Academic literature on the topic 'Surface-mediated interaction'
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Journal articles on the topic "Surface-mediated interaction"
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Hyldgaard, P., and T. L. Einstein. "Surface-state–mediated three-adsorbate interaction." Europhysics Letters (EPL) 59, no. 2 (July 2002): 265–71. http://dx.doi.org/10.1209/epl/i2002-00236-0.
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Ribeiro, Sylvie, Christina Puckert, Clarisse Ribeiro, Andreia C. Gomes, Michael J. Higgins, and Senentxu Lanceros-Méndez. "Surface Charge-Mediated Cell–Surface Interaction on Piezoelectric Materials." ACS Applied Materials & Interfaces 12, no. 1 (December 11, 2019): 191–99. http://dx.doi.org/10.1021/acsami.9b17222.
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HUANG, WEN-MIN, HSIN-HUA LAI, CHENG-HUNG CHANG, and HSIU-HAU LIN. "CARRIER-MEDIATED EXCHANGE COUPLING AND FERMI SURFACE TOPOLOGY." International Journal of Modern Physics B 22, no. 01n02 (January 20, 2008): 88–93. http://dx.doi.org/10.1142/s0217979208046098.
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We investigate the carrier-mediated exchange coupling between two ferromagnets, sandwiching an intermediate thin layer with Rashba interaction. The effective exchange coupling is obtained by integrating out the itinerant carriers. It turns out that the magnetic trends depend sensitively upon the topology of the Fermi surface. As the topology changes from “wedding cake” to “donut”, the mediated exchange goes from the oscillatory Ruderman-Kittel-Kasuya-Yosida to the non-collinear spiral interactions accordingly. It is rather surprising that the Fermi surface topology determines which type of magnetic interaction becomes dominant. Finally, we also discuss potential applications for carrier-mediated exchange coupling across the junction.
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Godfrey, H. P., D. A. Frenz, L. S. Canfield, S. K. Akiyama, and S. A. Newman. "Non-chemotactic translocation of phagocytic cells mediated by a fibronectin-related human lymphokine." Journal of Immunology 143, no. 11 (December 1, 1989): 3691–96. http://dx.doi.org/10.4049/jimmunol.143.11.3691.
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Abstract A fibronectin (FN)-related human lymphokine, macrophage agglutination factor (MAggF), agglutinates monocytes at femtomolar concentrations. Similar concentrations of MAggF translocate monocytes and neutrophils through artificial extracellular matrices by a non-chemotactic adhesive process not dependent on intracellular metabolism (matrix-driven translocation). As is the case with matrix-driven translocation mediated by other FN, MAggF-mediated translocation depends on interaction of the lymphokine amino-terminal heparin-binding domain with cell surface heparin-like molecules. In contrast, lymphokine-mediated agglutination involves interactions between the MAggF cell-binding domain and integrin FN receptors recognizing the Arg-Gly-Asp sequence. MAggF-mediated translocation and agglutination are also dependent on the lymphokine gelatin-binding domain. The extremely high activity of MAggF in translocating and agglutinating monocytes may result from cooperative interactions between multiple lymphokine domains and multiple classes of cell surface receptor molecules. We suggest that MAggF-mediated matrix-driven translocation could act independently of or in addition to chemotaxis in recruiting monocytes and neutrophils to a tissue site of T cell-mediated inflammation. Subsequent interaction of MAggF and monocyte FN receptor could then detain monocytes there.
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Hyldgaard, Per, and T. L. Einstein. "Surface-state mediated three-adsorbate interaction: electronic nature and nanoscale consequences." Surface Science 532-535 (June 2003): 600–605. http://dx.doi.org/10.1016/s0039-6028(03)00173-0.
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Huang, Lizhi, Jianfeng Jia, Hongwei Liu, Yong Yuan, Jian Zhao, Shuai Chen, Weibin Fan, Eric R. Waclawik, Huaiyong Zhu, and Zhanfeng Zheng. "Surface-mediated selective photocatalytic aerobic oxidation reactions on TiO2 nanofibres." RSC Advances 5, no. 70 (2015): 56820–31. http://dx.doi.org/10.1039/c5ra07518a.
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Sionov, Ronit Vogt, Chrystelle Lamagna, and Zvi Granot. "Recognition of Tumor Nidogen-1 by Neutrophil C-Type Lectin Receptors." Biomedicines 10, no. 4 (April 15, 2022): 908. http://dx.doi.org/10.3390/biomedicines10040908.
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Neutrophil-mediated cytotoxicity toward tumor cells requires cell contact and is mediated by hydrogen peroxide. We have recently shown that Cathepsin G expressed on the neutrophil surface interacts with tumor RAGE, and this interaction facilitates neutrophil cytotoxicity. Interruption of the Cathepsin G–RAGE interaction led to 50–80% reduction in cytotoxicity, suggesting that additional interactions are also involved. Here we show that blocking antibodies to the C-type lectin receptors (CLRs) Clec4e and Dectin-1, but not those to NKG2D, attenuated murine neutrophil cytotoxicity towards murine tumor cells, suggesting a contributing role for these CLRs in neutrophil recognition of tumor cells. We further observed that the CLRs interact with tumor Nidogen-1 and Hspg2, two sulfated glycoproteins of the basement membrane. Both Nidogen-1 and Hspg2 were found to be expressed on the tumor cell surface. The knockdown of Nidogen-1, but not that of Hspg2, led to reduced susceptibility of the tumor cells to neutrophil cytotoxicity. Altogether, this study suggests a role for CLR–Nidogen-1 interaction in the recognition of tumor cells by neutrophils, and this interaction facilitates neutrophil-mediated killing of the tumor cells.
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Zheng, Mingzhe, and Sen-itiroh Hakomori. "Soluble Fibronectin Interaction with Cell Surface and Extracellular Matrix Is Mediated by Carbohydrate-to-Carbohydrate Interaction." Archives of Biochemistry and Biophysics 374, no. 1 (February 2000): 93–99. http://dx.doi.org/10.1006/abbi.1999.1613.
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Bansal, Rajeev K. "Approximation of surface–groundwater interaction mediated by vertical streambank in sloping terrains." Journal of Ocean Engineering and Science 2, no. 1 (March 2017): 18–27. http://dx.doi.org/10.1016/j.joes.2016.10.002.
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Shin, Youngho, Sungjun Bae, and Woojin Lee. "Formation of surface mediated iron colloids during U(VI) and nZVI interaction." Advances in environmental research 2, no. 3 (September 25, 2013): 167–77. http://dx.doi.org/10.12989/aer.2013.2.3.167.
Full textDissertations / Theses on the topic "Surface-mediated interaction"
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Hara, Tomijiro. "Cell surface thioredoxin-1 : possible involvement in thiol-mediated leukocyte-endothelial cell interaction through lipid rafts." Kyoto University, 2007. http://hdl.handle.net/2433/135769.
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Usman, Jauhr. "Quantification of affinity mediated cell/surface interactions." Thesis, University of Bath, 1997. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362307.
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Venkatesh, Savitha. "Chitosan-mediated transfection and the role of cell surface interactions." Scholarly Commons, 1997. https://scholarlycommons.pacific.edu/uop_etds/2320.
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Transfection is the process of introducing DNA into cells and expression of the gene contained in the DNA. The DNA itself could be a functional gene, part of a gene, or a gene with the regulatory and transcribed sequences intact. The ability to transfect mammalian cells is a powerful tool that can be used to study the function and control of mammalian genes. Transfection of DNA into eukaryotic cells can be done in several ways. One of the methods of introducing foreign DNA into mammalian cells is known as cationic liposome-mediated transfection. Preliminary studies involved the development of a cationic lipid-mediated transfection method using HeLa cells and a plasmid that codes for ~-galactosidase. The cationic lipid used was Transfectam. Transfectam is a commercially available, cationic lipopolyamine. Chitosan, a cationic polymer of glucosamine, was used as an alternative transfecting agent and as a binding agent for polyanions. The transfection efficiency of chitosan was compared to that of Transfectam. Chitosan was found to be comparable to Transfectam in this regard. Polyanions of different chemical structures were used in a chitosan binding study. These include aurin tricarboxylic acid, calf thymus DNA and methyl green DNA. The kinetics of the binding interactions suggest that ionic interactions predominated. Based upon these findings, studies were performed to determine the nature of chitosan interactions with the cell surface. Chitosan beads were prepared to determine the interaction of chitosan with the cell membrane of He La cells and for the isolation of membrane proteins. Membrane proteins which bound to chitosan beads could be effectively eluted with a-0-mannopyranoside but not sodium chloride. Furthermore, HeLa cells bound to the chitosan beads could be eluted with aD- mannopyranoside but not sodium chloride. The results suggested that membrane bound proteins interact with chitosan through carbohydrate moiety interactions which may facilitate the transfection process.
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King, Malcolm Anthony Wallace. "Indirect substrate and surface state mediated interactions at surfaces : a case study of ethene adsorption on Cu{111}." Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615101.
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Peronio, Angelo. "A closer look at heterogeneous catalysis: reaction intermediates at the single-molecule level." Doctoral thesis, Università degli studi di Trieste, 2013. http://hdl.handle.net/10077/8577.
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2011/2012The present work pertains to the surface science approach to heterogeneous catalysis. In particular model systems for CO2 hydrogenation to methanol, and NO selective catalytic reduction, are investigated by means of a combined approach, where the molecular-level insight provided by a low-temperature scanning tunneling microscope is complemented by density functional theory (DFT) calculations of their electronic structure. To this end, the Inelastic Electron Tunneling Spectroscopy (STM-IETS) technique was introduced for the first time in our laboratory, a recent development which allows to measure the vibrational spectrum of individual molecules adsorbed on a surface. Regarding CO2, we provide single molecule imaging and characterization of CO2/Ni(110), chemisorbed with high charge transfer from the substrate, in an activated state that plays a crucial role in the hydrogenation process. We obtain a detailed characterization of the adsorption geometries and an estimate of the energies corresponding to the different adsorbed states. A consistent picture of CO2 chemisorption on Ni(110) is provided on the basis of the newly available information, yielding a deeper insight into the previously existing spectroscopic and theoretical data. In the Selective Catalytic Reduction (SCR) process, nitrogen oxide is selectively transformed to N2 by reductants such as ammonia. The specificity of this reaction was tentatively attributed to the formation of NH3-NO coadsorption complexes, as indicated by several surface science techniques. Here we characterize the NH3-NO complex at the atomic scale on the (111) surface of platinum, investigating the intermolecular interactions that tune the selectivity. The structures that arise upon coadsorption of NH3 and NO are analyzed in terms of adsorption sites, geometry, energetics and charge rearrangement. An ordered 2 × 2 adlayer forms, where the two molecules are arranged in a configuration that maximizes mutual interactions. In this structure, NH3 adsorbs on top and NO on fcc-hollow sites, leading to a cohesional stabilization of the extended layer by 0.29 eV/unit cell. The calculated vibrational energies of the individually-adsorbed species and of the coadsorption structure fit the experimental values found in literature within less than 6%. The characterizations and optimizations that had to be tackled in order to successfully perform STM-IETS measurement are eventually presented, focusing in particular on an original method which allows to increase the achieved resolution. Namely, the modulation broadening associated to phase-sensitive detection is reduced by employing a tailored modulation function, different from the commonly-used sinusoid. This method is not limited to STM-IETS, but can be easily applied whenever a lock-in amplifier is used to measure a second derivative.
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Pless, Elin. "Investigation of interactions with extracellular matrix proteins mediated by the CCP modules of the metabotropic GABAB receptor." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/5714.
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GABAB receptors are G-protein coupled receptors for the major inhibitory neurotransmitter in the mammalian central nervous system, γ-aminobutyric acid (GABA). The receptor is linked to a variety of disorders including epilepsy, pain, spasticity, drug addiction and cognitive impairment and is, therefore of major importance for drug discovery. The most abundant receptor isoforms GABABR1a and R1b differ by the presence in R1a of a pair of Nterminal extracellular complement control protein modules (CCP1 and CCP2) which - in other proteins - are generally involved in mediating specific protein-protein recognition. The CCP1 module contains disulphides but is natively disordered. In the current work, the yeast two-hybrid system was used to confirm an interaction of CCP1 of GABABR1a with the extracellular protein fibulin-2. Further work with the yeast twohybrid system extablished the novel interaction of the abundant extracellular matrix protein laminin, with GABABR1a CCP1, via its laminin globular (LG) domains. The laminin interaction was further characterised by surface plasmon resonance, demonstrating that several different domains are involved in the binding to the GABAB receptor CCPs. The primary binding site is located on laminin α5 LG4-5, but the E10 domains of the β1 chain and LG1-3 on α1 may also be involved. The pharmacological properties of the GABABR1a and R1b isoforms were studied by transient expression in Xenopus laevis oocytes. It was demonstrated that the agonist baclofen, as well as the antagonist CGP55845, appear to be more potent at GABABR1b compared to GABABR1a. Intriguingly, when recorded in the precence of laminin, GABABR1b/R2 expressing oocytes exhibited an increased baclofen-evoked response while the response in GABABR1a/R2 was completely abolished. In conclusion, the work demonstrates that laminin is a binding partner for GABABR1a CCPs. Such an interaction between the metabotropic GABA receptor and the extracellular matrix may lie behind the recently reported roles of GABA in neuronal migration and the laying down of neuronal circuitry during the development of parts of the central nervous system.
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Johansson, Malin. "Investigation of hPin1 mediated phosphorylation dependency in degradation control of c-Myc oncoprotein." Thesis, Linköpings universitet, Molekylär Bioteknik, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-92718.
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Cancer is the main cause of death in economically developed countries and the second leading cause of death in developing countries. Along with today’s knowledge that more than two hundred different diseases lie in the category of this prognosis there is an urge for more detailed and case-specific treatments to replace the dramatic actions of available radiation- and chemotherapy, which in many cases do not make a difference between healthy and cancer cells. The transcription factor and onco-protein c-Myc has, after being extensively studied during the past decades, become a prognostic marker for almost all cancer forms known. Still, many questions remain regarding how c-Myc interacts with its many different target proteins involved in cell-cycle regulation, proliferation and apoptosis. Current cell biology states that one of the regulating proteins, hPin1, interacts with c-Myc in a phosphorylation-dependent manner which appears to direct the correct timing of c-Myc activation and degradation through the ubiquitin/proteasome-pathway. The critical phosphorylation sites, T58 and S62, are located in the Myc-Box-I (MBI) region, a highly conserved sequence strongly coupled to aggressive tumourigenesis by hotspot mutations. Interestingly, preliminary results in the Sunnerhagen group suggested that MBI alone did not bind hPin1, suggesting hPin1 targeting a site distal from the residues to be phosphorylated. In this thesis, results from Surface Plasmon Resonance (SPR) and Nuclear Magnetic Resonance (NMR) show that the docking WW-domain of hPin1 binds unphosphorylated c-Myc at a region distal from the phosphorylation site, including residues 13-34. Furthermore, SPR experiments revealed that hPin1 binds unphosphorylated c-Myc with apparently greater affinity and with much slower kinetics than phosphorylated c-Myc. Thus, hPin1 recognition and interaction with c-Myc appears not to be dependent on phosphorylation of c-Myc prior binding. The newly identified binding region of c-Myc, located N-terminal of MBI, may further increase the understanding of protein degradation control and c-Myc function. The studies presented in this thesis provide a brick in the puzzle of c-Myc and hPin1 coupled oncogenesis for further development of new therapeutic strategies.
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Haakh, Harald Richard. "Fluctuation-mediated interactions of atoms and surfaces on a mesoscopic scale." Phd thesis, Universität Potsdam, 2012. http://opus.kobv.de/ubp/volltexte/2012/6181/.
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Thermal and quantum fluctuations of the electromagnetic near field of atoms and macroscopic bodies play a key role in quantum electrodynamics (QED), as in the Lamb shift. They lead, e.g., to atomic level shifts, dispersion interactions (Van der Waals-Casimir-Polder interactions), and state broadening (Purcell effect) because the field is subject to boundary conditions. Such effects can be observed with high precision on the mesoscopic scale which can be accessed in micro-electro-mechanical systems (MEMS) and solid-state-based magnetic microtraps for cold atoms (‘atom chips’).
A quantum field theory of atoms (molecules) and photons is adapted to nonequilibrium situations. Atoms and photons are described as fully quantized while macroscopic bodies can be included in terms of classical reflection amplitudes, similar to the scattering approach of cavity QED. The formalism is applied to the study of nonequilibrium two-body potentials. We then investigate the impact of the material properties of metals on the electromagnetic surface noise, with applications to atomic trapping
in atom-chip setups and quantum computing, and on the magnetic dipole contribution to the Van der Waals-Casimir-Polder potential in and out of thermal equilibrium. In both cases, the particular properties of superconductors are of high interest. Surface-mode contributions, which dominate the near-field fluctuations, are discussed in the context of the (partial) dynamic atomic dressing after a rapid change of a system parameter and in the Casimir interaction between two conducting plates, where nonequilibrium configurations can give rise to repulsion.Thermische und Quantenfluktuationen des elektromagnetischen Nahfelds von Atomen und makroskopischen Körpern spielen eine Schlüsselrolle in der Quantenelektrodynamik (QED), wie etwa beim Lamb-Shift. Sie führen z.B. zur Verschiebung atomarer Energieniveaus, Dispersionswechselwirkungen (Van der Waals-Casimir-Polder-Wechselwirkungen) und Zustandsverbreiterungen (Purcell-Effekt), da das Feld Randbedingungen unterliegt. Mikroelektromechanische Systeme (MEMS) und festkörperbasierte magnetische Fallen für kalte Atome (‘Atom-Chips’) ermöglichen den Zugang zu mesoskopischen Skalen, auf denen solche Effekte mit hoher Genauigkeit beobachtet werden können. Eine Quantenfeldtheorie für Atome (Moleküle) und Photonen wird an Nichtgleichgewichtssituationen angepasst. Atome und Photonen werden durch vollständig quantisierte Felder beschrieben, während die Beschreibung makroskopischer Körper, ähnlich wie im Streuformalismus (scattering approach) der Resonator-QED, durch klassische Streuamplituden erfolgt. In diesem Formalismus wird das Nichtgleich- gewichts-Zweiteilchenpotential diskutiert. Anschließend wird der Einfluss der Materialeigenschaften von normalen Metallen auf das elektromagnetische Oberflächenrauschen, das für magnetische Fallen für kalte Atome auf Atom-Chips und für Quantencomputer-Anwendungen von Bedeutung ist, sowie auf den Beitrag des magnetischen Dipolmoments zum Van der Waals-Casimir-Polder-Potential im thermisch- en Gleichgewicht und in Nichtgleichgewichtssituationen untersucht. In beiden Fällen sind die speziellen Eigenschaften von Supraleitern von besonderem Interesse. Beiträge von Oberflächenmoden, die die Feldfluktuationen im Nahfeld dominieren, werden im Kontext des (partiellen) dynamischen Dressing nach einer raschen Änderung eines Systemparameters sowie für die Casimir-Wechselwirkung zweier metallischer Platten diskutiert, zwischen denen in Nichtgleichgewichtssituationen Abstoßung auftreten kann.
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Tavares, Lucas Alves. "O envolvimento da proteína adaptadora 1 (AP-1) no mecanismo de regulação negativa do receptor CD4 por Nef de HIV-1." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/17/17136/tde-06012017-113215/.
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O Vírus da Imunodeficiência Humana (HIV) é o agente etiológico da Síndrome da Imunodeficiência Adquirida (AIDS). A AIDS é uma doença de distribuição mundial, e estima-se que existam atualmente pelo menos 36,9 milhões de pessoas infectadas com o vírus. Durante o seu ciclo replicativo, o HIV promove diversas alterações na fisiologia da célula hospedeira a fim de promover sua sobrevivência e potencializar a replicação. A rápida progressão da infecção pelo HIV-1 em humanos e em modelos animais está intimamente ligada à função da proteína acessória Nef. Dentre as diversas ações de Nef está a regulação negativa de proteínas importantes na resposta imunológica, como o receptor CD4. Sabe-se que esta ação resulta da indução da degradação de CD4 em lisossomos, mas os mecanismos moleculares envolvidos ainda são totalmente elucidados. Nef forma um complexo tripartite com a cauda citosólica de CD4 e a proteína adaptadora 2 (AP-2), em vesículas revestidas por clatrina nascentes, induzindo a internalização e degradação lisossomal de CD4. Pesquisas anteriores demonstraram que o direcionamento de CD4 aos lisossomos por Nef envolve a entrada do receptor na via dos corpos multivesiculares (MVBs), por um mecanismo atípico, pois, embora não necessite da ubiquitinação de carga, depende da ação de proteínas que compõem os ESCRTs (Endosomal Sorting Complexes Required for Transport) e da ação de Alix, uma proteína acessória da maquinaria ESCRT. Já foi reportado que Nef interage com subunidades dos complexos AP-1, AP-2, AP-3 e Nef não parece interagir com subunidades de AP-4 e AP-5. Entretanto, o papel da interação de Nef com AP-1 e AP-3 na regulação negativa de CD4 ainda não está totalmente elucidado. Ademais, AP-1, AP-2 e AP-3 são potencialmente heterogêneos devido à existência de isoformas múltiplas das subunidades codificadas por diferentes genes. Todavia, existem poucos estudos para demonstrar se as diferentes combinações de isoformas dos APs são formadas e se possuem propriedades funcionais distintas. O presente trabalho procurou identificar e caracterizar fatores celulares envolvidos na regulação do tráfego intracelular de proteínas no processo de regulação negativa de CD4 induzido por Nef. Mais especificamente, este estudo buscou caracterizar a participação do complexo AP-1 na modulação negativa de CD4 por Nef de HIV-1, através do estudo funcional das duas isoformas de ?-adaptina, subunidades de AP-1. Utilizando a técnica de Pull-down demonstramos que Nef é capaz de interagir com ?2. Além disso, nossos dados de Imunoblot indicaram que a proteína ?2-adaptina, e não ?1-adaptina, é necessária no processo de degradação lisossomal de CD4 por Nef e que esta participação é conservada para degradação de CD4 por Nef de diferentes cepas virais. Ademais, por citometria de fluxo, o silenciamento de ?2, e não de ?1, compromete a diminuição dos níveis de CD4 por Nef da membrana plasmática. A análise por imunofluorêsncia indireta também revelou que a diminuição dos níveis de ?2 impede a redistribuição de CD4 por Nef para regiões perinucleares, acarretando no acúmulo de CD4, retirados por Nef da membrana plasmática, em endossomos primários. A depleção de ?1A, outra subunidade de AP-1, acarretou na diminuição dos níveis celulares de ?2 e ?1, bem como, no comprometimento da eficiente degradação de CD4 por Nef. Além disso, foi possível observar que, ao perturbar a maquinaria ESCRT via super-expressão de HRS (uma subunidade do complexo ESCRT-0), ocorreu um acumulo de ?2 em endossomos dilatados contendo HRS-GFP, nos quais também detectou-se CD4 que foi internalizado por Nef. Em conjunto, os resultados indicam que ?2-adaptina é uma importante molécula para o direcionamento de CD4 por Nef para a via ESCRT/MVB, mostrando ser uma proteína relevante no sistema endo-lisossomal. Ademais, os resultados indicaram que as isoformas ?-adaptinas não só possuem funções distintas, mas também parecem compor complexos AP-1 com diferentes funções celulares, já que apenas a variante AP-1 contendo ?2, mas não ?1, participa da regulação negativa de CD4 por Nef. Estes estudos contribuem para o melhor entendimento dos mecanismos moleculares envolvidos na atividade de Nef, que poderão também ajudar na melhor compreensão da patogênese do HIV e da síndrome relacionada. Em adição, este trabalho contribui para o entendimento de processos fundamentais da regulação do tráfego de proteínas transmembrana no sistema endo-lisossomal.The Human Immunodeficiency Virus (HIV) is the etiologic agent of Acquired Immunodeficiency Syndrome (AIDS). AIDS is a disease which has a global distribution, and it is estimated that there are currently at least 36.9 million people infected with the virus. During the replication cycle, HIV promotes several changes in the physiology of the host cell to promote their survival and enhance replication. The fast progression of HIV-1 in humans and animal models is closely linked to the function of an accessory protein Nef. Among several actions of Nef, one is the most important is the down-regulation of proteins from the immune response, such as the CD4 receptor. It is known that this action causes CD4 degradation in lysosome, but the molecular mechanisms are still incompletely understood. Nef forms a tripartite complex with the cytosolic tail of the CD4 and adapter protein 2 (AP-2) in clathrin-coated vesicles, inducing CD4 internalization and lysosome degradation. Previous research has demonstrated that CD4 target to lysosomes by Nef involves targeting of this receptor to multivesicular bodies (MVBs) pathway by an atypical mechanism because, although not need charging ubiquitination, depends on the proteins from ESCRTs (Endosomal Sorting Complexes Required for Transport) machinery and the action of Alix, an accessory protein ESCRT machinery. It has been reported that Nef interacts with subunits of AP- 1, AP-2, AP-3 complexes and Nef does not appear to interact with AP-4 and AP-5 subunits. However, the role of Nef interaction with AP-1 or AP-3 in CD4 down-regulation is poorly understood. Furthermore, AP-1, AP-2 and AP-3 are potentially heterogeneous due to the existence of multiple subunits isoforms encoded by different genes. However, there are few studies to demonstrate if the different combinations of APs isoforms are form and if they have distinct functional properties. This study aim to identify and characterize cellular factors involved on CD4 down-modulation induced by Nef from HIV-1. More specifically, this study aimed to characterize the involvement of AP-1 complex in the down-regulation of CD4 by Nef HIV-1 through the functional study of the two isoforms of ?-adaptins, AP-1 subunits. By pull-down technique, we showed that Nef is able to interact with ?2. In addition, our data from immunoblots indicated that ?2- adaptin, not ?1-adaptin, is required in Nef-mediated targeting of CD4 to lysosomes and the ?2 participation in this process is conserved by Nef from different viral strains. Furthermore, by flow cytometry assay, ?2 depletion, but not ?1 depletion, compromises the reduction of surface CD4 levels induced by Nef. Immunofluorescence microscopy analysis also revealed that ?2 depletion impairs the redistribution of CD4 by Nef to juxtanuclear region, resulting in CD4 accumulation in primary endosomes. Knockdown of ?1A, another subunit of AP-1, resulted in decreased cellular levels of ?1 and ?2 and, compromising the efficient CD4 degradation by Nef. Moreover, upon artificially stabilizing ESCRT-I in early endosomes, via overexpression of HRS, internalized CD4 accumulates in enlarged HRS-GFP positive endosomes, where co-localize with ?2. Together, the results indicate that ?2-adaptin is a molecule that is essential for CD4 targeting by Nef to ESCRT/MVB pathway, being an important protein in the endo-lysosomal system. Furthermore, the results indicate that ?-adaptins isoforms not only have different functions, but also seem to compose AP-1 complex with distinct cell functions, and only the AP-1 variant comprising ?2, but not ?1, acts in the CD4 down-regulation induced by Nef. These studies contribute to a better understanding on the molecular mechanisms involved in Nef activities, which may also help to improve the understanding of the HIV pathogenesis and the related syndrome. In addition, this work contributes with the understanding of primordial process regulation on intracellular trafficking of transmembrane proteins.
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"Measuring the Surface-Surface Interactions Mediated by Proteins in a Physiological Solution." 2016. http://repository.lib.cuhk.edu.hk/en/item/cuhk-1292142.
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蛋白質與固體表面在生理環境中的相互作用是蘊涵於多種技術應用的一個基本現象，涉及了生物醫學植入體的塗層，靶向藥物運載以及生物感測器等應用。實際上，在許多生物醫學應用中，當材料進入組織或血液流體後，蛋白會第一時間吸附於其表面上，這會改變材料的表面性質，進而嚴重限制它們的實際應用。雖然過去幾十年在尋找抑制非特異性蛋白質吸附的理想表面方面已經取得了相當大的進展，但是我們對於蛋白質如何參與設計表面間相互作用的基本原理還知之甚少。本論文旨在理解在真正的生理溶液中蛋白質如何參與功能化表面間的相互作用，從而為良好控制蛋白質在生物醫學材料上的吸附和沉積提供基本資訊。具體來說，我們使用自主搭建的全內反射顯微鏡（TIRM）被動地監視許多單個膠體粒子與各種功能化表面相互作用下的布朗運動，從而產生相對應的勢能曲線。這些定量測量可以進一步幫助我們瞭解蛋白質調控作用下表面與表面間的主要作用力，目前我們對這方面的認知還是有限的。
首先，我們利用TIRM直接測量三種常見蛋白質（伴刀豆球蛋白A（ConA），牛血清白蛋白（BSA），溶菌酶（LYZ））修飾的的微米尺寸顆粒與大豆蛋白（SP）修飾玻璃表面之間的相互作用。我們的結果表明，蛋白層的吸附極大地影響了材料表面的電荷屬性，並且這些蛋白質官能表面之間的相互作用依賴於溶液的pH值，主要是通過靜電相互作用主導。
其次，我們通過動態光散射（DLS）和TIRM的組合研究了三種不同類型的改性表面在胎牛血清（FBS）中的相互作用，即：裸聚苯乙烯（PS）粒子和裸玻璃表面，BSA修飾的PS和玻璃表面，聚乙二醇（PEG）修飾PS和玻璃表面。DLS實驗表明，所有這三種修飾的PS表面在血清環境中很快會被蛋白層覆蓋，但與BSA修飾表面和裸露表面相比，PEG官能化的表面顯示出最小的蛋白質吸附量。對於TIRM測試，我們認為，對於裸露表面和BSA修飾表面，其相互作用主要是由空間排斥力，范德華引力和重力主導。然而，對於PEG修飾表面，由於兩個表面之間較長的作用距離，范德華力不再主導。
最後，我們從二氧化矽表面接枝聚[低聚（乙二醇）甲基丙烯酸甲酯]（POEGMA）聚合物刷，然後研究刷厚度和接枝密度對其與PS顆粒在血清環境中相互作用的影響。對於AFM測試，蛋白質吸附到POEGMA刷子表面上的量隨POEGMA刷厚度的增大而減小，表明POEGMA表面的抗蛋白性能隨刷厚度的增加而增強。通過TIRM測得的勢能曲線，可以發現，表面吸附的血清蛋白層一方面會因為不均一的缺陷導致橋接現象的產生，另一方面會由於均勻吸附而產生一定的空間排斥力。
The interaction of proteins with solid surfaces in a physiological environment is a fundamental phenomenon with implication for a wide variety of technological applications, ranging from coatings for biomedical implants, to targeted drug carries and biosensors. Actually, in many biomedical applications, the first event when a material enters tissue or blood fluids is protein adsorption on its surface and this has been shown to play an important role in changing the surface properties of the material, which further can severely limit their practical applications. Although considerable progress has been made over the last decades to find the ideal surface of which suppression the non-specific protein adsorption, the underlying principles of the role serum proteins play in the interactions with designed surfaces are poorly understood.
This thesis aims at understanding how proteins take part in interactions of various functionalized surfaces in a real physiological solution, thus providing fundamental information for well controlling the protein adsorption and deposition onto biomedical applications. Specifically, we use our established total internal reflection microscopy (TIRM) to passively monitor the Brownian excursions of many single colloidal particles, interacting with various functionalized surfaces to yield simultaneous interaction potential profiles. These quantitative measurements thus can help to understand the main forces responsible for the surface-surface interactions mediated by proteins in a physiological solution, a topic about which we have little knowledge.
Firstly, we utilized TIRM to directly measure the interactions between micron-sized particles decorated with three types of common proteins concanavalin A (ConA), bovine serum albumin (BSA), lysozyme (LYZ) and glass surface coated with soy proteins (SP). Our results show that the protein adsorption greatly affects the charge property of the surfaces and the interactions between those protein-functionalized surfaces depend on solution pH values and mainly dominated by electrostatic interaction forces.
Secondly, we studied the interactions between three different kinds of modified surfaces: namely bare polystyrene (PS) particle and bare glass surface, PS and glass surfaces both adsorbed with BSA, and PS and glass surfaces both coated with polyethylene glycol (PEG) in a fetal bovine serum (FBS) solution by a combination of dynamic light scattering (DLS) and TIRM. The DLS measurement showed that all three kinds of PS-coated surfaces were quickly covered by a layer of proteins when they were immersed in serum but PEG-functionalized surfaces showed a minimum protein adsorption compared with the BSA and bare surfaces. For TIRM measurements, we argue that the interactions were mainly governed by steric repulsion, van der Waals attraction and gravity in bare and BSA cases. However, in PEG case, van der Waal attraction might be absent due to a longer distance between two surfaces.
Finally, we grafted poly[oligo(ethylene glycol) methyl methacrylate] (POEGMA) polymer brushes from the bottom silica surfaces and study how brush thickness and graft density affect their interactions with PS particles in the serum environment. For AFM measurement, the amount of protein adsorption onto POEGMA brush surfaces decreases as the increase of POEGMA brush thickness, indicating that the anti-fouling properties of the POEGMA surfaces truly increase as the increase of brush thickness. The potential energy profiles analysis reveals that such adsorbed protein layer on both surfaces could contribute to mediate the interaction forces between the surfaces by exerting bridging effect caused by heterogeneous patches or steric repulsion caused by a homogeneous coverage.
Wang, Zhaohui.
Thesis Ph.D. Chinese University of Hong Kong 2016.
Includes bibliographical references (leaves ).
Abstracts also in Chinese.
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Books on the topic "Surface-mediated interaction"
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Simpson, Harry Jay. Interaction of sound with sound by novel mechanisms: Ultrasonic four-wave mixing mediated by a suspension and ultrasonic three-wave mixing at a free surface. 1992.
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Manchon, A., and S. Zhang. Theory of Rashba Torques. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198787075.003.0024.
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This chapter focuses on the theory of current-driven Rashba torque, a special type of spin–orbit mediated spin torque that requires broken spatial-inversion symmetry. This specific form of spin-orbit interaction enables the electrical generation of a non-equilibrium spin density that yields both damping-like and field-like torques on the local magnetic moments. We review the recent results obtained in (ferromagnetic and antiferromagnetic) two-dimensional electron gases, bulk magnetic semiconductors, and at the surface of topological insulators. We conclude by summarizing recent experimental results that support the emergence of Rashba torques in magnets lacking inversion symmetry.
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Kirchman, David L. Introduction to geomicrobiology. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198789406.003.0013.
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Geomicrobiology, the marriage of geology and microbiology, is about the impact of microbes on Earth materials in terrestrial systems and sediments. Many geomicrobiological processes occur over long timescales. Even the slow growth and low activity of microbes, however, have big effects when added up over millennia. After reviewing the basics of bacteria–surface interactions, the chapter moves on to discussing biomineralization, which is the microbially mediated formation of solid minerals from soluble ions. The role of microbes can vary from merely providing passive surfaces for mineral formation, to active control of the entire precipitation process. The formation of carbonate-containing minerals by coccolithophorids and other marine organisms is especially important because of the role of these minerals in the carbon cycle. Iron minerals can be formed by chemolithoautotrophic bacteria, which gain a small amount of energy from iron oxidation. Similarly, manganese-rich minerals are formed during manganese oxidation, although how this reaction benefits microbes is unclear. These minerals and others give geologists and geomicrobiologists clues about early life on Earth. In addition to forming minerals, microbes help to dissolve them, a process called weathering. Microbes contribute to weathering and mineral dissolution through several mechanisms: production of protons (acidity) or hydroxides that dissolve minerals; production of ligands that chelate metals in minerals thereby breaking up the solid phase; and direct reduction of mineral-bound metals to more soluble forms. The chapter ends with some comments about the role of microbes in degrading oil and other fossil fuels.
Book chapters on the topic "Surface-mediated interaction"
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Southam, Gordon. "Bacterial Surface-Mediated Mineral Formation." In Environmental Microbe-Metal Interactions, 257–76. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555818098.ch12.
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Ware, Carl F., and Jeanne L. Reade. "Functional Interactions of LFA-1, T8 and Alloantigen Surface Structures in T-Cell Mediated Cytotoxicity." In Advances in Experimental Medicine and Biology, 323–41. New York, NY: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-8326-0_22.
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Hagel, Lars. "Separation on the basis of chemistry." In Protein Purification Techniques. Oxford University Press, 2001. http://dx.doi.org/10.1093/oso/9780199636747.003.0011.
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Most chromatographic separations are based on chemical interaction between the solute of interest or impurities to be removed and the separation medium. The exception is separations based upon physical properties such as size (e.g. size exclusion chromatography) or transport in a force field (e.g. electrochromatography). The chemical interaction may be weak (e.g. employing van der Waals forces) or very strong (e.g. involving formation of chemical bonds as in covalent chromatography). Whenever separation is based upon attractive forces between the solute and the separation medium, we talk about adsorption chromatography (also when the solute is merely retarded). The chemical interaction between the solute and the adsorbent (the chromatography medium) is governed by the surface properties of the solute and the adsorbent and is in most cases mediated by the mobile phase or additives to the mobile phase. Macromolecules such as proteins display a variety of properties and, ideally, a selected set of properties is utilized for obtaining the required selectivity (i.e. relative separation from other solutes) using a separation medium of complementary properties. This chapter briefly reviews the different types of forces of interaction between solutes and surfaces commonly employed for chromatographic purifications, important properties of solvents, and some basic surface chemical properties of proteins. This, together with a description of some common types of chromatography modes provides a basis for a rational selection of separation mechanism for the purification of proteins and the choice of mobile phase composition to regulate the relative influence of different interaction mechanisms. The separation mechanisms are focused to adsorptive modes with the exception of affinity chromatography which is discussed in Chapter 9. The different attractive forces acting between molecular and particle surfaces include (1): • dispersion forces • electrostatic dipole interactions • electron donor-acceptor forces • formation of covalent bonds All these forces are due to interactions between electric charges (permanent or induced). Dispersion, or London forces, are caused by induced dipole-induced dipole interactions and are thus classified as a non-specific interaction. This type of non-polar interaction is the dominant force promoting dissolution of non-polar solutes in organic solvents.
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Kumar Chatterjee, Swapan, and Snigdha Saha. "Glycan and Its Role in Combating COVID-19." In Biotechnology to Combat COVID-19 [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97240.
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Newly identified beta-coronavirus i.e. the 2019 novel coronavirus is associated with a contagious transmittable respiratory disease called COVID-19. This disease has been declared as a “pandemic” by the World Health Organization (WHO). The entry of coronavirus in the human respiratory epithelial cells depends upon the interaction between host cell receptor ACE2 and viral S-glycoprotein. However, this type of molecular recognition in between cell surface receptors and envelope glycoproteins are mediated by specific glycan epitopes and attribute to viral entry through membrane fusion. Glycans are essential biomolecules made by all living organisms, have roles in serving structure, energy storage, and system regulatory purposes. The glycan shield plays a crucial role in concealing the surface S protein from molecular recognition. The immunomodulatory properties of Glycan-binding proteins (GBPs) like Lectins, build them as an attractive candidates for vaccine adjuvant. Investigations involving the complement system activation by the lectin pathway in COVID-19 and diseases are in need of the hour. The innate immune response involving complement system could have varied biological effects against an array of microbial infections. The advances in glycoprotein style methods especially immunomodulatory action of some lectins are necessary to boost the effectiveness of treatment of COVID-19 and other pandemics.
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Khaneja, Navin. "SQUID Magnetometers, Josephson Junctions, Confinement and BCS Theory of Superconductivity." In Magnetometers - Fundamentals and Applications of Magnetism. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.83714.
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A superconducting quantum interference device (SQUID) is the most sensitive magnetic flux sensor currently known. The SQUID can be seen as a flux to voltage converter, and it can generally be used to sense any quantity that can be transduced into a magnetic flux, such as electrical current, voltage, position, etc. The extreme sensitivity of the SQUID is utilized in many different fields of applications, including biomagnetism, materials science, metrology, astronomy and geophysics. The heart of a squid magnetometer is a tunnel junction between two superconductors called a Josephson junction. Understanding the work of these devices rests fundamentally on the BCS theory of superconductivity. In this chapter, we introduce the notion of local potential and confinement in superconductivity. We show how BCS ground state is formed from interaction of wave packets confined to these local potential wells. The starting point of the BCS theory of superconductivity is a phonon-mediated second-order term that describes scattering of electron pair at Fermi surface with momentum k i , − k i and energy 2 ℏ ω i to k j , − k j with energy 2 ℏ ω j . The transition amplitude is M = − d 2 ω d ω i − ω j 2 − ω d 2 , where d is the phonon scattering rate and ω d is the Debye frequency. However, in the presence of offset ω i − ω j , there is also a present transition between states k i , − k i and k j , − k i of sizable amplitude much larger than M . How are we justified in neglecting this term and only retaining M ? In this chapter, we show all this is justified if we consider phonon-mediated transition between wave packets of finite width instead of electron waves. These wave packets are in their local potentials and interact with other wave packets in the same well to form a local BCS state we also call BCS molecule. Finally, we apply the formalism of superconductivity in finite size wave packets to high Tc in cuprates. The copper electrons in narrow d-band live as packets to minimize the repulsion energy. The phonon-mediated coupling between wave packets (of width Debye energy) is proportional to the number of k-states in a packet, which becomes large in narrow d-band (10 times s-band); hence, d-wave Tc is larger (10 times s-wave). At increased doping, packet size increases beyond the Debye energy, and phonon-mediated coupling develops a repulsive part, destroying superconductivity at large doping levels.
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Murphy, Keith M. "Programming Politeness." In Rethinking Politeness with Henri Bergson, 121—C8.P104. Oxford University Press, 2022. http://dx.doi.org/10.1093/oso/9780197637852.003.0010.
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Abstract In his 1892 essay “Politeness”—a modest sort of “mirror for princes” addressed to students at one of France’s most acclaimed lycées—Henri Bergson described and promoted what amounts to a basic mechanics for harmonious interaction. He outlines three different forms of politeness, including “of minds,” “of manners,” and “of the heart,” each of which corresponds with the three most French of virtues—liberty, equality, and fraternity. The core of his argument is that through the enactment of politeness, whose effects are felt at multiple scales, from the interpersonal to the polity, a better and more just world will emerge. This argument resonates deeply with similar orientations in the world of design that also operate from a more contemporary position of social improvement. This chapter expands on its author’s earlier argument that design is a fundamental vector through which humans provision for each other the basic conditions for living. Bergson’s notion of politeness is used to show that debates about relative “goodness” or relative “badness” that haunt many design disciplines are, just below the surface, really debates about the ethical stances that humans take toward one other—but at one-degree removed, mediated through the forms of designed things. The discussion is organized around two complementary cases—“polite computing” and the design of “useable” software; and “hostile architecture” and the design of antagonistic spaces.
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Simons, Peter, and Charlotte M. Vines. "Analysis of GTP-Binding Protein–Coupled Receptor Assemblies by Flow Cytometry." In Flow Cytometry for Biotechnology. Oxford University Press, 2005. http://dx.doi.org/10.1093/oso/9780195183146.003.0022.
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GTP-binding protein–coupled receptors (GPCRs) represent the largest family of integral membrane signal-transducing molecules in the human genome, with estimates of at least 600 members. As such, they represent the targets of approximately 30%–50% of the prescription drugs on the market. They are involved in virtually every physiological process in the human body, with ligands including light, odorants, amines, peptides, proteins, lipids, and nucleotides. Binding of these ligands on the extracellular surface of the receptor leads to conformational changes within the receptor, resulting in a multitude of cellular responses. GPCRs, as their name implies, function through the actions of heterotrimeric GTP-binding proteins (G proteins). These G proteins then couple to a diverse array of effector molecules at the cell surface and inside the cell. GPCRs contain a common structural motif, with seven transmembrane alpha helices. With the recent description of the three-dimensional crystal structure of rhodopsin in its inactive state, a greater, though still incomplete, understanding of the functions of this receptor family has been achieved. In addition to the activation of G proteins, GPCRs undergo extensive regulation mediated primarily by a variety of kinases, including second messenger kinases and the family of G protein–coupled receptor kinases (GRKs). Following receptor phosphorylation by GRKs, additional proteins named arrestins associate with GPCRs. The traditional role of these molecules has been to serve as desensitizing agents, preventing further association of the receptor with G proteins. However, recent studies have demonstrated that arrestins can serve as adapters in the process of receptor internalization as well as scaffolds in the activation of numerous kinase pathways. Interactions between GPCRs and cellular proteins such as adaptins, rab GTPases, phosphatases, and ion channels have also been described. Thus, it has become apparent that understanding the interactions between GPCRs and their associated proteins is critical for any detailed understanding of receptor function. An overview of the activation and regulation of GPCRs is shown in figure 17.1 to provide a context for the approaches to be described in the remainder of this chapter.
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Bunker, Bruce C., and William H. Casey. "The Impact of Oxides on Environmental Chemistry." In The Aqueous Chemistry of Oxides. Oxford University Press, 2016. http://dx.doi.org/10.1093/oso/9780199384259.003.0027.
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The ancient Greek philosopher Empedocles defined our environments using the four basic elements of fire, earth, wind, and water. Although we now know there are at least 118 elements, of which 98 are naturally occurring, these ancient descriptions aptly describe the habitats on Earth that are occupied by oxides and living things. Many oxides that comprise Earth’s surface are born by the fire represented by the massive heat of Earth’s interior as mediated by plate tectonics. This heat produces the igneous rocks found in volcanoes and our major mountain chains. Water weathers these pristine rocks, which are gradually broken down to form earth, which includes the wide diversity of other rock types, soils, and sediments covering the surfaces of our continents and ocean floors. Weathered oxides in the form of dust are blown by wind and enter the atmosphere, where they influence the chemistry of the air we breathe and the rainfall that supports continental life. The chemical transformations of oxides are strongly influenced by all the environmental conditions they encounter in their life cycle (see Chapter 17). Conversely, the interactions between oxides, water, and organisms help define many of the environments that allow life on Earth to thrive. These interactions form the basis for this final chapter of our book. Oxides are present in all our planet’s major environments. In this chapter, we explore each of the environments defined by the ancient Greeks in descending order based on their distance from Earth’s core. The chapter progresses from the stratosphere (air) to continental surfaces (earth) to our oceans (water) and finally to the subsurface environments of subduction zones such as the Marianas Trench (fire). In each section, we highlight reactions involving the two most important classes of oxides in terms of their environmental impact, both of which are weathering products: (1) the clay minerals and (2) the redox-active colloids of iron and manganese oxides. Clay mineral reactions impact colloidal interactions (Chapter 8), ion exchange (Chapter 10), and the sequestration of environmental nutrients and contaminants. Reactions of the redox-active oxidates of iron and manganese are dominant in terms of reversible and often complex electrochemical (Chapter 11) and photochemical (Chapter 13) processes that take place in natural environments.
Conference papers on the topic "Surface-mediated interaction"
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Hertel, T., E. Knoesel, M. Wolf, and G. Ertl. "Time-Resolved Two-Colour Photoelectron Spectroscopy of Clean and Adsorbate Covered Metal Surfaces." In International Conference on Ultrafast Phenomena. Washington, D.C.: Optica Publishing Group, 1996. http://dx.doi.org/10.1364/up.1996.fe.45.
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The dynamics of photoexcited electrons and their interaction with adsorbates is of fundamental importance for many photostimulated reactions at metal surfaces. Such reactions are frequently mediated by 'hot' substrate electrons and the corresponding reaction cross sections will, therefore, depend critically on the charge carrier dynamics in the near surface region. On the other hand the perturbation of the local electronic structure by an adsorbate may allow to alter lifetimes of electronically excited states at surfaces.
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Li, Jianrong, Tianle Cheng, and Martin Y. M. Chiang. "Finite Element Modelling of Cell Adhesion Mediated by Receptor-Ligand Binding." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206297.
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The process of cell adhesion and spreading on the extracellular matrix (ECM) protein layer is mediated by the interaction of cell receptors and ECM ligands [1]. Receptors diffuse along the cell membrane surface and interact with ligands in ECM to form bonds. Cells spread and the adhesion zone grows as bond formation at the adhesion front increases to a critical level. This process involves coupling of reaction-diffusion and mechanical contact between cells and ECM. In this study, a novel numerical algorithm is developed to implement this coupling into the finite element method for modeling the process of cell adhesion and spreading. By taking the mass diffusion and the user-defined gap conductance features provided in a commercial FEM code, Abaqus [2], the process has been solved in an integrated and fully coupled manner. Preliminary results have been obtained from the simulation of cell spreading on a rigid substrate. The influence of glycocalyx layer (present at cell surface) on the adhesion development has also been incorporated into the modeling.
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Maciaszek, J. L., B. Andemariam, and G. Lykotrafitis. "Red Blood Cell Surface Receptor Expression of BCAM/Lu is Regulated by Protein Kinase A Activity." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14311.
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Irregular sickle red blood cells (RBCs) can contribute to the pathogenesis of vasoocclusion and other complications of sickle cell disease (SCD) via abnormal adherence to the vascular endothelium. It has previously been demonstrated that epinephrine enhances SCD RBC adhesion by activating the BCAM/Lu and ICAM-4 surface receptors [1–2]. Epinephrine acts on the RBC β2-adrenergic receptor, thereby activating Gas proteins that stimulate adenylyl cyclase (AC). This enzyme catalyzes the conversion of adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP), leading to protein kinase A (PKA) activation, an intermediate step in the upregulation of BCAM/Lu and ICAM-4 mediated adhesion. The interaction of BCAM/Lu with the α5 chain of laminin may contribute to vaso-occlusive events in SCD due to overexpression of BCAM on SCD RBCs.
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Dryjski, Maciej, Be-Sheng Kuo, and Thorir D. Bjornsson. "INTERACTION OF THROMBIN AND FACTOR Xa WITH BOVINE VASCULAR ENDOTHELIAL CELLS, SMOOTH MUSCLE CELLS AND RAT HEPATOMA CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644728.
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The inhibition of thrombin as well as of factor Xa has been thought to occur primarily in plasma through the neutralizing action of the serine protease inhibitor antithrombin III (AT-III). However, inhibition of thrombin and Xa by this mechanism may not be sufficient for effective elimination of these clotting factors in states of increased coagulation activity. The potential role of the vascular endothelium in the inhibition of clotting factor activities has therefore received attention in recent years. The aim of the present investigation was to characterize the binding and inhibition of thrombin and factor Xa to the vascular endothelial cell (EC), smooth muscle cell (SMC) and rat hepatoma cell (RHC) in vitro, as well as to evaluate the effects of plasma constituents upon the inhibition of these factors. Purified bovine thrombin and factor Xa were used. The enzymatic activities of both factors were assayed using chromogenic substrates. The cells were exposed for 5 U/ml thrombin or 0.5 U/ml factor Xa. After 10 minutes incubation, the initial thrombin activity in the solution had decreased by about 20% in case of EC and SMC and about 11% when incubated with RHC. Thrombin activity recovered from the cell surface amounted to 0.02 U/cm2. When the cells with the surface bound enzyme were incubated with defibrinogenated plasma or AT-III for 30 seconds, only about 10% and 25-40%, respectively, of initial activity could be found. In similar experiments with factor Xa, after 10 minutes incubation, the initial activity in the solution had decreased by 10%. Factor Xa activity recovered from the cell surface was 0.001 U/cm2. After 30 seconds exposure to AT-III, no cell surface related factor Xa activity was recovered, whereas 10% of the cell surface activity was recovered after incubation with defibrinogenated plasma. It is concluded that thrombin and factor Xa are taken up and inhibited by EC, SMC and RHC cell surfaces in similar ratios suggesting that cell surface-mediated inactivation of activated clotting factors is not restricted to vascular wall cells. The inactivation of factor Xa was dependent on AT-III, however, the inactivation of thrombin was further promoted by an additional unidentified plasma constituent
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Williams, T. J., M. Rampart, S. Nourshargh, P. G. Hellewell, S. D. Brain, and P. J. Jose. "INTERACTION OF POLYMORPHONUCLEAR LEUKOCYTES AND ENDOTHELIAL CELLS : FUNCTIONAL CONSEQUENCES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643985.
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The mechanisms involved in the accumulation of polymorphonuclear leukocytes (PMNs) in an inflammatory reaction are complex. A key phase in this process is the attachment of the PMN to the microvascular (venular in most tissues) endothelial cell, initiated by the extravascular generation of a chemical mediator. Experiments in vitro suggest that mediators, such as C5a, may act in vivo by stimulating the increased expression of the CD18 complex on the surface of the PMN within the venule lumen (1), whereas IL-1 may act by causing the expression of an adhesive molecule on the endothelial cell (2). In vitro the former process is rapid whereas the latter is slow in onset. We have measured the local accumulation of intravenously-injected Ulln-PMNs in response to intradermally-injected mediators in the rabbit, in order to investigate possible mechanisms in vivo. PMN accumulation was found to be rapid in onset in response to C5a, the rate of accumulation falling progressively to low levels by 4 hours. In contrast PMN accumulation in response to IL-1 was slow in onset, reaching a peak rate at 3-4 hours. Intradermal injection of the vasodilator prostaglandins PGI2; PGE2 and the neuropeptides VIP and CGRP caused a marked potentiation of the rate of leukocyte accumulation. PMN accumulation induced by C5a was associated with increased microvascular permeability, as indicated by the leakage of intravenously-injected 125I-albumin with a time-course in parallel with the rate of PMN accumulation enhanced by intradermally-injected vasodilators. Depletion of circulating PMNs abolishes these responses to C5a (3). In contrast, leukocyte accumulation induced by IL-1 was associated with little plasma protein leakage, even in the presence of intradermal vasodilators. This observation indicates that PMN emigration itself does not lead to increased microvascular permeability. C5a, but not IL-1, may stimulate emigrating PMNs to secrete an endogenous factor that increases permeability by an action on endothelial cells (3). This factor does not appear to be the phospholipid PAF (4). In contrast to the enhancing effects of local PGI2, intravenously-infused PGI2 inhibited PMN accumulation induced by C5a and IL-1, and plasma protein leakage induced by C5a (5). This effect is probably mediated by elevation of cyclic AMP in intravascular PMNs. We have shown that C5a stimulation of PMNs in contact with endothelial cells in vitro induces endothelial cell PGI2 secretion (6). Thus, PGI2 may be part of a negative feedback system in vivo to control interactions between PMNs and endothelial cells.These observations provide some clues to the intricacies of mechanisms of leukocyte accumulation in vivo.
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Savion, N., A. Gamliel, and N. Farzame. "THROMBIN INTERACTION WITH CULTURED AORTIC AND CAPILLARY ENDOTHELIAL CELLS: BINDING, INTERNALIZATION, DEGRADATION AND RELEASE OF PROTEASE NEXINS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644734.
Full textAbstract:
Thrombin (Th) binds specifically to confluent cultures of bovine aortic (ABAE) and brain capillary (BBC) endothelial cells. Saturation of 125I-Th binding is observed after 1 h exposure to the ligand and at an extracellular concentration of 0.5 and 1.0 µg/ml for ABAE and BBC cells, respectively. Under optimal conditions both ABAE and BBC cultures bind about 2 to 5 ng/106 cells, which represents about 20% of Th binding.to bovine corneal endothelial (BCE) cells. The cell associated 125I-Th in ABAE and BBC cells is internalized and degraded as described in BCE cells. The nature of the cell associated radioactivity is analyzed on SDS-polyacrylamide -gel electrophoresis and in ABAE and BBC cells about 30% of the I-Th appears in a complex with protease nexin I (PN I) while in BCE cells about 70% of the binding is mediated by PN I. ABAE cells possess 3 types of complexes, one which appears only on the cell surface with a molecular weight of 78 kDa, and two other complexes which appear only in the conditioned medium (CM) with molecular weights of 84 and 85 kDa. BBC and BCE cells demonstrate only one type of complex with a molecular weight of 77 kDa which appears both on the cell surface and in the CM. Preincubation of BCE cultures in the presence of Th is known to up-regulate the amount of PN I on the cell surface and in the CM, but this Th induced up-regulation effect is not observed in ABAE or BBC cells.The results described above indicate a difference between ABAE and BBC cells although both cell types growunder similar conditins and demonstrate similar morphological appearance. However, in both vascular endothelial cell types the total amount of PN I and its metabolism is relatively small compared to corneal endothelial cells. It, therefore, may indicate the lower capacity of vascular endothelial cells to control serine proteases activity at or near their cell surfaces as compared to corneal endothelial cells. This research was supported by a grant from the NationalCouncil for Research and Development, Israel and G.S.F. Munchen, Germany
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Castillo, R., G. Escolar, J. Monteagudo, A. Cases, M. Garrido, and A. Ordinas. "UREMIC PLASMA, AFTER INFUSION OF DESMOPRESSIN, IMPROVES THE INTERACTION OF NORMAL PLATELETS WITH VESSEL SUBENDOTHELIUM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644711.
Full textAbstract:
Desmopressin (DDAVP) shortened the bleeding time and increased the platelet retention on glass beads and the platelet interaction on subendothelium measured by the Baumgartner perfusion system in 11 uremic patients in whom the three tests were abnormal previous to the treatment (1).Patients were chosen at random out of a group of 30 with prolonged bleeding time and decreased platelet retention on glass beads. All tests were performed on blood drawn before and one and six hours after a single dose of DDAVP (0.4 μg/kg body weight). Perfusion experiments were carried out at a shear rate of 800 sec-1.Levels of VIII:C, VIIIR:Ag and RiCof were at the upper limit of normality before DDAVP and significantly increased one hour after treatment. The multimeric structure of vWF in pretreatment plasma was normal ; one hour after DDAVP larger multimers appeared.After injection of DDAVP, the perfusion studies using reconstituted blood with uremic PPP in presence of isolated normal platelets and washed red cells, showed a statistically increased surface coverage and platelet aggregate formation on subendothelium (p < 0.05 respectively when compared to the pretreatment values). In the same perfusion assays, the in vitro addition to pretreatment plasmas of 1 u/ml of purified vWF with normal multimeric structure, or purified VIII:C and vWF (1 u/ml each) did not modify the decreased platelet interaction on subendothelium.These results confirm the shortening of bleeding time by DDAVP in uremic patients and reveal an increase of platelet interaction on vessel subendothelium mediated by a factor present in PPP. Besides, they show that the effect of DDAVP in these patients is not due to the quantitative increase of the plasmatic vWF and FVIII.(1) Blood, 68, 2:337-342, 1986.
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Rosing, J., H. Speijer, J. W. P. Govers-Riemslag, and R. F. A. Zwaal. "THE EFFECT OF PROCOAGULANT PHOSPHOLIPID VESICLES WITH NET POSITIVE CHARGE ON THE ACTIVITY OF PROTHROMBINASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643839.
Full textAbstract:
It is generally thought that procoagulant phospholipid surfaces that promote the activation of vitamin K-dependent coagulation factors should have a net negative charge in order to promote calcium-dependent binding of the enzymes (FVIIa, FIXa and FXa) and substrates (prothrombin and FX) of the coagulation factor-activating complexes. Two models have been proposed to explain calcium-mediated association of vitamin K-dependent proteins with phospholipid: a) an electrostatic model, in which a positively-charged protein-calcium complex is attracted by a negatively-charged phospholipid surface and b) a chelation model in which a coordination complex is formed between calcium ions, γ-carboxyglutamic acids of the proteins and negatively-charged membrane phospholipids. To study the effect of the electrostatic potential of phospholipid vesicles on their activity in the pro-thrombinase complex the net charge of vesicles was varied by introduction of varying amounts of positively-charged stearylamine in the membrane surface. Introduction of 0-15 mole% stearylamine in phospholipid vesicles that contained 5 mole% phosphatidylseri-ne (PS) hardly affected their activity in prothrombin activation. Electrophoretic analysis showed that vesicles with > 5 mole% stearylamine had a net positive charge. The procoagulant activity of vesicles that contained phosphatidic acid, phosphatidylglyce-rol, phosphatidylinositol or phosphatidyl-glactate (PLac) as acidic phospholipid was much more effected by incorporation of stearylamine. Amounts of stearylamine that compensated the negative charge of acidic phospholipid caused considerable inhibition of the activity of the latter vesicles in prothrombin activation. The comparison of vesicles containing PS and PLac as acidic phospholipid is of special interest. PS and PLac only differ by the presence of NH+ 3-group in the serine moiety of PS. Thus, in spite of the fact that vesicles with PLac are more negatively charged than vesicles with PS, they are less procoagulant. Our results show that a) although procoagulant membranes have to contain acidic phospholipids there is no requirement for a net negative charge, b) the amino group of phosphatidylserine has an important function in the interaction of procoagulant membranes with vitamin K-dependent proteins and c) the chelation model can satisfactorily explain calcium-mediated lipid-protein association.
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Bastida, E., G. Escolar, R. Castillo, A. Ordinas, and J. J. Sixma. "FIBRONECTIN IS REQUIRED FOR PLATELET ADHESION AND FOR THROMBUS FORMATION ON SUBENDOTHELIUM AND COLLAGEN SURFACES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643558.
Full textAbstract:
Fibronectin (FN) plays a role in several adhesion mediated functions including the interaction of platelets with subendothelium.We investigated the role of plasma FN in platelet adhesion and platelet thrombus formation under flow conditions.To do this we used two different perfusion models:1)the annular chamber with α -chymotrypsin-treated rabbit vessel segments and 2)the flat chamber with coverslips coated with fibrillar purified human collagen type III.Perfusates consisted of washed platelets, and washed red blood celIs,suspended in normal or FN-depleted plasma.Perfusions were carried out for 10 min at shear rates of 300 or 1300 sec™1 Platelet deposition and thrombus dimensions were morphometrically evaluated by a computerized system. We found that depletion of plasma FN significantly reduced the percentage of total coverage surface and percentage of platelet thrombus, at both shear rates studied, and in both perfusion systems (p < 0.01)(p < 0.01).The dimensions of the platelet thrombi formed in perfusions at high shear rate were also significantly reduced in perfusions carried out with FN-depleted plasma.(p < 0.01). Addition of purified FN to FN-depleted perfusates restored all the values to those measured in the control perfusions.These results indicate that, in addition to supporting platelet adhesion to the subendothelium and to fibrillar collagen, FN contributes to platelet thrombus formation under flow conditions.
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Teo, Ka Yaw, Basma Ibrahim, Seungman Park, Yeo Yoon, and Bumsoo Han. "Enhanced Transmucosal Transport Using Osmolyte-Mediated Fluid-Matrix Interaction." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53102.
Full textAbstract:
Various drug delivery systems are developed to deliver therapeutic and diagnostic agents to tissues covered with mucus, such as airways, nasal cavity, or oral cavity [1]. However, the mucus, which present for protection of the tissues, significantly hinders the transport of these agents and ultimately mitigates their efficacy [2]. Several studies have been performed to improve the transmucosal transport by studying the transport rates of polymeric nanoparticles with various sizes and surface chemistry [3–5]. However, drug delivery systems with improved transmucosal transport capability are still highly desired.
Reports on the topic "Surface-mediated interaction"
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Yogev, David, Ricardo Rosenbusch, Sharon Levisohn, and Eitan Rapoport. Molecular Pathogenesis of Mycoplasma bovis and Mycoplasma agalactiae and its Application in Diagnosis and Control. United States Department of Agriculture, April 2000. http://dx.doi.org/10.32747/2000.7573073.bard.
Full textAbstract:
Mycoplasma bovis and M. agalactiae are two phylogenetically related mycoplasmas which cause economically significant diseases in their respective bovine or small ruminant hosts. These organisms cause persistent asymptomatic infections that can result in severe outbreaks upon introduction of carrier animals into susceptible herds. Little is known about the mechanisms underlying mycoplasma-host interaction, variation in virulence, or of the factors enabling avoidance of the host immune system. In recent years it has become apparent that the ability of pathogenic microorganisms to rapidly alter surface antigenic structures and to fine tune their antigenicity, a phenomena called antigenic variation, is one of the most effective strategies used to escape immune destruction and to establish chronic infections. Our discovery of a novel genetic system, mediating antigenic variation in M. bovis (vsp) as well as in M. agalactiae (avg) served as a starting point for our proposal which included the following objectives: (i) Molecular and functional characterization of the variable surface lipoproteins (Vsp) system of M. bovis and comparison with the Vsp-counterpart in M. agalactiae (ii) Determination of the role of Vsp proteins in the survival of M. bovis when confronted by host defense factors, (iii) Assessment of Vsp-based genetic and antigenic typing of M. bovis and M. agalactiae for epidemiology of infection and (iv) Improvement of diagnostic tests for M. bovis and M. agalactiae based on the vsp-and vsp-analogous systems. We have carried out an extensive molecular characterization of the vsp system and unravelled the precise molecular mechanism responsible for the generation of surface antigenic variation in M. bovis. Our data clearly demonstrated that the two pathogenic mycoplasma species possess large gene families encoding variable lipoprotein antigens that apparently play an important role in immune evasion and in pathogen-host interaction during infection. Phase variable production of these antigens was found to be mediated by a novel molecular mechanism utilizing double site-specific DNA inversions via an intermediate vsp configuration. Studies in model systems indicate that phase variation of VspA is relevant in interaction between M. bovis and macrophages or monocytes, a crucial stage in pathogenesis. Using an ELISA test with captured VspA as an antigen, phase variation was shown to occur in vivo and under field conditions. Genomic rearrangements in the avg gene family of M. agalactiae were shown to occur in vivo and may well have a role in evasion of host defences and establishment of chronic infection. An epidemiological study indicated that patterns of vsp-related antigenic variation diverge rapidly in an M. bovis infected herd. Marked divergence was also found with avg-based genomic typing of M. agalactiae in chronically infected sheep. However, avg-genomic fingerprints were found to be relatively homogeneous in different animals during acute stages of an outbreak of Contagious Agalactiae, and differ between unrelated outbreaks. These data support the concept of vsp-based genomic typing but indicate the necessity for further refinement of the methodology. The molecular knowledge on these surface antigens and their encoding genes provides the basis for generating specific recombinant tools and serological methods for serodiagnosis and epidemiological purposes. Utilization of these methods in the field may allow differentiating acutely infected herds from chronic herds and disease-free herds. In addition the highly immunogenic nature of these lipoproteins may facilitate the design of protective vaccine against mycoplasma infections.