Journal articles: 'Anti-adhesion'

1

Anonymous. "Anti-Adhesion Gel." Orthopedics 21, no. 4 (April 1998): 452. http://dx.doi.org/10.3928/0147-7447-19980401-13.

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2

Dedrick, Russell L., Patricia Walicke, and Marvin Garovoy. "Anti-adhesion antibodies." Transplant Immunology 9, no. 2-4 (May 2002): 181–86. http://dx.doi.org/10.1016/s0966-3274(02)00029-1.

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3

SIMMONS, D. "Anti-adhesion therapies." Current Opinion in Pharmacology 5, no. 4 (August 2005): 398–404. http://dx.doi.org/10.1016/j.coph.2005.02.009.

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4

Jothy, Serge, Sandra B. Munro, Lam LeDuy, Diane McClure, and Orest W. Blaschuk. "Adhesion or anti-adhesion in cancer: what matters more?" Cancer and Metastasis Reviews 14, no. 4 (December 1995): 363–76. http://dx.doi.org/10.1007/bf00690604.

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5

Clark, Wayne M., and Justin A. Zivin. "Anti-Adhesion Molecule Monoclonal Antibodies." CNS Drugs 6, no. 2 (August 1996): 90–99. http://dx.doi.org/10.2165/00023210-199606020-00002.

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6

Wiseman, David M. "Registries for anti-adhesion products?" Fertility and Sterility 85, no. 4 (April 2006): e7. http://dx.doi.org/10.1016/j.fertnstert.2006.01.005.

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7

Etzioni, Amos. "Anti adhesion molecules - Therapeutic applications." Pharmacological Research 31 (January 1995): 130. http://dx.doi.org/10.1016/1043-6618(95)86778-3.

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8

Wiseman, David M. "Registries for anti-adhesion products?" Fertility and Sterility 86, no. 3 (September 2006): 771. http://dx.doi.org/10.1016/j.fertnstert.2006.07.1462.

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9

Sahin, Mustafa, Murat Cakir, Fatih Mehmet Avsar, Ahmet Tekin, Tevfik Kucukkartallar, and Mehmet Akoz. "The Effects of Anti-Adhesion Materials in Preventing Postoperative Adhesion in Abdominal Cavity (Anti-Adhesion Materials for Postoperative Adhesions)." Inflammation 30, no. 6 (August 10, 2007): 244–49. http://dx.doi.org/10.1007/s10753-007-9043-1.

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10

Sheu, Shew-Meei, Bor-Shyang Sheu, Hsiao-Bai Yang, Huan-Yao Lei, and Jiunn-Jong Wu. "Anti-Lewis X Antibody Promotes Helicobacter pylori Adhesion to Gastric Epithelial Cells." Infection and Immunity 75, no. 6 (March 19, 2007): 2661–67. http://dx.doi.org/10.1128/iai.01689-06.

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ABSTRACT Lewis X (Lex) antigen is expressed on the human gastric mucosa and the O-specific chain of lipopolysaccharides of Helicobacter pylori. This antigen can induce autoantibodies, which may be involved in bacterial colonization and thus deserve further investigation. Flow cytometry was used to examine the effects of anti-Le monoclonal antibodies (MAbs) on H. pylori adhesion. A babA2 mutant was also constructed to evaluate the effect of an anti-Lex MAb on adhesion. The bacterial agglutination and in situ adhesion assays were used to confirm the anti-Lex MAb effect on H. pylori adhesion. This study revealed that an anti-Lex MAb, but not an anti-Leb MAb or an anti-Ley MAb, could enhance the adhesion of H. pylori strains that expressed high levels of Lex antigen to AGS cells. The enhancement was not found on an H. pylori strain with a low level of Lex antigen. Anti-Lex MAb could increase the adhesion of both the wild-type strain and its isogenic babA2 mutant to AGS cells. When AGS cells were pretreated with anti-Lex MAb, the adhesion of the babA2 mutant also increased. Only anti-Lex MAb could promote bacterial agglutination, and the in situ adhesion assay further confirmed that adding anti-Lex MAb resulted in denser bacterial adhesion on the gastric epithelia collected from clinical patients. These results suggest anti-Lex MAb could specifically enhance the adhesion abilities of H. pylori strains through a mechanism by which anti-Lex MAb promotes bacterial aggregation and mediates bivalent interaction (antigen-antibody-antigen) between bacteria and host cells.

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11

Lv, Mingchuan, Lipeng Song, Yuheng Li, Jiyu Liu, Yuyang Zhou, Jinming Liu, Xin Liu, and Jing Sun. "High quality anti-adhesion conductive electrotome." Materials Letters 313 (April 2022): 131750. http://dx.doi.org/10.1016/j.matlet.2022.131750.

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12

Barnes, Jo. "Sticking up for anti-adhesion molecules." Inpharma Weekly &NA;, no. 976 (March 1995): 9–10. http://dx.doi.org/10.2165/00128413-199509760-00016.

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13

Yadav, Ashok Kumar, Ashish Tyagi, Ashwani Kumar, Surbhi Panwar, Sunita Grover, Asha Chandola Saklani, Rajkumar Hemalatha, and Virender Kumar Batish. "Adhesion ofLactobacilliand their anti-infectivity potential." Critical Reviews in Food Science and Nutrition 57, no. 10 (April 16, 2015): 2042–56. http://dx.doi.org/10.1080/10408398.2014.918533.

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14

Lih, Eugene, Se Heang Oh, Yoon Ki Joung, Jin Ho Lee, and Dong Keun Han. "Polymers for cell/tissue anti-adhesion." Progress in Polymer Science 44 (May 2015): 28–61. http://dx.doi.org/10.1016/j.progpolymsci.2014.10.004.

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15

Roman, Horace, and Michel Canis. "Reply: Registries for anti-adhesion products?" Fertility and Sterility 85, no. 4 (April 2006): e8. http://dx.doi.org/10.1016/j.fertnstert.2006.01.006.

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16

Pan, C. T., T. L. Yang, C. H. Chao, Z. K. Wang, and P. R. Ni. "Study on Anti-Adhesion Layers Using AFM for Nanoimprint Process." Key Engineering Materials 661 (September 2015): 128–33. http://dx.doi.org/10.4028/www.scientific.net/kem.661.128.

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This study investigates how to improve the anti-adhesion issues between Silicon mold and nanostructures of hard polydimethylsiloxane (H-PDMS). A Silicon mold with different depths and widths was made using a focused ion beam (FIB). During the soft-lithography molding process, anti-adhesion layers were needed between the Silicon mold and H-PDMS samples to prevent the de-molding failure caused by the adhesion issues between the interfaces. This study adopts three methods to deposit anti-adhesion layers, such as liquid immersion, vapor deposition, and fluorine-doped diamond-like carbon (F-DLC) film. Perfluorooctyl-trichlorosilane (PFOTCS) was used as a mold-releasing agent for the liquid immersion and vapor deposition methods. The contact angles between each film were measured to determine the effect of anti-adhesion on the molding process. In addition, atomic force microscopy (AFM) was used to measure the adhesion force between the H-PDMS and anti-adhesion layers. The results show that the coatings of anti-adhesion layers are an effective approach to improve the formability of molding.

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17

Zhang, Yishu, Long Chen, and Hui Liu. "Study on ice adhesion of composite anti-/deicing component under heating condition." Advanced Composites Letters 29 (January 1, 2020): 2633366X2091244. http://dx.doi.org/10.1177/2633366x20912440.

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An anti-/deicing component of composite materials for wind turbine blades is usually carried out under heating conditions. In order to study the ice adhesion properties of composite anti-/deicing component under heating conditions, an experimental platform for measuring ice adhesion force on composites was set up. Based on the heating parameters such as the heating temperature, heating voltage, and heating time, the experiments of ice adhesion of composite anti-/deicing component under deicing conditions were designed by orthogonal analysis. In this article, ice adhesion forces on composite anti-/deicing component were measured at −9.74°C, −11.58°C, −14.1°C, and −16.84°C by the proposed experiment platform, and the real ice adhesion forces under various heating parameters were measured. Through the analysis of experimental data and fitting method, the relationship between various factors and ice adhesion on composite anti-/deicing component was expounded. The influence weight of each heating parameter on the ice adhesion was analyzed. In addition, the mathematical model of ice adhesion on composite anti-/deicing component under deicing condition was established to describe the influence of deicing variables on ice adhesion in the experiments. According to the fitting function of the experimental data, the relationship between the heat consumption of composite anti-/deicing component and ice adhesion force in the process of heating is in accordance with the inverse power exponential expression, which reveals the internal relationship between ice adhesion force and energy consumption.

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18

Lauener, R. P., R. S. Geha, and D. Vercelli. "Engagement of the monocyte surface antigen CD14 induces lymphocyte function-associated antigen-1/intercellular adhesion molecule-1-dependent homotypic adhesion." Journal of Immunology 145, no. 5 (September 1, 1990): 1390–94. http://dx.doi.org/10.4049/jimmunol.145.5.1390.

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Abstract Murine anti-CD14 mAb which recognize different CD14 epitopes induced marked homotypic adhesion of normal human monocytes. Induction of aggregation by anti-CD14 mAb required Mg2+, occurred at an optimal temperature of 37 degrees C, but not at 4 degrees C, and exhibited a kinetics which differed from adhesion triggered by IFN-gamma and anti-CD43 mAb. Monocyte adhesion induced by anti-CD14 mAb required neither Fcy gamma R engagement nor cross-linking of CD14, because adhesion was induced by F(ab)'2 fragments, as well as by monovalent F(ab) fragments of anti-CD14 mAb. mAb to CD11a, CD18, and intercellular adhesion molecule-1 (ICAM-1), but not antibodies to CD11b and CD11c, inhibited monocyte adhesion induced by CD14 engagement. These results indicate that CD14-dependent adhesion is mediated by lymphocyte function-associated Ag-1/ICAM-1 interactions. This was confirmed by the absence of aggregation in anti-CD14-stimulated cells from a patient with leukocyte adhesion deficiency. Monocyte adhesion upon CD14 engagement was blocked by an inhibitor of protein kinases, sphingosine. This suggests that protein kinases play a role in the intracellular signaling pathway(s) which couple CD14 to lymphocyte function-associated Ag-1/ICAM-1.

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19

Kuligowski, Michael P., Rain Y. Q. Kwan, Cecilia Lo, Cyndi Wong, Will G. James, Dorothee Bourges, Joshua D. Ooi, et al. "Antimyeloperoxidase antibodies rapidly induce α4-integrin–dependent glomerular neutrophil adhesion." Blood 113, no. 25 (June 18, 2009): 6485–94. http://dx.doi.org/10.1182/blood-2008-12-192617.

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Abstract Patients with antineutrophil cytoplasmic antibodies (ANCAs) frequently develop severe vasculitis and glomerulonephritis. Although ANCAs, particularly antimyeloperoxidase (anti-MPO), have been shown to promote leukocyte adhesion in postcapillary venules, their ability to promote adhesion in the glomerular vasculature is less clear. We used intravital microscopy to examine glomerular leukocyte adhesion induced by anti-MPO. In mice pretreated with LPS, 50 μg anti-MPO induced LFA-1–dependent adhesion in glomeruli. In concert with this finding, in mice pretreated with LPS, more than 80% of circulating neutrophils bound anti-MPO within 5 minutes of intravenous administration. However, even in the absence of LPS, more than 40% of circulating neutrophils bound anti-MPO in vivo, a response not seen in MPO−/− mice. In addition, a higher dose of anti-MPO (200 μg) induced robust glomerular leukocyte adhesion in the absence of LPS. The latter response was β2-integrin independent, instead requiring the α4-integrin, which was up-regulated on neutrophils in response to anti-MPO. These data indicate that anti-MPO antibodies bind to circulating neutrophils, and can induce glomerular leukocyte adhesion via multiple pathways. Lower doses induce adhesion only after an infection-related stimulus, whereas higher doses are capable of inducing responses in the absence of an additional inflammatory stimulus, via alternative adhesion mechanisms.

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20

Park, Heekyung, Seungho Baek, Hyun Kang, and Donghyun Lee. "Biomaterials to Prevent Post-Operative Adhesion." Materials 13, no. 14 (July 8, 2020): 3056. http://dx.doi.org/10.3390/ma13143056.

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Surgery is performed to treat various diseases. During the process, the surgical site is healed through self-healing after surgery. Post-operative or tissue adhesion caused by unnecessary contact with the surgical site occurs during the normal healing process. In addition, it has been frequently found in patients who have undergone surgery, and severe adhesion can cause chronic pain and various complications. Therefore, anti-adhesion barriers have been developed using multiple biomaterials to prevent post-operative adhesion. Typically, anti-adhesion barriers are manufactured and sold in numerous forms, such as gels, solutions, and films, but there are no products that can completely prevent post-operative adhesion. These products are generally applied over the surgical site to physically block adhesion to other sites (organs). Many studies have recently been conducted to increase the anti-adhesion effects through various strategies. This article reviews recent research trends in anti-adhesion barriers.

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21

Sharma, Rashmi P., Siddheshwar D. Raut, Vijaykumar V. Jadhav, Ambadas S. Kadam, and Rajaram S. Mane. "Anti-candida and anti-adhesion efficiencies of zinc ferrite nanoparticles." Materials Letters 237 (February 2019): 165–67. http://dx.doi.org/10.1016/j.matlet.2018.11.073.

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22

Harding, C. V., and E. R. Unanue. "Modulation of antigen presentation and peptide-MHC-specific, LFA-1-dependent T cell-macrophage adhesion." Journal of Immunology 147, no. 3 (August 1, 1991): 767–73. http://dx.doi.org/10.4049/jimmunol.147.3.767.

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Abstract Incubation of peritoneal macrophages in vitro before fixation increased their ability to present exogenous peptides to 3A9 T hybridoma cells. The enhanced level of presentation correlated with a greatly increased, peptide-specific adhesion of 3A9 cells to the macrophages, whereas peptide-independent adhesion was minimal and essentially unaltered. 3A9 cells exhibited rapid peptide-specific adhesion (plateau by 5 to 10 min) and deadhesion (complete reversal by 5 min). Peptide-specific adhesion was blocked by anti-I-Ak and anti-LFA-1. Interaction of T cell receptors and CD-4 with peptide-I-Ak complexes appeared to provide little direct contribution to the avidity of T cell-macrophage adhesion, but activated a LFA-1-mediated adhesion mechanism. In addition, anti-T cell receptor, anti-CD3, and anti-CD4 antibodies themselves activated LFA-1-dependent adhesion in the absence of peptide. Unlike the peptide-induced adhesion, this adhesion was similar for macrophages whether or not they were incubated in vitro before fixation. We conclude that the different macrophage populations supported LFA-1-mediated adhesion equally. Therefore, the enhancement of T cell stimulation observed after in vitro incubation of macrophages was due to increased peptide presentation and consequently increased triggering of LFA-1-mediated adhesion. Mechanisms may exist to regulate the effectiveness with which peptide-class II MHC complexes are displayed for T cell recognition.

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23

Eckert, Denise, Felicitas Rapp, Ayele T. Tsedeke, Jessica Molendowska, Robert Lehn, Markus Langhans, Claudia Fournier, Franz Rödel, and Stephanie Hehlgans. "ROS- and Radiation Source-Dependent Modulation of Leukocyte Adhesion to Primary Microvascular Endothelial Cells." Cells 11, no. 1 (December 27, 2021): 72. http://dx.doi.org/10.3390/cells11010072.

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Anti-inflammatory effects of low-dose irradiation often follow a non-linear dose–effect relationship. These characteristics were also described for the modulation of leukocyte adhesion to endothelial cells. Previous results further revealed a contribution of reactive oxygen species (ROS) and anti-oxidative factors to a reduced leukocyte adhesion. Here, we evaluated the expression of anti-oxidative enzymes and the transcription factor Nrf2 (Nuclear factor-erythroid-2-related factor 2), intracellular ROS content, and leukocyte adhesion in primary human microvascular endothelial cells (HMVEC) upon low-dose irradiation under physiological laminar shear stress or static conditions after irradiation with X-ray or Carbon (C)-ions (0–2 Gy). Laminar conditions contributed to increased mRNA expression of anti-oxidative factors and reduced ROS in HMVEC following a 0.1 Gy X-ray and 0.5 Gy C-ion exposure, corresponding to reduced leukocyte adhesion and expression of adhesion molecules. By contrast, mRNA expression of anti-oxidative markers and adhesion molecules, ROS, and leukocyte adhesion were not altered by irradiation under static conditions. In conclusion, irradiation of endothelial cells with low doses under physiological laminar conditions modulates the mRNA expression of key factors of the anti-oxidative system, the intracellular ROS contents of which contribute at least in part to leucocyte adhesion, dependent on the radiation source.

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24

Luscinskas, F. W., A. F. Brock, M. A. Arnaout, and M. A. Gimbrone. "Endothelial-leukocyte adhesion molecule-1-dependent and leukocyte (CD11/CD18)-dependent mechanisms contribute to polymorphonuclear leukocyte adhesion to cytokine-activated human vascular endothelium." Journal of Immunology 142, no. 7 (April 1, 1989): 2257–63. http://dx.doi.org/10.4049/jimmunol.142.7.2257.

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Abstract 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.

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25

Chiba, Ryuichi, Noriaki Nakagawa, Kazuhiro Kurasawa, Yoshiya Tanaka, Yasushi Saito, and Itsuo Iwamoto. "Ligation of CD31 (PECAM-1) on Endothelial Cells Increases Adhesive Function of vβ3 Integrin and Enhances β1 Integrin-Mediated Adhesion of Eosinophils to Endothelial Cells." Blood 94, no. 4 (August 15, 1999): 1319–29. http://dx.doi.org/10.1182/blood.v94.4.1319.

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Abstract We determined the role of the heterophilic interaction of vβ3 integrin on endothelial cells with CD31 on leukocytes in mediating leukocyte-endothelial cell interactions. Preincubation of interleukin-4 (IL-4)–stimulated human umbilical vein endothelial cells (HUVECs) with anti-CD31 monoclonal antibodies (MoAbs) enhanced eosinophil adhesion to the IL-4–stimulated HUVECs, and the endothelial CD31-induced enhancement of eosinophil adhesion to IL-4–stimulated HUVECs was prevented by anti–vascular cell adhesion molecule-1 (VCAM-1) MoAb and anti–very late activation antigen-4 (VLA-4) MoAb, but not by anti–intercellular adhesion molecule-1 (ICAM-1) MoAb, anti–lymphocyte function-associated antigen-1 (LFA-1) MoAb, anti–P-selectin MoAb, or anti–E-selectin MoAb. CD31 stimulation of HUVECs increased the adhesive function of vβ3 integrin to its ligand RGD peptide, the binding of which reached a maximum at 10 minutes after the stimulation, and the CD31-induced vβ3 integrin activation on HUVECs was inhibited by inhibitors of protein kinase C and phosphatidylinositol 3 kinase (PI3-kinase). Furthermore, anti-vβ3 integrin MoAb and RGD peptide as well as soluble CD31 inhibited endothelial CD31-induced enhancement of eosinophil adhesion to IL-4–stimulated HUVECs. However, anti-vβ3 integrin MoAb had no significant inhibitory effect on the eosinophil adhesion to IL-4–stimulated or unstimulated HUVECs without CD31 stimulation of HUVECs. Finally, CD31 stimulation of eosinophils increased the adhesive function of 4β1 integrin (VLA-4) to its ligand fibronectin and their adhesion to IL-4–stimulated HUVECs in a VLA-4–dependent manner. These results indicate that CD31-mediated inside-out signaling activates vβ3 integrin on endothelial cells, that the heterophilic vβ3 integrin/CD31 interaction induces β1 integrin-mediated adhesion of eosinophils to endothelial cells, and that the heterophilic interaction itself is not significantly involved in firm adhesion of eosinophils to endothelial cells.

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26

Chiba, Ryuichi, Noriaki Nakagawa, Kazuhiro Kurasawa, Yoshiya Tanaka, Yasushi Saito, and Itsuo Iwamoto. "Ligation of CD31 (PECAM-1) on Endothelial Cells Increases Adhesive Function of vβ3 Integrin and Enhances β1 Integrin-Mediated Adhesion of Eosinophils to Endothelial Cells." Blood 94, no. 4 (August 15, 1999): 1319–29. http://dx.doi.org/10.1182/blood.v94.4.1319.416k28_1319_1329.

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We determined the role of the heterophilic interaction of vβ3 integrin on endothelial cells with CD31 on leukocytes in mediating leukocyte-endothelial cell interactions. Preincubation of interleukin-4 (IL-4)–stimulated human umbilical vein endothelial cells (HUVECs) with anti-CD31 monoclonal antibodies (MoAbs) enhanced eosinophil adhesion to the IL-4–stimulated HUVECs, and the endothelial CD31-induced enhancement of eosinophil adhesion to IL-4–stimulated HUVECs was prevented by anti–vascular cell adhesion molecule-1 (VCAM-1) MoAb and anti–very late activation antigen-4 (VLA-4) MoAb, but not by anti–intercellular adhesion molecule-1 (ICAM-1) MoAb, anti–lymphocyte function-associated antigen-1 (LFA-1) MoAb, anti–P-selectin MoAb, or anti–E-selectin MoAb. CD31 stimulation of HUVECs increased the adhesive function of vβ3 integrin to its ligand RGD peptide, the binding of which reached a maximum at 10 minutes after the stimulation, and the CD31-induced vβ3 integrin activation on HUVECs was inhibited by inhibitors of protein kinase C and phosphatidylinositol 3 kinase (PI3-kinase). Furthermore, anti-vβ3 integrin MoAb and RGD peptide as well as soluble CD31 inhibited endothelial CD31-induced enhancement of eosinophil adhesion to IL-4–stimulated HUVECs. However, anti-vβ3 integrin MoAb had no significant inhibitory effect on the eosinophil adhesion to IL-4–stimulated or unstimulated HUVECs without CD31 stimulation of HUVECs. Finally, CD31 stimulation of eosinophils increased the adhesive function of 4β1 integrin (VLA-4) to its ligand fibronectin and their adhesion to IL-4–stimulated HUVECs in a VLA-4–dependent manner. These results indicate that CD31-mediated inside-out signaling activates vβ3 integrin on endothelial cells, that the heterophilic vβ3 integrin/CD31 interaction induces β1 integrin-mediated adhesion of eosinophils to endothelial cells, and that the heterophilic interaction itself is not significantly involved in firm adhesion of eosinophils to endothelial cells.

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27

May, Andreas E., Franz-Josef Neumann, Albert Schömig, and Klaus T. Preissner. "VLA-4 (α4β1) engagement defines a novel activation pathway for β2 integrin–dependent leukocyte adhesion involving the urokinase receptor." Blood 96, no. 2 (July 15, 2000): 506–13. http://dx.doi.org/10.1182/blood.v96.2.506.

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Abstract During acute inflammatory processes, β2 and β1 integrins sequentially mediate leukocyte recruitment into extravascular tissues. We studied the influence of VLA-4 (very late antigen-4) (4β1) engagement on β2 integrin activation-dependent cell-to-cell adhesion. Ligation of VLA-4 by the soluble chimera fusion product vascular cell adhesion molecule-1 (VCAM-1)–Fc or by 2 anti-CD29 (β1 chain) monoclonal antibodies (mAb) rapidly induced adhesion of myelomonocytic cells (HL60, U937) to human umbilical vein endothelial cells (HUVECs). Cell adhesion was mediated via β2 integrin (LFA-1 and Mac-1) activation: induced adhesion to HUVECs was inhibited by blocking mAbs anti-CD18 (70%-90%), anti-CD11a (50%-60%), or anti-CD11b (60%-70%). Adhesion to immobilized ligands of β2 integrins (intercellular adhesion molecule-1 [ICAM-1], fibrinogen, keyhole limpet hemocyanin) as well as to ICAM-1–transfected Chinese hamster ovary cells, but not to ligands of β1 integrins (VCAM-1, fibronectin, laminin, and collagen), was augmented. VCAM-1–Fc binding provoked the expression of the activation-dependent epitope CBRM1/5 of Mac-1 on leukocytes. Clustering of VLA-4 through dimeric VCAM-1–Fc was required for β2 integrin activation and induction of cell adhesion, whereas monovalent VCAM-1 or Fab fragments of anti-β1 integrin mAb were ineffective. Activation of β2 integrins by 4β1 integrin ligation (VCAM-1–Fc or anti-β1 mAb) required the presence of urokinase receptor (uPAR) on leukocytic cells, because the removal of uPAR from the cell surface by phosphatidylinositol-specific phospholipase C reduced cell adhesion to less than 40%. Adhesion was reconstituted when soluble recombinant uPAR was allowed to reassociate with the cells. Finally, VLA-4 engagement by VCAM-1–Fc or anti-β1 integrin mAb induced uPAR-dependent adhesion to immobilized vitronectin as well. These results elucidate a novel activation pathway of β2 integrin–dependent cell-to-cell adhesion that requires 4β1 integrin ligation for initiation and uPAR as activation transducer.

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28

May, Andreas E., Franz-Josef Neumann, Albert Schömig, and Klaus T. Preissner. "VLA-4 (α4β1) engagement defines a novel activation pathway for β2 integrin–dependent leukocyte adhesion involving the urokinase receptor." Blood 96, no. 2 (July 15, 2000): 506–13. http://dx.doi.org/10.1182/blood.v96.2.506.014k41_506_513.

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During acute inflammatory processes, β2 and β1 integrins sequentially mediate leukocyte recruitment into extravascular tissues. We studied the influence of VLA-4 (very late antigen-4) (4β1) engagement on β2 integrin activation-dependent cell-to-cell adhesion. Ligation of VLA-4 by the soluble chimera fusion product vascular cell adhesion molecule-1 (VCAM-1)–Fc or by 2 anti-CD29 (β1 chain) monoclonal antibodies (mAb) rapidly induced adhesion of myelomonocytic cells (HL60, U937) to human umbilical vein endothelial cells (HUVECs). Cell adhesion was mediated via β2 integrin (LFA-1 and Mac-1) activation: induced adhesion to HUVECs was inhibited by blocking mAbs anti-CD18 (70%-90%), anti-CD11a (50%-60%), or anti-CD11b (60%-70%). Adhesion to immobilized ligands of β2 integrins (intercellular adhesion molecule-1 [ICAM-1], fibrinogen, keyhole limpet hemocyanin) as well as to ICAM-1–transfected Chinese hamster ovary cells, but not to ligands of β1 integrins (VCAM-1, fibronectin, laminin, and collagen), was augmented. VCAM-1–Fc binding provoked the expression of the activation-dependent epitope CBRM1/5 of Mac-1 on leukocytes. Clustering of VLA-4 through dimeric VCAM-1–Fc was required for β2 integrin activation and induction of cell adhesion, whereas monovalent VCAM-1 or Fab fragments of anti-β1 integrin mAb were ineffective. Activation of β2 integrins by 4β1 integrin ligation (VCAM-1–Fc or anti-β1 mAb) required the presence of urokinase receptor (uPAR) on leukocytic cells, because the removal of uPAR from the cell surface by phosphatidylinositol-specific phospholipase C reduced cell adhesion to less than 40%. Adhesion was reconstituted when soluble recombinant uPAR was allowed to reassociate with the cells. Finally, VLA-4 engagement by VCAM-1–Fc or anti-β1 integrin mAb induced uPAR-dependent adhesion to immobilized vitronectin as well. These results elucidate a novel activation pathway of β2 integrin–dependent cell-to-cell adhesion that requires 4β1 integrin ligation for initiation and uPAR as activation transducer.

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29

Lyu, Yuan, Wadie D. Mahauad-Fernandez, and Chioma M. Okeoma. "Development and Characterization of the Shortest Anti-Adhesion Peptide Analogue of B49Mod1." Molecules 25, no. 5 (March 6, 2020): 1188. http://dx.doi.org/10.3390/molecules25051188.

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Inhibition of cancer cell adhesion is an effective approach to killing adherent cancer cells. B49 and its analog B49Mod1 peptides, derived from the extracellular domain (ECD) of bone marrow stromal antigen 2 (BST-2), display anti-adhesion activity on breast cancer cells. However, the minimal sequence required for this anti-adhesion activity is unknown. Here, we further characterized the anti-adhesion activity of B49Mod1. We show that the anti-adhesion activity of B49Mod1 may require cysteine-linked disulfide bond and that the peptide is susceptible to proteolytic deactivation. Using structure-activity relationship studies, we identified an 18-Mer sequence (B18) as the minimal peptide sequence mediating the anti-adhesion activity of B49Mod1. Atomistic molecular dynamic (MD) simulations reveal that B18 forms a stable complex with the ECD of BST-2 in aqueous solution. MD simulations further reveal that B18 may cause membrane defects that facilitates peptide translocation across the bilayer. Placement of four B18 chains as a transmembrane bundle results in water channel formation, indicating that B18 may impair membrane integrity and form pores. We hereby identify B18 as the minimal peptide sequence required for the anti-adhesion activity of B49Mod1 and provide atomistic insight into the interaction of B18 with BST-2 and the cell membrane.

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Leung, Yvette, and Remo Panaccione. "Anti-Adhesion Molecule Strategies for Crohn Disease." BioDrugs 22, no. 4 (2008): 259–64. http://dx.doi.org/10.2165/00063030-200822040-00005.

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Ofek, I. "Toward anti-adhesion therapy for microbial diseases." Trends in Microbiology 4, no. 8 (August 1996): 297–99. http://dx.doi.org/10.1016/0966-842x(96)30023-1.

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Chen, Huaxin, Yongchang Wu, Huiyun Xia, Zhen Zhang, and Teng Yuan. "Anti-freezing asphalt concrete: ice-adhesion performance." Journal of Materials Science 53, no. 7 (December 14, 2017): 4781–95. http://dx.doi.org/10.1007/s10853-017-1866-z.

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Stocks, S. C., and M. A. Kerr. "Stimulation of neutrophil adhesion by antibodies recognizing CD15 (LeX) and CD15-expressing carcinoembryonic antigen-related glycoprotein NCA-160." Biochemical Journal 288, no. 1 (November 15, 1992): 23–27. http://dx.doi.org/10.1042/bj2880023.

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The carbohydrate antigen, CD15 (Le(X)), and its sialylated derivative have recently been shown to be involved in the binding of neutrophils to the endothelial lectins, E-selectin and P-selectin. Neutrophil NCA-160, a carcinoembryonic antigen (CEA)-related glycoprotein, is the major carrier of CD15, which is also expressed on the common beta 2 chain of leucocyte integrins. Rabbit IgG antibodies directed against CEA, which cross-react with neutrophil NCAs, increase the adhesion of neutrophils to plastic. This effect is also observed with F(ab')2 and Fab antibody fragments and a monoclonal antibody (mAb) recognizing the same antigen. Anti-CD15 mAbs inhibit adhesion at higher concentrations, but augment adhesion at lower concentrations. Anti-CEA and anti-CD15 antibodies cause the homotypic adhesion of neutrophils demonstrable by light microscopy and flow cytometry. Anti-(integrin beta 2 chain) mAbs inhibit both adhesion to plastic and homotypic adhesion. These results suggest that binding of ligand to NCA-160 is able to trigger neutrophil adhesion events which have been shown to be integrin mediated. Anti-CD15 mAbs do not, however, induce a respiratory burst from neutrophils.

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Lo, S. K., G. A. Van Seventer, S. M. Levin, and S. D. Wright. "Two leukocyte receptors (CD11a/CD18 and CD11b/CD18) mediate transient adhesion to endothelium by binding to different ligands." Journal of Immunology 143, no. 10 (November 15, 1989): 3325–29. http://dx.doi.org/10.4049/jimmunol.143.10.3325.

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Abstract Upon stimulation with C5a, TNF, or phorbol dibutyrate (PDB), polymorphonuclear leukocytes (PMN) exhibit first an increase then a decrease in adhesion to unstimulated endothelial cells (EC). Essentially all of this adhesion is mediated by the CD18 family of leukocyte integrins on PMN. To determine the individual roles of CD11a/CD18 (LFA-1), CD11b/CD18 (CR3, Mac-1) and CD11c/CD18 (p150,95) in adhesion of PDB-stimulated PMN to unstimulated EC, mAb against the CD11 chains were used. mAb against CD11a or CD11b each blocked adhesion of PMN to EC by approximately 50%, but mAb against CD11c had no effect. Inasmuch as a combination of anti-CD11a and CD11b mAb completely blocked adhesion, it appears that CD11a/CD18 and CD11b/CD18 make approximately equal contributions to binding, and CD11c does not participate. Anti-CD11a or CD11b each blocked adhesion by about 50% throughout the transient time course of PDB-stimulated adhesion, indicating that the capacity of each of these receptors to bind EC is transiently activated by PDB. We next examined the role of ICAM-1 on EC as a ligand for CD18. Two anti-ICAM-1 mAb (LB-2 and 84H10) each inhibited PMN adhesion in a dose-dependent fashion, reaching a maximal inhibition of approximately 50%. Anti-ICAM-1 mAb blocked the CD11a/CD18-dependent portion of adhesion because concomitant use of anti-CD11a and anti-ICAM-1 did not cause additive inhibition. In contrast, anti-CD11b plus anti-ICAM-1 resulted in complete blockade of adhesion. This result suggests that CD11a/CD18 recognizes ICAM-1 on EC, but CD11b/CD18 recognizes a different ligand(s). To determine if CD11b CD18 has the ability to recognize ICAM-1, human macrophages were plated on culture surfaces coated with purified ICAM-1. Interaction of CD11a/CD18 with the surface-bound ICAM-1 resulted in selective down-modulation of CD11a/CD18 from the apical portion of the macrophages. In contrast, ICAM-1-coated surfaces did not down-modulate CD11b/CD18. The data suggest that CD11b/CD18 does not recognize ICAM-1, and that this receptor functions in adhesion of PMN to EC by recognizing novel ligand(s) on EC.

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Sachs, Ulrich J. H., Triantafyllos Chavakis, Lin Fung, Alexander Lohrenz, Jürgen Bux, Angelika Reil, Andreas Ruf, and Sentot Santoso. "Human alloantibody anti-Mart interferes with Mac-1–dependent leukocyte adhesion." Blood 104, no. 3 (August 1, 2004): 727–34. http://dx.doi.org/10.1182/blood-2003-11-3809.

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AbstractThe CD11b/CD18 integrin plays a crucial role in cell-cell adhesion processes. Recently, we described a case of severe neonatal alloimmune neutropenia (NAIN) caused by an alloantibody against a variant of the CD11b subunit (Mart alloantigen). Allele-specific transfected cells allowed us to demonstrate that an H61R point mutation is directly responsible for the formation of Mart epitopes. No difference in the adhesion capability between H61 and R61 homozygous neutrophils was observed. Functional analysis showed that anti-Mart inhibited Mac-1–dependent adhesion of neutrophils and monocytic U937 cells to fibrinogen, intercellular adhesion molecule-1 (ICAM-1), receptor for advanced glycation end product (RAGE), and glycoprotein Ibα but not to junctional adhesion molecule-C or urokinase plasminogen activator receptor (uPAR). Accordingly, anti-Mart blocked neutrophil and U937 cell adhesion to endothelial cells and platelet-leukocyte aggregate formation in whole blood under high shear. Other sera of anti-Mart from mothers of infants without NAIN did not show inhibitory properties. We conclude that anti-Mart antibodies with different functional properties exist. This is supported by our findings that anti-Mart antibodies have different abilities to inhibit cell-cell adhesion, to enhance the respiratory burst of neutrophils, and to recognize different epitopes at the N-terminal region of CD11b. In conclusion, some anti-Mart alloantibodies interfere with Mac-1–dependent cellular functions of neutrophils, cause NAIN, and may be used as tools for studying Mac-1–dependent functions.

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Wang, Liying, Guangji Li, Yinlei Lin, Zixun Zhang, Zhifeng Chen, and Shuqing Wu. "A strategy for constructing anti-adhesion surfaces based on interfacial thiol–ene photoclick chemistry between DOPA derivatives with a catechol anchor group and zwitterionic betaine macromolecules." Polymer Chemistry 7, no. 30 (2016): 4964–74. http://dx.doi.org/10.1039/c6py01043a.

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Lee, Hee Jung, Seung Min Hyun, Hak Joo Lee, Dae Geun Choi, Dong Il Lee, and Eung Sug Lee. "Adhesion Promoter and Anti-Sticking Layer Effects on Adhesion Properties Using Symmetric AFM Probe." Advanced Materials Research 26-28 (October 2007): 1113–16. http://dx.doi.org/10.4028/www.scientific.net/amr.26-28.1113.

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The reliable reproducibility of nano patterns or other nano structures is one of many issues in the nano-imprint lithography process. An important prerequisite for reproducibility is suitable adhesion properties of adhesion promoters or anti-sticking layer. In this study, rhombus shaped symmetrical probe with a flat tip was developed and fabricated using MEMS fabrication technique. For the experimental setup of the adhesion test using a UV curable PAK01 resin coated AFM tip with several adhesion promoters, the flat tip is covered by PAK01 resist using micromanipulator. Anti-sticking layers of silane agents were prepared on the tip by vapor deposition method. Adhesion force between various adhesion promoters (GPTS, APMDS, APTS, DUV30J, O2 planairzation) and PAK01 resist and the force between anti-sticking layer (FOTS, DDMS) and PAK01 resist were evaluated using the force-distance mode of AFM. Adhesion force of GPTS and FOTS are about 7180 nN and 1660 nN, respectively.

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Titu, Aurel Mihail, Sandor Ravai-Nagy, and Alina Bianca Pop. "Research on the Influence of Coating Technologies on Adhesion Anti-Corrosion Layers in the Case of Al7175 Aluminum Alloy." Coatings 13, no. 6 (June 6, 2023): 1054. http://dx.doi.org/10.3390/coatings13061054.

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A key element in ensuring the service life and strength of aluminum alloys in many industrial applications is the adhesion of anti-corrosion coatings. The aim of this study is to analyze how coating processes affect the adhesion of anti-corrosion coatings on aluminum alloy 7175. In other words, the influence of the nature of the elementary layers that form the anti-corrosion coating was studied for the following: the anodic layer, the primer, and the topcoat. To learn more about the different coating technologies and how they affect adhesion, a thorough literature review was carried out. In addition, a case study using electrocoating and thermal spraying was conducted to show the impact of coating processes on adhesion. The results showed that electrodeposition, as opposed to thermal spraying, improved the adhesion of anti-corrosion coatings. In the case of the aluminum alloy analyzed, there is a significant difference in terms of the adhesion strength of the anti-corrosion coatings. This resistance is influenced by both the anodic coating (BSA TSA SAA) and the type of primer and topcoat used (water-based or solvent-based). The correct choice of anode coat and primer and topcoat can lead to an increase (or decrease) in the adhesion strength of the paint coat by 20%. In conclusion, this study highlights how crucial it is to select the best coating process to maximize the adhesion and durability of aluminum alloys under corrosion conditions.

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Jun, In-Jung, Jong Won Chae, Mi Hwa Chung, and Eun Mi Choi. "Unexpected Intraocular Inflammation Following the Use of Anti-Adhesion Agents, Mediclore® - A Case Report." Scholars Journal of Medical Case Reports 12, no. 02 (February 15, 2024): 188–91. http://dx.doi.org/10.36347/sjmcr.2024.v12i02.014.

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Several cases of unexpected intraocular inflammation have been reported following the use of anti-adhesion agents, including Mediclore®. However, anti-adhesion agents are now used in many surgeries because of their effectiveness in preventing postoperative adhesions. Awareness of the relationship between postoperative intraocular inflammation and anti-adhesion agents is important to avoid unnecessary evaluations. Two women experienced congestion and pain in both eyes after undergoing gynecological surgery using robotic and laparoscopic techniques under general anesthesia. They were diagnosed with anterior uveitis and episcleritis, and the cause was considered to be an anti-adhesion agent after excluding other factors and ophthalmic examinations. Here, we report two cases of intraocular inflammation after surgery and describe the clinical importance of anterior uveitis and episcleritis.

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Xie, Qiang, Tianhui Hao, Jifeng Zhang, Chao Wang, Rongkui Zhang, and Hui Qi. "Anti-Icing Performance of a Coating Based on Nano/Microsilica Particle-Filled Amino-Terminated PDMS-Modified Epoxy." Coatings 9, no. 12 (November 20, 2019): 771. http://dx.doi.org/10.3390/coatings9120771.

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Coatings with anti-icing performance possess hydrophobicity and low ice adhesion strength, which delay ice formation and make ice removal easier. In this paper, the anti-icing performance of nano/microsilica particle-filled amino-terminated PDMS (A-PDMS)-modified epoxy coatings was investigated. In the process, the influence of the addition of A-PDMS on the hydrophobicity and ice adhesion strength was investigated. Furthermore, the influences of various weight ratios of nanosilica/microsilica (Rn/m) on the hydrophobicity and ice adhesion strength of the coating were investigated. Hydrophobicity was evaluated by contact angle (CA) and contact angle hysteresis (CAH) tests. Ice adhesion strength was measured by a centrifugal adhesion test. The addition of A-PDMS markedly increased hydrophobicity and decreased ice adhesion. The size combination of particles obviously affects hydrophobicity but has little effect on ice adhesion. Finally, X-ray photoelectron spectroscopy (XPS) and scanning electron microscopy (SEM) were used to reveal the anti-icing mechanism of the coatings.

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Hamid, Adila A., Amilia Aminuddin, Nur Najmi Mohamad Anuar, Nur Izzati Mansor, Mohd Faizal Ahmad, Mohammed S. M. Saleh, Mohd Helmy Mokhtar, and Azizah Ugusman. "Persicaria minor (Huds.) Opiz Prevents In Vitro Atherogenesis by Attenuating Tumor Necrosis Factor-α-Induced Monocyte Adhesion to Human Umbilical Vein Endothelial Cells." Life 12, no. 10 (September 20, 2022): 1462. http://dx.doi.org/10.3390/life12101462.

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Persicaria minor (Huds.) Opiz is an herb with anti-inflammatory, antioxidant, and anti-atherosclerosis effects. Nevertheless, the mechanism underlying its anti-atherosclerosis effect is poorly comprehended. This in vitro study assessed the protective effects of standardized aqueous extract of P. minor leaves (PM) on tumor necrosis factor-α (TNF-α)-induced monocyte adhesion to human umbilical vein endothelial cells (HUVEC), which is one of the pivotal early steps in atherogenesis. The results showed that PM decreased the mRNA and protein expression of cellular adhesion molecules, vascular adhesion molecule-1 and intercellular adhesion molecule-1, resulting in reduced adhesion of monocytes to HUVEC. Additionally, PM inhibited nuclear factor kappaB (NF-κB) activation as indicated by reduced NF-κB p65 levels in TNF-α-induced HUVEC. Overall, PM could prevent in vitro atherogenesis by inhibiting NF-κB activation and adhesion of monocytes to HUVEC. The effects of PM are probably mediated by its bioactive compound, quercetin-3-O-glucuronide. The findings may provide a rationale for the in vivo anti-atherosclerosis effect of PM, and support its potential use in atherosclerosis.

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Geiger, Timothy M., Patricia L. Roberts, Thomas E. Read, Peter W. Marcello, David J. Schoetz, and Rocco Ricciardi. "Has the Use of Anti-Adhesion Barriers Affected the National Rate of Bowel Obstruction?" American Surgeon 77, no. 6 (June 2011): 773–77. http://dx.doi.org/10.1177/000313481107700636.

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In this study, we analyzed temporal trends in anti-adhesion barrier application and admission rates for small bowel obstruction. We used data from the Nationwide Inpatient Sample and identified patients with ICD-9 codes for “application or administration of anti-adhesion barrier substances” from October 2002 through December 2007. Next, we identified cases of bowel obstruction coded from January 1997 through December 2007. We then used Kendall correlation analyses and the Joinpoint regression program to evaluate changes in trends. From October 1, 2002 through December 31, 2007, a total of 28,014 patients had an anti-adhesion barrier substance applied. During the study period, application of anti-adhesion barriers increased from 0.7 applications per 100,000 to 2.6 applications per 100,000 population (Joinpoint and Kendall; P < 0.002). Since 1997 there has been a steady rise in hospitalizations for bowel obstruction, increasing from 18.3 cases per 100,000 to 19.8 cases per 100,000 population (Joinpoint and Kendall; P < 0.002). In conclusion, the application of anti-adhesion barriers has increased significantly since 2002, yet bowel obstructions continue to be a major health problem.

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Zhao, Kaihui, Peng Li, Changfan Zhang, Jing He, Xiangfei Li, and Jianhua Liu. "Optimal Utilization of Adhesion Force for Heavy-Haul Electric Locomotive Based on Extremum Seeking with Sliding Mode and Asymmetric Barrier Lyapunov Function." Journal of Advanced Transportation 2019 (January 23, 2019): 1–15. http://dx.doi.org/10.1155/2019/6270515.

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An optimal utilization of adhesion force based on extremum seeking with sliding mode (SMES) and asymmetric barrier Lyapunov function (ABLF) is proposed for heavy-haul electric locomotives (HHELs), which can eliminate the wheel skidding at optimal adhesion point and achieves maximum traction for HHELs. First, the state equation of wheel-rail adhesion control system is described. The optimal utilization of adhesion force and anti-slip control are analyzed considering the condition changes at the wheel-rail surface. Then, the nonsingular terminal sliding mode observer (NTSMO) is designed to achieve the accurate adhesion coefficient of the wheel-rail. Finally, the SMES method for HHEL is developed to obtain the optimal slip speed and the maximum adhesion coefficient of the uncertain wheel-rail surface. Meanwhile, the ABLF controller is designed to achieve anti-slip control for HHELs in the optimal adhesion state. Comparing with the conventional differential acceleration control (DAC) method, the simulations and experiments verify that the proposed method can achieve optimal adhesion anti-slip control with quick dynamic response, and the HHEL achieves maximum traction.

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Hoshino, M., and Y. Nakamura. "The effect of inhaled sodium cromoglycate on cellular infiltration into the bronchial mucosa and the expression of adhesion molecules in asthmatics." European Respiratory Journal 10, no. 4 (April 1, 1997): 858–65. http://dx.doi.org/10.1183/09031936.97.10040858.

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There is no direct evidence of the anti-inflammatory effect of inhaled sodium cromoglycate (SCG). To investigate whether inhaled SCG has any effect on cellular infiltration into the bronchial mucosa and the expression of adhesion molecules in patients with asthma, biopsies of the bronchial mucosa were taken from nine patients with atopic bronchial asthma before and after treatment with inhaled SCG (8 mg x day(-1)) from a metered-dose inhaler (MDI). Eosinophils were stained with anti-EG2, neutrophils with anti-NP57, mast cells with anti-AA1, T-lymphocytes with anti-CD4, CD8 and CD3, and macrophages with anti-CD68. Intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), endothelial leucocyte adhesion molecule-1 (ELAM-1) and P-selectin were stained at the same time as adhesion molecules expressed in vascular endothelium. The intensity of ICAM-1 expression in the bronchial epithelium was also evaluated. The numbers of eosinophils, mast cells, T-lymphocytes and macrophages were significantly reduced as a result of SCG administration, and the expression of ICAM-1, VCAM-1 and ELAM-1 was also significantly inhibited. A significant correlation was found between ICAM-1 expression and T-lymphocytes and between VCAM-1 expression and eosinophils. It was concluded that sodium cromoglycate does have an effect on the infiltration of the bronchial mucosa by inflammatory cells and also on the expression of adhesion molecules.

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Nasu, K., T. Ishida, M. Setoguchi, Y. Higuchi, S. Akizuki, and S. Yamamoto. "Expression of wild-type and mutated rabbit osteopontin in Escherichia coli, and their effects on adhesion and migration of P388D1 cells." Biochemical Journal 307, no. 1 (April 1, 1995): 257–65. http://dx.doi.org/10.1042/bj3070257.

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Recombinant wild-type rabbit osteopontin (rOP) and the protein with an aspartate-to-glutamate transposition induced by a point mutation in the rabbit OP cDNA within the Gly-Arg-Gly-Asp-Ser (GRGDS) sequence were expressed in Escherichia coli and purified to homogeneity. P388D1 cells bound rOP in a saturable manner. rOP induced adhesion and haptotaxis of P388D1 cells, whereas mutated rabbit OP (rOPmut) did not. Anti-rOP IgG F(ab′)2 and synthetic GRGDS peptide inhibited rOP-mediated adhesion and haptotaxis of P388D1 cells. Fibronectin (FN)-mediated adhesion of P388D1 cells was markedly inhibited in the presence of fluid-phase rOP. Adhesion of P388D1 cells to rOP was significantly inhibited by anti-[alpha-subunits of VLA4 (alpha 4) and VLA5 (alpha 5)] monoclonal antibodies (mAbs), but not by anti-[alpha-subunit of vitronectin (VN) receptor (alpha V) or Mac-1 (alpha M)] mAb. Adhesion of P388D1 cells to FN and VN was significantly inhibited by anti-alpha V mAb but not anti-alpha 4, -alpha 5 or -alpha M mAb. Haptotaxis of P388D1 cells to rOP was significantly inhibited by anti-alpha V mAb, but not by anti-alpha 4, -alpha 5 and alpha M mAbs, whereas that to FN showed no inhibition with all three mAbs. Haptotaxis of P388D1 cells to VN was significantly inhibited by anti-alpha 5 and -alpha V mAbs but not by anti-alpha 4 and -alpha M mAbs. Similar features of inhibition of adhesion and haptotaxis of P388D1 cells to human OP were observed by mAbs. rOP had no chemotactic effect on P388D1 cells. Significant polymorphonuclear leucocyte migration was observed 3-12 h after intradermal injection of rOP into rabbits.

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Campanero, M. R., P. Sánchez-Mateos, M. A. del Pozo, and F. Sánchez-Madrid. "ICAM-3 regulates lymphocyte morphology and integrin-mediated T cell interaction with endothelial cell and extracellular matrix ligands." Journal of Cell Biology 127, no. 3 (November 1, 1994): 867–78. http://dx.doi.org/10.1083/jcb.127.3.867.

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Leukocyte activation is a complex process that involves multiple cross-regulated cell adhesion events. In this report, we investigated the role of intercellular adhesion molecule-3 (ICAM-3), the third identified ligand for the beta 2 integrin leukocyte function-associated antigen-1 (LFA-1), in the regulation of leukocyte adhesion to ICAM-1, vascular cell adhesion molecule-1 (VCAM-1), and the 38- and 80-kD fragments of fibronectin (FN40 and FN80). The activating anti-ICAM-3 HP2/19, but not other anti-ICAM-3 mAb, was able to enhance T lymphoblast adhesion to these proteins when combined with very low doses of anti-CD3 mAb, which were unable by themselves to induce this phenomenon. In contrast, anti-ICAM-1 mAb did not enhance T cell attachment to these substrata. T cell adhesion to ICAM-1, VCAM-1, FN40, and FN80 was specifically blocked by anti-LFA-1, anti-VLA alpha 4, and anti-VLA alpha 5 mAb, respectively. The activating anti-ICAM-3 HP2/19 was also able to specifically enhance the VLA-4- and VLA-5-mediated binding of leukemic T Jurkat cells to VCAM-1, FN40, and FN80, even in the absence of cooccupancy of the CD3-TcR complex. We also studied the localization of ICAM-3, LFA-1, and the VLA beta 1 integrin, by immunofluorescence microscopy, on cells interacting with ICAM-1, VCAM-1 and FN80. We found that the anti-ICAM-3 HP2/19 mAb specifically promoted a dramatic change on the morphology of T lymphoblasts when these cells were allowed to interact with those adhesion ligands. Under these conditions, it was observed that a large cell contact area from which an uropod-like structure (heading uropod) was projected toward the outer milieu. However, when T blasts were stimulated with other adhesion promoting agents as the activating anti-VLA beta 1 TS2/16 mAb or phorbol esters, this structure was not detected. The anti-ICAM-3 TP1/24 mAb was also unable to induce this phenomenon. Notably, a striking cell redistribution of ICAM-3 was induced specifically by the HP2/19 mAb, but not by the other anti-ICAM-3 mAb or the other adhesion promoting agents. Thus, ICAM-3 was almost exclusively concentrated in the most distal portion of the heading uropod whereas either LFA-1 or the VLA beta 1 integrin were uniformly distributed all over the large contact area. Moreover, this phenomenon was also observed when T cells were specifically stimulated with the HP2/19 mAb to interact with TNF alpha-activated endothelial cells.(ABSTRACT TRUNCATED AT 400 WORDS)

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Gutsaeva, Diana R., James B. Parkerson, Shobha D. Yerigenahally, Jeffrey C. Kurz, Robert G. Schaub, Tohru Ikuta, and C. Alvin Head. "Inhibition of cell adhesion by anti–P-selectin aptamer: a new potential therapeutic agent for sickle cell disease." Blood 117, no. 2 (January 13, 2011): 727–35. http://dx.doi.org/10.1182/blood-2010-05-285718.

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Abstract Adhesive interactions between circulating sickle red blood cells (RBCs), leukocytes, and endothelial cells are major pathophysiologic events in sickle cell disease (SCD). To develop new therapeutics that efficiently inhibit adhesive interactions, we generated an anti–P-selectin aptamer and examined its effects on cell adhesion using knockout-transgenic SCD model mice. Aptamers, single-stranded oligonucleotides that bind molecular targets with high affinity and specificity, are emerging as new therapeutics for cardiovascular and hematologic disorders. In vitro studies found that the anti–P-selectin aptamer exhibits high specificity to mouse P-selectin but not other selectins. SCD mice were injected with the anti–P-selectin aptamer, and cell adhesion was observed under hypoxia. The anti–P-selectin aptamer inhibited the adhesion of sickle RBCs and leukocytes to endothelial cells by 90% and 80%, respectively. The anti–P-selectin aptamer also increased microvascular flow velocities and reduced the leukocyte rolling flux. SCD mice treated with the anti–P-selectin aptamer demonstrated a reduced mortality rate associated with the experimental procedures compared with control mice. These results demonstrate that anti–P-selectin aptamer efficiently inhibits the adhesion of both sickle RBCs and leukocytes to endothelial cells in SCD model mice, suggesting a critical role for P-selectin in cell adhesion. Anti–P-selectin aptamer may be useful as a novel therapeutic agent for SCD.

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Adler, S., and X. Chen. "Anti-Fx1A antibody recognizes a beta 1-integrin on glomerular epithelial cells and inhibits adhesion and growth." American Journal of Physiology-Renal Physiology 262, no. 5 (May 1, 1992): F770—F776. http://dx.doi.org/10.1152/ajprenal.1992.262.5.f770.

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Cell-matrix interactions play an important role in regulating cell growth and metabolic activity and potentially in maintaining the integrity of the glomerular filtration barrier. The effect of anti-Fx1A antibody (Ab), the pathogenetic Ab of passive Heymann nephritis, on the interaction of cultured rat glomerular visceral epithelial cells (GEC) with matrix components was examined in an effort to determine whether it affects cell adhesion. Affinity chromatography demonstrated that anti-Fx1A recognizes an alpha 3 beta 1-integrin-type matrix receptor on GEC. Anti-Fx1A inhibited the adhesion of GEC to several substrates (collagen IV approximately equal to collagen I less than laminin approximately equal to fibronectin) in a dose-dependent manner and produced reversible cell detachment and "rounding up" when added to adherent cells. Maximal inhibition of adhesion was similar with anti-Fx1A and anti-beta 1, and competition studies showed no additive effects between anti-Fx1A and anti-beta 1 in inhibiting adhesion, suggesting that the effect of anti-Fx1A on GEC adhesion is attributable to its anti-beta 1 activity. Anti-Fx1A Ab also inhibited the growth of GEC in culture without evidence of cytotoxicity, and cells resumed normal growth on removal of Ab. These studies suggest that anti-Fx1A Ab can bind to matrix receptors on GEC, resulting in inhibition of cell attachment and growth, as well as producing detachment of cells that are already adherent. Interference with GEC-glomerular basement membrane interactions in vivo might have significant effects on glomerular permeability to proteins.

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Barthel, Steven R., Douglas S. Annis, Deane F. Mosher, and Mats W. Johansson. "Differential Engagement of Modules 1 and 4 of Vascular Cell Adhesion Molecule-1 (CD106) by Integrins α4β1 (CD49d/29) and αMβ2 (CD11b/18) of Eosinophils." Journal of Biological Chemistry 281, no. 43 (August 30, 2006): 32175–87. http://dx.doi.org/10.1074/jbc.m600943200.

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We have studied adhesion of eosinophils to various forms of vascular cell adhesion molecule 1 (VCAM-1, CD106), an integrin counter-receptor implicated in eosinophil recruitment to the airway in asthma. Full-length 7d-VCAM-1, with seven immunoglobulin-like modules, contains integrin-binding sites in modules 1 and 4. The alternatively spliced six-module protein, 6d-VCAM-1, lacks module 4. In static assays, unactivated purified human blood eosinophils adhered similarly to recombinant soluble human 6d-VCAM-1 and 7d-VCAM-1 coated onto polystyrene microtiter wells. Further experiments, however, revealed differences in recognition of modules 1 and 4. Antibody blocking indicated that eosinophil adhesion to 6d-VCAM-1 or a VCAM-1 construct containing only modules 1–3, 1–3VCAM-1, is mediated by α4β1 (CD49d/29), whereas adhesion to a construct containing modules 4–7, 4–7VCAM-1, is mediated by bothα4β1 andαMβ2 (CD11b/18). Inhibitors of phosphoinositide 3-kinase, which block adhesion of eosinophils mediated by αMβ2, blocked adhesion to 4–7VCAM-1 but had no effect on adhesion to 6d-VCAM-1. Consistent with the antibody and pharmacological blocking experiments, eosinophilic leukemic cell lines lacking αMβ2 did not adhere to 4–7VCAM-1 but did adhere to 6d-VCAM-1 or 1–3VCAM-1. Activation of eosinophils by interleukin (IL)-5 enhanced static adhesion to 6d-VCAM-1, 7d-VCAM-1, or 4–7VCAM-1; IL-5-enhanced adhesion to all 3 constructs was blocked by anti-αMβ2. Adhesion of unstimulated eosinophils to 7d-VCAM-1 under flow conditions was inhibited by anti-α4 or anti-αM. IL-5 treatment decreased eosinophil adhesion to 7d-VCAM-1 under flow, and anti-αM had the paradoxical effect of increasing adhesion. These results demonstrate that αMβ2 modulatesα4β1-mediated eosinophil adhesion to VCAM-1 under both static and flow conditions.

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Evangelista, V., S. Manarini, S. Rotondo, N. Martelli, R. Polischuk, JL McGregor, G. de Gaetano, and C. Cerletti. "Platelet/polymorphonuclear leukocyte interaction in dynamic conditions: evidence of adhesion cascade and cross talk between P-selectin and the beta 2 integrin CD11b/CD18." Blood 88, no. 11 (December 1, 1996): 4183–94. http://dx.doi.org/10.1182/blood.v88.11.4183.4183.

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Abstract Adhesion between platelets and polymorphonuclear leukocytes (PMN) is a key event in thrombosis and inflammation. Double color fluorescence- activated cell sorter (FACS) analysis was used to determine the extent and kinetics of adhesion of thrombin-activated platelets to resting or activated PMN when mixed cell populations were incubated in dynamic conditions. Activated platelets bound very rapidly to PMN. Mixed cell conjugates reached a maximum at 1 minute and were reversible within 10 minutes. Platelet/PMN adhesion required both Ca2+ and Mg2+ and was markedly increased by the presence of Mn2+. The latter made mixed cell conjugates stable up to 10 minutes. Adhesion of platelets required metabolic activity of PMN and was abolished by tyrosine kinase inhibitors. Furthermore, adhesion of platelets to PMN resulted in binding of a monoclonal antibody (MoAb 24) known as beta 2 integrins “activation reporter.” When PMN were activated by exogenous stimuli, the adhesion of platelets was markedly increased: fMLP induced a rapid and transient effect, while PMA resulted in a slower, but stable, increase in mixed conjugates formation. The hypothesis that activated PMN beta 2 integrins are able to bind a counter-receptor on platelets was directly demonstrated by the increase of mixed cell conjugates following PMN treatment with KIM127 and KIM185, two anti-CD18 antibodies able to induce the active conformation of beta 2 integrins. Consistently, two other anti-CD18, as well as an anti-CD11b inhibitory antibody abolished platelet/PMN adhesion. PMN beta 2 integrin activation was not the only mechanism for activated platelet/PMN adhesion to occur: indeed, this phenomenon could also be inhibited by two anti-P-selectin antibodies. Resting platelets did not adhere to resting PMN, but markedly adhered to fMLP-or PMA-activated PMN. Resting platelet/fMLP-activated PMN adhesion was abolished by anti-CD18 antibodies, but not by anti-P-selectin antibodies. In conclusion, activated platelet/PMN interaction can be modeled as an adhesion cascade involving a P-selectin-dependent recognition step and a functional signal. The latter proceeds through tyrosine kinase activation and enables a beta 2 integrin-dependent adhesion to a not yet identified counter-receptor constitutively expressed on platelet surface.

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Journal articles on the topic 'Anti-adhesion'

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