36 resultados para Adhesion

em Deakin Research Online - Australia


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In this paper wool and polyester fabrics were pretreated with atmospheric plasma glow discharge (APGD) to improve the ability of the substrate to bond with anthraquinone-2-sulfonic acid doped conducting polypyrrole coating. A range of APGD gas mixtures and treatment times were investigated. APGD treated fabrics were tested for surface contact angle, wettability and surface energy change. Effect of the plasma treatment on the binding strength was analyzed by studying abrasion resistance, surface resistivity and reflectance. Investigations showed that treated fabrics exhibited better hydrophilicity and increased surface energy. Surface treatment by an APGD gas mixture of 95% helium/5% nitrogen yielded the best results with respect to coating uniformity, abrasion resistance and conductivity.


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Cerebral amyloid angiopathy (CAA) is a major feature of Alzheimer's disease pathology. In CAA, degeneration of vascular smooth muscle cells (VSMCs) occurs close to regions of the basement membrane where the amyloid protein (Aβ) builds up. In this study, the possibility that Aβ disrupts adhesive interactions between VSMCs and the basement membrane was examined. VSMCs were cultured on a commercial basement membrane substrate (Matrigel). The presence of Aβ in the Matrigel decreased cell-substrate adhesion and cell viability. Full-length oligomeric Aβ was required for the effect, as N- and C-terminally truncated peptide analogues did not inhibit adhesion. Aβ that was fluorescently labelled at the N-terminus (fluo-Aβ) bound to Matrigel as well as to the basement membrane heparan sulfate proteoglycan (HSPG) perlecan and laminin. Adhesion of VSMCs to perlecan or laminin was decreased by Aβ. As perlecan influences VSMC viability through the extracellular signal-regulated kinase (ERK)1/2 signalling pathway, the effect of Aβ1–40 on ERK1/2 phosphorylation was examined. The level of phospho-ERK1/2 was decreased in cells following Aβ treatment. An inhibitor of ERK1/2 phosphorylation enhanced the effect of Aβ on cell adhesion. The studies suggest that Aβ can decrease VSMC viability by disrupting VSMC–extracellular matrix (ECM) adhesion.

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The β7 integrins α4β7 and Eβ7 play key roles in forming the gut-associated lymphoid tissue, and contribute to chronic inflammation. The α4β7 integrin-mediated adhesion of activated lymphocytes is largely due to a transient increase in avidity from ligand-induced clustering of α4β7 at the cell-surface. Here, we report that L and D enantiomers of a cell-permeable peptide YDRREY encompassing residues 735-740 of the cytoplasmic tail of the β7 subunit inhibit the adhesion of T cells to β7 integrin ligands. The YDRREY peptide abrogated mucosal addressin cell adhesion molecule-1-induced clustering of α4β7 on the surface of activated T cells. A mutated form of the YDRREY peptide carrying either single or double conservative mutations at Tyr735Phe and Tyr740Phe was unable to inhibit T cell adhesion, suggesting that both tandem tyrosines are critical for activity. The YDRREY peptide was bound and phosphorylated by focal adhesion kinase and src, which may serve to sequester cytoskeletal proteins to the cytoplasmic domain of 4β7. The quasi-palindromic sequence YDRREY within the β7 cytoplasmic tail constitutes a cell adhesion regulatory domain that modulates the interaction of β7-expressing leukocytes with their endothelial and epithelial ligands. Cell-permeable peptidomimetics based on this motif have utility as anti-inflammatory reagents for the treatment of chronic inflammatory disease.

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Mucosal vascular addressin cell adhesion molecule-1 (MAdCAM-1) is predominantly expressed on high endothelial venules in inflamed tissues where it assists with leucocyte extravasation. Here we report that MAdCAM-1 has the potential to be more widely expressed outside the endothelial cell lineage than previously appreciated. Thus, MAdCAM-1 RNA transcripts and cell-surface protein were expressed by NIH 3T3 fibroblasts following activation with tumour necrosis factor-alpha (TNF-alpha), and by freshly isolated and cultured primary mouse splenic and tail fibroblasts in the absence of TNF-alpha stimulation. They were constitutively expressed by B16F10 melanoma cells, and expression was enhanced by cell activation with TNF-alpha. Mucosal vascular addressin cell adhesion molecule-1 was expressed on the apical surface of isolated cells, but became predominantly localized to cell junctions in confluent cell monolayers, suggesting it may play a role in the homotypic aggregation of cells. Tumour necrosis factor-alpha enhanced the expression of a firefly luciferase reporter directed by the MAdCAM-1 promoter in NIH 3T3 and B16F10 cells. A DNA fragment extending from nt -1727 to -673 was sufficient to confer cell-type selective expression. Mucosal vascular addressin cell adhesion molecule-1 expressed by NIH 3T3 cells was biologically active, as it supported the adhesion of TK-1 T cells in an alpha4beta7-dependent fashion. The expression of MAdCAM-1 by fibroblasts, and melanomas suggests MAdCAM-1 may play a role in regulating host responses in the periphery, leucocyte transmigration across nonendothelial boundaries, or the homotypic interactions of some malignant melanomas.

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A role for α4 and β7 integrins in mediating leucocyte entry into the central nervous system in the multiple sclerosis (MS)-like disease experimental autoimmune encephalomyelitis (EAE) has been demonstrated. However, the individual contributions of their respective ligands mucosal addressin cell adhesion molecule-1 (MAdCAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-cadherin expressed on the blood-brain barrier has not been determined. In the present paper, it is shown that an antibody directed against MAdCAM-1, the preferential ligand for α4β7, effectively prevented the development of a progressive, non-remitting, form of EAE, actively induced by injection of myelin oligodendrocyte glycoprotein peptide (MOG(35-55)) autoantigen. Combinational treatment with both anti-MAdCAM-1, VCAM-1, and intercellular adhesion molecule-1 (ICAM-1) (ligand for integrin lymphocyte function-associated antigen (LFA)-1) mAbs led to more rapid remission than that obtained with anti-MAdCAM-1 antibody alone. However, neither MAdCAM-1 monotherapy, nor combinational antibody blockade was preventative when administered late in the course of disease progression. In conclusion, MAdCAM-1 plays a major contributory role in the progression of chronic EAE and is a potential therapeutic target for the treatment of MS. Critically, antivascular addressin therapy must be given eaA role for alpha4 and beta7 integrins in mediating leucocyte entry into the central nervous system in the multiple sclerosis (MS)-like disease experimental autoimmune encephalomyelitis (EAE) has been demonstrated. However, the individual contributions of their respective ligands mucosal addressin cell adhesion molecule-1 (MAdCAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-cadherin expressed on the blood-brain barrier has not been determined. In the present paper, it is shown that an antibody directed against MAdCAM-1, the preferential ligand for alpha4beta7, effectively prevented the development of a progressive, non-remitting, form of EAE, actively induced by injection of myelin oligodendrocyte glycoprotein peptide (MOG(35-55)) autoantigen. Combinational treatment with both anti-MAdCAM-1, VCAM-1, and intercellular adhesion molecule-1 (ICAM-1) (ligand for integrin lymphocyte function-associated antigen (LFA)-1) mAbs led to more rapid remission than that obtained with anti-MAdCAM-1 antibody alone. However, neither MAdCAM-1 monotherapy, nor combinational antibody blockade was preventative when administered late in the course of disease progression. In conclusion, MAdCAM-1 plays a major contributory role in the progression of chronic EAE and is a potential therapeutic target for the treatment of MS. Critically, antivascular addressin therapy must be given early in the course of disease prior to the establishment of irreversible damage if it is to be effective, as a single treatment modality.

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Most industrially applied polymer resins and composites have low surface free energy and lack polar functional groups on their surface, resulting in inherently poor adhesion properties. A strong research momentum to understand polymer adhesion in the last decade has been motivated by the growing needs of the automotive and aerospace industries for better adhesion of components and surface coatings. This paper reviews the recent research efforts on polymer adhesion with a special focus on adhesion mechanisms. It starts with an introduction to adhesion with explanatory notes on adhesion phenomena. Recent research on the adhesion mechanisms of mechanical coupling, chemical bonding and thermodynamic adhesion is then discussed. The area of adhesion promoters is reviewed with the focus on plasma and chemical treatments, along with direct methods for adhesion measurement. The topics of polymer blends and reactive polymerization are considered and the interactions with adhesion mechanisms are reported. The concluding section provides recommendations regarding future research on the contentious aspects of currently accepted adhesion mechanisms and on strategies for enhancing polymer adhesion strength.

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A new fabric with potential in medical textiles has been developed by application of a surface coating on wool using pulsed plasma polymerization of HMDSO. This coating enabled a controllable MVTR and surface adhesion. MVTR in the range recommended for optimum wound healing was obtained by varying frequency, monomer pressure and deposition time. Lower surface adhesion was achieved. Peeling tests, contact angle measurements, SPM force curves and ATR FT-IR were used to characterize the surfaces for both wool and a PE model substrate. All these results were consistent with a decrease in surface energy after PP-HMDSO treatment. ATR FT-IR results showed a siloxane film with less organic Si(CH3)n groups and more SiOSi cross-links.

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Geckos have extraordinary wall-climbing ability because of the millions of hairs with micro/nano fibrillar structures on their feet. Mimicking gecko's feet is of scientific and engineering importance for development of physical adhesion materials and devices. The design of gecko-inspired physical adhesives seems to be geometry dominated. In this study, Finite Element Method (FEM) has been used to analyse the vertical peel-off force of polyporpylene (PP) nanofibres having different fibre dimensions, inclining angels and contact areas on a flat glass substrate. It has been found that the main parameters affecting the frictional adhesion are fibre diameter and fibre aspect ratio, the inclining angle between the fibre and the substrate surface, and the intimate contact areas. Our analysis has shown that PP nanofibres with a diameter of less than 200nm can generate less peel-off force than fibres of larger diameters, indicating more stable adhesion with the glass substrate for thinner fibres. A bent fibre with more intimate contact area can bear more shear force than a straight fibre with less contact area. Also, under the same shear loading, fibres with an inclining angle of less than 30° provide a low peel off force.

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A central composite rotatable design (CCRD) method was used to investigate the performance of the accelerated thermomolecular adhesion process (ATmaP), at different operating conditions. ATmaP is a modified flame-treatment process that features the injection of a coupling agent into the flame to impart a tailored molecular surface chemistry on the work piece. In this study, the surface properties of treated polypropylene were evaluated using X-ray photoelectron spectroscopy (XPS) and time-of-flight secondary ion mass spectrometry (ToF-SIMS). All samples showed a significant increase in the relative concentration of oxygen (up to 12.2%) and nitrogen (up to 2.4%) at the surface in comparison with the untreated sample (0.7% oxygen and no detectable nitrogen) as measured by XPS. ToF-SIMS and principal components analysis (PCA) showed that ATmaP induced multiple reactions at the polypropylene surface such as chain scission, oxidation, nitration, condensation, and molecular loss, as indicated by changes in the relative intensities of the hydrocarbon (C3H7+ , C3H5+ , C4H7+, and C5H9+), nitrogen and oxygen-containing secondary ions (C2H3O+, C3H8N+, C2H5NO+, C3H6NO+, and C3H7NO+). The increase in relative intensity of the nitrogen oxide ions (C2H5NO+ and C3H7NO+) correlates with the process of incorporating oxides of nitrogen into the surface as a result of the injection of the ATmaP coupling agent.

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The main challenges in the manufacture of composite materials are low surface energy and the presence of silicon-containing contaminants, both of which greatly reduce surface adhesive strength. In this study, carbon fiber (CF) and E-glass epoxy resin composites were surface treated with the Accelerated Thermo-molecular adhesion Process (ATmaP). ATmaP is a multiaction surface treatment process where tailored nitrogen and oxygen functionalities are generated on the surface of the sample through the vaporization and atomization of n-methylpyrrolidone solution, injected via specially designed flame-treatment equipment. The treated surfaces of the polymer composites were analyzed using XPS, time of flight secondary ion mass spectrometry (ToF-SIMS), contact angle (CA) analysis and direct adhesion measurements. ATmaP treatment increased the surface concentration of polar functional groups while reducing surface contamination, resulting in increased adhesion strength. XPS and ToF-SIMS showed a significant decrease in silicon-containing species on the surface after ATmaP treatment. E-glass composite showed higher adhesion strength than CF composite, correlating with higher surface energy, higher concentrations of nitrogen and CO functional groups (from XPS) and higher concentrations of oxygen and nitrogen-containing functional groups (particularly C2H3O+ and C2H5NO+ molecular ions, from ToF-SIMS).

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Interfacial chemistry and adhesion between titanium dioxide (TiO2) nanotube layers and titanium (Ti) substrates were studied in this Article. TiO2 nanotube layers were produced on pure Ti by anodization and annealed in air for different time durations. The adhesion of the TiO2 nanotube layers was then investigated by Rockwell C indentation test. Results show that adhesion of TiO2 nanotube layers improved with the extension of annealing time. This improvement in adhesion of TiO2 nanotube layers was analyzed from the viewpoint of interfacial chemistry using energy dispersive X-ray spectrometry (EDS) and X-ray photoelectron spectroscopy (XPS). It suggests that more Ti-O bonds formed in the interface after annealing, and this led to the improved adhesion of the TiO2 nanoube layers.

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Two curved surfaces of molecularly smooth mica are brought into contact under a controlled load, and their deformed shape is measured using optical interference fringes of equal chromatic order. This technique allows exceptionally accurate measurements of surface profiles at separations down to a molecular scale. Contact between the surfaces can be made either adhesive or nonadhesive by suitable choice of the medium between them. Results have been obtained in both cases and compared with the theories of Hertz (nonadhesive contact) and Johnson, Kendall, and Roberts (adhesive contact).

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Simultaneous measurements of surface force and surface charge demonstrate strong attraction due to the spontaneous transfer of electrical charge from one smooth insulator (mica) to another (silica) as a result of simple, nonsliding contact in dry nitrogen. The measured surface charge densities are 5 to 20 millicoulombs per square meter after contact. The work required to separate the charged surfaces is typically 6 to 9 joules per square meter, comparable to the fracture energies of ionic-covalent materials. Observation of partial gas discharges when the surfaces are approximately 1 micrometer apart gives valuable insight into the charge separation processes underlying static electrical phenomena in general.