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Letteratura scientifica selezionata sul tema "Wound healing Physiology"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 31 gennaio 2023

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Articoli di riviste sul tema "Wound healing Physiology"

1

Strodtbeck, Frances. "Physiology of wound healing." Newborn and Infant Nursing Reviews 1, no. 1 (March 2001): 43–52. http://dx.doi.org/10.1053/nbin.2001.23176.

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2

Rhee, John S., David Hom, and Timothy Lian. "Wound Healing and Flap Physiology." Otolaryngology–Head and Neck Surgery 143, no. 5 (November 2010): 718. http://dx.doi.org/10.1016/s0194-5998(10)02297-7.

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3

Silver, I. A. "The physiology of wound healing." Journal of Wound Care 3, no. 2 (March 2, 1994): 106–9. http://dx.doi.org/10.12968/jowc.1994.3.2.106.

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4

Flanagan, M. "The physiology of wound healing." Journal of Wound Care 9, no. 6 (June 2000): 299–300. http://dx.doi.org/10.12968/jowc.2000.9.6.25994.

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5

Rhee, John S., David Hom, and Timothy Lian. "Wound Healing and Flap Physiology." Otolaryngology - Head and Neck Surgery 143, no. 5 (November 2010): 718. http://dx.doi.org/10.1016/j.otohns.2010.09.045.

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6

Young, Alistair, and Clare-Ellen McNaught. "The physiology of wound healing." Surgery (Oxford) 29, no. 10 (October 2011): 475–79. http://dx.doi.org/10.1016/j.mpsur.2011.06.011.

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7

Harper, Daniel, Alistair Young, and Clare-Ellen McNaught. "The physiology of wound healing." Surgery (Oxford) 32, no. 9 (September 2014): 445–50. http://dx.doi.org/10.1016/j.mpsur.2014.06.010.

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8

Singh, Shailendra, Alistair Young, and Clare-Ellen McNaught. "The physiology of wound healing." Surgery (Oxford) 35, no. 9 (September 2017): 473–77. http://dx.doi.org/10.1016/j.mpsur.2017.06.004.

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9

Hunt, Thomas K. "The physiology of wound healing." Annals of Emergency Medicine 17, no. 12 (December 1988): 1265–73. http://dx.doi.org/10.1016/s0196-0644(88)80351-2.

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10

Norris, Susan O’Brien, Barbara Provo, and Nancy A. Stotts. "Physiology of Wound Healing and Risk Factors that Impede the Healing Process." AACN Advanced Critical Care 1, no. 3 (November 1, 1990): 545–52. http://dx.doi.org/10.4037/15597768-1990-3010.

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Abstract (sommario):

In the critically ill patient, wound repair can be impeded by processes inherent to the illness, its treatment, and the critical care environment. This vulnerability to wound complications increases patient morbidity and mortality as well as length of stay, resource consumption, and hospital cost. The physiology of wound healing and factors that impede wound repair are discussed. Those factors commonly seen in critical illness include advanced age, diabetes mellitus, compromised immunocompetence, inadequate perfusion, and oxygenation, infection, malnutrition, obesity, and preoperative illness. Knowledge of management of the physiologic factors that affect wound healing enables the nurse to maximize tissue repair and prevent wound complications

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Tesi sul tema "Wound healing Physiology"

1

Rippon, Mark Geoffrey. "The physiology of wound healing." Thesis, Manchester Metropolitan University, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240980.

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2

Kesl, Shannon Lynn. "Metabolic Therapy for Age-Dependent Impaired Wound Healing." Scholar Commons, 2016. http://scholarcommons.usf.edu/etd/6104.

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Chronic wounds represent an under-acknowledged socioeconomic epidemic, affecting 1.8 million new patients per year and costing the US health care system upwards of $25 billion annually. This substantial cost is rapidly growing due to a disproportionate occurrence in the ever-aging population. Key features associated with age-related impairment of wound healing include limited energy and nutrient exchange, unremitting inflammations, increased reactive oxygen species (ROS), and diminished blood flow. Most chronic wound therapies target specific molecular mechanisms; however, there are often multiple mitigating factors that prevent normal wound closure. This is likely one reason most wound therapies are minimally effective. In the standard American diet, carbohydrates are broken down for fuel (glucose). While fasting, starvation, and calorie or carbohydrate restriction, beta-oxidation of stored fats in the liver produces ketone bodies (primarily acetoacetate (AcAc) and β-hydroxybutyrate (βHB) to serve as energy metabolites for extra-hepatic tissues. In addition to enhancing metabolic physiology, ketone bodies have recently been discovered to have signaling properties that are independent of their function as energy metabolites. Here we present the evidence for a novel method of inducing therapeutic ketosis via exogenous ketone supplementation to promote enhanced ischemic wound healing in young and aged Fischer 344 rats. Preliminary mechanistic studies demonstrated that exogenous ketone supplementation enhanced wound healing via increasing proliferation and migration, decreasing lactate production, and decreasing ROS production as well as affecting inflammatory cytokines and growth factors. We conclude that exogenous ketone supplementation will be an effective, cost efficient, low toxicity therapy to promote enhancement of wound healing in an aged population.

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3

Andreatta-Van, Leyen Sheila. "Experimental approaches for enhancing wound healing and inhibiting tumor growth." Case Western Reserve University School of Graduate Studies / OhioLINK, 1994. http://rave.ohiolink.edu/etdc/view?acc_num=case1061557930.

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4

Mari, Walid Omran Dr. "Extracellular Microvesicles as a Novel Biomarker for Wound Healing." Wright State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=wright1495270509788421.

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5

Menke, Nathan. "A COMPUTATIONAL BIOLOGY APPROACH TO THE ANALYSIS OF COMPLEX PHYSIOLOGY: COAGULATION, FIBRINOLYSIS, AND WOUND HEALING." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/2093.

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The birth of complexity research derives from the logical progression of advancement in the scientific field afforded by reductionist theory. We present in silico models of two complex physiological processes, wound healing and coagulation/fibrinolysis based on two common tools in the study of complex physiology: ordinary differential equations (ODE) and Agent Based Modeling (ABM). The strengths of these two approaches are well-suited in the analysis of clinical paradigms such as wound healing and coagulation. The complex interactions that characterize acute wound healing have stymied the development of effective therapeutic modalities. The use of computational models holds the promise to improve our basic approach to understanding the process. We have modified an existing ordinary differential equation model by 1) evolving from a systemic model to a local model, 2) the incorporation of fibroblast activity, and3) including the effects of tissue oxygenation. Possible therapeutic targets, such as fibroblast death rate and rate of fibroblast recruitment have been identified by computational analysis. This model is a step toward constructing an integrative systems biology model of human wound healing. The coagulation and fibrinolytic systems are complex, inter-connected biological systems with major physiological roles. We present an Agent Based Modeling and Simulation (ABMS) approach to these complex interactions. This ABMS method successfully reproduces the initiation, propagation, and termination of blood clot formation and its lysis in vitro due to the activation of either the intrinsic or extrinsic pathways. Furthermore, the ABMS was able to simulate the pharmacological effects of two clinically used anticoagulants, warfarin and heparin, as well as the physiological effects of enzyme deficiency/dysfunction, i.e., hemophilia and antithrombin III-heparin binding impairment, on the coagulation system. The results of the model compare favorably with in vitro experimental data under both physiologic and pathophysiologic conditions. Our computational systems biology approach integrates reductionist experimental data into a cohesive model that allows rapid evaluation of the effects of multiple variables. Our ODE and AMBS models offer the ability to generate non-linear responses based on known relationships among variables and in silico modeling of mechanistic biological rules on computer software, respectively. Simulations of normal and disease states as well as effects of therapeutic intervention demonstrate the potential uses of computer simulation. Specifically, models may be applied to hypothesis generation and biological advances, discovery of new diagnostic and therapeutic options, platforms to test novel therapies, and opportunities to predict adverse events during drug development. The ultimate aim of such models is creation of bedside simulators that allow personalized, individual medicine; however, a myriad of opportunities for scientific advancement are opened through in silico experimentation.

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Roach, Necrisha. "The Development of a Novel Multi-dimensional Product for Wound Healing Applications." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/2131.

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A characteristic feature of chronic wounds is a prolonged inflammatory response as well as susceptibility to infection. Studies have shown that during the inflammatory response, there is a significant increase in the levels of neutrophil-derived enzymes. The purpose of this work was to determine whether the anionic macromolecule polystyrene sulfonate (PSS) and five of its salt forms, namely PSS-calcium, PSS-chlorhexidine, PSS-doxycycline, PSS-glutathione and PSS-silver are able to inhibit the activity of three of the enzymes whose levels are elevated in chronic wounds: elastase, cathepsin G and myeloperoxidase. In addition to the enzyme inhibition study, the various formulations’ antimicrobial properties were analyzed by evaluating their ability to inhibit the growth of three common clinical isolates: Staphylococcus aureus, Pseudomonas aeruginosa and Acinetobacter baumanii. It is worthy to note that the structure of PSS makes it a very flexible platform to which other molecules can be added in order to address a variety of “targets” as well as tailor quantitative strength. The results from this project showed that purified PSS and the various salt derivatives were able to inhibit elastase and cathepsin G activity. In addition, three of the therapeutic cations attached to PSS: silver, doxycycline and chlorhexidine retained their intrinsic antimicrobial properties without having an adverse effect on healthy tissue. In summary, this study demonstrated that PSS possessed an intrinsic ability to inhibit a number of proteases and that it could also be used as a delivery vehicle for other compounds with potential therapeutic value.

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Marshall, Nicholas John. "The influence of insulin-like growth factor 1 and its analogues on fibroblasts and dermal wound healing." Title page, table of contents and synopsis only, 1998. http://web4.library.adelaide.edu.au/theses/09MD/09mdm3685.pdf.

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Includes bibliography (leaves 191-219). Examines the levels of insulin-like growth factor and the presence of IGF binding proteins in human wound fluid. Tests the potency of IGF-1 and 2 analogues in in vitro models of fibroblast activity and their effect on healing in normal and diabetic rodent wounds. Shows that IGF-1, IGF-2 and their binding proteins are present in fluid from a partial thickness cutaneous wound; that the binding proteins negatively modulate the activity of insulin-like growth factors in vitro, but that the IGFs do not necessarily show enhanced activity in vivo at the wound site if binding protein affinity is decreased. Discusses possible roles of these binding proteins in wound repair.

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8

Sinno, Hani. "Role of collagen, complement C3, and C5 on cutaneous wound healing: topical formulation, preparation, and «in-vivo» evaluation in experimental rats." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66713.

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The growing rates of problematic wounds in the population and the subsequent increase in morbidity and mortality warrant further understanding of wound healing and the development of therapeutic agents targeted to alleviate these devastating concerns. The complement system is composed of bactericidal and hemolytic proteins that increase capillary leakage and inflammatory cell migration. It allows for an anaphylactic reaction and the recruitment of inflammatory cells. Fibroblast recruitment and subsequent collagen deposition in wounds is responsible for wound healing and is regulated by inflammatory cells. However, little is known about role the complement system may have on wound healing strength. This work investigates the effects of the topical application of collagen, complements C3 and C5 in varied formulations on the paired surgical skin incision rat model. These potential findings may help further enhance the understanding of wound healing and allow for a novel therapeutic approach for the treatment of patients.<br>Les plaies aigues et chroniques sont associées à des taux de morbidité et mortalité importantes, et c'est pourquoi il est important de réaliser des études approfondies qui permettraient de développer des agents thérapeutiques qui stimulent la guérison de plaie. Le lien entre le système de complément et la guérison de plaies est encore méconnu. Le système de complément est composé de protéines bactéricides et hémolytiques qui augmentent la fuite capillaire tout en stimulant la migration de cellules. Il permet une réaction anaphylactique en recrutant des cellules inflammatoires telles que les fibroblastes suivis par la déposition de collagène au site de la plaie; ensemble celles-ci participent activement à la guérison et sont par la suite modulées par d'autres cellules inflammatoires. Cette étude analyse les effets de l'application topique de collagène, de compléments C3 et C5 sous diverses formes, au site de la plaie. Le modèle expérimental sélectionné a été réalisé par l'application d'une incision chirurgicale sur la peau dorsale du rat. Ces futurs résultats amélioreront notre compréhension de la guérison de plaies tout en permettant le développement d'une approche thérapeutique originale pour le traitement des patients atteints de plaies aigues et chroniques.

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9

Robertson, James Gray. "Insulin-like growth factors and insulin-like growth factor binding proteins in wounds /." Title page, contents and abstract only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09phr6509.pdf.

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10

Horobin, Adele Jayne. "Maggots and wound healing : the effects of Lucilia sericata larval secretions upon interactions between human dermal fibroblasts and extracellular matrix proteins." Thesis, University of Nottingham, 2005. http://eprints.nottingham.ac.uk/11516/.

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The introduction of necrophagous fly larvae (maggots) into chronic wounds for the purpose of inducing healing is an ancient practice that has recently undergone a renaissance in Western medicine. Through clinical observations, maggots are broadly recognised to debride the wound of necrotic tissue, cleanse the wound of infection and promote granulation tissue formation. Despite such recognition, little research at the biological level has been undertaken to identify the mechanisms by which maggots accomplish such feats. The dermal fibroblast is a major cellular component of granulation tissue and as such, its migration into the wound plays a vital role in new tissue growth. Fibroblast migration is directed by the composition of the extracellular matrix. Maggot secretions contain proteolytic enzymes that are active against a variety of extracellular matrix proteins which are present at the wound site. Hence, this thesis focused upon the effects of maggot secretions on human dermal fibroblast adhesion and migration in the presence of common extracellular matrix proteins. This was with the aim of elucidating the mechanisms by which maggots stimulate tissue formation within the wound and from there, developing new products that may be used to promote wound healing. Experiments showed that maggot secretions modulated fibroblast adhesion to tissue culture plastic surfaces and to surfaces coated with collagen and particularly fibronectin. Modification of the protein-coated surface by enzymes present within the secretion appeared to play a role. Fibroblast migration upon a fibronectin-coated surface was enhanced in the presence of maggot secretions. The same also occurred in the presence of a higher concentration of secretions when the cells were located within a three-dimensional environment comprising collagen gel and fibronectin. Evidence suggested that this may have been associated with enhanced matrix re-modelling.

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Libri sul tema "Wound healing Physiology"

1

Cutting, Keith F. Wound physiology & moist wound healing. Holsworthy: Medical Communications UK, 2003.

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2

Peter, Altmeyer, ed. Wound healing and skin physiology. New York: Springer-Verlag, 1994.

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3

Altmeyer, Peter, Klaus Hoffmann, Stephan el Gammal, and Jerry Hutchinson, eds. Wound Healing and Skin Physiology. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-77882-7.

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4

Comprehensive wound management. 2nd ed. Thorofare, NJ: SLACK Inc., 2010.

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5

The care of wounds: A guide for nurses. Oxford: Blackwell Scientific Publications, 1994.

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6

Dealey, Carol. The Care of Wounds. New York: John Wiley & Sons, Ltd., 2008.

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7

Percival, Steven L. Microbiology of wounds. Boca Raton, FL: CRC Press, 2010.

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8

A, Bryant Ruth, and International Association for Enterostomal Therapy., eds. Acute and chronic wounds: Nursing management. St. Louis: Mosby Year Book, 1992.

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9

Heino, Jyrki, and Veli-Matti Ka ha ri. Cell invasion. Georgetown, Tex: Landes Bioscience, 2002.

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10

Bianca, C. Towards a mathematical theory of complex biological systems. Singapore: World Scientific, 2011.

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Capitoli di libri sul tema "Wound healing Physiology"

1

Hatz, R. A., R. Niedner, W. Vanscheidt, and W. Westerhof. "Physiology of Wound Healing." In Wound Healing and Wound Management, 1–16. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-79195-6_1.

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2

Theoret, Christine. "Physiology of Wound Healing." In Equine Wound Management, 1–13. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781118999219.ch1.

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3

Horch, Raymund E., Oliver Bleiziffer, and Ulrich Kneser. "Physiology and Wound Healing." In Plastic and Reconstructive Surgery, 3–10. London: Springer London, 2010. http://dx.doi.org/10.1007/978-1-84882-513-0_1.

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4

Gupta, Ankit. "Classification of Wounds and the Physiology of Wound Healing." In Wound Healing Research, 3–53. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-2677-7_1.

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5

Mayya, Chaithra, Sumit Kharbhanda, Ashadul Haque, and Dhiraj Bhatia. "Mechanisms of Collective Cell Migration in Wound Healing: Physiology and Disease." In Wound Healing Research, 55–74. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-2677-7_2.

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6

Cohen, I. K., and J. H. Haynes. "Fetal Wound Repair." In Wound Healing and Skin Physiology, 27–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-77882-7_3.

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7

Toia, Francesca, Fernando Rosatti, and Adriana Cordova. "Wound Healing: Physiology and Pathology." In Textbook of Plastic and Reconstructive Surgery, 15–25. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-82335-1_2.

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Wadström, T., and Å. Ljungh. "Pathogenesis of Wound Infections." In Wound Healing and Skin Physiology, 393–411. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-77882-7_38.

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9

Rompel, R., and J. Petres. "Wound Healing in Oncologic Dermatosurgery." In Wound Healing and Skin Physiology, 551–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-77882-7_53.

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Abatangelo, G., P. Brun, and R. Cortivo. "Collagen Metabolism and Wound Contraction." In Wound Healing and Skin Physiology, 71–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-77882-7_7.

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Atti di convegni sul tema "Wound healing Physiology"

1

Pryse, Kenneth M., Teresa M. Abney, Guy M. Genin, and Elliot L. Elson. "Probing Cytoskeletal Mechanics Using Biochemical Inhibitors." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19451.

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Quantifying the mechanics of the cytoskeletons of living cells is important for understanding several physiologic and pathologic cellular functions, such as wound healing and cellular migration in cancer. Our laboratory develops three-dimensional tissue constructs for assaying cytoskeletal mechanics in controlled conditions. These tissue constructs consist of defined components such as chick embryo fibroblasts and reconstituted rat tail collagen; fibroblasts remodel the collagen extracellular matrix (ECM) and develop a structural environment representative of that which would exist in a natural tissue. Our protocol for quantifying the microscale mechanics of the proteins that comprise the cytoskeleton involves mechanical testing of a tissue construct first in a bath that contains nutrition medium to support the active physiologic functioning of the cells, and next in the presence of inhibitors that selectively eliminate specific cytoskeletal structures. By solving an inverse homogenization problem, the mechanical functioning of these proteins at the cellular level can be estimated. Here, we present a combination of mechanical testing and imaging results to quantify the effects of specific inhibitors on cytoskeletal and extracellular matrix form and function.

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2

Sharma, Puja, Kevin Sheets, and Amrinder S. Nain. "The Influence of Polymeric Fiber Stiffness and Alignment on Cytoplasmic Bleb Dynamics and Migration of Glioblastoma Multiforme Cells." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80923.

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Cell migration is a tightly regulated phenomenon necessary for regular physiologic processes such as wound healing, immune response, embryonic development, growth, and regeneration [1–3]. Consequences of abnormal migratory behaviors include autoimmune diseases and metastasis during cancer progression [4, 5]. Described as one of the hallmarks of cancer, metastasis is a complex multistep process, and is responsible for 90% of cancer deaths in humans. A better understanding of the process of metastasis is of paramount importance in developing efficient cancer treatment therapies and drugs [6].

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Grabowski, F. E. "RHEOLOGY AND PRIMARY HEMOSTASIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643986.

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Overview The adhesion-aggregation of platelets to a site of vessel wall injury is a quintessential blood flow phenomenon. Firstly, platelets are driven to the vicinity of the vessel wall by a form of convective diffusion in which red cells both mechanically augment the effective platelet diffusivity (Turitto et al., Ind. Eng. Chem. Fund. 11:216-223, 1972; Grabowski et al., Ind. Eng. Chem. Fund. 11:224-232, 1972) and enhance the near-wall piatelet concentration (Ti11es and Eckstein, Microvasc Res., In press, 1987). Secondly, red cells subjected to physiologic shear forces are capable of secreting sufficient adenine nucleotides to induce primary platelet aggregation without themselves undergoing frank lysis (Reimers et al, Blood 64:1200-1206, 1984). This "humoral" effect of erythrocytes is likely to contribute to primary hemostasis in a shear stress-dependent manner. Thirdly, endothelial cells are able to modulate platelet aggregation at a site of vessel injury by producing prostacyclin (and perhaps other antithrombotic substances) in a manner which increases with vessel shear rate (Grabowski et al, Blood 62:301a, 1983); production for a large range of arterial shear rates appears to be limited by plasma-borne substrate (arachidonate). This manner of production ensures a concentration of prostacyclin in the near-wall region which remains relatively independent of shear rate.Imaging primary hemostasis. In our work, epi-fluorescence videomicroscopy has allowed real time imaging of platelet adhesion-aggregation to a simulated vessel wall injury. The injury model is an endothelial cell monolayer (ECM) across which, prior to ECM exposure to flowing blood, a 6-0 sterile suture is drawn in a direction transverse to flow. Microinjuries result which measure 70 ± 15μm (Mean ± SD) in width. The fluorescent label is the TAB murine monoclonal antibody (courtesy of Dr. R.P. McEver) directed against human platelet GPIIB, together with a fluorescein-conjugated goat F(ab')2 against murine inmunoglobulin. The injured ECM's, grown to confluence on rectangular cover glasses precoated with microfibrillar collagen, comprise one wall of a flow chamber mounted on a vertical microscope stage. On microinjury sites and at shear rates of 100 to 700 sec-1, computer-enhanced video images show adherence, remodelling and growth of chains of platelet aggregates. Aligned with the flow direction, these chains have a spacing of approximately 30)im, a length similar to the average endothelial cell diameter. One may speculate that such chains provide a scaffold for wound healing insofar as they are likely rich in agents chemotactic for leukocytes and in platelet-derived growth factor.Modulatory role of endothelium. When the ECM's are pre treated with 1.0 mM FC lysine acetyl sal icy late (LA), aggregate length increases (P<0.001) up totwo-fold, outflow levels by RIA of serum thromboxane B2 increase (8 of 8 paired runs), and outflow levels of prostacyclin by RIA for 6-Keto PGFiot decrease (5 of 7 paired runs). The Table gives data for one of four similar experiments at 270 sec-1 and following five minutes of flow. These data imply that products of ECM which are inhibitable by aspirin modulate local adhesion-aggregation; their inhibition, as by vasculitis or drugs, may give rise to thrombotic states.Bleeding disorders. Aggregate length is reduced in von Willebrand's disease (4 patients), Hermansky-Pudlak syndrome (2 patients), and after 300 mg oral aspirin (Tablet 4 donors). The reduction in the first two, however, is greater (P<0.01) than that for oral aspirin. With oral aspirin, further, there is a paradoxic increase in the percent platelet coverage of the injury area. Summary. Rheology has profound effects on the rate, structure, and modulation of primary hemostasis. Many of these effects can be studied via real-time, epi-fluorescence videomicroscopy of platelet adhesion-aggregation to a site of injury to an endothelial cell monolayer exposed to flowing blood. The model described has application to the study of thrombotic and hemostatic disorders and unstable angina.

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