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Nasal packing is frequently used after septoplasty and some complications caused by nasal packing are unavoidable. A nasal septal retainer has recently been developed. We evaluated the safety and clinical efficacy of the retainer in septoplasty, and the subjective symptoms of patients with the retainer were compared with Merocel nasal packing. A prospective, randomized, controlled study was performed in patients who had undergone septoplasty. In total, 39 patients were randomized to receive Merocel (n = 17) or the retainer (n = 22) after septoplasty. The deviation of nasal septum and nasal mucosa was evaluated by endoscopy. The clinical efficacy and subjective symptoms were compared using the visual analog scale. During the packing/retaining period, the mean scores of headache, nasal obstruction, epiphora, and facial pressure in the retainer group were significantly lower than in the Merocel group (P

Background Long noncoding RNAs (lncRNAs) are involved in a variety of human immune diseases. However, the expression profile and precise function of lncRNAs in allergic rhinitis (AR) remain unknown. In the present study, genome-wide analysis of lncRNA expression was performed in the nasal mucosa tissue and mRNA regulatory relationship was examined among patients with or without AR. Methods Microarray assays were performed and the differential expressions of lncRNAs or mRNA were verified through RT-PCR. The lncRNA functions were annotated using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). The potential regulatory relationships between lncRNAs and the co-expressed mRNAs were analyzed using Cytoscape software. The expressions of specific lncRNAs and mRNAs were examined using an in vitro cell model. Results A total of 57 lncRNAs and 127 mRNAs were dysregulated in the nasal mucosa tissue of patients with AR, compared to those of patients without AR (fold change > 2.0 and P P Conclusion The results of the present study suggest that lncRNAs participate in the biological pathways related to AR. Leukocyte transepithelial migration may be a potential target for lncRNAs to regulate allergic inflammation and CXCL12/CXCR4 axis plays an important role in the inflammatory process of AR.

Additional file 1: Table S1. Clinical characteristics of AR and non-AR patients.

// Chongze Yuan 1, 2, * , Hong Hu 1, 2, * , Muyu Kuang 1, 2, * , Zongwei Chen 4 , Xiaoting Tao 1, 2 , Shengjian Fang 1, 2 , Yihua Sun 1, 2 , Yawei Zhang 1, 2 and Haiquan Chen 1, 2, 3 1 Department of Thoracic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China 2 Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China 3 Institutes of Biomedical Sciences, Fudan University, Shanghai, China 4 Department of Thoracic Surgery, Zhongshan Hospital, Shanghai, China * These authors have contributed equally to this work Correspondence to: Yihua Sun, email: Sun_yihua76@hotmail.com Yawei Zhang, email: zhangyawei68@hotmail.com Haiquan Chen, email: hqchen1@yahoo.com Keywords: lung cancer; ChIP-seq; super enhancer; RAI14; targeted therapy Abbreviations: SE: super enhancer; TE: typical enhancer; TKIs: tyrosine kinase inhibitors; ChIP-seq: Chromatin Immunoprecipitation followed by high-throughput DNA sequencing; NSCLC: non-small cell lung cancer Received: December 23, 2016 Accepted: September 23, 2017 Published: October 27, 2017 ABSTRACT Purpose: Tyrosine kinase inhibitors (TKIs) are widely used to treat lung adenocarcinoma patients with EGFR mutations or ALK -fusions. However, patients with wild-type genes or TKIs-resistant mutations lack effective therapeutic targets. Extensive studies reveal that super enhancer (SE), a large cis -regulatory element, is associated with key oncogenes in a variety of cancers. By comparing the effect of SE on lung adenocarcinoma cell lines with normal cell line, this work attempts to find new biomarkers and potential therapeutic targets for lung adenocarcinoma. Experimental Design: Chromatin Immunoprecipitation (ChIP) followed by high-throughput DNA sequencing (ChIP-seq) of H3K27ac (acetylation on lysine 27 of histone 3) was performed in lung adenocarcinoma cell lines SPC-A1 and SCH-1153. The differences in SE distribution were then analyzed among SPC-A1, SCH-1153, A549 and normal human lung fibroblasts (NHLF) to identify SE-associated oncogenes. The expression of SE-associated oncogenes was then detected by RNA-seq and further verified in 71 patients by real-time PCR. Results: SE associated with many new oncogenes in lung adenocarcinoma, among which, RAI14 was up-regulated in A549 and 31 of 71 patients. High expression of RAI14 could inhibit cell proliferation, indicating its potential as a new biomarker for lung adenocarcinoma.

Peroxisome proliferator-activated receptor gamma (PPAR γ), is important in the immunoregulation of the allergic response. Mast cells are the most important inflammatory cells in immediate hypersensitivity and allergic diseases. However, there is limited information regarding the effects of PPAR γ on mast cell maturation. In the present study, mouse bone marrow‑derived mast cells (BMMCs) were cultured in interleukin (IL)‑3 and stem cell factor (SCF), in the presence or absence of the PPAR γ agonist, pioglitazone (PIO). The expression levels of the tyrosine kinase receptor CD117 and the high affinity IgE receptor FceRI α, were assessed by flow cytometry, cell viability was assessed by Alamar‑Blue assay and histamine release was determined by measuring the activity of β‑hexosaminidase. IL‑3 and SCF are required for the development of mast cells in vitro. PIO dose‑dependently inhibited the expression of CD117 and FceRI α, and the maturation of BMMCs. Treatment with PIO additionally inhibited the formation of granules and reduced the expression of β‑hexosaminidase. In addition, reverse transcription‑polymerase chain reaction analysis revealed that BMMCs treated with PIO expressed a lower level of mast cell protease (MCP)‑6 mRNA and PIO treatment enhanced the level of PPAR γ mRNA. Furthermore, PIO induced mast cell progenitor apoptosis. PPAR γ agonists may maintain mast cell homeostasis by inhibiting maturation of their precursors. The inhibitory effects of PPAR γ agonists include suppression of the activation of mast cells and a decrease in mast cell function in the inflammatory response. Therefore, PPAR γ agonists may serve as effective anti-inflammatory reagents in the treatment of allergic reactions.

Allergic rhinitis (AR) is a common chronic inflammatory condition. It has been previously indicated that oxidative stress may contribute to allergic inflammation, including AR. Although molecular hydrogen (H2), an antioxidative agent, has been effective in treatment of numerous oxidative stress-associated diseases, the effect of inhalation of a high concentration of H2 on AR remains unknown. In the current study, female BALB/c mice were sensitized with ovalbumin (OVA) followed by intranasal OVA challenge to establish an animal model of AR. Mice were subjected to exposure to H2 and the inert gas helium at different frequencies and durations. The frequencies of sneezing/scratching and the body weights of mice were recorded. Histological analysis and multiplex cytokine assays were performed to evaluate the effects of H2 on AR. Challenge with OVA induced significant nasal mucosa inflammation. H2 inhalation reduced the infiltration of inflammatory cells into mucosa and lowered the levels of interleukin (IL)-5, IL-13 and monocyte chemoattractant protein-1 in serum. H2 inhalation slightly increased the level of interferon-γ, however the difference was not statistically significant. Treatment with H2 limited the weight increase in healthy mice and reversed the weight loss in mice with AR. Furthermore, H2 inhalation induced a therapeutic effect on AR in a dose-dependent manner. The current results demonstrate that H2 may demonstrate a therapeutic value for allergic diseases.