1,721,028 research outputs found
Dataset supporting article entitled "Correlative 3D Imaging and Microfluidic Modelling of Human Pulmonary Lymphatics using Immunohistochemistry and High-resolution μCT"
No full textThis dataset supports the article entitled "Correlative 3D Imaging and Microfluidic Modelling of Human Pulmonary Lymphatics using Immunohistochemistry and High-resolution μCT" and includes:
20x human lung lymphatics Immunohistochemistry data files
2x COMSOL result modelling files
Location of the micro-CT data set used in this article
This dataset, approx 98Gb, is available on request via the webform at https://library.soton.ac.uk/datarequest </span
"3-Dimensional Imaging and Mathematical Modelling of Human Pulmonary Lymphatics"
No full textThis raw data contributes to the University of Southampton Doctoral thesis entitled "3-Dimensional Imaging and Mathematical Modelling of Human Pulmonary Lymphatics" </span
Mata
Full text linkMata is a system for medical image data management. It allows for a highly modular image management workflow supporting large file sizes. The name Mata derives from 'medicine' and 'data'.
The work has been described in Wollatz, L., Scott, M., Johnston, S. J., Lackie, P. M. & Cox, S. J. (2018) 'Curation of Image Data for Medical Research', Proc. 14th Int. IEEE Conf. eScience</span
LungJ v0.5.1
No full textLungJ is an ImageJ/ Fiji plug-in, designed to solve many tasks related to the processing of very large 3D images with a specific target at medical mu-CT scans of lungs.</span
Altered microRNA expression profile during epithelial wound repair in bronchial epithelial cells
No full textBasic science and pathophysiology of ocular allergy
No full textOcular allergy includes several clinical subtypes ranging from the mild seasonal allergic conjunctivitis to the potentially sight-threatening atopic keratoconjunctivitis. Current therapies, particularly for the severe forms of disease, need to be more localized and with fewer side effects. For this to be achieved, it requires a better understanding of the basic mechanisms involved. In this chapter, recent findings are discussed that suggest that it is important to take an integrated approach, including both immune and structural elements of the eye. This provides potential new strategies for therapy, addressing the influence of structural cells in disease. These might influence the immune processes that take place and, as the structural cells are precisely localized, topical application is likely to be effective
Epithelial repair is inhibited by an ?1,6-fucose binding lectin
No full textThe effective repair of damage to the airway epithelium is essential to maintain the ability to exclude airborne particulates and protect against potential pathogens. Carbohydrates on the cell surface have an important role in cell-cell and cell substrate interactions. Using a model of repair with airway epithelial-derived cells of the 16HBE 14o(-) cell line, we have examined the effect of the Aleuria aurantia lectin (AAL), which binds very selectively to ?(1,6)-linked fucose residues. Addition of unconjugated or FITC-labeled AAL reduced the rate of epithelial repair to approximately one-third of control values as measured by image analysis while cell viability was maintained. Pulse labeling with AAL-FITC for 30 min followed by incubation in AAL-free medium caused similar inhibition of repair but could be reversed by addition of fucose up to 7 h after AAL removal. By confocal microscopy, AAL binding was found to be on the apical, but not basolateral, surfaces of cells, and internalization of the labeled lectin was seen. Preincubation of the lectin with fucose prevented this effect. Ulex europeaus I lectin, which is also fucose specific, resulted in similar binding to the cells and internalization, but it did not affect the speed of the repair process. We conclude that ?(1,6)-fucose binding sites play an important role in epithelial repair. Better understanding of this process will provide a deeper insight into the crucial mechanisms of epithelial repair.<br/
Inflammatory cytokines can enhance CD44-mediated airway epithelial cell adhesion independently of CD44 expression
No full textIn airways, the cell surface molecule CD44 is upregulated on bronchial epithelial cells in areas of damage. We have shown that a blocking standard CD44 (CD44s) antibody caused a 77% (± 19%) inhibition of cell migration at 3 h after mechanical damage and decreased epithelial cell repair of cells grown on cell culture filter inserts. With the use of primary human bronchial epithelial cells and the bronchial epithelial cell line 16HBE 14o-, a CD44s antibody inhibited >95% (P < 0.01) of cell binding to hyaluronic acid (HA). The cytokines TNF-?, IFN-?, IL-1?, and IL-4 stimulated a 2- to 3.5-fold increase in CD44-dependent cell binding to HA. IFN-? treatment did not increase CD44 expression as assessed by flow cytometry, although phorbol myristate acetate treatment did. This indicates that IFN-?-induced cell binding to HA did not require increased CD44 expression. These data indicate that CD44 is important for bronchial epithelial cell binding to HA and that cytokines known to be expressed in inflammation can increase HA binding independently of the level of CD44 expression
TGF-? isoform release and activation during in vitro bronchial epithelial wound repair
No full textRestitution of an epithelial layer after environmental or biological damage is important to maintain the normal function of the respiratory tract. We have investigated the role of transforming growth factor (TGF)-beta isoforms in the repair of layers of 16HBE 14o- bronchial epithelial-derived cells after damage by multiple scoring. ELISA showed that both latent TGF-beta 1 and TGF-beta 2 were converted to their active forms 2 h after wounding. Time-lapse microscopy showed that the addition of TGF-beta 1, but not TGF-beta 2, progressively increased the rate of migration of damaged monolayers at concentrations down to 250 pg/ml. This increase was blocked by addition of a neutralizing TGF-beta 1 antibody. Phase-contrast microscopy and inhibition of proliferation with mitomycin C showed that proliferation was not required for migration. These results demonstrate that conversion of latent to active TGF-beta 1 and TGF-beta 2 during in vitro epithelial wound repair occurs quickly and that TGF-beta 1 speeds epithelial repair. A faster repair may be advantageous in preventing access of environmental agents to the internal milieu of the lung although the production of active TGF-beta molecules may augment subepithelial fibrosis
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