624 research outputs found
Expression of MUC5AC and MUC5B mucins in normal and cystic fibrosis lung
AbstractHypersecretion of airway mucus is a characteristic feature of chronic airway diseases like cystic fibrosis (CF) and leads via impairment of the muco-ciliary clearance and bacterial superinfection to respiratory failure. The major components of the mucus matrix forming family of mucins in the airways are MUC5AC and MUC5B. To investigate the expression of these glycoproteins in CF, immunohistochemistry was carried out on trachea, bronchi and peripheral lung obtained from CF patients and compared to normal lung tissues. MUC5AC immunohistochemistry demonstrated signals in goblet cells of the epithelial lining. Also, goblet cells inside glandular secretory ducts revealed MUC5AC-positive staining. In comparison to those from normal subjects, CF sections were characterized by inflammatory changes and goblet cell hyperplasia, resulting in increased numbers of MUC5AC-positive cells. Immunohistochemical staining for MUC5B showed abundant staining of submucosal glands and epithelial goblet cells. Inside the glands, the immunoreactivity was restricted to glandular mucous cells. MUC5AC and MUC5B are expressed in the same histological pattern in CF compared to normal tissues with an increase of MUC5AC-positive cells due to goblet cell hyper- and metaplasia
Dexamethasone inhibits ozone-induced gene expression of macrophage inflammatory protein-2 in rat lung
AbstractTo address the potential role of the chemokine macrophage inflammatory protein-2 (MIP-2) in airway inflammation, we examined whether MIP-2 may play a role in ozone-induced neutrophilic inflammation of airways and its modulation by dexamethasone in rat lung. Following ozone exposure, MIP-2 mRNA expression in the lung peaked at 2 h after exposure and slowly declined thereafter. Dexamethasone suppressed ozone-induced MIP-2 mRNA expression and neutrophil accumulation in the lung. We suggest that the MIP-2 mRNA induction may switch on the neutrophilic influx observed in this model of lung inflammation. Furthermore, the MIP-2 expression is regulated by dexamethasone which may represent one of the mechanisms by which glucocorticoids exert their potent anti-inflammatory properties
Determining the structure of Ru(0001) from low-energy electron diffraction of a single terrace
While a perfect hcp (0001) surface has three-fold symmetry, the diffraction
patterns commonly obtained are six-fold symmetric. This apparent change in
symmetry occurs because on a stepped surface, the atomic layers on adjacent
terraces are rotated by 180 degrees. Here we use a Low-Energy Electron
Microscope to acquire the three-fold diffraction pattern from a single hcp Ru
terrace and measure the intensity-vs-energy curves for several diffracted
beams. By means of multiple scattering calculations fitted to the experimental
data with a Pendry R-factor of 0.077, we find that the surface is contracted by
3.5(+-0.9) at 456 K.Comment: 10 pages, 4 figures. Corrected some typos, added more details.
Accepted for publication in Surface Science (Letters
Análise teórico-experimental de ligações parafusadas com enrijecedores de alma em perfis de aço formados a frio
Lipid-laden bronchoalveolar macrophages in asthma and chronic cough
SummaryBackgroundThe presence of lipids in alveolar macrophages (AMs) may impair their phagocytic response, and determine airway inflammation and obstruction.ObjectiveTo determine the factors such as severity of asthma, chronic cough, airway inflammation and obesity that may influence the presence of lipids in lung macrophages.MethodsBronchoalveolar lavage fluid (BALF) was obtained from 38 asthmatics (21 severe and 17 mild/moderate), 16 subjects with chronic cough and 11 healthy control subjects. The presence of lipids in macrophages was detected using an Oil-red-O stain and an index of lipid-laden macrophages (LLMI) was obtained.ResultsLLMI scores were higher in healthy subjects (median 48 [IQR 10–61]) and the severe asthma group (37 [11.5–61]) compared to mild/moderate asthmatics (7 [0.5–37]; p < 0.05 each). Subjects reporting a history of gastro-oesophageal reflux disease (GORD) had higher LLMI values (41.5 [11.3–138] versus 13 [0–39.3], p = 0.02). There was no significant correlation between LLMI and chronic cough, BAL cell differential counts, FEV1, FEV1/FVC or body mass index (BMI).ConclusionsThe reduced LLMI in mild/moderate asthma may be related to lower incidence of GORD. However, this was not related to the degree of airflow obstruction, obesity or airway inflammation
Bounds for graph regularity and removal lemmas
We show, for any positive integer k, that there exists a graph in which any
equitable partition of its vertices into k parts has at least ck^2/\log^* k
pairs of parts which are not \epsilon-regular, where c,\epsilon>0 are absolute
constants. This bound is tight up to the constant c and addresses a question of
Gowers on the number of irregular pairs in Szemer\'edi's regularity lemma.
In order to gain some control over irregular pairs, another regularity lemma,
known as the strong regularity lemma, was developed by Alon, Fischer,
Krivelevich, and Szegedy. For this lemma, we prove a lower bound of
wowzer-type, which is one level higher in the Ackermann hierarchy than the
tower function, on the number of parts in the strong regularity lemma,
essentially matching the upper bound. On the other hand, for the induced graph
removal lemma, the standard application of the strong regularity lemma, we find
a different proof which yields a tower-type bound.
We also discuss bounds on several related regularity lemmas, including the
weak regularity lemma of Frieze and Kannan and the recently established regular
approximation theorem. In particular, we show that a weak partition with
approximation parameter \epsilon may require as many as
2^{\Omega(\epsilon^{-2})} parts. This is tight up to the implied constant and
solves a problem studied by Lov\'asz and Szegedy.Comment: 62 page
Role of non-coding RNAs in maintaining primary airway smooth muscle cells
BACKGROUND: The airway smooth muscle (ASM) cell maintains its own proliferative rate and contributes to the inflammatory response in the airways, effects that are inhibited by corticosteroids, used in the treatment of airways diseases. OBJECTIVE: We determined the differential expression of mRNAs, microRNAs (miRNAs) and long noncoding RNA species (lncRNAs) in primary ASM cells following treatment with a corticosteroid, dexamethasone, and fetal calf serum (FCS). METHODS: mRNA, miRNA and lncRNA expression was measured by microarray and quantitative real-time PCR. RESULTS: A small number of miRNAs (including miR-150, −371-5p, −718, −940, −1181, −1207-5p, −1915, and −3663-3p) were decreased following exposure to dexamethasone and FCS. The mRNA targets of these miRNAs were increased in expression. The changes in mRNA expression were associated with regulation of ASM actin cytoskeleton. We also observed changes in expression of lncRNAs, including natural antisense, pseudogenes, intronic lncRNAs, and intergenic lncRNAs following dexamethasone and FCS. We confirmed the change in expression of three of these, LINC00882, LINC00883, PVT1, and its transcriptional activator, c-MYC. We propose that four of these lincRNAs (RP11-46A10.4, LINC00883, BCYRN1, and LINC00882) act as miRNA ‘sponges’ for 4 miRNAs (miR-150, −371-5p, −940, −1207-5p). CONCLUSION: This in-vitro model of primary ASM cell phenotype was associated with the regulation of several ncRNAs. Their identification allows for in-vitro functional experimentation to establish causality with the primary ASM phenotype, and in airway diseases such as asthma and chronic obstructive pulmonary disease (COPD)
Educating a global workforce?
In the public rhetoric, at least, education is the answer to most, if not all, the questions raised by the global knowledge-based economy. In this chapter we begin an examination of what education promises the global workforce, and what the global workforce, and the knowledgebased economy, might reasonably ask of education. Different perspectives on the knowledgebased economy imply different constructions of ‘knowledge’. Workers are characterised within these frameworks as ‘knowledge workers’ (an elite), or, perhaps, ‘knowledgeable workers’ (the non-elite majority) and questions arise around what they are required to learn, to know, and to be able to do. The global knowledge-based economy produces profound challenges to workrelated education at every level. While these challenges manifest themselves in uniquely local ways at specific local sites, they are produced, and must be addressed, in contexts that are uncompromisingly global. If work-related education is to contribute to positive outcomes for people and for local communities we (workers, corporations, educators, researchers, policy makers, politicians and international organisations) must find new ways to pay attention to the ways in which a workforce in the knowledge-based economy can be understood to be ‘global’ as well as ‘local’, and what workers need to be able to know and be able to do to move across and within these spatial and temporal domains
Transcriptome analysis shows activation of circulating CD8 T cells in patients with severe asthma
Background: Although previous studies have implicated tissue CD4 T cells in the development and maintenance of the inflammatory response in asthmatic patients, little is known about the role of CD8 T cells. There is now accumulating evidence that microRNAs and other noncoding RNAs are important regulators of T-cell function. Objectives: We sought to use transcriptomics to determine the activation state of circulating CD4 and CD8 T cells in patients with nonsevere and severe asthma. Methods: mRNA and noncoding RNA expression in circulating T cells was measured by means of microarray, quantitative real-time PCR, or both. Results: Comparison of mRNA expression showed widespread changes in the circulating CD8 but not CD4 T cells from patients with severe asthma. No changes were observed in the CD4 and CD8 T cells in patients with nonsevere asthma versus those in healthy control subjects. Bioinformatics analysis showed that the changes in CD8 T-cell mRNA expression were associated with multiple pathways involved in T-cell activation. As with mRNAs, we also observed widespread changes in expression of noncoding RNA species, including natural antisense, pseudogenes, intronic long noncoding RNAs (lncRNAs), and intergenic lncRNAs in CD8 T cells from patients with severe asthma. Measurement of the microRNA expression profile showed selective downregulation of miR-28-5p in CD8 T cells and reduction of miR-146a and miR-146b in both CD4 and CD8 T cells. Conclusions: Severe asthma is associated with the activation of circulating CD8 T cells but not CD4 T cells. This response is correlated with the downregulation of miR-146a/b and miR-28-5p, as well as changes in the expression of multiple species of lncRNA that might regulate CD8 T-cell function. © 2011 American Academy of Allergy, Asthma & Immunology
Identification and Specification of the Mouse Skeletal Stem Cell
SummaryHow are skeletal tissues derived from skeletal stem cells? Here, we map bone, cartilage, and stromal development from a population of highly pure, postnatal skeletal stem cells (mouse skeletal stem cells, mSSCs) to their downstream progenitors of bone, cartilage, and stromal tissue. We then investigated the transcriptome of the stem/progenitor cells for unique gene-expression patterns that would indicate potential regulators of mSSC lineage commitment. We demonstrate that mSSC niche factors can be potent inducers of osteogenesis, and several specific combinations of recombinant mSSC niche factors can activate mSSC genetic programs in situ, even in nonskeletal tissues, resulting in de novo formation of cartilage or bone and bone marrow stroma. Inducing mSSC formation with soluble factors and subsequently regulating the mSSC niche to specify its differentiation toward bone, cartilage, or stromal cells could represent a paradigm shift in the therapeutic regeneration of skeletal tissues
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