or no music) and text language (within-participants variable: L1 or L2) on reading comprehension of college students in East China. A total of 90 participants (50 females) were screened into non- listeners (n = 45) and listeners (n = 45), and then were randomly assigned to one of three groups: Mandarin pop music group (n = 30), English pop music group (n = 30) and no music group (n = 30). The results showed that reading comprehension performance was negatively affected by music with lyrics compared to the no music condition. Furthermore, Chinese/English reading comprehension was reduced more by pop music in the same language as the written texts. As expected, non-listeners were more negatively affected by music with lyrics than listeners. For both listeners and non-listeners, average reading comprehension accuracy rates were the lowest in the condition of music with native language lyrics. Overall, our research findings indicate that listening to pop music with lyrics reduces reading comprehension performance. However, listening to background music cause much less distraction if the students commonly listen to music while reading. The current study supports the duplex-mechanism account of auditory distraction.

FGF2 cooperates with IL-17 to promote autoimmune inflammation.

IL-17 is a pro-inflammatory cytokine implicated a variety of autoimmune diseases. We have recently reported that FGF2 cooperates with IL-17 to protect intestinal epithelium during dextran sodium sulfate (DSS)-induced colitis. Here, we report a pathogenic role of the FGF2-IL-17 cooperation in the pathogenesis of autoimmune arthritis. Combined treatment with FGF2 and IL-17 synergistically induced ERK activation as well as the production of cytokines and chemokines in human synovial intimal resident fibroblast-like synoviocytes (FLS). Furthermore, ectopic expression of FGF2 in mouse joints potentiated IL-17-induced inflammatory cytokine and chemokine production in the tissue. In the collagen-induced arthritis (CIA) model, while ectopic expression of FGF2 in vivo exacerbated tissue inflammation and disease symptom in the wild-type controls, the effect was largely blunted in Il17a -/- mice. Taken together, our study suggests that FGF2 cooperates with IL-17 to promote the pathogenesis of autoimmune arthritis by cooperating with IL-17 to induce inflammatory response.

The microRNA miR-23b suppresses IL-17-associated autoimmune inflammation by targeting TAB2, TAB3 and IKK-α.

Inflammatory cytokines such as interleukin-17 (IL-17) promote inflammatory autoimmune diseases. Although several microRNAs (miRNAs) have been shown to regulate autoimmune pathogenesis by affecting lymphocyte development and function, the role of miRNAs in resident cells present in inflammatory lesions remains unclear. Here we show that miR-23b is downregulated in inflammatory lesions of humans with lupus or rheumatoid arthritis, as well as in the mouse models of lupus, rheumatoid arthritis or multiple sclerosis. IL-17 downregulates miR-23b expression in human fibroblast-like synoviocytes, mouse primary kidney cells and astrocytes and is essential for the downregulation of miR-23b during autoimmune pathogenesis. In turn, miR-23b suppresses IL-17-, tumor necrosis factor α (TNF-α)- or IL-1ß-induced NF-κB activation and inflammatory cytokine expression by targeting TGF-ß-activated kinase 1/MAP3K7 binding protein 2 (TAB2), TAB3 and inhibitor of nuclear factor κ-B kinase subunit α (IKK-α) and, consequently, represses autoimmune inflammation. Thus, IL-17 contributes to autoimmune pathogenesis by suppressing miR-23b expression in radio-resident cells and promoting proinflammatory cytokine expression.