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Firm Adhesion (firm + adhesion)
Selected AbstractsSynthesis and function of the fibrous layers covering the eggs of Siphlonurus lacustris (Ephemeroptera, Siphlonuridae)ACTA ZOOLOGICA, Issue 1 2001Elda Gaino Abstract Ultrastructural analysis (transmission and electron scanning microscopy) of the eggs of the mayfly Siphlonurus lacustris (Eaton) showed that they are wrapped in a thick coat composed of a network of tightly entwined filaments. Groups of twisted filaments form slightly uplifted buttons that are scattered on the coat surface. After experimentally induced egg deposition, egg,water interaction promotes marked cohesion of the eggs and their firm adhesion to the substrate. Egg masses include numerous gametes; the covering of those located close to the substrate greatly extends to anchor the whole mass. Eggs removed from the coat reveal a slightly punctuated smooth chorion and tagenoform micropyles (three to five). The coat increases egg size by about 20%. The lack of female reproductive accessory glands in Ephemeroptera transfers the synthesis of the adhesive coats to the follicle cells, which are typically competent for insect egg shell deposition (vitelline envelope and chorionic layers). This covering results from electron-dense granules that give rise to filaments progressively organized to form superimposed layers variously orientated around the egg. In addition to egg adhesion to the substrate, a trophic function and protection from shear stress are postulated for this covering. [source] Differential Roles of CD36, ICAM-1, and P-selectin in Plasmodium falciparum Cytoadherence In VivoMICROCIRCULATION, Issue 6 2007Bryan G. Yipp ABSTRACT Cytoadherence of Plasmodium falciparum -infected red blood cells (IRBCs) on human microvascular endothelium is mediated by synergistic adhesive interactions with different adhesion molecules in vitro. Here, the authors used a unique human/severe combined immunodeficient (SCID) mouse chimeric model to directly visualize IRBC,endothelial interactions in an intact human microvasculature in vivo. Stimulation of human skin grafts with 100 ng TNF-, for 4 h led to a dramatic reduction in the distance rolled by IRBCs before arrest, so that the majority of IRBCs adhered directly to the endothelium with a 1.8-fold increase in the number of adherent cells. The decrease in rolling distance and increase in adhesion could be reversed by anti-ICAM-1. More importantly, the effect of TNF-, could be seen only in the presence of CD36. A further increase in adhesion by 4.9-fold was observed after 24 h of TNF-, stimulation. The increase could be reversed by anti-ICAM-1, but not anti-VCAM-1. In histamine-stimulated grafts, the rolling flux fraction and adhesion increased by 2.8- and 1.6-fold, respectively. The increases were attributable to P-selectin as an inhibitory anti-P-selectin antibody abrogated both the increased rolling flux fraction and firm adhesion. These findings indicate that in addition to CD36, ICAM-1, and P-selectin are major contributors to the dynamic process of IRBC adhesion by different mechanisms in vivo. [source] Platelet Recruitment in the Murine Hepatic Microvasculature During Experimental Sepsis: Role of NeutrophilsMICROCIRCULATION, Issue 2 2006GEORG SINGER ABSTRACT Objectives: Sepsis is a major clinical problem that often results in the dysfunction or failure of multiple organs, including the liver. While inflammatory cell activation has been implicated as an early critical event in sepsis-induced liver dysfunction, there is growing evidence for the involvement of activated platelets in this pathologic process. Methods: Intravital microscopy was used in this study to assess the magnitude and time course of platelet adhesion in the liver microcirculation during experimental sepsis and to determine whether the platelet accumulation is linked to leukocyte infiltration. The adhesion of platelets and leukocytes in terminal hepatic venules (THV) and sinusoids was quantified at 2, 4, and 6 h after abdominal sepsis induced by cecal ligation and puncture (CLP). Results: While the rolling and firm adhesion of platelets and leukocytes in THV were not altered in the first 2 h after CLP, platelet recruitment was observed at 4 h and further elevated at 6 h after CLP. Leukocyte adhesion in THV exhibited a similar time course. A similar accumulation of blood cells in sinusoids was noted after CLP. This was accompanied by an increased number of nonperfused sinusoids. CLP-induced leukocyte and platelet recruitment in THV and sinusoids was attenuated in mice rendered neutropenic with anti-neutrophil serum. Conclusion: These findings indicate that sepsis is associated with a neutrophil-dependent recruitment of platelets in the liver microcirculation that impairs sinusoidal perfusion and may contribute to the liver dysfunction associated with sepsis. [source] Possible Steps Involved in the Transition to Stationary Adhesion of Rolling Neutrophils: A Brief ReviewMICROCIRCULATION, Issue 6 2000C. WAYNE SMITHArticle first published online: 26 JAN 2010 ABSTRACT The transition from rolling to firm adhesion is a phenomenon frequently observed when neutrophils are interacting with activated endothelium in vitro or in vivo under physiologically relevant shear stress. The mechanisms leading to this activation are poorly understood, though selectin-dependent tethering and CD18-integrin-dependent adhesion are known to be involved. This transition may involve a sequence of interactions that trigger sufficient integrin activation to allow cell arrest under flow. Recent evidence is reviewed in support of the concept that integrin (Mac-1 and LFA-1) activation results from signaling that occurs through selectin binding, chemotactic factor stimulation, and, possibly, LFA-1 binding. [source] Increased Sensitivity to the C-X-C Chemokine CINC/gro in a Model of Chronic InflammationMICROCIRCULATION, Issue 2 2000Brent Johnston ABSTRACT Objective: The C-C chemokine MCP-1 elicits significant neutrophil emigration in rats with chronic adjuvant-induced inflammation, but not in naive animals. We examined responses to the C-X-C chemokine CINC/gro to determine whether this class of chemokine elicits altered neutrophil responses during chronic inflammation. Methods: CINC/gro was superfused over mesenteric venules of naive rats or animals with chronic adjuvant-induced vasculitis. Antibodies were used to characterize adhesive mechanisms. Results: CINC/gro elicited leukocyte transendothelial migration in adjuvantimmunized rats at 100-fold lower concentrations than required to elicit transmigration in naive animals. In both groups, neutrophils constituted >95% of the leukocytes recruited by CINC/gro. Using in vitro chemotaxis assays, neutrophils from control and adjuvant-immunized rats responded equally to CINC/gro, suggesting differences in migration were not related to neutrophil phenotype. Differences in adhesion molecule usage were noted in vivo. In control animals, CD18 antibodies blocked CINC/gro-induced neutrophil adhesion and emigration. In adjuvant-immunized animals, an ,4 -integrin antibody reduced adhesion and emigration, while a CD18 antibody selectively inhibited emigration. Conclusions: This study demonstrates increased sensitivity to a C-X-C chemokine in a model of chronic inflammation, implicates the ,4 -integrin in neutrophil adhesion, and demonstrates that CD18 mediates leukocyte transendothelial migration independent from firm adhesion. [source] Anti-adhesive Membrane for Pleural CavityARTIFICIAL ORGANS, Issue 3 2010Yasuharu Noishiki Abstract An anti-adhesive membrane containing a large amount of glycerin was developed for lung surgery and was tested in the pleural cavity of six dogs. The test membranes were put between the lung and the chest wound of the pleural cavity wall to separate them. In five of the animals, no adhesion was observed after 3 weeks in the area where the membrane had been inserted, but the area without the membrane showed firm adhesion between the lung and the pleural cavity wall. A sixth animal observed for 3 months also showed no adhesion. Seprafilm, which is the product of choice for peritoneal surgeries, was used as a control in six dogs. Seprafilm could not prevent adhesion in the pleural cavity of all six animals after 3 weeks observation. The new test membrane contained glycerin, which gathered and dispersed abundant water. Together with this, growth factors are also dispersed, resulting in dilution of excessive growth factors at the wound sites. In general, fibroblasts do not migrate in an extremely hydrous gel matrix. Migration of fibroblasts into the membrane is minimized, resulting in the prevention of formation of adhesion tissue composed of fibroblasts and collagen fibers. From the results, we assume that water can prevent adhesion after surgery. [source] Leukocyte rolling is exclusively mediated by P-selectinin colonic venulesBRITISH JOURNAL OF PHARMACOLOGY, Issue 7 2002Ming Xiu Wan The objective of the present study was to examine the role of the endothelial selectins (i.e. P- and E-selectin) in leukocyte-endothelium interactions in colonic venules by use of intravital microscopy. Balb/c mice were exposed to dextran sodium sulphate (DSS) in the drinking water for 5 days or treated intraperitoneally (i.p.) with tumour necrosis factor-, (TNF-,) for 3 h. In DSS-treated mice, mRNA of both P- and E-selectin were expressed and leukocyte rolling and adhesion was increased to 27±3 cells min,1 and 36±8 cells mm,1, respectively. An anti-P-selectin antibody abolished DSS-induced leukocyte rolling, whereas an antibody against E-selectin had no effect. Established leukocyte adhesion was insensitive to inhibition of the selectins. DSS markedly increased production of TNF-, in the colon. TNF-, increased leukocyte rolling to 22±3 cells min,1 and adhesion to 45±4 cells mm,1. Only inhibition of P-selectin significantly reduced (>94%) leukocyte rolling provoked by TNF-,. Leukocyte adhesion was not changed by late anti-P-selectin antibody treatment. In contrast, pretreatment with the anti-P-selectin antibody not only abolished leukocyte rolling but also completely inhibited firm adhesion in response to TNF-,. This study demonstrates that P-selectin plays an important role in leukocyte rolling in colonic venules, both in experimental colitis and when stimulated with TNF-,. Moreover, P-selectin-dependent leukocyte rolling was found to be a precondition for TNF-,-induced firm adhesion. Thus, these findings suggest that P-selectin may be a key target to reduce pathological recruitment of inflammatory cells in the colon. British Journal of Pharmacology (2002) 135, 1749,1756; doi:10.1038/sj.bjp.0704638 [source] | ||||||||||