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At least 163 records · Page 9Linked to original sources
PubMed1998

Evaluation of polyethylene glycol/polylactic acid films in the prevention of adhesions in the rabbit adhesion formation and reformation sidewall models.

OBJECTIVE: To assess the efficacy of bioresorbable films consisting of various polyethylene glycol 6000 and polylactic acid block copolymers on the formation and reformation of adhesions in rabbit models of adhesion development between the sidewall to the adjacent cecum and bowel. The composition of the different polymers was expressed by the number of monomeric units in the block, namely, ethylene oxide (EO) and lactic acid (LA), respectively. DESIGN: Studies of the efficacy of EO/LA films were conducted in rabbit sidewall adhesion formation studies in the presence and absence of blood and in rabbit adhesion reformation studies. REPEL (Life Medical Sciences, Edison, NJ), a film of EO/LA ratio 3.0 manufactured under commercial conditions, was also tested in these animal models. SETTING: University-based laboratory. ANIMALS: New Zealand white rabbits. INTERVENTION(S): Placement of films of various EO/LA ratios at the site of injury to the parietal peritoneum. MAIN OUTCOME MEASURE(S): Adhesion formation and reformation. RESULT(S): Films of various EO/LA ratios, Seprafilm (Genzyme, Cambridge, MA) and Interceed (Johnson and Johnson Medical, Arlington, TX) placed over an area of excised sidewall at the time of initial injury were highly efficacious in the prevention of adhesion formation. A film of EO/LA ratio 3.7, in contrast with Interceed, was also shown to maintain maximal efficacy in the reduction of adhesion formation in the presence of blood. Further, a film of EO/LA ratio 3.0 produced under commercial conditions, REPEL, was highly efficacious in reducing adhesion development in the rabbit models of adhesion and reformation. CONCLUSION(S): These studies suggest that bioresorbable EO/LA films reduced adhesion development in rabbit models of adhesion formation and reformation.

Abdomen↗
PubMed1998

Staphylococcal enterotoxin-A-induced in-vitro adhesion of HL-60 cells to endothelial cells involves both selectin and integrin families of cell adhesion molecules.

In-vivo exposure to the bacterial superantigen Staphylococcal enterotoxin-A (SEA) induces an inflammatory response characterized by rapid extravasation of leucocytes and release of excessive amounts of cytokines. We have utilized an in-vitro adhesion assay to understand the molecular mechanisms responsible for SEA-induced extravasation of leucocytes. Stimulation of human umbilical cord endothelial cells (HUVEC) with increasing concentrations of recombinant SEA (rSEA) did not influence the in-vitro adhesion of HL-60 cells to HUVEC, whereas stimulation of HUVEC by interleukin (IL)-1beta supported adhesion of HL-60 cells. Increased adhesion of HL-60 cells to HUVEC was noted upon stimulation of endothelium with culture medium obtained from human peripheral blood mononuclear cells (PBM) stimulated with recombinant SEA for 24 (CM-SEA 24 h), 72 (CM-SEA 72 h) and 120 h (CM-SEA 120 h), but not after stimulation with culture medium obtained from control human peripheral blood mononuclear cells (CM), suggesting that soluble factors present in the supernatants play a major role in SEA-induced cell adhesion. While CM-SEA 24 and 72 h induced both a rapid (4 h) and delayed type of adhesion, CM-SEA 120 h only induced a delayed type of adhesion. Stimulation of PBM by SEA resulted in increased levels of IL-1beta, IL-2 and interferon (IFN)-gamma after 24h. Further stimulation for 72-120h resulted in a significant increase in the levels of IL-1beta, IFN-gamma and tumour necrosis factor (TNF). Stimulation of PBM with SEA also resulted in increased levels of soluble and L-selectin in the cell supernatants. Increased cell-surface expression of E-selectin, ICAM-1, HLA-DR and VCAM-1 was detected on HUVEC stimulated with CM-SEA media. While E-selectin and VCAM were induced on HUVEC within a few hours, induction of ICAM and HLA-DR required a longer induction period. Adhesion of HL-60 cells to HUVEC treated with CM-SEA was inhibited by monoclonal antibodies (MoAbs) against both the selectin and integrin families of cell adhesion molecules, suggesting that multiple pathways contribute to SEA-induced leucocyte extravasation. The results suggested that selectin-dependent adhesion was more prominent during the early phase while integrin-induced adhesion occurred at a later stage.

Antibodies, Monoclonal↗
PubMed2004

Cortactin associates with N-cadherin adhesions and mediates intercellular adhesion strengthening in fibroblasts.

The regulation of N-cadherin-mediated intercellular adhesion strength in fibroblasts is poorly characterized; this is due, in part, to a lack of available quantitative models. We used a recombinant N-cadherin chimeric protein and a Rat 2 fibroblast, donor-acceptor cell model, to study the importance of cortical actin filaments and cortactin in the strengthening of N-cadherin adhesions. In wash-off assays, cytochalasin D (1 microM) reduced intercellular adhesion by threefold, confirming the importance of cortical actin filaments in strengthening of N-cadherin-mediated adhesions. Cortactin, an actin filament binding protein, spatially colocalized to, and directly associated with, nascent N-cadherin adhesion complexes. Transfection of Rat-2 cells with cortactin-specific, RNAi oligonucleotides reduced cortactin protein by 85% and intercellular adhesion by twofold compared with controls (P<0.005) using the donor-acceptor model. Cells with reduced cortactin exhibited threefold less N-cadherin-mediated intercellular adhesion strength compared with controls in wash-off assays using N-cadherin-coated beads. Immunoprecipitation and immunoblotting showed that N-cadherin-associated cortactin was phosphorylated on tyrosine residue 421 after intercellular adhesion. While tyrosine phosphorylation of cortactin was not required for recruitment to N-cadherin adhesions it was necessary for cadherin-mediated intercellular adhesion strength. Thus cortactin, and phosphorylation of its tyrosine residues, are important for N-cadherin-mediated intercellular adhesion strength.

Actins↗
PubMed2006

Adhesiolysis in severe and reccurent cases of adhesions related disorder (ARD) - a novel approach utilizing lift (gasless) laparoscopy and SprayGel adhesion barrier.

We investigated the feasibility and outcome of adhesiolysis in patients with severe and reccurent adhesions using lift (gasless) laparoscopy and a SprayGel adhesion barrier at the Institute for Endoscopic Gynecology (EndoGyn). The design included a prospective evaluation of lift (gasless) laparoscopic adhesiolysis in combination with a SprayGel adhesion barrier. A new score for bowel adhesions was developed and applied. All 35 patients with severe and reccurent adhesions underwent a lift-laparoscopic adhesiolysis with the Abdo-Lift and SprayGel adhesion barrier, a second-look laparoscopy at Day 7 and, in case of continuation of pain, a third-look laparoscopy within 6 months after the initial surgery. All patients were operated upon without conversion to laparotomy. The reduction in the adhesion score of adhesions at the second-look laparoscopy was overall (sum) 89.8% (90.1% reduction in extent, 89.3% reduction in severity, and 89.9% reduction in grade). Five patients (14.3%) had a third-look laparoscopy within 6 months after the initial surgery, in which four cases of adhesion reformation were confirmed. However, the scores were reduced compared to the initial surgery, especially in grade (94.2%) and severity (93.2%). In these analyses, SprayGel was uniquely effective in improving the success rates of adhesiolysis when combined with lift (gasless) laparoscopy and good hemostasis techniques. Adhesiolysis with Abdo-Lift and SprayGel had unparalleled efficacy in the adhesiolysis procedure even in those patients in whom other solutions have not worked. An overall reduction of adhesions by 89.9% at second-look laparoscopy was found. Even if five patients (14.3%) required a third-look laparoscopy where four cases of adhesion reformation were confirmed, the scores were reduced when compared to the initial surgery, especially in grade and severity.

Adult↗
PubMed1989

Endothelial-leukocyte adhesion molecule-1-dependent and leukocyte (CD11/CD18)-dependent mechanisms contribute to polymorphonuclear leukocyte adhesion to cytokine-activated human vascular endothelium.

We have examined the contributions of endothelial-leukocyte adhesion molecule-1 (ELAM-1) and the complex of leukocyte surface adhesion molecules designated CD11/CD18 to the adhesion of human polymorphonuclear leukocytes (PMN) to cultured human endothelial cells (HEC), activated by rIL-1 beta for 4 or 24 h. Inhibition of PMN attachment to IL-1-activated HEC was measured in a quantitative in vitro monolayer adhesion assay, after treatment with mAb directed to ELAM-1 (mAb H18/17), and to CD11a (mAb L11), CD11b (mAb 44), CD11c (mAb L29), and CD18 (mAb 10F12), alone or in combination. Pretreatment of activated HEC with mAb H18/7 inhibited PMN adhesion by 47 +/- 8% whereas control mAb had no effect. CD11/CD18-directed mAb significantly blocked PMN adhesion to activated HEC (anti-CD11a, 40 +/- 3%; anti-CD11b, 34 +/- 4%; anti-CD18, 78+/- 6% inhibition). The combination of mAb H18/7 and each of the various anti-CD11/CD18 mAb resulted in greater inhibition of PMN adhesion than any Mab alone. After 24 h of rIL-1 beta treatment, when ELAM-1 was markedly decreased but elevated PMN adhesion was still observed, mAb H18/7 had no effect on PMN adhesion. At this time, CD11/CD18-dependent adhesive mechanisms predominated and a CD11c-dependent mechanism became apparent (anti-CD11a, 67 +/- 4% inhibition; anti-CD11b, 45 +/- 9%; anti-CD11c, 26 +/- 6%; anti-CD18, 97 +/- 1%). In summary, PMN adhesion to IL-1-activated HEC involves both CD11/CD18-dependent mechanisms and an ELAM-1-dependent mechanism, and the relative contribution of these varies at different times of IL-1-induced HEC activation. The additive blocking observed at 4 h with mAb H18/7 in combination with CD11/CD18-directed Mab implies that members of the CD11/CD18 complex do not function as an obligate ligand(s) for ELAM-1.

Antibodies, Monoclonal↗
PubMed1988

Assessment of intraperitoneal adhesion formation in a rat model: can a procoagulant substance prevent adhesions?

Previous studies have shown oxidized cellulose to decrease adhesion formation in rats. A recent report showed a decrease in adhesions after application of a fibrin sealant containing thrombin, fibrinogen, and aprotinin, raising the question of whether procoagulants block adhesions by something other than a mechanical barrier effect. To assess the value of a procoagulant in preventing adhesion formation, we compared the efficacy of thrombin with that of oxidized cellulose in decreasing postoperative adhesions in rats. Eighty-five Sprague-Dawley rats underwent midline abdominal incisions and subsequent removal of a small area of right anterior abdominal wall peritoneum. Defects were left open or were closed with interrupted sutures and then treated with thrombin, oxidized cellulose, or nothing. Results obtained at postmortem seven days later showed a decrease in adhesion number and severity among animals treated with oxidized cellulose. No such effect was noted in the thrombin group. No treatment increased adhesion formation. We conclude that although oxidized cellulose appears to be of some benefit in decreasing postoperative adhesion formation in the rat, thrombin alone shows no similar effect. Further conclusions regarding adhesion induction, histologic correlates of adhesion formation, and validity of some methods of adhesion analysis are also addressed.

Animals↗
PubMed1996

Analysis of platelet adhesion to a collagen-coated surface under flow conditions: the involvement of glycoprotein VI in the platelet adhesion.

Platelet adhesion to the exposed surface of the extracellular matrix in flowing blood is the first and critical reaction for in vivo thrombus formation. However, the mechanism of this in vivo platelet adhesion has yet to be studied extensively. One of the reasons for this is the lack of a practical assay method for assessing platelet adhesion under flow conditions. We have devised an assay method (the fluorescent adhesion assay) that is based on the technique originally reported by Hubbell and McIntire (Biomaterials 7:354, 1986) with some modifications to make it more amenable for assaying small samples and have developed an analysis method to quantify the extent of platelet adhesion and aggregation from fluorescence images by using a computer-assisted image analysis system. In our assay, platelet adhesion, expressed as the percentage of the area covered by adhered platelets, was found to increase biphasically as a function of time. In the first phase, platelets interacted with the coated collagen, transiently stopping on the surface; we called this reaction the temporary arrest. In the second phase, platelets adhered much more rapidly and permanently on the surface, and this adhesion was dependent on the shear rate; platelets formed aggregates in this phase. We used our assay to analyze the effects of platelet aggregation inhibitors on platelet adhesion. All three examined inhibitors, EDTA (10 mmol/L), antiglycoprotein (GP) IIb/IIIa, and GRGDS peptide (1 mmol/L), inhibited the second phase adhesion in flowing blood. Furthermore, GPVI-deficient platelets also showed defective second-phase adhesion under the same conditions. These results suggested that GPIIb/IIIa activation and GPVI contribute to the reaction inducing the second phase. The second-phase adhesion has been extensively investigated, and the consensus is that this reaction is mainly attributable to the platelet-platelet interaction. In this report, we were able to detect an earlier reaction, the temporary arrest. This temporary arrest would reflect the fast and weak interaction between platelet GPIb/IX and collagen-von Willebrand factor complexes on the collagen-coated surface.

Blood Platelets↗
PubMed1998

Interference of nonsteroidal antiinflammatory drugs with very late activation antigen 4/vascular cells adhesion molecule 1-mediated lymphocyte-endothelial cell adhesion.

OBJECTIVE: To study the effect of nonsteroidal antiinflammatory drugs (NSAIDs) on the adhesion of peripheral blood lymphocytes (PBL) to activated human umbilical vein endothelial cells (HUVEC) under conditions that resemble blood flow. METHODS: Assays of adhesion of PBL to HUVEC or recombinant vascular cell adhesion molecule 1 (rVCAM-1), intercellular adhesion molecule 1 (ICAM-1), and E-selectin were performed under continuous rotation at 37 degrees C. The phenotype of PBL subpopulations attached was characterized by flow cytometry. Lymphocytes were pretreated with different doses (5-100 microg/ml) of aceclofenac, diclofenac, indomethacin, or piroxicam or with inhibitory monoclonal antibodies (MAb) prior to the adhesion assays. The effect of NSAIDs on lymphocyte adhesion molecules was assessed by flow cytometry. To determine whether NSAIDs interfere with the affinity state of very late activation antigen 4 (VLA-4) integrin, we studied the effect of these drugs on the appearance of a beta1 activation-dependent epitope recognized by the HUTS21 MAb both on human T lymphoblasts and on synovial fluid lymphocytes (SFL). RESULTS: In the flow-resembling model, PBL-HUVEC adhesion was mainly mediated by the VLA-4/ VCAM-1 adhesion pathway. The major PBL subset attached was the CD3+, CD45RO+ memory T cell, with CD49d(high) expression. Aceclofenac, diclofenac, and indomethacin, but not piroxicam, were able to inhibit PBL adhesion to HUVEC or rVCAM-1. However, the quantitative expression of VLA-4 was not affected by treatment of PBL with any of the NSAIDs studied. On T lymphoblasts and SFL, mostly CD45RO+ cells, the expression of the beta1 activation-dependent epitope detected by HUTS21 MAb was significantly decreased by aceclofenac, diclofenac, and indomethacin. CONCLUSION: Some NSAIDs are able to inhibit the adhesion of PBL to HUVEC under conditions that resemble blood flow by interfering with the conformational change in VLA-4 that increases its affinity for VCAM-1.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1995

Reduction of monocyte adhesion to xenogenic tissue by endothelialization: an adhesion molecule and time-dependent mechanism.

Great interest has been shown for the seeding of autologous endothelial cells on prosthetic materials. We investigated the inflammatory and immunogenic properties of xenogeneic tissue before and after seeding with cultured human great saphenous vein endothelial cells in vitro. Adhesion of monocytes to xenogeneic tissue with or without endothelium and the endothelial cell expression of E-selectin, intercellular adhesion molecule 1, vascular adhesion molecule 1, and major histocompatibility complex class II antigens were investigated 1, 3, and 7 days after seeding. Both monocyte adhesion and endothelial adhesion molecule expression were relatively high 1 day after seeding and were significantly lowered after 3 to 7 days. There was no difference between monocyte adhesion and adhesion molecule expression on viable or nonviable xenogeneic tissue. Monocyte adhesion and adhesion molecule expression increased after interleukin-1 beta or interferon-gamma stimulation of the endothelial cells. The results suggest that human endothelial cells exhibit an early proinflammatory and immunogenic activity immediately after seeding. Three and 7 days after seeding, the endothelialized surface is less adhesive for monocytes as compared with nonendothelialized tissue. These findings have implications when cultured or intraoperatively recruited endothelial cells are used clinically.

Animals↗
PubMed2006

Effect of simulated pulpal pressure on dentin permeability and adhesion of self-etch adhesives.

OBJECTIVES: Dentin bonds made with one-bottle etch-and-rinse and self-etch adhesives are affected by the formation of interfacial blisters, porosities and deterioration. The first objective of this study was to evaluate the fluid flow through resin-dentin interfaces created by self-etching adhesives applied to deep dentin using a replica technique and by directly measuring dentin permeability (P). The second objective was to examine the effect of intrapulpal pressure on the microtensile bond strength of these adhesives. METHODS: A fluid-transport model was used to measure the fluid permeability (%P) through different adhesives. Impressions of bonded dentin were taken with a polyvinylsiloxane impression material to monitor fluid transudation from the surface of the adhesive. Positive replicas were fabricated for SEM examination. Two groups of resin-bonded specimens (pulpal pressure versus no pulpal pressure) were created for microtensile bond strength evaluation. Adhesive application was performed under 0 cm H(2)O. Pulpal pressure group was submitted to 20 cm H(2)O of pulpal pressure during build-up procedures. RESULTS: Clearfil Protect Bond exhibited the lowest permeability and fewest numbers of fluid droplets over the surface of the bonded dentin. G-Bond and Clearfil-S3 Bond were more permeable than Clearfil Protect Bond. One Up Bond F was the most permeable adhesive. A highly significant correlation was observed between the relative permeability of these adhesives (%P) and the number of fluid droplets on the adhesive surfaces. The application of pulpal pressure significantly reduced bond strength. SIGNIFICANCE: Resin-dentin bonds created by contemporary self-etch adhesives are susceptible to fluid permeation induced by pulpal pressure. HEMA-based adhesives showed the largest reductions in bond strengths after pulpal pressure application.

Acid Etching, Dental↗
PubMed2005

Assessing the effect of latex particle size and distribution on the rheological and adhesive properties of model waterborne acrylic pressure-sensitive adhesives films.

The adhesive and rheological properties of model acrylic pressure-sensitive adhesive (PSA) films prepared from high solid emulsions with different particle sizes and distributions have been investigated with a customized probe tack apparatus. For each emulsion, the monomer composition and gel content were kept constant but different average particle sizes and distributions were used. Adhesive films 100 microm thick were then prepared from these emulsions and their rheological properties in the linear regime and adhesive properties were systematically characterized. Surprisingly, both the rheological and adhesive properties were found to be very dependent on the initial latex particle size distribution. A series of experiments were carried out to assess the adhesive properties of films made from blends of small- and large-particle-size latexes. Using the probe tack test, a maximum in adhesion energy of the dry films was found for 60% of small particles in the blend, a composition clearly different from that giving a minimum viscosity of the latex implying that optimizing for properties may not be equivalent to optimizing for processing in these adhesive applications. Finally, the adhesive properties of two multimodal latexes with different particle size distributions were investigated. Both gave significantly higher adhesion energies and clear evidence of a fibrillar detachment process. This important result suggests that the spatial distribution of gel domains in the dry film and the molecular connectivity between those gel domains also play an important role in controlling its adhesive properties.

Journal Article↗
PubMed1991

[A study of the adhesive resins used in adhesion bridges].

UNLABELLED: We suspected that the composition of stiffened adhesive resins may cause adhesion bridges to drop out. In this study, by using a scanning type electron microscope, we observed the breaking sides of the adhesive resin after the tension test. We also examined the surfaces of the resin that we cut and ground after it had hardened, and the surfaces of the adhesion bridges that dropped out. RESULTS: 1) RESULTS of the tension test. No significant differences between the adhesive resins were observed. We noticed no significant differences between the metal surface treatment methods. 2) Observations of the breaking side after the tension test. When we examined Panavia EX, we observed flaking of the metallic side and the tooth enamel. We noticed that the surface was smooth regardless of the method of preprocessing the metal. But the surface of the adhesive resin was bumpy, and we found bubbles of different sizes on the resin surfaces. When we examined Super-Bond C&B, we observed flaking of the metallic side and the tooth enamel, and the surfaces were smooth regardless of the method of preprocessing the metal. Unlike Panavia EX, however, we found various hollows, big and small, like the bubbles on the smooth surfaces of Super-Bond C&B. 3) Observations of the abrasive surface of stiffened adhesive resins. With an ambient temperature of 15 and 28 degrees, we found many minute hollows like bubbles on the abrasive surfaces of Panavia EX and Super-Bond C&B. 4) Observations of the surface of the bonding materials of the adhesion bridges which dropped out. We found bumpy surfaces on the adhesive resin which remained on the metallic side of the adhesion bridges, whichever position the adhesion bridges dropped out of.

Boron Compounds↗
PubMed2005

Quantitative measurement of changes in adhesion force involving focal adhesion kinase during cell attachment, spread, and migration.

Focal adhesion kinase (FAK) is a critical protein for the regulation of integrin-mediated cellular functions and it can enhance cell motility in Madin-Darby canine kidney (MDCK) cells by hepatocyte growth factor (HGF) induction. We utilized optical trapping and cytodetachment techniques to measure the adhesion force between pico-Newton and nano-Newton (nN) for quantitatively investigating the effects of FAK on adhesion force during initial binding (5 s), beginning of spreading (30 min), spreadout (12 h), and migration (induced by HGF) in MDCK cells with overexpressed FAK (FAK-WT), FAK-related non-kinase (FRNK), as well as normal control cells. Optical tweezers was used to measure the initial binding force between a trapped cell and glass coverslide or between a trapped bead and a seeded cell. In cytodetachment, the commercial atomic force microscope probe with an appropriate spring constant was used as a cyto-detacher to evaluate the change of adhesion force between different FAK expression levels of cells in spreading, spreadout, and migrating status. The results demonstrated that FAK-WT significantly increased the adhesion forces as compared to FRNK cells throughout all the different stages of cell adhesion. For cells in HGF-induced migration, the adhesion force decreased to almost the same level (approximately 600 nN) regardless of FAK levels indicating that FAK facilitates cells to undergo migration by reducing the adhesion force. Our results suggest FAK plays a role of enhancing cell adhesive ability in the binding and spreading, but an appropriate level of adhesion force is required for HGF-induced cell migration.

Animals↗
PubMed2003

Avidity modulation activates adhesion under flow and requires cooperativity among adhesion receptors.

An early step in activation of leukocyte adhesion is a release of integrins from cytoskeletal constraints on their diffusion, leading to rearrangement and, consequently, increased avidity. Static adhesion assays using purified ligand as a substrate have demonstrated that very low doses of cytochalasin D disconnect beta2-integrins from their cytoskeletal links, allowing rearrangement and activating adhesion. The adhesion process in blood vessels is poorly simulated by these assays, however, for two reasons: leukocyte adhesion to endothelium 1), occurs in the presence of blood flow and 2), involves the simultaneous interactions of multiple sets of adhesion molecules. We investigated the effect of cytochalasin D, at concentrations that increase integrin diffusion but do not alter leukocyte shape and surface features, on adhesion of leukocytes to endothelial cells under flow. Cytochalasin D increased the number of rolling cells, the number of firmly adherent cells, and the duration of both rolling and firm adhesion. These effects required endothelial cell expression of ICAM-1, the ligand for leukocyte beta2-integrins. The beta2-integrin-ICAM-1 interaction alone was not sufficient, however. Experiments using purified substrates demonstrated that avidity effects on activation of adhesion under flow require functional cooperativity between integrins and other adhesion receptors.

Animals↗
PubMed1998

Efficacy of tray adhesives for the adhesion of elastomer rubber impression materials to impression modeling plastics for border molding.

STATEMENT OF PROBLEM: Tray adhesive, which is used for the adhesion of elastomer rubber impression materials to a custom resin tray, lowers the retention of the impression materials to the impression modeling plastics, as some ingredients of tray adhesive make the impression modeling plastic soft and tacky. PURPOSE: The efficacy of tray adhesive, which is used for the adhesion of elastomer rubber impression materials to a custom resin tray, on the adhesion between elastomer rubber impression material and impression modeling plastic was investigated. MATERIAL AND METHODS: Four silicone rubber impression materials (two addition reaction types and two condensation reaction types), two polysulfide rubber impression materials, and one impression modeling plastic were used in this study. Tensile strength between elastomer rubber impression material and impression modeling plastic with or without the application of tray adhesive was evaluated. RESULTS: Although tray adhesives for both addition reaction type and both condensation reaction type of silicone impression materials and one tray adhesive for polysulfide rubber impression material increased the tensile strength between the impression material and impression modeling plastic, one tray adhesive for polysulfide rubber impression material decreased the tensile strength when sufficient drying time was not applied.

Adhesiveness↗
PubMed2001

Type XIII collagen: a novel cell adhesion component present in a range of cell-matrix adhesions and in the intercalated discs between cardiac muscle cells.

Recent analysis of type XIII collagen surprisingly showed that it is anchored to the plasma membranes of cultured cells via a transmembrane segment near its amino terminus. Here we demonstrate that type XIII collagen is concentrated in cultured skin fibroblasts and several other human mesenchymal cell lines in the focal adhesions at the ends of actin stress fibers, co-localizing with the known focal adhesion components talin and vinculin. This co-occurrence was also observed in rapidly forming adhesive structures of spreading and moving fibroblasts and in disrupting focal adhesions following microinjection of the Rho-inhibitor C3 transferase into the cells, suggesting that type XIII collagen is an integral focal adhesion component. Moreover, it appears to have an adhesion-related function since cell-surface expression of type XIII collagen in cells with weak basic adhesiveness resulted in improved cell adhesion on selected culture substrata. In tissues type XIII collagen was found in a range of integrin-mediated adherens junctions including the myotendinous junctions and costameres of skeletal muscle as well as many cell-basement membrane interfaces. Some cell-cell adhesions were found to contain type XIII collagen, most notably the intercalated discs in the heart. Taken together, the results strongly suggest that type XIII collagen has a cell adhesion-associated function in a wide array of cell-matrix junctions.

Animals↗
PubMed1999

Does soluble intercellular adhesion molecule-1 (ICAM-1) affect neutrophil activation and adhesion following ischaemia-reperfusion?

OBJECTIVES: To examine the effect of reperfusion plasma and sICAM-1 on neutrophil integrin expression and neutrophil adhesion to determine if sICAM-1 has a potential role in the regulation of neutrophil adhesion. MATERIALS: Twenty-seven patients, 17 men and 10 women undergoing femorodistal surgery. Blood was taken preoperatively and from the femoral vein following the release of the cross-clamp. Neutrophils were obtained from five volunteers and incubated with phosphate buffered saline (PBS), preoperative plasma or reperfusion plasma with and without sICAM-1. Neutrophil expression of CD11b and adhesion were measured. MAIN RESULTS: Neutrophil CD11b expression did not change following incubation in the three media. Neutrophil adhesion increased significantly following exposure to reperfusion plasma compared to PBS or preoperative plasma (45.5 adhesion vs. 12.75%, p < 0.01 Mann-Whitney U-test). Soluble ICAM-1 decreased CD11b expression and adhesion in neutrophils exposed to reperfusion plasma only (CD11b expression fell from 15.9 to 3.4 mcf, p < 0.01 Mann-Whitney U-test and adhesion fell to 11.6% cells adhered, p < 0.01). CONCLUSION: An increase in CD11b expression is not required for an increase in neutrophil adhesion. The change in neutrophil adhesion produced by reperfusion plasma can be blocked by sICAM-1. Soluble ICAM-1 may have a physiological role in the regulation of neutrophil adhesion.

Aged↗
PubMed1999

Elevated serum intercellular adhesion molecule-1 and vascular adhesion molecule-1 among patients with stable angina pectoris who suffer cardiovascular death or non-fatal myocardial infarction.

AIMS: Inflammatory mechanisms have been implicated in the pathogenesis of atherosclerosis. Cell adhesion molecules, expressed on endothelial cells and leukocytes, mediate transendothelial migration of leukocytes into the vessel wall, but also circulate in soluble forms. In the present study we related soluble cell adhesion molecules to the risk of suffering a cardiovascular death or a non-fatal myocardial infarction (cardiovascular death/myocardial infarction) in a substudy to the Angina Prognosis Study in Stockholm (APSIS). METHODS AND RESULTS: Soluble intercellular adhesion molecule-1, vascular adhesion molecule-1 and E-selectin were measured in serum collected on inclusion in the APSIS study. During follow-up, seven patients suffered non-fatal myocardial infarction or cardiovascular death, whereas 86 patients were event-free. Cardiovascular death/myocardial infarction was associated with elevated intercellular adhesion molecule-1 (354+/-142 vs 282+/-62ng x ml-1;P<0.01) and vascular adhesion molecule-1 (538+/-138 vs 433+/-135ng x ml-1;P =0.05), and E-selectin levels tended to be higher (72+/-54 vs 49+/-20ng x ml-1). Clinical risk factors (history of hypertension, previous myocardial infarction, diabetes and smoking) were more abundant in the event group. Subgroup analyses showed that hypertension, smoking or male sex were associated with elevated intercellular adhesion molecule-1, whereas previous myocardial infarction or male sex were associated with elevated vascular adhesion molecule-1. CONCLUSION: Patients with stable angina pectoris who developed cardiovascular death/myocardial infarction had elevated serum levels of soluble cell adhesion molecules, indicating increased inflammatory activity. The value of soluble cell adhesion molecules as prognostic markers in patients with stable ischaemic heart disease merits further study.

Aged↗