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Books on the topic 'Foam cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 March 2023

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1

Bottalico, Lori A. Regulation and consequences of macrophage foam cell formation. [New York]: [Columbia University], 1993.

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2

Pop-Iliev, Remon. Processing of fine-cell polypropylene foams in compounding-based rotational foam molding. Ottawa: National Library of Canada, 1999.

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3

Panno, Joseph. The cell: Exploring nature's first life-form. New York, NY: Facts on File, 2010.

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4

Panno, Joseph. The cell: Exploring nature's first life form. New York, NY: Facts on File, 2010.

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5

Bilodeau, Andre. Building your hull with the bead & cove foam system using core cell foam. [S.l.]: A. Bilodeau, 1997.

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6

J, Bereiter-Hahn, Anderson O. Roger 1937-, and Reif Wolf-Ernst, eds. Cytomechanics: The mechanical basis of cell form and structure. Berlin: Springer-Verlag, 1987.

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7

Cell wall deficient forms: Stealth pathogens. 3rd ed. Boca Raton, Fla: CRC Press, 2001.

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8

Cell wall deficient forms: Stealth pathogens. 2nd ed. Boca Raton, Fla: CRC Press, 1993.

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9

Bereiter-Hahn, J. Cytomechanics: The Mechanical Basis of Cell Form and Structure. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987.

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10

Pivar, Stuart. On the origin of form: Evolution by self-organization. Berkeley, Calif: North Atlantic Books, 2009.

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11

Cheung, Kwok Keung. Processing of fine-cell polypropylene foams in extrusion. Ottawa: National Library of Canada, 1996.

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12

Lemberg, Kathryn. Ferroptosis: A Novel Form of Cancer Cell Death Induced by the Small Molecule Erastin. [New York, N.Y.?]: [publisher not identified], 2011.

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13

Sagolla, Dom. 140 characters: A style guide for the short form. Hoboken, N.J: John Wiley & Sons, 2009.

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14

Sagolla, Dom. 140 characters: A style guide for the short form. Hoboken, N.J: John Wiley & Sons, 2009.

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15

Zwischen Beethoven und Brahms: Die Violoncello-Sonate im 19. Jahrhundert. Kassel: Bärenreiter, 2006.

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16

Cohen, Norman. Biology (Biology: Form & Function). Hodder Arnold H&S, 1991.

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17

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
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18

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
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19

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.
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20

Elger, Marlies, and Wilhelm Kriz. The renal glomerulus. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0043.

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The glomerulus performs its functions with three major cell types. Endothelial cells and visceral epithelial cells (podocytes) lie on the inside and outside of the glomerular basement membrane, and together these three structures form the glomerular filtration barrier. Mesangial cells sit in the axial region. Pathologies of all these regions and cell types can be identified. Parietal epithelial cells lining Bowman’s capsule participate in crescent formation, and at the tubular pole some of these cells seem to represent a stem cell population for tubular cells and podocytes. The extraglomerular mesangium and juxtaglomerular apparatus complete the description of the glomerular corpuscle. The structure of these elements, and how they relate to function, are illustrated in detail.
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21

Read, Nick D. Fungal cell structure and organization. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0004.

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Human pathogenic fungi produce three basic ‘cell’ types: hyphae, yeast cells, and spores. The organization and subcellular structure of these different cell types and their modes of growth and formation are reviewed. Growth and form is the consequence of how new cell surface is formed. This is generated by the delivery of vesicles to the surface which provides new membrane and the enzymes for cell wall synthesis. To generate these various cell types, the pathway of vesicle secretion to the surface has to be carefully regulated. These vesicles have to be transported through the cell by the cytoskeleton, and in filamentous cells these vesicles accumulate at a supply centre called the Spitzenkörper before docking and fusion with the hyphal apex. Ultimately, membrane is also endocytosed and recycled behind actively expanding regions of the fungal surface. These various processes are described and particular emphasis is given to the structural and organizational features of fungal cells that play roles in their pathogenesis and virulence.
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22

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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23

Lutgens, Esther, Marie-Luce Bochaton-Piallat, and Christian Weber. Atherosclerosis: cellular mechanisms. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0013.

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Atherosclerosis is a lipid-driven, chronic inflammatory disease of the large and middle-sized arteries that affects every human being and slowly progresses with age. The disease is characterized by the presence of atherosclerotic plaques consisting of lipids, (immune) cells, and debris that form in the arterial intima. Plaques develop at predisposed regions characterized by disturbed blood flow dynamics, such as curvatures and branch points. In the past decades, experimental and patient studies have revealed the role of the different cell-types of the innate and adaptive immune system, and of non-immune cells such as platelets, endothelial, and vascular smooth muscle cells, in its pathogenesis. This chapter highlights the roles of these individual cell types in atherogenesis and explains their modes of communication using chemokines, cytokines, and co-stimulatory molecules.
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24

Lopez-Sanchez, Carmen, Virginio Garcia-Lopez, Gary C. Schoenwolf, and Virginio Garcia-Martinez. From epiblast to mesoderm: elaboration of a fate map for cardiovascular progenitors. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0003.

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The origin and migration of cardiovascular progenitors have been identified using multiple cell fate mapping techniques monitoring marked epiblast cells through time at carefully defined stages of early gastrulation. These studies have revealed that ordered groups of cells from the epiblast move into the anterior region of the primitive streak, and then migrate anterior laterally to define the first heart field in the mesodermal layer. Subsequently, the right and left components of the first heart field fuse into a single straight heart at the embryonic midline. Additional cells derived from the second heart field are added to the cardiac tube and contribute to further heart development. Heterotopic and heterochronic transplantation studies have revealed that cardiac precursor cells are plastic and do not form a specific subpopulation of the cardiac mesoderm. Specification of the heart fields occurs after ingression of precardiac cells through the primitive streak.
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25

Bereiter-Hahn, J., and O. R. Anderson. Cytomechanics: The Mechanical Basis of Cell Form and Structure. Springer, 1987.

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26

Smorygo, Oleg. Open Cell Foams As Substrates for the Design of Structured Catalysts, Solid Oxide Fuel Cells and Supported Asymmetric Membranes. Nova Science Publishers, Incorporated, 2020.

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27

Smorygo, Oleg, Vladislav Sadykov, and Ljudmila Bobrova. Open Cell Foams as Substrates for the Design of Structured Catalysts, Solid Oxide Fuel Cells and Supported Asymmetric Membranes. Nova Science Publishers, Incorporated, 2016.

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28

Cell Biology Laboratory Manual: Form, Function and Diversity Cell Life. Kendall Hunt Publishing Company, 2022.

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29

Mattman, Lida H. Cell Wall Deficient Forms: Stealth Pathogens. Taylor & Francis Group, 2000.

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30

Mattman, Lida H. Cell Wall Deficient Forms: Stealth Pathogens. Taylor & Francis Group, 2000.

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31

Mattman, Lida H. Cell Wall Deficient Forms: Stealth Pathogens, Fourth Edition. CRC, 2009.

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32

Mattman, Lida H. Cell Wall Deficient Forms: Stealth Pathogens. Taylor & Francis Group, 2009.

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33

Gopinath, Sumanth. Ringtone Dialectic: Economy and Cultural Form. MIT Press, 2013.

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34

Gopinath, Sumanth. Ringtone Dialectic: Economy and Cultural Form. MIT Press, 2013.

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35

Pleniceanu, Oren, and Benjamin Dekel. Kidney stem cells. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0344.

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End-stage renal failure is a major cause of death with currently only dialysis and transplantation available as therapeutic options, each with its own limitations and drawbacks. To allow regenerative medicine-based kidney replacement therapies and due to the fact that neither haematopoietic stem cells nor mesenchymal stem cells, the most accessible human stem cells, can be used to derive genuine nephron progenitors, much attention has been given to finding adult renal stem cells. Several candidates for this have been described, but their true identity as stem or progenitor cells and their potential use in therapy has not yet been shown. However, the analysis of embryonic renal stem cells, specifically stem/progenitor cells that are induced into the nephrogenic pathway to form nephrons until the 34th week of gestation, has been much more conclusive.
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36

Isaacs, John D., and Philip M. Brown. Rituximab and abatacept. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0083.

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Two biologics that target cells have been licensed to treat rheumatoid arthritis (RA). Rituximab is a chimeric monoclonal antibody (mAb) against CD20 that depletes B cells; abatacept is a soluble form of CTLA-4 that blocks costimulation and interferes with T-cell function. Both drugs alleviate signs and symptoms of RA and have been shown to retard radiographic progression. Rituximab is licensed for use following failure of tumour necrosis factor (TNF) blockade whereas abatacept's licence permits it use as a first-line biologic. In the United Kingdom, however, the National Institute for Health and Clinical Excellence (NICE) restricts the use of abatacept to patients who develop adverse effects with rituximab or in whom rituximab is contraindicated. As with other biologics, the use of either drug is associated with an enhanced risk of serious infections; additionally, rituximab in particular can cause infusion reactions, requiring prophylaxis. By targeting cells that are central to RA pathogenesis, these drugs provide important additional therapeutic options for patients with RA.
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37

Levitan, Irwin B., and Leonard K. Kaczmarek. The Neuron. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199773893.001.0001.

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The Fourth Edition of The Neuron provides a comprehensive first course in the cell and molecular biology of nerve cells. It begins with properties of the many newly discovered ion channels that have emerged through mapping of the genome and which shape the way a single neuron generates varied patterns of electrical activity. It also covers the molecular mechanisms that convert electrical activity into the secretion of neurotransmitter hormones at synaptic junctions between neurons. It discusses the biochemical pathways that are linked to the action of neurotransmitters and that can alter the cellular properties of neurons or sensory cells that transduce information from the outside world into the electrical code used by neurons, and the rapidly expanding knowledge of the molecular factors that induce an undifferentiated cell to become a neuron, and then guide it to form appropriate synaptic connections with its partners. Also addressed is the role of ongoing experience and activity in shaping these connections, and the mechanisms thought to underlie the phenomena of learning and memory.
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38

Kühn, Wolfgang, and Gerd Walz. The molecular basis of ciliopathies and cyst formation. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0303.

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Abnormalities of the cilium, termed ‘ciliopathies’, are the prime suspect in the pathogenesis of renal cyst formation because the gene products of cystic disease-causing genes localize to them, or near them. However, we only partially understand how cilia maintain the geometry of kidney tubules, and how abnormal cilia lead to renal cysts, and the diverse range of diseases attributed to them. Some non-cystic diseases share pathology of the same structures. Although still incompletely understood, cilia appear to orient cells in response to extracellular cues to maintain the overall geometry of a tissue, thereby intersecting with the planar cell polarity (PCP) pathway and the actin cytoskeleton. The PCP pathway controls two morphogenetic programmes, oriented cell division (OCD) and convergent extension (CE) through cell intercalation that both seem to play a critical role in cyst formation. The two-hit theory of cystogenesis, by which loss of the second normal allele causes tubular epithelial cells to form kidney cysts, has been largely borne out. Additional hits and influences may better explain the rate of cyst formation and inter-individual differences in disease progression. Ciliary defects appear to converge on overlapping signalling modules, including mammalian target of rapamycin and cAMP pathways, which can be targeted to treat human cystic kidney disease irrespective of the underlying gene mutation.
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39

Clarke, Noel W. Metastatic disease in prostate cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0068.

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Metastases are the predominant cause of morbidity and death from prostate cancer (CaP). The tendency for cells to migrate from the primary site, enter the vascular/lymphatic circulation, and implant/grow at secondary sites is the principal discriminator of aggressive form indolent disease. But this process is poorly understood. Cells enter the circulation in increasing number as the disease progresses, impinging on endothelial surfaces, particularly in red bone marrow where they bind and transmigrate, forming early cell colonies. This requires chemo-attractants and nutrients enabling cellular survival. Established metastases thrive independently, disrupting local tissue, as characterized by progressive replacement of red bone marrow and disruption of skeletal architecture. Bone disruption includes massive overstimulation of both osteoblasts and osteoclasts, inducing synchronous over-production of abnormal bone and gross osteolysis.
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40

Dettman, Robert, Juan Antonio Guadix, Elena Cano, Rita Carmona, and Ramón Muñoz-Chápuli. The multiple functions of the proepicardial/epicardial cell lineage in heart development. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0020.

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The epicardium is the outer cell layer of the vertebrate heart. In recent years, both the embryonic and adult epicardium have revealed unsuspected peculiarities and functions, which are essential for cardiac development. In this chapter we review the current literature on the epicardium, and describe its evolutionary origin, the mechanisms leading to the induction of its extracardiac progenitor tissue, the proepicardium, and the way in which the proepicardium is transferred to the heart to form the epicardium. We also describe the epicardial epithelial–mesenchymal transition from which mesenchymal cells originate, and the developmental fate of these cells, which contribute to the vascular, interstitial, valvular, and adipose tissue. Finally, we review the molecular interactions established between the epicardium and the myocardium, which are key for myocardial development and can also play a role in cardiac homeostasis. This chapter highlights how the epicardium has become a major protagonist in cardiac biology.
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41

Pitzalis, Costantino, Frances Humby, and Michael P. Seed. Synovial pathology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0052.

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Synovial pathology is seen in a variety of disease states, including rheumatoid arthritis (RA), osteoarthritis (OA), psoriatic arthritis, and systemic lupus erythmatosus (SLE). This chapter highlights recent advances that characterize the cellular composition of these tissues according to surface markers and chemokine and cytokine expression, and describes synovial functional status and response to therapeutics. In RA, after initiation, pannus migrates over and under cartilage, and into subchondral bone, in a destructive process. Cartilage-pannus junction (CPJ) is characterized as invasive or 'quiescent' or 'indistinct'. Invasive CPJ can comprise macrophages, fibroblast-like synoviocytes (FLS), mast cells, and/or neutrophils. CPJ activity is related to the state of activation of the overlying subintima. Subintimal inflammation can be graded to a variety of degrees (I–IV) according to established criteria and is illustrated. In some RA synovia, cellular aggregates organize into ectopic lymphoid structures (ELS) through the expression of lymphorganogenic signals, to exhibit T- or B-cell zones accompanied by dendritic cells and lymphangiogenesis. ELS synthesize rheumatoid factor (RF) and anti-citrullinated peptide antibodies (ACAP), considered to be indicative of aggressive disease. The selective cellular expression of macrophage and dendritic cell chemokines and cytokines such as TNF, GMCSF, TGFβ‎, IL-1, IL-6, IL-23, and chemokines can be seen in synovia, to form a regulated and cooperative environment that sustains the cellular organization and pathological function. Important to this process are FLS and CD68+ macrophages. CD68 expression correlates with disease severity and can be useful as a surrogate marker of disease modifying activity of therapeutics, such as anti-TNF and anti-B-cell biologics.
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42

Kidder. Technology and Applications of Closed Cell Foams Seminar Notes. Technomic Pub Co, 1991.

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43

Cohen, Norman. Cell Structure, Function and Metabolism ; Biology, Form and Function. CBS Publishers & Distributors, 1997.

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44

Cytomechanics: The Mechanical Basis of Cell Form and Structure. Springer, 2011.

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45

The ringtone dialectic: Economy and cultural form. The MIT Press, 2013.

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46

Ronco, Pierre M. Kidney involvement in plasma cell dyscrasias. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0150.

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Monoclonal proliferations of the B-cell lineage are characterized by abnormal and uncontrolled expansion of a single clone of B cells at different maturation stages, with a variable degree of differentiation to immunoglobulin-secreting plasma cells. Therefore, they are usually associated with the production and secretion in blood of a monoclonal immunoglobulin and/or a fragment thereof which may become deposited in tissues. These deposits can take the form of casts (in myeloma cast nephropathy), crystals (in myeloma-associated Fanconi syndrome), fibrils (in light-chain and exceptional heavy-chain amyloidosis), or granular precipitates (in monoclonal immunoglobulin deposition disease). They may disrupt organ structure and function, inducing life-threatening complications. All of the pathologic entities related to immunoglobulin deposition principally involve the kidney, which is not only explained by the high levels of renal plasma flow and glomerular filtration rate, but also by the sieving properties of the glomerular capillary wall and by the prominent role of the renal tubule in LC handling and catabolism.The different renal (and other) manifestations are related to the unique physicochemical characteristics of each paraprotein or immunoglobulin fragment, and the rate of their production.
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47

Hanahan, Donald J. A Guide to Phospholipid Chemistry. Oxford University Press, 1997. http://dx.doi.org/10.1093/oso/9780195079814.001.0001.

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This book provides a concise introduction to phospholipid chemistry and is intended for a broad audience of biologists, biochemists, and graduate students. Developed as part of a graduate course on lipids, this book also serves as a reference for laboratory investigators on signal transduction and biological membranes. The first part of the text is devoted to an orientation to the chemical nature of lipids in general, how they are thought to be associated in the cell, and the methodology by which the cellular lipids (including the phospholipids) can be recovered from cells and subjected to an initial identification. Subsequent chapters characterize the choline-containing phospholipids, including the sphingolipids, the non-choline containing phospholipids, and finally, the so-called minor phospholipids. The latter compounds, which act as agonists or lipid chemical mediators on cells, form a vanguard of a new category of biologically active substances and have set the study of cellular phospholipids on a new and exiting course. Most importantly, this book provides a basis for further inquiry on these complicated molecules, showing that although the compounds are unique, with care and understanding, they can be studied with ease
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48

Crawshaw, Anjali. Sarcoidosis and other granulomatous lung disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0138.

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Sarcoidosis is a multisystem disorder characterized by the formation of non-caseating granulomas in many tissues. A granuloma is an organized aggregate of immune cells; it forms in response to an antigenic stimulus. It contains abnormal macrophages (epithelioid histiocytes, which often fuse to form multinucleated giant cells), lymphocytes, neutrophils, eosinophils, fibroblasts, and collagen.
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49

Lee, Chang-Dong Patrick. Extrusion processing of low-bulk density, microcellular, open-cell thermoplastic foams. 2006.

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50

Jacobson, Dean. Microbial Life: An Illustrated Guide To Single Cell Diversity Form, And Function. Cambridge University Press, 2008.

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