Bibliographies thématiques / Molecular adhesion

Littérature scientifique sur le sujet « Molecular adhesion »

Auteur : Grafiati
Publié le 8 juin 2024

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Articles de revues sur le sujet "Molecular adhesion"

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Mentzer, S. J., D. V. Faller et S. J. Burakoff. « Interferon-gamma induction of LFA-1-mediated homotypic adhesion of human monocytes. » Journal of Immunology 137, no 1 (1 juillet 1986) : 108–13. http://dx.doi.org/10.4049/jimmunol.137.1.108.

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Abstract Cell-cell adhesion plays an important role in monocyte function. To investigate the molecular basis for monocyte adhesion, we used recombinant interferon-gamma to induce the formation of homotypic monocyte adhesions. The induction of homotypic adhesions correlated with the increased expression of the LFA-1 membrane molecule. LFA-1 surface expression was increased twofold, whereas expression levels of other monocyte surface molecules including CR3 and p150,95 were unchanged. The direct involvement of LFA-1 in monocyte adhesion was addressed by anti-LFA-1 monoclonal antibody inhibition of homotypic adhesions. Two monoclonal antibodies to distinct epitopes on the LFA-1 alpha-chain completely inhibited homotypic adhesions. Antibodies to a variety of other monocyte surface molecules, often present at higher cell surface density than LFA-1, did not inhibit homotypic adhesion. A panel of monoclonal antibodies that recognized different functional epitopes on the LFA-1 alpha-chain inhibited homotypic monocyte in a hierarchy identical to that observed in previous studies of cell-mediated cytotoxicity. These findings suggest that LFA-1 serves an adhesive function for human mononuclear phagocytes. In addition to providing a molecular basis for homotypic monocyte adhesions, the results suggest a more general role for LFA-1 in monocyte adhesion reactions.
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Willaert, Ronnie G., Yeseren Kayacan et Bart Devreese. « The Flo Adhesin Family ». Pathogens 10, no 11 (28 octobre 2021) : 1397. http://dx.doi.org/10.3390/pathogens10111397.

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The first step in the infection of fungal pathogens in humans is the adhesion of the pathogen to host tissue cells or abiotic surfaces such as catheters and implants. One of the main players involved in this are the expressed cell wall adhesins. Here, we review the Flo adhesin family and their involvement in the adhesion of these yeasts during human infections. Firstly, we redefined the Flo adhesin family based on the domain architectures that are present in the Flo adhesins and their functions, and set up a new classification of Flo adhesins. Next, the structure, function, and adhesion mechanisms of the Flo adhesins whose structure has been solved are discussed in detail. Finally, we identified from Pfam database datamining yeasts that could express Flo adhesins and are encountered in human infections and their adhesin architectures. These yeasts are discussed in relation to their adhesion characteristics and involvement in infections.
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Taylor, James T., Rebekka Harting, Samer Shalaby, Charles M. Kenerley, Gerhard H. Braus et Benjamin A. Horwitz. « Adhesion as a Focus in Trichoderma–Root Interactions ». Journal of Fungi 8, no 4 (6 avril 2022) : 372. http://dx.doi.org/10.3390/jof8040372.

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Fungal spores, germlings, and mycelia adhere to substrates, including host tissues. The adhesive forces depend on the substrate and on the adhesins, the fungal cell surface proteins. Attachment is often a prerequisite for the invasion of the host, hence its importance. Adhesion visibly precedes colonization of root surfaces and outer cortex layers, but little is known about the molecular details. We propose that by starting from what is already known from other fungi, including yeast and other filamentous pathogens and symbionts, the mechanism and function of Trichoderma adhesion will become accessible. There is a sequence, and perhaps functional, homology to other rhizosphere-competent Sordariomycetes. Specifically, Verticillium dahliae is a soil-borne pathogen that establishes itself in the xylem and causes destructive wilt disease. Metarhizium species are best-known as insect pathogens with biocontrol potential, but they also colonize roots. Verticillium orthologs of the yeast Flo8 transcription factor, Som1, and several other relevant genes are already under study for their roles in adhesion. Metarhizium encodes relevant adhesins. Trichoderma virens encodes homologs of Som1, as well as adhesin candidates. These genes should provide exciting leads toward the first step in the establishment of beneficial interactions with roots in the rhizosphere.
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TAKASHIMA, Yoshinori, Motofumi OSAKI, Tomoko SEKINE, Yasushi SHOJIMA et Akira HARADA. « Materials Adhesion Based on Molecular Adhesive Techniques ». Journal of The Adhesion Society of Japan 54, no 6 (1 juin 2018) : 201–11. http://dx.doi.org/10.11618/adhesion.54.201.

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Young, Katherine A., Laura Biggins et Hayley J. Sharpe. « Protein tyrosine phosphatases in cell adhesion ». Biochemical Journal 478, no 5 (10 mars 2021) : 1061–83. http://dx.doi.org/10.1042/bcj20200511.

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Adhesive structures between cells and with the surrounding matrix are essential for the development of multicellular organisms. In addition to providing mechanical integrity, they are key signalling centres providing feedback on the extracellular environment to the cell interior, and vice versa. During development, mitosis and repair, cell adhesions must undergo extensive remodelling. Post-translational modifications of proteins within these complexes serve as switches for activity. Tyrosine phosphorylation is an important modification in cell adhesion that is dynamically regulated by the protein tyrosine phosphatases (PTPs) and protein tyrosine kinases. Several PTPs are implicated in the assembly and maintenance of cell adhesions, however, their signalling functions remain poorly defined. The PTPs can act by directly dephosphorylating adhesive complex components or function as scaffolds. In this review, we will focus on human PTPs and discuss their individual roles in major adhesion complexes, as well as Hippo signalling. We have collated PTP interactome and cell adhesome datasets, which reveal extensive connections between PTPs and cell adhesions that are relatively unexplored. Finally, we reflect on the dysregulation of PTPs and cell adhesions in disease.
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Labbate, Maurizio, Hua Zhu, Leena Thung, Rani Bandara, Martin R. Larsen, Mark D. P. Willcox, Michael Givskov, Scott A. Rice et Staffan Kjelleberg. « Quorum-Sensing Regulation of Adhesion in Serratia marcescens MG1 Is Surface Dependent ». Journal of Bacteriology 189, no 7 (19 janvier 2007) : 2702–11. http://dx.doi.org/10.1128/jb.01582-06.

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ABSTRACT Serratia marcescens is an opportunistic pathogen and a major cause of ocular infections. In previous studies of S. marcescens MG1, we showed that biofilm maturation and sloughing were regulated by N-acyl homoserine lactone (AHL)-based quorum sensing (QS). Because of the importance of adhesion in initiating biofilm formation and infection, the primary goal of this study was to determine whether QS is important in adhesion to both abiotic and biotic surfaces, as assessed by determining the degree of attachment to hydrophilic tissue culture plates and human corneal epithelial (HCE) cells. Our results demonstrate that while adhesion to the abiotic surface was AHL regulated, adhesion to the HCE cell biotic surface was not. Type I fimbriae were identified as the critical adhesin for non-QS-mediated attachment to the biotic HCE cell surface but played no role in adhesion to the abiotic surface. While we were not able to identify a single QS-regulated adhesin essential for attachment to the abiotic surface, four AHL-regulated genes involved in adhesion to the abiotic surface were identified. Interestingly, two of these genes, bsmA and bsmB, were also shown to be involved in adhesion to the biotic surface in a non-QS-controlled fashion. Therefore, the expression of these two genes appears to be cocontrolled by regulators other than the QS system for mediation of attachment to HCE cells. We also found that QS in S. marcescens regulates other potential cell surface adhesins, including exopolysaccharide and the outer membrane protein OmpX. We concluded that S. marcescens MG1 utilizes different regulatory systems and adhesins in attachment to biotic and abiotic surfaces and that QS is a main regulatory pathway in adhesion to an abiotic surface but not in adhesion to a biotic surface.
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Bach, Cuc T. T., Sarah Creed, Jessie Zhong, Maha Mahmassani, Galina Schevzov, Justine Stehn, Lauren N. Cowell et al. « Tropomyosin Isoform Expression Regulates the Transition of Adhesions To Determine Cell Speed and Direction ». Molecular and Cellular Biology 29, no 6 (5 janvier 2009) : 1506–14. http://dx.doi.org/10.1128/mcb.00857-08.

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ABSTRACT The balance of transition between distinct adhesion types contributes to the regulation of mesenchymal cell migration, and the characteristic association of adhesions with actin filaments led us to question the role of actin filament-associating proteins in the transition between adhesive states. Tropomyosin isoform association with actin filaments imparts distinct filament structures, and we have thus investigated the role for tropomyosins in determining the formation of distinct adhesion structures. Using combinations of overexpression, knockdown, and knockout approaches, we establish that Tm5NM1 preferentially stabilizes focal adhesions and drives the transition to fibrillar adhesions via stabilization of actin filaments. Moreover, our data suggest that the expression of Tm5NM1 is a critical determinant of paxillin phosphorylation, a signaling event that is necessary for focal adhesion disassembly. Thus, we propose that Tm5NM1 can regulate the feedback loop between focal adhesion disassembly and focal complex formation at the leading edge that is required for productive and directed cell movement.
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Saed, Ghassan M., et Michael P. Diamond. « Molecular Characterization of Postoperative Adhesions : The Adhesion Phenotype ». Journal of the American Association of Gynecologic Laparoscopists 11, no 3 (août 2004) : 307–14. http://dx.doi.org/10.1016/s1074-3804(05)60041-2.

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Willaert, Ronnie. « Adhesins of Yeasts : Protein Structure and Interactions ». Journal of Fungi 4, no 4 (27 octobre 2018) : 119. http://dx.doi.org/10.3390/jof4040119.

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The ability of yeast cells to adhere to other cells or substrates is crucial for many yeasts. The budding yeast Saccharomyces cerevisiae can switch from a unicellular lifestyle to a multicellular one. A crucial step in multicellular lifestyle adaptation is self-recognition, self-interaction, and adhesion to abiotic surfaces. Infectious yeast diseases such as candidiasis are initiated by the adhesion of the yeast cells to host cells. Adhesion is accomplished by adhesin proteins that are attached to the cell wall and stick out to interact with other cells or substrates. Protein structures give detailed insights into the molecular mechanism of adhesin-ligand interaction. Currently, only the structures of a very limited number of N-terminal adhesion domains of adhesins have been solved. Therefore, this review focuses on these adhesin protein families. The protein architectures, protein structures, and ligand interactions of the flocculation protein family of S. cerevisiae; the epithelial adhesion family of C. glabrata; and the agglutinin-like sequence protein family of C. albicans are reviewed and discussed.
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Simmons, David L. « Dissecting the modes of interactions amongst cell adhesion molecules ». Development 119, Supplement (1 décembre 1993) : 193–203. http://dx.doi.org/10.1242/dev.119.supplement.193.

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The process of cell adhesion can be mediated by more than SO molecules. Fortunately, most of these can be grouped into a small number of super families. For example, more than half of all leukocyte adhesion molecules are members of the immunoglobulin super-family. The principles of cell-cell adhesion are reviewed including: kinetics and equilibria; on/off rates; affinities/avidities; homotypic/heterotypic interactions; mapping and delineation of binding sites. These principles are illustrated with two CAMs: firstly the interaction of the homotypic epithelial/myeloid adhesins CD66, and the endothelial adhesin, CD31, and secondly the heterotypic adhesins ICAM-1, 2 and 3, which interact with the leukocyte integrin LFA-1.
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Thèses sur le sujet "Molecular adhesion"

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Townsend, Paul Andrew. « The molecular basis of osteoblast adhesion ». Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263651.

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Lougheed, Caroline. « Targeting focal adhesion signaling in cancer and acquired resistance to focal adhesion kinase inhibitors ». Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=94996.

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In cancer progression, the development of metastases is characteristic of late stage disease and makes treatment and cure more difficult. In order for metastasis to occur, cancer cells must gain motile and invasive phenotypes. As one of the keystone proteins involved in cell motility and invasion, Focal Adhesion Kinase (FAK) has emerged as a good therapeutic target for the inhibition of metastases via targeted drug design and small molecule inhibitors. Accordingly, a small molecule inhibitor has recently been developed against FAK activation and signaling. However, drug resistance is common among targeted therapies. Development and classification of drug resistant cells elucidated the possible mechanism behind FAK inhibitor resistance such that second-line therapy drugs can be designed to overcome or avoid resistance. The overall data presented herein support the role of FAK as an important drug target in cancer metastasis as well as provide insight and direction for future FAK inhibitor design.
Dans la progression du cancer, le développement de métastases est caractéristique de la phase terminale et rend le traitement difficile. Afin que des métastases se dévelopment, les cellules cancéreuses doivent acquérir de la motilité ainsi qu'un phénotype invasif. Considéré come l'une des plus importantes protéines participant dans la motilité cellulaire, la prot éine Focal Adhesion Kinase (FAK) a émergé comme une bonne cible thérapeutique pour l'inhibition de métastases par la création de drogues ciblées et de petites molécules inhibitrices. Par conséquent, une molécule inhibitrice de l'activation de FAK et sa signalisation a été récemment développée. Cependant, J'ai demontré que la résistance est commune parmis ces drogues. Le dévelopement et la classification des clones de cellules résistantes ont permi d'élucider un mécanisme impiquant en partie une amplification de l'activité FAK; ce mécanisme permetter a de découvrir des analogues de deuxième génération pour surmonter ou éviter la résistance. L'ensemble de données présentées ci-dessous supportet le rôle de FAK comme une cible importante dans la prévention de métastases et exposent les futur directions pour contourner la résistance aux inhibiteurs de FAK.
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Harrison, O. J. « The molecular mechanism of cadherin-mediated adhesion ». Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.603783.

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My work examines the role of a conserved tryptophan residue, Trp2, in the adhesive domain of cadherins that has been shown to be essential for their adhesive function. Structural studies have shown Trp2 to be integrated into its own cadherin domain, integrated into the domain an opposing cadherin molecule, or freed from the domain and exposed to solvent. Until now, the physiological relevance of these structures has been controversial. Using conformation specific antibodies I show that Trp2 integrates into the domain fold of its own cadherin molecule in physiological conditions, but that this integration is not stable owing to structural constraints imposed by calcium binding to the cadherin. This raises the possibility that Trp2 could participate in intermolecular interactions during adhesion by inserting into opposing cadherins in what is referred to as the strand exchange model of cadherin adhesion. This model is tested directly by introducing cysteine substitutions into opposing cadherins such that disulphide bonds can form between them during adhesion only if they engage in strand exchange. The results provide clear evidence that strand exchange is central to adhesion by classical cadherins. Further results demonstrate that exchange of Trp2 in this way is stabilised by formation of a salt bridge. By disrupting this salt bridge with point mutations we find that if the tendency of Trp2 to integrate into its own domain and thus be unavailable for adhesion is inhibited, adhesion can be greatly enhanced. Our results thus define the mechanism of cadherin adhesion as a dynamic balance between the conflicting tendencies of Trp2 to engage in intramolecular and intermolecular interactions.
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Minett, William T. « Cell adhesion on synthetic polymer substrates ». Thesis, Aston University, 1986. http://publications.aston.ac.uk/14512/.

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Cho, Jae Youl. « Molecular mechanism of CD98 function ». Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249677.

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Wu, Tao. « Structure-function analysis of vascular tethering molecules using atomic force microscope ». Diss., Atlanta, Ga. : Georgia Institute of Technology, 2008. http://hdl.handle.net/1853/31844.

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Thesis (Ph.D)--Mechanical Engineering, Georgia Institute of Technology, 2009.
Committee Chair: Zhu, Cheng; Committee Member: Barry, Bridgette; Committee Member: Boyan, Barbara; Committee Member: McEver, Rodger; Committee Member: McIntire, Larry. Part of the SMARTech Electronic Thesis and Dissertation Collection.
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Eriksson, Malin. « The Influence of Molecular Adhesion on Paper Strength ». Doctoral thesis, Stockholm, Department of Fibre and Polymer Technology, School of Chemical Science and Engineering, KTH, Royal Institute of Technlology, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-4101.

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Buehler, Betul. « Molecular Adhesion and Friction at Elastomer/Polymer Interfaces ». University of Akron / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=akron1164649632.

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Killock, David James. « Molecular characterisation of L-selectin-dependent adhesion and signalling ». Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.512055.

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Gideonsson, Pär. « Helicobacter pylori : molecular insights into regulation of adhesion properties ». Doctoral thesis, Umeå universitet, Institutionen för medicinsk kemi och biofysik, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-120466.

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Helicobacter pylori infects the human stomach and triggers an inflammatory response that damages the gastric tissue. This host-pathogen interplay has dire consequences as up to 20 % of infected individuals develop peptic ulcer disease or gastric cancer. Given that half of the world’s population is infected, the number of afflicted humans is staggering and also tells that H. pylori is extremely efficient in spreading and maintaining infection. To enable persistent infection many factors play a role, but one important feature of H. pylori is its impressive ability to adhere to the slimy gastric mucus layer and the underlying epithelial cells. This occurs mainly via the BabA and SabA proteins that bind ABO/Leb- and sLex/sLea-antigens. I have in my thesis studied how these two proteins are utilized and regulated. H. pylori transcription is in part controlled by two-component systems (TCSs) that use a sensor protein and a DNA-binding response regulator. We have studied how these systems control sabA and to some extent babA and indeed found a better map of how sabA and babA is regulated at the transcriptional level. We also found that variations in a polynucleotide T-tract located in the sabA promotor could fine-tune SabA expression/ sLex-binding. Thus we have exposed how strict regulation by TCSs combined with stochastic processes together shapes attachment in the bacterial population. As the buffering mucus layer is constantly exfoliated, placing H. pylori in bactericidal acid, we hypothesized that low pH should abrogate adhesion. SabA expression was indeed repressed in low pH, however BabA expression remained unaffected. The BabA/ Leb-binding was instead directly reversibly hampered by low pH and the degree of pH sensitivity was strain dependent and encoded in the BabA sequence. We believe that the pH dependent loss of binding is one key factor H. pylori utilizes to maintain persistent infection. BabA is divided in generalists that bind ABO antigens and specialists that only bind blood group (bg) O. We co-crystalized BabA bound to these receptors and established the structural basis for generalist vs. specialist discrimination. We furthermore found a disulfide-clasped loop (CL2) in the center of the binding domain crucial for binding. Breaking CL2 with N-Acetylcysteine (NAC) disrupted binding and H. pylori infection mice experiments revealed inflammatory reduction upon NAC-treatment. In sum, I have in my thesis dissected how H. pylori controls its adhesive abilities and how intrinsic properties in binding can be exploited for therapeutic purposes.
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Livres sur le sujet "Molecular adhesion"

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A, Horton Michael, dir. Molecular biology of cell adhesion molecules. Chichester : Wiley, 1996.

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Pigott, Rod. The adhesion molecules. London : Academic Press London, 1993.

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Switalski, Lech, Magnus Höök et Edwin Beachey, dir. Molecular Mechanisms of Microbial Adhesion. New York, NY : Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3590-3.

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Madilyn, Fletcher, dir. Bacterial adhesion : Molecular and ecological diversity. New York : Wiley, 1996.

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M, Edelman Gerald, Cunningham Bruce A et Thiery Jean-Paul, dir. Morphoregulatory molecules. New York : Wiley, 1990.

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1957-, Ley Klaus, dir. Adhesion molecules : Function and inhibition. Basel : Birkhäuser, 2007.

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Michael, Horton, dir. The adhesion molecule factsbook. 2e éd. San Diego, CA : Academic Press, 2000.

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Kendall, Kevin. Molecular adhesion and its applications : The sticky universe. New York : Kluwer Academic/Plenum Publishers, 2001.

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Berezin, V. A. Structure and function of the neural cell adhesion molecule NCAM. New York : Springer, 2010.

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Berezin, V. A. Structure and function of the neural cell adhesion molecule NCAM. New York : Springer, 2010.

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Chapitres de livres sur le sujet "Molecular adhesion"

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Baig, Abdul Mannan. « Acanthamoeba Adhesion ». Dans Molecular Food Microbiology, 339–57. 3e éd. First edition. | Boca Raton : Taylor & Francis, 2021. | : CRC Press, 2021. http://dx.doi.org/10.1201/9781351120388-27.

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Zhao, Ya-Pu, Feng-Chao Wang et Mei Chi. « Molecular Dynamics Simulation and Molecular Orbital Method ». Dans Handbook of Adhesion Technology, 1349–84. Berlin, Heidelberg : Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-01169-6_52.

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Zhao, Ya-Pu, Feng-Chao Wang et Mei Chi. « Molecular Dynamics Simulation and Molecular Orbital Method ». Dans Handbook of Adhesion Technology, 1559–95. Cham : Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-55411-2_52.

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Zhao, Ya-Pu, Feng-Chao Wang et Mei Chi. « Molecular Dynamics Simulation and Molecular Orbital Method ». Dans Handbook of Adhesion Technology, 1–38. Cham : Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-42087-5_52-2.

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Allen, Timothy Craig, et Philip T. Cagle. « Cell Adhesion Molecules ». Dans Molecular Pathology Library, 19–28. Boston, MA : Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-89626-7_3.

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Allen, Timothy Craig, et Philip T. Cagle. « Cell Adhesion Molecules ». Dans Molecular Pathology Library, 22–39. New York, NY : Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-72430-0_3.

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Shanahan, M. E. R., P. Schreck et J. Schultz. « Role of Molecular Dissipation in Elastomer Adhesion ». Dans Adhesion 13, 48–61. Dordrecht : Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-010-9082-7_4.

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Covault, Jonathan. « Cell Adhesion ». Dans Molecular Biology of Membrane Transport Disorders, 11–45. Boston, MA : Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1143-0_2.

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Humphries, Martin J. « Cell Adhesion Assays ». Dans Methods in Molecular Biology, 203–10. Totowa, NJ : Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-413-1_14.

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Arnaout, M. Amin. « Molecular Basis for Leukocyte Adhesion Molecule Deficiency ». Dans Blood Cell Biochemistry, 335–46. Boston, MA : Springer US, 1993. http://dx.doi.org/10.1007/978-1-4757-9534-9_13.

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Actes de conférences sur le sujet "Molecular adhesion"

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Mofrad, Mohammad R. K. « Molecular Mechanosensors and Focal Adhesion Mechanotransduction ». Dans ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19707.

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Cellular response to mechanical stimulation is mediated by both biochemical mechanisms via changes in gene expression and by biophysical mechanisms via mechanically induced changes in specific molecules’ structure and function. These mechanically responsive molecules can be described as the cell’s mechanosensors and can function to initiate processes such as focal adhesion formation. A series of molecular dynamics investigations explore the mechanosensor function of key molecules involved in focal adhesion formation and cytoskeletal dynamics.
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Nishino, Hiroki, Kohei Kanamori, Yoshikatsu Kimoto, Kazuma Okada et Akio Yonezu. « Fracture Behavior of Alumina/Epoxy Resin Interface and Effect of Water Molecules by Using Molecular Dynamics Using Reaction Force Field (ReaxFF) ». Dans ASME 2021 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2021. http://dx.doi.org/10.1115/imece2021-69109.

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Abstract Adhesion bonding of metals and polymers is attracting attention as an innovative bonding technology to realize high functionality and weight reduction of various mechanical parts and structural materials. This technology has been significantly demanded with the rapid development of multi-materials in recent years. However, it has been reported that natural oxide film and hydroxide film are formed on the metal surface, resulting in the change in adhesion, especially degradation of adhesion is sometimes accelerated by water molecules at the interface. The mechanism of adhesion degradation is still unclear. In this study, the interface between metal and resin was modeled using the molecular dynamics (MD) simulation to investigate how the moisture (water molecules) on the interfacial surface affects the adhesion. This study varied the amount of water molecules at the interface and investigated how water molecules affect the adhesive strength subjected to uni-axial tensile loading. In addition, the potential energy around the interface was calculated, and the adhesion mechanism with respected to water molecules was carefully discussed.
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Zhenyu Yang, Quan Ren et Ya-Pu Zhao. « Molecular dynamics simulation of the bio-adhesion in molecular motors ». Dans 2005 IEEE International Conference on Robotics and Biomimetics - ROBIO. IEEE, 2005. http://dx.doi.org/10.1109/robio.2005.246291.

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Golji, Javad, et Mohammad R. K. Mofrad. « Focal Adhesion Mechanotransduction : Molecular Events Leading to Vinculin Activation ». Dans ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19711.

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Focal adhesions are formed as a molecular glue linking cytoskeletal actin filaments to the extracellular matrix (ECM). They are formed at the site of mechanical stimulation (1) and involve and initial recruitment of talin and vinculin to ECM bound integrin molecules at the site of external stimulation. Talin recruitment and its force-induced activation and subsequent interaction with vinculin have been extensively studied (2–4). Vinculin is natively in an auto-inhibited conformation and its activation involves removal of a steric hindrance preventing binding of Vt with actin (5) (Figure 1). Several hypotheses have been put forth regarding vinculin activation and its subsequent interaction with actin: 1) vinculin activation requires only interaction with talin at domain 1 (D1) (6), 2) a simultaneous interaction with both actin and talin is necessary to achieve vinculin activation (7), 3) once activated vinculin interacts with actin via an electrostatic interaction between Vt and two regions on F-actin (5). Each of these hypotheses is evaluated through molecular dynamics simulation and analysis.
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Lefeng Wang, Weibin Rong et Lining Sun. « Elastic-plastic adhesive contact of fractal microparts surfaces with low adhesion parameters ». Dans 2008 3rd IEEE International Conference on Nano/Micro Engineered and Molecular Systems. IEEE, 2008. http://dx.doi.org/10.1109/nems.2008.4484402.

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Chong, W. W. F., M. Teodorescu et H. Rahnejat. « Prediction of Load and Shear of Ultra-Thin Multi-Species Surface Films ». Dans ASME 2012 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/detc2012-71317.

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Unless protected by an inert gas atmosphere, micro-scale conjunctions are often separated by molecularly-thin adhered films. Therefore, predicting contact load, friction or adhesion, must consider the contribution of this layer to the overall contact problem. The contribution of an adhered layer can be accounted for using a simplified solution (e.g. an adjustment to the energy of adhesion to account for the liquid film). However, these methods cannot account for layers consisting of multiple species of molecules. The most common approach, which accounts for inter-molecular forces between molecules of various species, is a molecular dynamics simulation. However, this is time consuming, and therefore, often limited for small volumes of fluid and small scale contacts. The current paper proposes an alternative approach, where the pressure and shear between two smooth surfaces separated by an ultra-thin film is predicted using a statistical mechanics based model. This method accounts for the chemical structure of each species of molecules comprising the ultra-thin film, their concentration, intermolecular forces and adsorption to the wall. This approach is very fast, therefore, it can be easily included in a larger scale code predicting the behavior of the entire micro-scale mechanism. It was found that for a specified material of the solid boundary the model can predict the optimal concentration of each species of molecule in the intervening ultra-thin film, to minimize friction or adhesion.
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de Boer, M. P., J. A. Knapp, J. M. Redmond, T. A. Michalske et R. Maboudian. « Adhesion, Adhesion Hysteresis and Friction in MEMS Under Controlled Humidity Ambients ». Dans ASME 1998 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1998. http://dx.doi.org/10.1115/imece1998-1145.

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Abstract In surface micromachining, compliant structures and high surface to volume ratios render surface properties such as adhesion and friction critical parameters in system reliability. The adhesion and friction of polycrystalline silicon (polysilicon) MEMS structures depends strongly on the ambient to which they are subjected. This dependence is reduced, but not eliminated, when molecular coatings are applied to their surfaces. From measured adhesion energy (Γ, J/m2) for uncoated beams, we demonstrate that capillary condensation produces an exponential dependence of adhesion on relative humidity (RH). For coated beams, we demonstrate that after substantial exposure to high RH ambients, adhesion begins to vary along the length of the beam. This implies a localized breakdown mechanism of the molecular coating. Finally, we present data on a new structure to measure friction in MEMS. With this structure, we can infer slip on a nanometer length scale.
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Kukreti, Sharad, Larry V. McIntire et C. Wayne Smith. « Molecular Mechanisms of Monocyte Adhesion to Cytokine Stimulated Endothelial Cells Under Physiological Flow Conditions ». Dans ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0238.

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Abstract This study investigates the underlying mechansisms of monocyte adhesion to both short term (IL-1β, 4 hr) and long term (IL-4, 24 hr) activated endothelial cells. At a wall shear stress of 2 dynes/cm2, monocytes appear to use multiple pathways for primary and secondary adhesion to IL-1β, 4 hr stimulated endothelial cells. However, on IL-4 24 hr stimulated HUVECs, VLA-4/VCAM-1 was the dominant mechanism for monocyte adhesion. Upon additional histamine exposure of IL-4, 24 hr treated endothelial cells, both P-selectin and VLA-4 were involved and had to blocked simultaneously to abolish monocyte adhesion. A combination of IL-1+IL-4 (24 hr) treatment resulted in a complete loss of the primary adhesive mechanism under flow conditions whereas secondary adhesion remained intact as indicated by static experiments.
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Lee, Lieng-Huang. « New perspectives in polymer adhesion mechanisms--importance of diffusion and molecular bonding in adhesion ». Dans SPIE's 1993 International Symposium on Optics, Imaging, and Instrumentation, sous la direction de Eric A. Norland et Kenneth M. Liechti. SPIE, 1993. http://dx.doi.org/10.1117/12.158592.

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Chen, K. Y., Y. L. Yeh, C. C. Wang, M. J. Jang et C. W. Lee. « To determine the adhesion by using AFM and the adhesive material volume estimation ». Dans 2009 IEEE 3rd International Conference on Nano/Molecular Medicine and Engineering (NANOMED). IEEE, 2009. http://dx.doi.org/10.1109/nanomed.2009.5559125.

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Rapports d'organisations sur le sujet "Molecular adhesion"

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Patterson, James E. Molecular Basis of Adhesion. Fort Belvoir, VA : Defense Technical Information Center, août 2012. http://dx.doi.org/10.21236/ada567127.

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Rabolt, J. F. Structural Determination of the Factors Which Influence Molecular Adhesion to Polymer Surfaces. Fort Belvoir, VA : Defense Technical Information Center, août 1997. http://dx.doi.org/10.21236/ada329127.

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Morrison, Mark, et Joshuah Miron. Molecular-Based Analysis of Cellulose Binding Proteins Involved with Adherence to Cellulose by Ruminococcus albus. United States Department of Agriculture, novembre 2000. http://dx.doi.org/10.32747/2000.7695844.bard.

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At the beginning of this project, it was clear that R. albus adhered tightly to cellulose and its efficient degradation of this polysaccharide was dependent on micromolar concentrations of phenylacetic acid (PAA) and phenylpropionic acid (PPA). The objectives for our research were: i) to identify how many different kinds of cellulose binding proteins are produced by Ruminococcus albus; ii) to isolate and clone the genes encoding some of these proteins from the same bacterium; iii) to determine where these various proteins were located and; iv) quantify the relative importance of these proteins in affecting the rate and extent to which the bacterium becomes attached to cellulose. BARD support has facilitated a number of breakthroughs relevant to our fundamental understanding of the adhesion process. First, R. albus possesses multiple mechanisms for adhesion to cellulose. The P.I.'s laboratory has discovered a novel cellulose-binding protein (CbpC) that belongs to the Pil-protein family, and in particular, the type 4 fimbrial proteins. We have also obtained genetic and biochemical evidence demonstrating that, in addition to CbpC-mediated adhesion, R. albus also produces a cellulosome-like complex for adhesion. These breakthroughs resulted from the isolation (in Israel and the US) of spontaneously arising mutants of R. albus strains SY3 and 8, which were completely or partially defective in adhesion to cellulose, respectively. While the SY3 mutant strain was incapable of growth with cellulose as the sole carbon source, the strain 8 mutants showed varying abilities to degrade and grow with cellulose. Biochemical and gene cloning experiments have been used in Israel and the US, respectively, to identify what are believed to be key components of a cellulosome. This combination of cellulose adhesion mechanisms has not been identified previously in any bacterium. Second, differential display, reverse transcription polymerase chain reaction (DD RT-PCR) has been developed for use with R. albus. A major limitation to cellulose research has been the intractability of cellulolytic bacteria to genetic manipulation by techniques such as transposon mutagenesis and gene displacement. The P.I.'s successfully developed DD RT- PCR, which expanded the scope of our research beyond the original objectives of the project, and a subset of the transcripts conditionally expressed in response to PAA and PPA have been identified and characterized. Third, proteins immunochemically related to the CbpC protein of R. albus 8 are present in other R. albus strains and F. intestinalis, Western immunoblots have been used to examine additional strains of R. albus, as well as other cellulolytic bacteria of ruminant origin, for production of proteins immunochemically related to the CbpC protein. The results of these experiments showed that R. albus strains SY3, 7 and B199 all possess a protein of ~25 kDa which cross-reacts with polyclonal anti-CbpC antiserum. Several strains of Butyrivibrio fibrisolvens, Ruminococcus flavefaciens strains C- 94 and FD-1, and Fibrobacter succinogenes S85 produced no proteins that cross-react with the same antiserum. Surprisingly though, F. intestinalis strain DR7 does possess a protein(s) of relatively large molecular mass (~200 kDa) that was strongly cross-reactive with the anti- CbpC antiserum. Scientifically, our studies have helped expand the scope of our fundamental understanding of adhesion mechanisms in cellulose-degrading bacteria, and validated the use of RNA-based techniques to examine physiological responses in bacteria that are nor amenable to genetic manipulations. Because efficient fiber hydrolysis by many anaerobic bacteria requires both tight adhesion to substrate and a stable cellulosome, we believe our findings are also the first step in providing the resources needed to achieve our long-term goal of increasing fiber digestibility in animals.
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Press, Michael F. Molecular Mechanism for Loss of Cell Adhesion in HER-2/neu Overexpressing Tumor Cells. Fort Belvoir, VA : Defense Technical Information Center, juillet 2001. http://dx.doi.org/10.21236/ada400616.

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Press, Michael F. Molecular Mechanism for Loss of Cell Adhesion in HER-2/neu Overexpressing Tumor Cells. Fort Belvoir, VA : Defense Technical Information Center, juillet 2002. http://dx.doi.org/10.21236/ada410189.

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Press, Michael F. Molecular Mechanism for Loss of Cell Adhesion in HER-2/neu Overexpressing Tumor Cells. Fort Belvoir, VA : Defense Technical Information Center, juillet 2004. http://dx.doi.org/10.21236/ada428250.

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Dixon, David Adams. Final Report : Molecular Basis for Microbial Adhesion and Geochemical Surface Reactions : A Study Across Scales. Office of Scientific and Technical Information (OSTI), juin 2013. http://dx.doi.org/10.2172/1084736.

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Morrison, Mark, Joshuah Miron, Edward A. Bayer et Raphael Lamed. Molecular Analysis of Cellulosome Organization in Ruminococcus Albus and Fibrobacter Intestinalis for Optimization of Fiber Digestibility in Ruminants. United States Department of Agriculture, mars 2004. http://dx.doi.org/10.32747/2004.7586475.bard.

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Improving plant cell wall (fiber) degradation remains one of the highest priority research goals for all ruminant enterprises dependent on forages, hay, silage, or other fibrous byproducts as energy sources, because it governs the provision of energy-yielding nutrients to the host animal. Although the predominant species of microbes responsible for ruminal fiber degradation are culturable, the enzymology and genetics underpinning the process are poorly defined. In that context, there were two broad objectives for this proposal. The first objective was to identify the key cellulosomal components in Ruminococcus albus and to characterize their structural features as well as regulation of their expression, in response to polysaccharides and (or) P AA/PPA. The second objective was to evaluate the similarities in the structure and architecture of cellulosomal components between R. albus and other ruminal and non-ruminal cellulolytic bacteria. The cooperation among the investigators resulted in the identification of two glycoside hydrolases rate-limiting to cellulose degradation by Ruminococcus albus (Cel48A and CeI9B) and our demonstration that these enzymes possess a novel modular architecture specific to this bacterium (Devillard et al. 2004). We have now shown that the novel X-domains in Cel48A and Cel9B represent a new type of carbohydrate binding module, and the enzymes are not part of a ceiluiosome-like complex (CBM37, Xu et al. 2004). Both Cel48A and Cel9B are conditionally expressed in response to P AA/PPA, explaining why cellulose degradation in this bacterium is affected by the availability of these compounds, but additional studies have shown for the first time that neither PAA nor PPA influence xylan degradation by R. albus (Reveneau et al. 2003). Additionally, the R. albus genome sequencing project, led by the PI. Morrison, has supported our identification of many dockerin containing proteins. However, the identification of gene(s) encoding a scaffoldin has been more elusive, and recombinant proteins encoding candidate cohesin modules are now being used in Israel to verify the existence of dockerin-cohesin interactions and cellulosome production by R. albus. The Israeli partners have also conducted virtually all of the studies specific to the second Objective of the proposal. Comparative blotting studies have been conducted using specific antibodies prepare against purified recombinant cohesins and X-domains, derived from cellulosomal scaffoldins of R. flavefaciens 17, a Clostridium thermocellum mutant-preabsorbed antibody preparation, or against CbpC (fimbrial protein) of R. albus 8. The data also suggest that additional cellulolytic bacteria including Fibrobacter succinogenes S85, F. intestinalis DR7 and Butyrivibrio fibrisolvens Dl may also employ cellulosomal modules similar to those of R. flavefaciens 17. Collectively, our work during the grant period has shown that R. albus and other ruminal bacteria employ several novel mechanisms for their adhesion to plant surfaces, and produce both cellulosomal and non-cellulosomal forms of glycoside hydrolases underpinning plant fiber degradation. These improvements in our mechanistic understanding of bacterial adhesion and enzyme regulation now offers the potential to: i) optimize ruminal and hindgut conditions by dietary additives to maximize fiber degradation (e.g. by the addition of select enzymes or PAA/PPA); ii) identify plant-borne influences on adhesion and fiber-degradation, which might be overcome (or improved) by conventional breeding or transgenic plant technologies and; iii) engineer or select microbes with improved adhesion capabilities, cellulosome assembly and fiber degradation. The potential benefits associated with this research proposal are likely to be realized in the medium term (5-10 years).
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Chen, Chen, Peng Chen, Xia Liu et Hua Li. Combined 5-Fluorouracil and Low Molecular Weight Heparin for the Prevention of Postoperative Proliferative Vitreoretinopathy in Patients with Retinal Detachment. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, août 2021. http://dx.doi.org/10.37766/inplasy2021.8.0117.

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Review question / Objective: The aim of this meta-analysis is to evaluate the efficacy and safety of intraoperative infusion of combined 5-fluorouracil and low molecular weight heparin (LMWH) for the prevention of postoperative proliferative vitreoretinopathy in patients with retinal detachment. Condition being studied: Postoperative proliferative vitreoretinopathy (PVR) is the primary cause of failure of retinal reattachment surgery. 5-fluorouracil (5-FU) inhibits the proliferation of fibroblasts, and suppresses collagen contraction. On the other hand, heparin reduces fibrin exudation, and inhibits the adhesion and migration of retinal pigment epithelial cells. We conduct this comprehensive literature search and meta-analysis to address whether intraoperative infusion of combined 5-FU and LWMH improves the primary success rate of pars plana vitrectomy, as well as reduces postoperative PVR. Our study aims to provide clinical evidence for retinal surgeons concerning their choice of intraoperative medication.
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Doyle, Jesse D., Nolan R. Hoffman et M. Kelvin Taylor. Aircraft Arrestor System Panel Joint Improvement. U.S. Army Engineer Research and Development Center, août 2021. http://dx.doi.org/10.21079/11681/41342.

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Aircraft Arresting Systems (AAS) for military applications utilize sacrificial panels made of Ultra-High Molecular Weight polyethylene (UHMWPE) that are embedded into the pavement beneath the AAS cable to protect the pavement from cable damage. Problems have been observed with the materials and practices used to seal the UHMWPE panel joints from water and debris. Data obtained from laboratory and field studies were used make improvements to current practice for sealing UHMWPE panel joints. The study evaluated four joint-sealant materials, eight alternative surface treatment and preparation techniques to promote adhesion to UHMWPE, and seven joint-edge geometries. Bond-strength testing of joint-sealant specimens was conducted in the laboratory, followed by field evaluation of construction techniques. Field performance of the joint systems was monitored for 24 months after installation. Additionally, a thermal response model was developed to refine the joint design dimensions. Results confirmed that the best material to use was self-leveling silicone joint sealant. It was recommended that a dovetail groove be cut into the edge of UHMW panels to provide positive mechanical interlock and to reduce adhesive failures of the sealant. It was also recommended that the panel-to-panel joint-sealant reservoir be widened to prevent sealant compression damage.
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