Relevant bibliographies by topics / Leukocyte-endothelial

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Leukocyte-endothelial'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Leukocyte-endothelial"

1

Harlan, JM. "Leukocyte-endothelial interactions." Blood 65, no. 3 (March 1, 1985): 513–25. http://dx.doi.org/10.1182/blood.v65.3.513.513.

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Harlan, JM. "Leukocyte-endothelial interactions." Blood 65, no. 3 (March 1, 1985): 513–25. http://dx.doi.org/10.1182/blood.v65.3.513.bloodjournal653513.

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MIYASAKA, Masayuki. "Leukocyte-Endothelial Cell Interactions." Japanese Journal of Thrombosis and Hemostasis 1, no. 6 (1990): 465–74. http://dx.doi.org/10.2491/jjsth.1.465.

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Carlos, TM, and JM Harlan. "Leukocyte-endothelial adhesion molecules." Blood 84, no. 7 (October 1, 1994): 2068–101. http://dx.doi.org/10.1182/blood.v84.7.2068.2068.

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Abstract In the 9 years since the last review on leukocyte and endothelial interactions was published in this journal many of the critical structures involved in leukocyte adherence to and migration across endothelium have been elucidated. With the advent of cell and molecular biology approaches, investigations have progressed from the early descriptions by intravital microscopy and histology, to functional and immunologic characterization of adhesion molecules, and now to the development of genetically deficient animals and the first phase I trial of “anti-adhesion” therapy in humans. The molecular cloning and definition of the adhesive functions of the leukocyte integrins, endothelial members of the Ig gene superfamily, and the selectins has already provided sufficient information to construct an operative paradigm of the molecular basis of leukocyte emigration. The regulation of these adhesion molecules by chemoattractants, cytokines, or chemokines, and the interrelationships of adhesion pathways need to be examined in vitro and, particularly, in vivo. Additional studies are required to dissect the contribution of the individual adhesion molecules to leukocyte emigration in various models of inflammation or immune reaction. Certainly, new adhesion structures will be identified, and the current paradigm of leukocyte emigration will be refined. The promise of new insights into the biology and pathology of the inflammatory and immune response, and the potential for new therapies for a wide variety of diseases assures that this will continue to be an exciting area of investigation.
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Carlos, TM, and JM Harlan. "Leukocyte-endothelial adhesion molecules." Blood 84, no. 7 (October 1, 1994): 2068–101. http://dx.doi.org/10.1182/blood.v84.7.2068.bloodjournal8472068.

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In the 9 years since the last review on leukocyte and endothelial interactions was published in this journal many of the critical structures involved in leukocyte adherence to and migration across endothelium have been elucidated. With the advent of cell and molecular biology approaches, investigations have progressed from the early descriptions by intravital microscopy and histology, to functional and immunologic characterization of adhesion molecules, and now to the development of genetically deficient animals and the first phase I trial of “anti-adhesion” therapy in humans. The molecular cloning and definition of the adhesive functions of the leukocyte integrins, endothelial members of the Ig gene superfamily, and the selectins has already provided sufficient information to construct an operative paradigm of the molecular basis of leukocyte emigration. The regulation of these adhesion molecules by chemoattractants, cytokines, or chemokines, and the interrelationships of adhesion pathways need to be examined in vitro and, particularly, in vivo. Additional studies are required to dissect the contribution of the individual adhesion molecules to leukocyte emigration in various models of inflammation or immune reaction. Certainly, new adhesion structures will be identified, and the current paradigm of leukocyte emigration will be refined. The promise of new insights into the biology and pathology of the inflammatory and immune response, and the potential for new therapies for a wide variety of diseases assures that this will continue to be an exciting area of investigation.
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Wild, Martin K., and M. Gabriele Bixel. "Leukocyte?endothelial cell interactions." FEBS Journal 273, no. 19 (October 2006): 4375–76. http://dx.doi.org/10.1111/j.1742-4658.2006.05436.x.

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Harlan, John. "Leukocyte-Mediated Endothelial Injury." Journal of Vascular and Interventional Radiology 9, no. 4 (July 1998): 675–77. http://dx.doi.org/10.1016/s1051-0443(98)70352-5.

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McEver, Rodger P. "Leukocyte—endothelial cell interactions." Current Biology 2, no. 11 (November 1992): 620. http://dx.doi.org/10.1016/0960-9822(92)90185-d.

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McEver, Rodger P. "Leukocyte—endothelial cell interactions." Current Opinion in Cell Biology 4, no. 5 (October 1992): 840–49. http://dx.doi.org/10.1016/0955-0674(92)90109-p.

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Bevilacqua, M. P. "Endothelial-Leukocyte Adhesion Molecules." Annual Review of Immunology 11, no. 1 (April 1993): 767–804. http://dx.doi.org/10.1146/annurev.iy.11.040193.004003.

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Dissertations / Theses on the topic "Leukocyte-endothelial"

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Williams, Marcie Renee. "Leukocyte and endothelial gene expression: response to endothelial stimulation and leukocyte transmigration." Diss., Georgia Institute of Technology, 2009. http://hdl.handle.net/1853/33817.

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Leukocyte transmigration is a critical step of the inflammatory process. In this project I have examined leukocyte responses to transmigration and endothelial responses to both chemical and mechanical stimuli which are known to be involved in leukocyte transmigration. My work has identified ~2500 differentially expressed genes following endothelial exposure to interleukin-1 beta (IL1β). Interestingly, IL1β induces up-regulation of claudin-1 and pre-b-cell colony enhancing factor and down-regulation of claudin-5 and occludin, which are all involved in maintaining endothelial cell-cell junctions. Analysis of endothelial cell (EC) transcriptional changes following neutrophil transmigration found few differentially expressed genes in comparison to IL1β treated ECs; indicating that the effects of transmigration on ECs are minimal in comparison to the global transcriptional changes induced by IL1β. Atherosclerosis, characterized by monocyte accumulation within the vessel lumen, is found in regions of flow reversal and low time averaged oscillatory shear stress. I have examined the effects of this type of shear stress on endothelial cell gene expression. My data indicates that most genes differentially expressed under these conditions are controlled by low average shear stress rather than flow reversal. These differentially expressed genes are involved in regulating the cell cycle and the immune response. My work shows that cell proliferation is increased following exposure to low steady shear stress or exposure to reversing oscillatory flow in comparison to high steady shear stress. Additionally monocyte adhesion is increased following exposure of ECs to reversing oscillatory flow. My work has also examined the impact of transmigration on monocyte gene expression. I have identified genes which are differentially expressed in monocytes by exposure to EC secretions, monocyte/EC contact, and diapedesis. I have also shown that freshly isolated human monocytes have reduced apoptosis following transmigration. Surprisingly, I also found that monocytes had reduced expression of anti-microbial peptides following transmigration. Overall my work identifies important endothelial and leukocyte transcriptional responses to the process of transmigration which extends from cytokine stimulation through diapedesis.
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Jenkins, Yvonne. "Leukocyte - endothelial interactions in allograft rejection." Thesis, University of Newcastle Upon Tyne, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.430338.

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Toothill, Valerie. "Leukocyte-endothelial cell interactions in inflammatory disease." Thesis, Open University, 1992. http://oro.open.ac.uk/57401/.

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For established manufacturing nations, increased competitive pressure has been the way of life since the late 1970s. For the most part however, production decision making in manufacturing industry has not changed to meet these new challenges. It usually takes a subordinate strategic role to the marketing and finance functions with the consequence that it accepts a reactive role in the corporate debate. The outcome is that strategic initiatives and developments are predominantly based on corporate marketing-decisions at the "front end" with manufacturing being forced to react at the "back end" of the debate. Since manufacturing managers come late into these discussions, it is difficult for them to successfully influence corporate decisions. All too often, the result is the formulation and later development of strategies which manufacturing is unable to successfully support. That is not to say that this happens for want of trying - strong is the work ethic in the manufacturing culture. However, if the basic link between the manufacturing processes and infrastructure (ie manufacturing strategy) and the market is not strategically sound, then the business will suffer. There are many reasons why manufacturing is typically reactive in the strategic debate. One important factor is the lack of appropriate concepts and language with which to explain or contribute to corporate decisions. This research has been undertaken to help redress this deficiency. The work began in the early 1980s. Upto that time, both the professional and academic contributions to the field of manufacturing strategy principally concerned statements which highlighted the problem and alerted manufacturing industry as a whole to its size and potential. However, there were in addition some important early pointers as to ways of overcoming the inadequacy of production's contribution to strategy formulation as well as some alternative approaches which firms needed to consider as ways of improving their overall performance. The inability of the production executive to contribute appropriate functional inputs provided the stimulus to undertake this work and to endeavour to build on initial insights as a way of taking forward the subject area of manufacturing strategy. The core of this thesis concerns these developments. Reported here are three contributions to this field of study all of which have been tested in different firms and are increasingly being used by academics, consultants and businesses as a way of helping to gain essential insights into what is a complex problem. The three facets are: • Typically, corporate strategies are composites of functional statements which are inadequately debated one with another in order to understand and test the coherence of the approaches proposed. The result is that the opportunity to fashion corporate strategies supported by all the functions within a business is not adequately pursued. In addition, the necessity to develop corporate strategy in this way and the advantages which ensue have gone unrecognised • The reactive role of manufacturing results in a lack of strategic direction within this function. As a result, typical developments and investments tend to take the form of operational responses undertaken without strategic context. One outcome of the research is a methodology which provides a way in which a business can develop a manufacturing strategy which links manufacturing developments and investments to the needs of its agreed markets. Two applications of this are provided in Chapter 4 • It is most important for an industrial company to recognise that it is attempting to support the inherently changing nature of its markets with manufacturing investments the characteristics of which are fixed in nature and will not change without further investments and developments. Product profiling is a methodology for enabling companies to assess the current level of match between its markets and manufacturing and to recognise the extent to which decisions will effect this in the future. Examples of its application illustrating different sources of mismatch are given in Chapter 5.
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Hart, Stephanie Hall Burridge Keith W. T. "Vascular endothelial cadherin phosphorylation modulates endothelial cell permeability and leukocyte transendothelial migration." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,2069.

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Thesis (M.S.)--University of North Carolina at Chapel Hill, 2008.
Title from electronic title page (viewed Feb. 17, 2009). "... in partial fulfillment of the requirements for the degree of Master of Science in the Department of Pharmacology." Discipline: Pharmacology; Department/School: Medicine.
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Gautam, Narinder. "Mechanisms for leukocyte-mediated adjustment of endothelial barrier function /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4794-5/.

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Grooby, Warwick L. "Studies of endothelial and leukocyte cell adhesion molecules in renal transplantation /." Title page, contents and summary only, 1996. http://web4.library.adelaide.edu.au/theses/09PH/09phg876.pdf.

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Gao, Dingcheng. "On the pathophysiological significance of CD154-CD40 mediated leukocyte endothelial cell interaction." Doctoral thesis, [S.l.] : [s.n.], 2003. http://webdoc.sub.gwdg.de/diss/2003/gao/gao.pdf.

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Ehrnfelt, Cecilia. "In vitro models of xenograft rejection : studies on leukocyte-endothelial cell interactions /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-807-6/.

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Buckley, Christopher Dominic. "Molecular analysis of IgSF-integrin interactions : their role in leukocyte endothelial adhesion." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320117.

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Ismail, Hodan. "Vascular endothelial growth factor and angiopoietin-1 regulate leukocyte adhesion to endothelial cells through the nuclear receptor Nur77." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=107844.

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Vascular endothelial growth factor (VEGF) and angiopoietin 1 (Ang-1) are critical regulators of angiogenesis. Additionally, both have been found to participate in inflammatory processes: VEGF as a pro-inflammatory and Ang-1 as an anti-inflammatory mediator. Nur77 is a member of a family of orphan receptors (NR4A) that includes Nurr1 and Nor1 and plays a role in regulating vascular inflammation; however, this has yet to be fully understood. The aim of this study was to evaluate whether Nur77 expression in endothelial cells (ECs) serves as a negative feedback mechanism designed to inhibit NFkappaB induction, dampen VEGF-induced E-selectin and VCAM1 expression and enhanced leukocyte adhesion to ECs, and mediate the suppression of EC activation induced by Ang-1 treatment.Treatment of human umbilical vein endothelial cells (HUVECs) with either VEGF or Ang-1 significantly and transiently induced Nur77 expression and enhanced PKD-dependent HDAC7 phosphorylation and mobilization from the nucleus to the cytosol. HUVECs transduced with adenoviruses expressing mutated HDAC7 or a dominant-negative PKD1 inhibited VEGF-, but not Ang-1-, induced Nur77 expression. Inhibition of PI3K and ERK1/2 resulted in the suppression of Ang-1-induced Nur77 expression whereas the inhibition of JNK resulted in significantly greater induction of Nur77 by Ang-1. NFκB binding activity and gel shift assays revealed that Nur77 inhibits VEGF-induced NFκB activity. Overexpression of Nur77 showed titre-dependent upregulation of IκBα mRNA and protein expressions that was not evident in HUVECs transduced with viruses expressing a dominant-negative form of Nur77 (Ad-dnNur77). Functionally, Nur77 was found to suppress VEGF-induced mRNA and protein expressions of the adhesion molecules E-selectin and VCAM1. Importantly, the role of Nur77 in cytokine-induced leukocyte adhesion to ECs was examined. Adherence of U937 cells to HUVECs activated by VEGF was suppressed by overexpressing Nur77 whereas the loss of Nur77 by siRNA interference resulted in augmentation of adhesion. Interestingly, Ang1 was able to dampen VEGF-induced monocyte adhesion to HUVEC monolayers. I conclude that Nur77 plays an important role in providing a negative feedback mechanism designed to attenuate VEGF-induced pro-inflammatory responses through selective inhibition of NFκB activation. Furthermore, Nur77, in part, may be vital to the Ang-1 anti-inflammatory response.
Les facteurs de croissance endothélials vasculaires (VEGF) et l'angiopoïétine 1 (Ang-1) sont de régulateurs essentiels de l'angiogénèse. En outre, tous les deux ont été découverts pour leur participation dans le processus d'inflammation: VEGF comme pro-infammatoire et Ang-1 comme médiateur anti-inflammatoire. Nur77 est un membre de la famille des récepteurs orphelins (NR4A) qui comprend Nurr1 and Nor1 et jouent un rôle dans la régulation de l'inflammation vasculaire; toutefois cela n'est pas encore totalement compris. Le but de cette étude était d'évaluer si l'expression de Nur77 dans les cellules endothéliales (ECs) sert de mécanisme de rétroaction négatif conçu pour inhiber l'induction de NFκB en réduisant l'expression de la E-selectin et de VCAM1 induite par VEGF, ainsi que l'adhésion des leucocytes aux ECs, et pour agir en médiateur de la suppression de l'activation des ECs induite par le traitement avec Ang-1. Le traitement des cellules endothéliales humaines de la veine ombilicale (HUVECs) soit avec VEGF ou Ang-1 induit de façon significative et transitoire l'expression de Nur77 et augmente la Phosphorylation de HDAC7 PKD dépendante et la mobilisation du noyau vers le cytosol. Les HUVECs transduits avec les adénovirus exprimant HDAC7 muté ou un dominant négatif PKD1 inhibent VEGF, mais pas l'expression de Nur77 induit par Ang-1. L'inhibition de la PI3K et de ERK1/2 aboutit à la suppression de l'expression de Nur77 induit par Ang-1 alors que l'inhibition de JNK résulte de façon significative en une plus grande induction de Nur77 par Ang-1. L'essai d'activité de liaison de NFκB ainsi que celui du gel de retardation révèlent que Nur77 inhibe l'activité de NFκB induit par VEGF. La surexpression de Nur77 a montré une sur-régulation dépendante de la titration de l'ARNm et de l'expression protéique de IκBα, pas évidente avec les HUVECs transduites avec les virus exprimant la forme dominante négative de Nur77 (Ad-dnNur77). J'ai trouvé que Nur77 réprimait l'ARNm et l'expression protéique de E-selectin and VCAM1 induit par VEGF. De façon importante, le rôle de Nur77 dans l'adhésion des leucocytes aux ECs induits par les cytokines a été examiné. L'adhérence des cellules U937 aux HUVECs activées par VEGF était réprimée par la surexpression de Nur77 alors que la perte de Nur77 par l'ARNsi d'interférence résulte dans une augmentation de l'adhésion. De manière intéressante, Ang-1 était capable d'amortir l'adhésion aux monocouches de HUVECs induite par VEGF. Je conclus que Nur77 joue un rôle important en fournissant un mécanisme de rétroaction négatif conçu pour atténuer la réponse pro-infammatoire induite par VEGF à travers l'inhibition sélective de l'activation de NFκB. Par ailleurs Nur77 en partie, peut être vital pour les réponses anti-inflammatoires d'Ang-1.
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Books on the topic "Leukocyte-endothelial"

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Dietmar, Vestweber, ed. The Selectins: Initiators of leukocyte endothelial adhesion. Australia: Harwood Academic Publishers, 1997.

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Collins, Tucker, ed. Leukocyte Recruitment, Endothelial Cell Adhesion Molecules, and Transcriptional Control. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1565-4.

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Tucker, Collins, ed. Leukocyte recruitment, endothelial cell adhesion molecules, and transcriptional control: Insights for drug discovery. Boston: Kluwer Academic Publishers, 2001.

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Tucker, Collins, ed. Leukocyte recruitment, endothelial cell adhesion molecules, and transcriptional control: Insights for drug discovery. Boston, Mass: Kluwer Academic Publishers, 2001.

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Tucker, Collins, ed. Leukocyte recruitment, endothelial cell adhesion molecules, and transcriptional control: Insights for drug discovery. Boston: Kluwer Academic Publishers, 2001.

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Tucker, Collins, ed. Leukocyte recruitment, endothelial cell adhesion molecules, and transcriptional control: Insights for drug discovery. Boston: Kluwer Academic Publishers, 2001.

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Cale, Alexander Ronald John. Vascular reactivity during acute rejection of canine single lung allografts: Therole of Leukocyte-endothelial cell interactions. Manchester: University of Manchester, 1996.

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Vestweber, Dietmar. Selectins: Initiators of Leukocyte Endothelial Adhesion (Advances in Vascular Biology). Harwood Academic Publishers, 1997.

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Walpola, Piyal Lasitha. The influence of shear stress on endothelial leukocyte adhesion molecule expression. 1995.

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Collins, Tucker. Leukocyte Recruitment, Endothelial Cell Adhesion Molecules, and Transcriptional Control: Insights for Drug Discovery. Springer, 2012.

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Book chapters on the topic "Leukocyte-endothelial"

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Winn, Robert K., Charles L. Rice, Nicholas B. Vedder, William J. Mileski, and John M. Harlan. "Leukocyte-Mediated Endothelial Injury." In Endothelial Cell Dysfunctions, 141–52. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4899-0721-9_8.

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Varani, James. "Leukocyte-Endothelial Cell Interactions." In Vascular Endothelium, 127–35. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3736-6_12.

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Buckley, Christopher D., David H. Adams, and David L. Simmons. "Soluble Leukocyte-Endothelial Adhesion Molecules." In Physiology of Inflammation, 285–302. New York, NY: Springer New York, 2001. http://dx.doi.org/10.1007/978-1-4614-7512-5_15.

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Etzioni, Amos. "Adhesion Molecules in Leukocyte Endothelial Interaction." In Toward Anti-Adhesion Therapy for Microbial Diseases, 151–57. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0415-9_17.

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Gonzalez, Norberto C., and John G. Wood. "Leukocyte-endothelial interactions in environmental hypoxia." In Advances in Experimental Medicine and Biology, 39–60. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4757-3401-0_5.

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Lefer, David J., and Steven P. Jones. "Leukocyte-Endothelial Interactions Following Myocardial Ischemia." In Molecular Basis for Microcirculatory Disorders, 427–38. Paris: Springer Paris, 2003. http://dx.doi.org/10.1007/978-2-8178-0761-4_22.

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Vestweber, Dietmar. "Molecular Mechanisms of Endothelial Leukocyte Association." In Vascular Endothelium, 9–20. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4899-0133-0_2.

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Redl, H., G. Schlag, and I. Marzi. "Leukocyte-Endothelial Interactions in Trauma and Sepsis." In Update in Intensive Care and Emergency Medicine, 124–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84827-8_9.

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Redl, H., G. Schlag, H. P. Dinges, R. Kneidinger, and J. Davies. "Leukocyte-Endothelial Interactions in Trauma and Sepsis." In Host Defense Dysfunction in Trauma, Shock and Sepsis, 277–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77405-8_29.

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Alexander, J. Steven, and Alireza Minagar. "Endothelial Cell-Leukocyte Interactions During CNS Inflammation." In Inflammatory Disorders of the Nervous System, 1–16. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-905-2:001.

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Conference papers on the topic "Leukocyte-endothelial"

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Bevilacqua, M. A., and M. A. Gimbrone. "LEUKOCYTE-ENDOTHELIAL INTERACTIONS: IMPLICATIONS FOR INFLAMMATION AND COAGULATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642948.

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A rapidly increasing body of data indicates that the vascular endothelium plays an active role in the development of inflammatory and thrombotic processes. Our laboratory has focused on the modulation of certain endothelial cell functions by inflammatory/immune mediators. Initially, we demonstrated that human monocyte derived interleukin-1 (hmIL-1) can act directly on cultured human endothelial cells (HEC) to increase the expression of tissue factor procoagulant activity in a time- and protein-synthesis dependent fashion (J. Exp. Med. 160:618, 1984). Increased expression of HEC tissue factor was also elicited with recombinant IL-1α (rlL-lα), rIL-1 β, and recombinant human tumor necrosis factor (rTNF), as well as with bacterial endotoxin (1 ipopolysaccharide, LPS) (Am. J. Pathol. 121:393, 1985; Proc. Natl. Acad. Sci. USA 83:4533, 1986). The kinetics of the HEC tissue factor responses to these stimuli were similar, demonstrating a rapid use rise to peak activity at ~ 4 hr, and a decline toward basal levels by 24 hr. This characteristic decline in tissue factor PCA after prolonged incubation with IL-1 or TNF was accompanied by selective endothelial hyporesponsiveness to the initially stimulating monokine. Interestingly, the effects of IL-1 and TNF were found to be additive even at apparent maximal doses of the individual monokines. We have also examined the effects of IL-1 and other mediators on HEC production of fibrinolytic components (J. Clin. Invest. 78:587, 1986). HEC monolayers which had been treated for 24 hr with IL-1 or TNF exhibited decreased tissue type plasminogen activator (tPA) and increased plasminogen activator inhibitor (PAI) as assessed in functional and immunological assays. Thus, certain inflammatory mediators such as IL-1 and TNF can act on vascular endothelial cells to induce the expression of tissue factor in a rapid and transient fashion, and to decrease the expression of fibrinolytic activity in a more prolonged fashion. In a parallel series of studies, we have demonstrated that IL-1, TNF and LPS also act on HEC to increase the adhesion of polymorphonuclear leukocytes (PMN), monocytes and the related cell lines HL-60 and U937 (J. Clin. Invest. 76:2003, 1985; Fed. Proc. 46:405A, 1987). The kinetics of this modulation of HEC adhesiveness parallel that of the change in tissue factor PCA. Recently, we have developed two monoclonal antibodies (mAb), H4/18 and H18/7, which identify a surface antigen expressed on monokine- and LPS-stimulated HEC but not on unstimulated HEC. The mediator specificity, kinetics, and protein synthesis-dependence of the expression of this antigen correlate with increased HEC adhesiveness for leukocytes. Neither mAb binds to unstimulated or stimulated PMN, HL-60 cells or dermal fibroblasts. H18/7 inhibits the adhesion of PMN (>50%) and HL-60 cells (>60%) to stimulated HEC by comparison to isotype matched control mAb; H4/18 also inhibits HL-60 adhesion but to a lesser extent. H4/18 and H18/7 immunoprecipitate the same polypeptides from biosynthetically-1abeled monokine-stimulated HEC, but not unstimulated HEC. We have designated this inducible endothelial cell surface protein, endothelial-leukocyte adhesion molecule-1 (E-LAM 1). Thus, vascular endothelium can be activated by inflammatory/immune mediators to express both prothrombotic and pro-inflammatory functions. In vivo, these endothelial responses may contribute to a variety of pathophysiologic processes.
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Gimbrone, M. A., M. P. Bevilacqua, and M. E. Wheeler. "ENDOTHELIAL-DEPENDENT MECHANISMS OF LEUKOCYTE ADHESION: ROLE OF MONOKINES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643983.

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Localized adhesion of peripheral blood leukocytes to the vessel wall is an essential component of inflammatory reactions. There is increasing experimental evidence that vascular endothelial cells play an active role in this process. Our laboratory has been especially interested in defining endothelial-dependent mechanisms of leukocyte adhesion, and the role of leukocyte products in their modulation. We have reported1 that purified natural human monocyte-derived interleukin 1 (IL-1) can act directly on cultured human endothelial cells (HEC) to dramatically increase the adhesiveness of their surfaces for human polymorphonuclear leukocytes (PMN), monocytes and the related cell lines HL-60 and U937. This effect was concentration-, time- (onset≅30 min; peak≅4h) , and protein/RNA-synthesis-requiring, and, in selective pretreatment/fixation experiments, was shown to be mediated primarily through the endothelial cell. To better define this inducible endothelial pro-adhesive mechanism, we have developed a series of murine monoclonal antibodies directed against monokine-stimulated HEC surfaces. One of these antibodies (H4/18) recognizes an endothelial cell surface structure which is induced by IL-1 (and certain other cytokines)2 in a similar fashion (kinetics, concentration - dependence, sensitivity to metabolic inhibitors) as the pro-adhesive surface change for leukocytes. H4/18 partially blocks HD-60 cell adhesion to monokine-treated HEC, and, in vivo, labels human vascular endothelium at sites of experimental delayed hypersensitivity reactions4. A second monoclonal antibody (H18/7)5 significantly blocks the adhesion of both HL-60 cells and PMN to monokine-treated HEC. Monoclonal antibodies H4/18 and H18/7 appear to recognize the same inducible surface structure as assessed by immunoprecipitation of extracts of metabolically labeled, monokine-stimulated HEC. We have designated this monokine-inducible, endothelial-leukocyte adhesion molecule "E-IAM 1". IL-1 treated HEC cultures (in contrast to sham-treated control cultures) generate a soluble leukocyte adhesion inhibitor (LAI)6,7. LAI acts on PMN to inhibit their adhesion to hyperadhesive endothelial monolayers as well as to serum-coated plastic surfaces, but does not inhibit PMN activation by chemotactic stimuli (LTB4, f-met-leu-phe). IAI appears to differentially inhibit adhesion of peripheral blood leukocytes, isolated from the same donor, to hyperadhesive HEC (PMN > monocytes; lymphocytes, no effect), and does not inhibit HL-60 cell-HEC adhesion. Endothelial production of IAI is time-dependent (peak 5-6 h.), and blocked by cycloheximide but not by aspirin. Preliminary characterization indicates that LAI is nonsedimentable (250,000 xg, 45 min), nondialyzable (>10 kD), stable to heat (80°C, 30 min) and acid (pH 2) and is precipitable by ammonium sulphate (60-80% saturation). Thus, this endothelial-derived inhibitory activity, which appears to be distinct from PGI2 or other cyclooxygenase products, blocks leukocyte adhesion without globally suppressing leukocyte function. Further characterization of the cellular and molecular mechanisms regulating the endothelial expression of E-LAM 1 and LAI should contribute to our understanding of the active role of the vascular wall in the inflammatory process.1. Bevilacqua et al. (1985); J. Clin. Invest.76:2003.2. Cotran et al. (1986); J. Exp. Med. 164:661.3. Bevilacqua et al. (1987); Fed. Proc. (in press).4. Wheeler et al. (1986); Fed. Proc. 45:1725.5. Wheeler et al. (1987); Fed. Proc. (in press).
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3

Shao, Jin-Yu, and Baoyu Liu. "Cellular Membrane Tether Retraction: Experiment and Model." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80760.

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During leukocyte rolling on the endothelium, membrane tethers can be extracted simultaneously from both leukocytes and endothelial cells because of the force imposed by the blood flow [1]. Tether extraction has been shown to stabilize leukocyte rolling by increasing the lifetime of the adhesive selectin-ligand bonds that mediate leukocyte rolling [2]. Over the past two decades, tether extraction has been studied extensively, both experimentally and theoretically. In contrast, much less is known about tether retraction.
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Lei, Xiaoxiao, Michael B. Lawrence, and Cheng Dong. "Mechanics of Cell Rolling Adhesion in Shear Flow." In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0284.

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Abstract Leukocyte rolling along endothelial cells is a critical step of leukocyte-endothelium interaction, which plays important roles in tissue inflammation and wound healing [1]. The occurrence of rolling results from the dynamic balance of hemodynamic shearing force acting on the cell and adhesive bond force between cell and endothelium, while the balance strongly depends on the leukocyte deformability [2]. The objective of this study is to elucidate the effects of (1) hydrodynamic shear stress, (2) cell deformation, and (3) surface adhesion strength on the rolling adhesion event through in vitro experiment and theoretical simulation.
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Khismatullin, Damir B., and George A. Truskey. "Three-Dimensional Computational Modeling of Leukocyte Rolling and Adhesion." In ASME 2006 2nd Joint U.S.-European Fluids Engineering Summer Meeting Collocated With the 14th International Conference on Nuclear Engineering. ASMEDC, 2006. http://dx.doi.org/10.1115/fedsm2006-98555.

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Recruitment of leukocytes into sites of acute and chronic inflammation is a vital component of the innate immune response in humans and plays an important role in cardiovascular diseases, such as ischemia-reperfusion injury and atherosclerosis. Leukocytes extravasate into the inflamed tissue through a multi-step process, which involves initial contact of a leukocyte with activated endothelium (tethering or capture), leukocyte rolling, firm adhesion, and transendothelial migration. We developed a computational fluid dynamics algorithm for fully three-dimensional transient simulations of multiphase viscoelastic problems. The algorithm was applied to model leukocyte rolling and adhesion in a parallel-plate flow chamber. In the model, the leukocyte is a viscoelastic cell with the nucleus located in the intracellular space and cylindrical microvilli distributed over the cell membrane. Leukocyte-endothelial cell interactions are mediated by cell adhesion molecules expressed on the tips of leukocyte microvilli and on endothelium. We show that the model can predict both shape changes and velocities of rolling leukocytes under physiological flow conditions. Results of this study indicate that viscosity of the cytoplasm is a critical parameter of leukocyte adhesion, affecting the cell’s ability to roll on endothelium.
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6

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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7

Kandasamy, Kathirvel, and Kaushik Parthasarathi. "Lipopolysaccharide (LPS)-Induced Leukocyte Retention In Pulmonary Microvessels: Role Of Endothelial Cytosolic Calcium." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5515.

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8

Koon, Amber N., Maria A. Kern, Lindon H. Young, Edward Iames, Robert Barsotti, and Qian Chen. "Effects of Modulating eNOS Activity on Leukocyte-Endothelial Interactions in Rat Mesenteric Postcapillary Venules." In The Twenty-Third American and the Sixth International Peptide Symposium. Prompt Scientific Publishing, 2013. http://dx.doi.org/10.17952/23aps.2013.038.

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9

Graham, Drew A., Danil V. Dobrynin, Alexander Fridman, Gary Friedman, and Alisa Morss Clyne. "A Pin-to-Hole Spark Discharge Plasma Generates Nitric Oxide and Can Be Safely Applied to an Endothelial Cell Monolayer." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206764.

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Endothelial cells line all blood vessels and regulate many homeostatic functions (e.g. platelet aggregation, vascular tone, vascular cell proliferation, leukocyte adhesion) by production of the signaling molecule nitric oxide (NO). NO bioavailability and thus endothelial cell function are compromised in many chronic disease states, including diabetes mellitus and its associated micro- and macrovascular complications (e.g. impaired wound healing and atherosclerosis, respectively) [1]. In the specific case of diabetic wound healing, application of exogenous NO to the diseased tissue may help restore critical NO-mediated processes and could positively impact healing and overall patient health [2]. We have developed a novel pin-to-hole spark discharge plasma device that generates NO and can be applied to cultured endothelial cells with minimal cell injury or death. We propose that this plasma device represents a promising novel method for topical NO application.
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Pham, Hung T., Robert Barsotti, Amber N. Koon, Brian Rueter, Lindon H. Young, and Qian Chen. "The Role of NADPH Oxidase on L-NAME-Induced Leukocyte-Endothelial Interactions in Rat Mesenteric Postcapillary Venules." In The Twenty-Third American and the Sixth International Peptide Symposium. Prompt Scientific Publishing, 2013. http://dx.doi.org/10.17952/23aps.2013.066.

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