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The association of the SH protein with respiratory syncytial virus (RSV) particles was examined in HEp2 cells and human ciliated nasal epithelial cells. Imaging of infected cells demonstrated the presence of the SH protein in virus filaments, and analysis of purified RSV particles revealed a SH protein species whose size was consistent with the glycosylated SH protein. Although the SH protein was detected in virus filaments it was not required for virus filament formation. Analysis of RSV-infected ciliated cells also revealed that the SH protein was trafficked into the cilia, and this correlated with reduced cilia density on these cells. Reduced cilia loss was not observed on ciliated cells infected with a RSV isolate that failed to express the SH protein. These data provide direct evidence that the SH protein is trafficked into virus particles, and suggests that the SH protein may also promote cilia dysfunction on nasal epithelial cells.

Additional file 1: Table S1. Clinical characteristics of patients with and without asthma.Table S2. Real-time quantitative PCR primer sequences of mouse and human genes.

Supplemental Material for Microarray Assay Reveals Ciliary Abnormalities of the Allergic Nasal Mucosa by Yang Peng MD Wei-jie Guan MD, PhD Zhen-chao Zhu MD Kai Sen Tan PhD Zhuo Chen MD Hai-yu Hong MD, PhD Xiao-xue Zi PhD Anand Kumar Andiappan MD Li Shi MD, PhD Qin-tai Yang MD, PhD De-Yun Wang MD, PhD Qian-hui Qiu MD, PhD in American Journal of Rhinology & Allergy

Additional file 1: Table S1. Summary of characteristics from CRSwNP patients co-existence with AR elucidated by using IF staining. Table S2. dMIQE checklist for demonstrating the methods to perform quantitative polymerase chain reaction.

EMSA competition of PU.1 (ETS family) and YY1 consensus probes with rs612529 probes. EMSA experiments were performed with radiolabeled probes representing the consensus binding sequence of PU.1 and YY1. A EMSA competition experiment with consensus PU.1-probe. Nuclear extracts from primary monocytes were exposed to radiolabeled PU.1 consensus alone (lane 1) or together with excess of unlabeled PU.1 consensus probes (lane 2), PU.1 mutant probes (lane 3), or increasing amounts of rs612529 C (lanes 4–6) or T probes (lanes 7–9). The competitors were added to the binding reactions at increasing concentrations prior to the incubation with probe. B EMSA competition experiment with consensus YY1-probe. Radiolabeled YY1 probe was used alone (lane 1) or with excess of unlabeled YY1 probe (lane 2), YY1 mutant probe (lane 3), or increasing amounts of rs612529 C (lanes 4–7) or T probes (lanes 8–11). (PDF 243 kb)

Oligonucleotide sequences of probes used in EMSA experiments. The table lists the sequence of oligonucleotides used as radiolabeled probes or as cold competitors in EMSA. VSTM1 C and T probe sequences represent the two allelic variants of a 25-bp region in the VSTM1 promoter containing the rs612529 SNP. Consensus and mutant oligonucleotides are based on consensus binding sites of the respective transcription factor. (PDF 51Â kb)

Gating strategy for the flow cytometry analysis of SIRL-1 expression on whole blood samples. Whole blood samples stained with antibodies specific for CCR3, CD16, CD123, CD14, FcÎľRIÎą, and HLA-DR were counterstained with either anti-SIRL-1 or isotype-matched control antibody. Gates allowing the simultaneous analysis of the SIRL-1 staining on neutrophils, eosinophils, basophils, monocytes, mDC, pDC, B cells, and NK & T cells are indicated. (PDF 210Â kb)

In silico prediction of transcription factors with allele-specific binding to rs612529. The web based prediction tools JASPAR (A) and TRANSFAC (B) were used to identify potential transcription factor binding sites in the VSTM1 promoter region affected by the allelic variations of rs612529 T/C. Only sites predicted with a binding score greater than 5.0 (JASPAR) and 0.9 (TRANSFAC) were selected for further analysis. The nucleotide underlined in red indicates the location of rs612529 within binding motif of the respective TF. Yellow shaded rows indicate transcription factors predicted to be highly specific for T allele.5. (PDF 55Â kb)

Model on the potentiating effect of a regulatory CpG-SNP. A Conventional vs. regulatory CpG-SNPs. The methylation of CpG pairs results in the condensation of chromatin due to a tighter packaging of the histone-DNA complexes (open circle: non-methylated CpG, closed circle: methylated CpG). While a conventional CpG-SNP can assist this process by providing only one additional allele-dependent methylation site (middle panel), a regulatory CpG-SNP (such as rs612529) modulates the recruiting of CpG-modifying enzymes (right panel). In the case of rs612529, this seems to be mediated by the allele-specific binding of PU.1 to the T allele of the CpG-SNP. In monocytes PU.1 was reported to bind the demethylase Tet-2. B Potentiating effect. Recruitment of Tet-2 mediates the chromatin-opening by facilitating the demethylation of all CpG pairs in the vicinity. The epigenetic effect is allele-specific (T allele) and direction of the direction probably cell-typeâ dependent. (PDF 415Â kb)

VSTM1 promoter sequence. The sequence of the region 411 bases upstream of the TSS and 282 bases downstream (untranslated region, Exon1, and part of Intron 1 of VSTM1 transcript) was obtained from UCSC genome browser ( https://genome.ucsc.edu/ ). The location of rs612529 T/C (underlined) as well as of each CpG site is indicted (red bold font). The transcription start site is indicated by â TSS,â the translational start by the start codon ATG. The transcribed region is indicated by small letters. Primers for bisulfite sequencing (F1/F2 and B1/B2) as well as the primer pair used for rs612529 genotyping and ChiP analysis are indicated by empty arrows. (PDF 161Â kb)

This article shows that in spherical polar coordinates, some noncentral separable potentials have supersymmetry and shape invariance in the r and θ dimensions, we choose Hartmann potential and ring-shaped oscillator as two important examples, thus in principle the energy eigenvalues and energy eigenfunctions of such the potentials in the r and θ dimensions can be obtained by the method of supersymmetric quantum mechanics. Here we use an alternative method to get the required results.

Background The Toll-like receptor proteins are important in host defense and initiation of the innate and adaptive immune responses. A number of studies have identified associations between genetic variation in the Toll-like receptor genes and allergic disorders such as asthma and allergic rhinitis. The present study aim to search for genetic variation associated with allergic rhinitis in the Toll-like receptor genes. Methods A first association analysis genotyped 73 SNPs in 182 cases and 378 controls from a Swedish population. Based on these results an additional 24 SNPs were analyzed in one Swedish population with 352 cases and 709 controls and one Chinese population with 948 cases and 580 controls. Results The first association analysis identified 4 allergic rhinitis-associated SNPs in the TLR7-TLR8 gene region. Subsequent analysis of 24 SNPs from this region identified 7 and 5 significant SNPs from the Swedish and Chinese populations, respectively. The corresponding risk-associated haplotypes are significant after Bonferroni correction and are the most common haplotypes in both populations. The associations are primarily detected in females in the Swedish population, whereas it is seen in males in the Chinese population. Further independent support for the involvement of this region in allergic rhinitis was obtained from quantitative skin prick test data generated in both populations. Conclusions Haplotypes in the TLR7-TLR8 gene region were associated with allergic rhinitis in one Swedish and one Chinese population. Since this region has earlier been associated with asthma and allergic rhinitis in a Danish linkage study this speaks strongly in favour of this region being truly involved in the development of this disease.

Objectives: We have conducted this study to assess (1) the existence of prevention programmes for AR as developed by professional and health care organizations in Asia- Pacific countries; (2) any discrepancies in local guidelines in comparison to ARIA, or within and across these countries. Study design: Web search study. Methodology: We have conducted a study using Web search in accordance with the perspective of physicians or patients for the relevant prevention and pharmacotherapy guidelines in the management of AR as developed by professional and health care organizations in Asia-Pacific countries/regions. Results: National allergy (AR and/or asthma) preventive programs are found in only 6 out of 17 (22.2%) countries (excluding Japan and South Korea). There exist several aspects of discrepancies in existing educational programs such as in (1) allergic disease (asthma or AR) that the guidelines focus on; (2) targeted age groups (children or adults); and (3) breadth and depth of coverage, such as for particular inhalant allergens or food allergies only. Based on the information provided by MIMS website (updated in 2011 by UBM Medica, London, United Kingdom) and the MIMS proven by the country’s local health authority, controversies exist in recommended minimum age, doses and potential side-effects of many commonly used 2nd-generation antihistamines and intranasal corticosteroids. Conclusion: This is the first study that demonstrates discrepancies and a lack of public education programmes for AR prevention and management in Asia-Pacific countries/regions.

The stringent requirements on size and power consumption constrain the conventional hearing aid devices from providing the patients an economic and user friendly solution, specifically for better noise cancellation. With the advancements in technologies such as integrated circuits design, wireless communications and digital signal processing techniques, the wireless hearing aids having multi-microphones, analog, digital and mixed signals and radio frequency signals processing circuits, DSP and programmable units seem to be promising to provide enhanced performance. The focus of this paper is about the system simulation of a typical wireless hearing aid using Agilent Advanced Design System#8482;. The behavioral modeling features are exploited to enable the whole system simulations including electro-acoustic transducers. A few system level simulation results are included.

Gating strategy for monocytes expressing FcγRIII, FcεRIα, or FcαR. PBMCs were stained with antibodies specific for FcγRIII (CD16), FceRIα, FcαR (CD89), and CD14 together with anti-SIRL-1, or isotype-matched control antibody. Monocytes were gated based on scatter properties (SSC-A and FSC-A) and live/dead-staining (AmCyan). Gates for FcγRIII+ monocytes, FcεRIα + monocytes, and FcαR+ monocytes are indicated in plots displaying the CD14 staining vs. the respective Fc-receptor. (PDF 297 kb)

Cohorts used in the study. The data for this study were collected from seven different cohorts. Four of these cohorts were established for the functional association studies (eQTL, FACS analysis, ROS assay, DNA methylation, and ChiP assay), while the three other cohorts were used for the genetic association studies with atopic dermatitis (AD). Size of the cohorts as well as ethnicity and appropriate reference are provided for each cohort. (PPTX 80Â kb)

Cohorts used in the study. The data for this study were collected from seven different cohorts. Four of these cohorts were established for the functional association studies (eQTL, FACS analysis, ROS assay, DNA methylation, and ChiP assay), while the three other cohorts were used for the genetic association studies with atopic dermatitis (AD). Size of the cohorts as well as ethnicity and appropriate reference are provided for each cohort. (PPTX 80Â kb)

Gating strategy for monocytes expressing FcγRIII, FcεRIα, or FcαR. PBMCs were stained with antibodies specific for FcγRIII (CD16), FceRIα, FcαR (CD89), and CD14 together with anti-SIRL-1, or isotype-matched control antibody. Monocytes were gated based on scatter properties (SSC-A and FSC-A) and live/dead-staining (AmCyan). Gates for FcγRIII+ monocytes, FcεRIα + monocytes, and FcαR+ monocytes are indicated in plots displaying the CD14 staining vs. the respective Fc-receptor. (PDF 297 kb)