Mexicanolide limonoids from the seeds of Khaya ivorensis with antimicrobial activity.

The methanol extract of the seeds of Khaya ivorensis afforded two new mexicanolide limonoids, ivorensines A and B (1 and 2), together with one known compound, ruageanin D (3). The structures of the isolated compounds were established based on 1 D and 2 D (1H-1H COSY, HMQC, and HMBC) NMR spectroscopy, in addition to high resolution mass spectrometry. The isolated limonoids were tested in vitro for antimicrobial potentials against 5 pathogenic microorganisms. As a result, compounds 1-3 exhibited antimicrobial activity against the tested Gram negative bacteria at the minimum inhibitory concentration values less than 50 µg/ml.

[Research on Quantitative Method for the Determination of Carbon Isotopic Composition of CO2 with Micro-Laser Raman Spectroscopy].

In this study, a series of 12CO2/N2 and 13CO2/N2 binary mixtures with various molar fraction ratios were synthesized. It was found that the Raman peak area ratios were proportional to molar fraction ratios. The linearity of the working curves was very good. Moreover, the slopes of working curves were regarded as Raman quantification factor (F12CO2 and F13CO2). The natural fluids only containing 12CO2 and N2 composition in the gas phase have been applied to estimate their molar fraction ratios when F12CO2 is 1.163 49. As F13CO2 and F12CO2 are equal to 1.610 86 and 1.163 49, their ratio (F13CO2/F12CO2) is 1.384 5. Based on the study of principles and feasibility of the method of laser Raman spectroscopy, the molar fraction ratio C12/C13 would be calculated using the product of A12CO2/A13CO2 (the ratio of Raman peak area) and F13CO2/F12CO2. In addition, man-made inclusions with known molar fraction ratios (C12/C13) were presented to testify the validity and precision of the method. The possibility of quantifying carbon isotopic composition of CO2 with Micro-Laser Raman Spectroscopy is demonstrated.

MicroRNA expression profile of mature dendritic cell in chronic rhinosinusitis.

OBJECTIVE: Chronic rhinosinusitis (CRS), which includes CRS without nasal polyposis (CRSsNP) and with nasal polyposis (CRSwNP), shows imbalance of helper T cells (Th) and regulatory T cells (Treg). The balance of Th and Treg cells is orchestrated by dendritic cells (DCs). Recent studies show functions of DCs can be regulated by microRNAs (miRNAs or miRs). This study is aimed to investigate miRNAs expression profiles of peripheral blood DCs in CRS. METHODS: Peripheral blood samples of 30 patients with CRS and 7 patients with nasal septum deviation alone were collected. CD14(+) monocytes were isolated from these samples and differentiated into dendritic cells (DCs). Small RNAs were extracted from mature DCs and reversely transcribed into cDNA by Mir-XTM miRNA First-Strand synthesis method. MiRNA microarrays were used for miRNA expression analysis. Microarray results were validated by real-time PCR performed on five top list target genes. RESULTS: MiRNA microarrays showed that DCs from different types of patients have different sets of differential expressed miRNAs when comparing with Controls; they also share 31 commonly changed miRNAs among all three groups of CRS patients. Of these 31 miRNAs, 5 miRNAs were up-regulated and 25 miRNAs were down-regulated in all three types of CRS, while MiR-1290 was down-regulated in CRSsNP but up-regulated in both atopic CRSwNP and non-atopic CRSwNP. CONCLUSIONS: By comparing miRNA gene expression patterns in 3 types of CRS patients, we have been able to identify candidate miRNAs that might mediate the core pathogenesis of CRS through regulating dendritic cells. These miRNAs could serve as potential therapeutic targets for CRS.

Effects of Integrative Neuromuscular Training Combined With Regular Tennis Training Program on Sprint and Change of Direction of Children.

OBJECTIVE: The aim of this study was to investigate the effects of integrative neuromuscular training (NMT) on sprint and the ability to change direction for children who are between the ages of 7 and 8 and beginning to play tennis. METHODS: Thirty-two participants were randomized into a training group (TG; n = 16) and a control group (CG; n = 16). All participants attended tennis classes twice a week for a continuous 8 weeks. In addition, the TG received NMT (e.g., 20-m sprints, running at four corners, rope ladder drills, etc.), which progressed in difficulty every 2 weeks. Pre-intervention and post-intervention measurements, including a 30-m sprint test, a 5-10-5 test, and a 3 × 10 m shuttle run test, were assessed by a Smartspeed laser timing gate system, while the spider agility test was evaluated with a stopwatch. RESULTS: Two-way repeated measures ANOVA found significant differences in the interaction between time and group among variables measured. Results were as follows: time in the 30 m sprint (F = 13.467, 95% CI = 7.163-7.506, p = 0.001, η 2 p = 0.310, Δ = 0.42 s); 5-10-5 test (F = 13.975, 95% CI = 8.696-9.017, p = 0.001, η 2 p = 0.318, Δ = 0.78 s); 3 × 10 m shuttle run (F = 7.605, 95% CI = 11.213-11.642, p = 0.01, η 2 p = 0.202, Δ = 0.77 s); and spider agility test (F = 34.555, 95% CI = 28.258-29.670, p < 0.001, η 2 p = 0.535, Δ = 3.96 s). The results demonstrated a greater decrease in sprint and change of direction (COD) time among the TG than the CG from pre-intervention to post-intervention. CONCLUSION: A regular tennis training combined with NMT program could produce greater improvement in a player's sprint and ability to change direction when introduced to childhood tennis beginners in a sensitive period, compared to tennis class intervention only.

IL-37 attenuates allergic process via STAT6/STAT3 pathways in murine allergic rhinitis.

Allergic rhinitis (AR) is a common upper airway allergic disease caused by allergens triggering a type 2 immune response. The imbalance of CD4+ T cell subsets is the essential immunological feature of AR, which is mainly characterized by the predominance of T helper (Th) 2 cells. Recent studies indicated that the anti-inflammatory factor interleukin (IL)-37 is involved in the immune regulation of AR. However, the mechanism of IL-37 acts on AR has not been fully elucidated. Thus, we sought to assess the protective role of IL-37 in AR and further explore the possible mechanism. An ovalbumin (OVA)-induced AR murine model was established. After IL-37 treatment, the allergic symptoms (sneezes and nasal rubbings), nasal mucosal infiltration with eosinophils, and serum IgE production were found significantly attenuated. For CD4+ T cell subsets, the proliferation and differentiation of Th2 and Th17 cells were restrained. The relevant effector cytokines of IL-4, IL-5, IL-6, and IL-17a protein expression and transcription factors GATA3 and RORγt mRNA levels were obviously decreased. However, IL-37 had no significant effect on Th1 and Treg response including in IFN-γ, IL-10, T-bet, and Foxp3 expression. Furthermore, IL-37 was found down-regulated the STAT6, STAT3, phospho-STAT6, and phospho-STAT3 expression. In conclusion, IL-37 alleviates allergic inflammation in AR possibly through repressing STAT6 and STAT3 signaling pathways.

Increased expression of IL-1R8 and a possible immunomodulatory role of its ligand IL-37 in allergic rhinitis patients.

Allergic rhinitis (AR) is a chronic inflammatory airway disease that is caused by an abnormal T cell response. T helper (Th)-17 cells and Th2 cells are the CD4+ T cell subsets implicated in the pathogenesis of AR. The suppression of excessive responses of these Th17 and Th2 cells has been reported to be an effective therapeutic approach to treat AR patients, and continuous efforts are being undertaken to find new methods to modulate the function of these cells. Recent studies have shown that IL-1R8 and its ligand IL-37 negatively regulate the immune response. In this study, we investigated the immunomodulatory the roles of IL-37/IL-1R8 axis in AR patients. We found that IL-1R8 expression was very low on dendritic cells (DCs) and resting CD4+ T cells but increased strongly on CD4+ T cells following T cell activation. Furthermore, IL-1R8 expression on CD4+ T cells was markedly higher in AR patients than in healthy controls. The IL-1R8 ligand IL-37 could act on CD4+ T cells to inhibit IL-17 and IL-4 production but could not influence DC-induced IL-17- and IL-4-producing CD4+ T cell responses. Meanwhile, recombinant IL-37 (rIL-37) did not influence IL-6, IL-1ß, and IL-10 production by DCs and expression of co-stimulatory molecules (including CD80, CD40, CD86 and HLA-DR) in DCs. Thus, IL-37 may regulate aberrant T cell immune response of allergic rhinitis mainly through CD4+ T cells, not DCs. The immunomodulatory roles of the IL-37/IL-1R8 axis indicate the therapeutic potential of this axis in AR.

Ovol2 gene inhibits the Epithelial-to-Mesenchymal Transition in lung adenocarcinoma by transcriptionally repressing Twist1.

BACKGROUND: Associated with recent achievements in therapy for advanced lung adenocarcinoma, there will still be an unmet medical need for effective treatment of stage IIIb/IV, and the prognosis of lung cancer is not optimistic till now. OBJECTIVE: In order to obtain some essential evidences for a potential targeted therapy in lung adenocarcinoma, the effects of Ovol2 gene on Epithelial-to-Mesenchymal Transition (EMT) was observed and the probable mechanisms were analyzed. METHODS: Ovol2 expression was previously evaluated by immunochemistry in lung adenocarcinoma tissue, and Ovol2 was overexpressed by lentivirus infection in A549 cells. Subsequently, the migration and invasion ability of A549 cells was tested by Transwell and Wound healing experiments. The mRNA level of genes correlated to EMT was detected by Real-time PCR, and the expression of reasonable makers was probed by Western Blot. Finally, rescue experiment, Luciferase assay, and chromatin immunoprecipitation assay were performed to explore the probable mechanisms. RESULTS: After treated with Ovol2 overexpression, the expression level of E-cadherin was increased, while the expression level of Vimentin and Twist1 was declined not only in the mRNA level but also in the protein level. Moreover, we found that Ovol2 represses transcription of Twist1 by binding to its promoter directly. Wound healing and Transwell assays indicate that the migration and invasion ability were downregulated by Ovol2 in A549 cells. CONCLUSION: Ovol2 can suppress migration and invasion ability of A549 cells, and prevent EMT by inhibition of Twist1 transcription directly.

ING5 inhibits epithelial-mesenchymal transition in breast cancer by suppressing PI3K/Akt pathway.

Epithelial-mesenchymal transition (EMT) is a crucial step in tumor progression and has an important role during cancer invasion and metastasis. The proteins of the inhibitor of growth (ING) candidate tumor suppressor family are involved in multiple cellular functions such as cell cycle regulation and apoptosis. ING5 is a member of the family. However, the role of ING5 in breast cancer is still unclear. Thus, the aim of this study is to explore the role of ING5 in breast cancer. In the present study, we showed that ING5 is involved in the pathogenesis of breast cancer. ING5 is down-regulated in breast cancer tissues and cell lines. Overexpression of ING5 significantly inhibited breast cancer cell migration, invasion, and EMT phenotype, moreover, overexpression of ING5 significantly the phosphorylation of PI3K and Aktin in breast cancer cells. In conclusion, our findings show that ING5 can efficiently inhibit the EMT progression in breast cancer cells by suppressing PI3K/Akt signaling pathway. Therefore, ING5 may be a good molecular target for the prevention and treatment of breast cancer.