Books on the topic 'Glycoproteins Receptors'

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1

T, Preissner Klaus, ed. Biology of vitronectins and their receptors: Proceedings of the First International Vitronectin Workshop, Rauischholzhausen Castle, Marburg, Germany, 25-28 August, 1993. Amsterdam: Excerpta Medica, 1993.

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2

Murphy, Natalie P. Coronary thrombosis and thrombolysis: The role of platelet glycoprotein IIb/IIIa. Dublin: University College Dublin, 1996.

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3

Pharand, Chantal. The use of platelet glycoprotein IIB/IIIA receptor antagonists in the management of unstable angina and non-st-elevation myocardial infarction: A critical evaluation. [Toronto?: s.n., 2000.

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4

E, Vance Dennis, and Vance Jean E, eds. Biochemistry of lipids, lipoproteins, and membranes. Amsterdam: Elsevier, 1991.

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5

Rich, Tina. Toll and Toll-Like Receptors : : An Immunologic Perspective. Springer, 2010.

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6

Rich, Tina. Toll and Toll-Like Receptors : : An Immunologic Perspective. Springer London, Limited, 2007.

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7

Preissner, Klaus T., and Sylvia Rosenblatt. Biology of Vitronectins and Their Receptors: Proceedings of the First International Vitronectin Workshop, Rauischholzhausen Castle, Marburg, Germany (International Congress Series). Elsevier Science Pub Co, 1993.

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8

Zona Pellucida Domain Proteins. John Wiley and Sons Ltd, 2016.

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9

Toll and Toll-Like Receptors:: An Immunologic Perspective (Molecular Biology Intelligence Unit). Springer, 2005.

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10

Jarvie, Keith Roger. The glycoprotein nature of dopamine D1 and D2 receptors. 1990.

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11

Michael, Lincoff A., and Topol Eric J. 1954-, eds. Platelet glycoprotein IIb/IIIa receptor inhibitors in cardiovascular disease. Totowa, N.J: Humana Press, 1999.

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12

Badimon, Lina, Felix C. Tanner, Giovanni G. Camici, and Gemma Vilahur. Pathophysiology of thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0018.

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Ischaemic heart disease and stroke are major causes of death and morbidity worldwide. Coronary and cerebrovascular events are mainly a consequence of a sudden thrombotic occlusion of the vessel lumen. Arterial thrombosis usually develops on top of a disrupted atherosclerotic plaque because of the exposure of thrombogenic material, such as collagen fibrils and tissue factor (TF), to the flowing blood. TF, either expressed by subendothelial cells, macrophage- and/or vascular smooth muscle-derived foam-cells in atherosclerotic plaques, is a key element in the initiation of thrombosis due to its ability to induce thrombin formation (a potent platelet agonist) and subsequent fibrin deposition at sites of vascular injury. Adhered platelets at the site of injury also play a crucial role in the pathophysiology of atherothrombosis. Platelet surface receptors (mainly glycoproteins) interact with vascular structures and/or Von Willebrand factor triggering platelet activation signalling events, including an increase in intracellular free Ca2+, exposure of a pro-coagulant surface, and secretion of platelet granule content. On top of this, interaction between soluble agonists and platelet G-coupled protein receptors further amplifies the platelet activation response favouring integrin alpha(IIb)beta(3) activation, an essential step for platelet aggregation. Blood-borne TF and microparticles have also been shown to contribute to thrombus formation and propagation. As thrombus evolves different circulating cells (red-blood cells and leukocytes, along with occasional undifferentiated cells) get recruited in a timely dependent manner to the growing thrombus and further entrapped by the formation of a fibrin mesh.
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13

Tanner, Jerome Edward. Analysis of Epstein-Barr virus glycoproteins GP350/220: Role of virus receptor attachment and cell entry. 1988.

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14

Hullinger, Gordon A. A gp135 cellular receptor mediates infection of caprine synovial membrane cells by the lentivirus caprine arthritis-encephalitis virus. 1993.

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15

Alexander, D. J., N. Phin, and M. Zuckerman. Influenza. Edited by I. H. Brown. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0037.

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Influenza is a highly infectious, acute illness which has affected humans and animals since ancient times. Influenza viruses form the Orthomyxoviridae family and are grouped into types A, B, and C on the basis of the antigenic nature of the internal nucleocapsid or the matrix protein. Infl uenza A viruses infect a large variety of animal species, including humans, pigs, horses, sea mammals, and birds, occasionally producing devastating pandemics in humans, such as in 1918 when it has been estimated that between 50–100 million deaths occurred worldwide.There are two important viral surface glycoproteins, the haemagglutinin (HA) and neuraminidase (NA). The HA binds to sialic acid receptors on the membrane of host cells and is the primary antigen against which a host’s antibody response is targeted. The NA cleaves the sialic acid bond attaching new viral particles to the cell membrane of host cells allowing their release. The NA is also the target of the neuraminidase inhibitor class of antiviral agents that include oseltamivir and zanamivir and newer agents such as peramivir. Both these glycoproteins are important antigens for inducing protective immunity in the host and therefore show the greatest variation.Influenza A viruses are classified into 16 antigenically distinct HA (H1–16) and 9 NA subtypes (N1–9). Although viruses of relatively few subtype combinations have been isolated from mammalian species, all subtypes, in most combinations, have been isolated from birds. Each virus possesses one HA and one NA subtype.Last century, the sudden emergence of antigenically different strains in humans, termed antigenic shift, occurred on three occasions, 1918 (H1N1), 1957 (H2N2) and 1968 (H3N2), resulting in pandemics. The frequent epidemics that occur between the pandemics are as a result of gradual antigenic change in the prevalent virus, termed antigenic drift. Epidemics throughout the world occur in the human population due to infection with influenza A viruses, such as H1N1 and H3N2 subtypes, or with influenza B virus. Phylogenetic studies have led to the suggestion that aquatic birds that show no signs of disease could be the source of many influenza A viruses in other species. The 1918 H1N1 pandemic strain is thought to have arisen as a result of spontaneous mutations within an avian H1N1 virus. However, most pandemic strains, such as the 1957 H2N2, 1968 H3N2 and 2009 pandemic H1N1, are considered to have emerged by genetic re-assortment of the segmented RNA genome of the virus, with the avian and human influenza A viruses infecting the same host.Influenza viruses do not pass readily between humans and birds but transmission between humans and other animals has been demonstrated. This has led to the suggestion that the proposed reassortment of human and avian influenza viruses takes place in an intermediate animal with subsequent infection of the human population. Pigs have been considered the leading contender for the role of intermediary because they may serve as hosts for productive infections of both avian and human viruses, and there is good evidence that they have been involved in interspecies transmission of influenza viruses; particularly the spread of H1N1 viruses to humans. Apart from public health measures related to the rapid identification of cases and isolation. The main control measures for influenza virus infections in human populations involves immunization and antiviral prophylaxis or treatment.
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16

Barros, Rodrigo José Saraiva de, Tereza Cristina de Brito Azevedo, Carla de Castro Sant’Anna, Marianne Rodrigues Fernandes, Leticia Martins Lamarão, and Rommel Mario Rodríguez Burbano. Grupos sanguíneos e anticorpos anti-eritrocitários de importância transfusional. Brazil Publishing, 2020. http://dx.doi.org/10.31012/978-65-5861-112-7.

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Immunohematology is an area dedicated to the study of the interactions of the immune system and blood cells in transfusion practice. Blood transfusion is a therapeutic technique that has been widely used since the 17th century. The transfusion medicine aims to repair the pathological needs of blood components in the living organism, be it red blood cells, plasma, platelets, clotting factors, among others. Despite being a therapeutic means, transfusion of blood components can be considered at risk because it is a biological material and due to the transfusion immunological reactions that can be caused during or after the moment of transfusion. In the surface structure of red blood cells, numerous molecules of a protein, glycoprotein or glycolipid nature are found, which are also called membrane antigens that make up structures and perform transport functions, as receptors, as adhesion, enzymatic and / or complement regulatory molecules. The formation of these antigens occurs by an approximate amount of 39 genes involved in their production, of which 282 different antigens are organized in more than 30 blood group systems. This antigenic diversity is a major cause of the formation of irregular anti-erythrocyte antibodies. Therefore, with the increase in blood transfusions in surgeries, transplants and clinical treatment of cancer and other chronic diseases, a significant increase in the occurrence of alloimmunizations in polytransfused patients began to be observed. Such biological phenomena motivated us to carry out this study and the antigenic diversity motivated us to elaborate this small compendium where we also describe the main blood groups.
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