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Books on the topic 'Endothelin receptor'

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Published: 31 January 2023

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1

Barton, Matthias. Endothelin in renal physiology and disease. Basel: Karger, 2011.

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2

Mondo, John Paul Di. Isolation and sequencing of the rat endothelin-A receptor (ETA) gene. Ottawa: National Library of Canada, 1996.

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3

Pollock, David M., and Robert F. Highsmith, eds. Endothelin Receptors and Signaling Mechanisms. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-11672-2.

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4

NATO, Advanced Study Institute on Vascular Endothelium: Receptors and Transduction Mechanisms (1988 Porto Karras Chalkidikē Greece). Vascular endothelium: Receptors and transduction mechanisms. New York: Plenum Press, 1989.

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5

Boyd, Ryan. Expression and function of endothelin and its receptors in vascular adventitial fibroblasts. St. Catharines, Ont: Brock University, Faculty of Applied Health Sciences, 2007.

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6

Hunt, Jennifer Ann. Characterization of thromboxane receptors on a bovine aortic endothelial cell line. Birmingham: University of Birmingham, 1991.

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7

Inoue, Michitoshi. Regulation of coronary blood flow. London: Springer-Verlag, 1991.

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8

Warner, Timothy D. Endothelin and Its Inhibitors. Springer Berlin / Heidelberg, 2012.

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9

Warner, Timothy D. Endothelin and Its Inhibitors. Springer London, Limited, 2012.

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10

Endothelin and Its Inhibitors. Springer, 2001.

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11

Endothelin receptors: From the gene to the human. CRC Press, 1995.

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12

R, Ruffolo Robert, ed. Endothelin receptors: From the gene to the human. Boca Raton, Fla: CRC Press, 1995.

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13

Transcriptional regulation of the endothelin A receptor: Possible developmental and pathophysiological implications. Ottawa: National Library of Canada, 2000.

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14

Highsmith, Robert F. Endothelin: Molecular Biology, Physiology, and Pathology. Humana Press, 2014.

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15

F, Highsmith Robert, ed. Endothelin: Molecular biology, physiology, and pathology. Totowa, N.J: Humana Press, 1998.

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16

Highsmith, Robert F. Endothelin: Molecular Biology, Physiology, and Pathology. Humana Press, 2010.

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17

Highsmith, Robert F. Endothelin: Molecular Biology, Physiology, and Pathology. Humana Press, 2013.

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18

Pollock, D. M. Endothelin Receptors And Signaling Mechanisms (Biotechnology Intelligence Unit). Edited by D. M. Pollock. SPRINGER-VERLAG, 1998.

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19

Pollock, David M. Endothelin Receptors and Signaling Mechanisms. Springer, 2013.

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20

Highsmith, Robert F., and David M. Pollock. Endothelin Receptors and Signaling Mechanisms. Springer London, Limited, 2013.

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21

Vergnaud, Sophie, David Dobarro, and John Wort. Pulmonary vasculature. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199657742.003.0017.

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A 16-year-old girl with a diagnosis of diffuse cutaneous systemic sclerosis is referred to a specialist pulmonary hypertension centre with a history of progressive breathlessness, reduced exercise tolerance, and raised pulmonary pressures on transthoracic echocardiogram. She is found to have pulmonary arterial hypertension on right cardiac catheterization and is started on sildenafil, a phosphodiesterase-5 inhibitor, which stabilizes her condition. An endothelin receptor antagonist is added, which provides some initial symptomatic improvement. She continues to deteriorate over a period of 5 years, ultimately requiring intravenous prostanoids, the only treatment to provide a real symptomatic and haemodynamic improvement. This chapter explores the physiology and pathophysiology of pulmonary arterial hypertension, its classification, the means of investigation and diagnosis, who to refer to specialist centres, and the concepts behind current and future treatment strategies.
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22

Catravas, J. Vascular Endothelium: Receptors and Transduction Mechanisms. Springer, 2013.

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23

Catravas, J. Vascular Endothelium: Receptors and Transduction Mechanisms. Springer London, Limited, 2013.

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24

Dhaun, Neeraj, and David J. Webb. Endothelins and their antagonists in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0114_update_001.

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The endothelins (ETs) are a family of related peptides of which ET-1 is the most powerful endogenous vasoconstrictor and the predominant isoform in the cardiovascular and renal systems. The ET system has been widely implicated in both cardiovascular disease and chronic kidney disease (CKD). ET-1 contributes to the pathogenesis and maintenance of hypertension and arterial stiffness, as well endothelial dysfunction and atherosclerosis. By reversal of these effects, ET antagonists, particularly those that block ETA receptors, may reduce cardiovascular risk. In CKD patients, antagonism of the ET system may be of benefit in improving renal haemodynamics and reducing proteinuria, effects seen both in animal models and in some human studies. Data suggest a synergistic role for ET receptor antagonists with angiotensin-converting enzyme inhibitors in lowering blood pressure, reducing proteinuria, and in animal models in slowing CKD progression. However, in clinical trials, fluid retention or cardiac failure has caused concern and these agents are not yet ready for general use for risk reduction in CKD.
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25

Huang, Kui. Vascular Endothelial Growth Factor Receptors in Angiogenesis. Uppsala Universitet, 2001.

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26

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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27

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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28

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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29

McCourt, Peter A. G. Hyaluronan Receptors of Liver Endothelial Cells, Their Purification and Characterisation. Uppsala Universitet, 1999.

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30

Lars, Edvinsson, and Uddman Rolf, eds. Vascular innervation and receptor mechanisms: New perspectives. San Diego: Academic Press, 1993.

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31

Whitworth, Caroline, and Stewart Fleming. Malignant hypertension. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0216.

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Malignant hypertension (MH) is recognized clinically by elevated blood pressure together with retinal haemorrhages or exudates with or without papilloedema (grades III or IV hypertensive retinopathy); and may constitute a hypertensive emergency or crisis when complicated by evidence of end-organ damage including microangiopathic haemolysis, encephalopathy, left ventricular failure, and renal failure. Though reversible, it remains a significant cause of end-stage renal failure, and of cardiovascular and cerebrovascular morbidity and mortality in developing countries.MH can complicate pre-existing hypertension arising from diverse aetiologies, but most commonly develops from essential hypertension. The absolute level of blood pressure appears not to be critical to the development of MH, but the rate of rise of blood pressure may well be relevant in the pathogenesis. The pathogenesis of this transformation remains unclear.The pathological hallmark of MH is the presence of fibrinoid necrosis (medial vascular smooth muscle cell necrosis and fibrin deposition within the intima) involving the resistance arterioles in many organs. Fibrinoid necrosis is not specific to MH and this appearance is seen in other conditions causing a thrombotic microangiopathy such as haemolytic uraemic syndrome, scleroderma renal crisis, antiphospholipid syndrome, and acute vascular rejection post transplant. MH can both cause a thrombotic microangiopathy (TMA) but can also complicate underlying conditions associated with TMA.The pathophysiological factors that interact to generate and sustain this condition remain poorly understood. Risk factors include Afro-Caribbean race, smoking history, younger age of onset of hypertension, previous pregnancy, and untreated hypertension associated with non-compliance or cessation of antihypertensive therapy.Evidence from clinical studies and animal models point to a central role for the intrarenal renin–angiotensin system (RAS) in MH; there is good evidence for renal vasoconstriction and activation of the renal paracrine RAS potentiating MH once established; however, there may also be a role in the predisposition of MH suggested by presence of increased risk conferred by an ACE gene polymorphism in humans and polymorphisms for both ACE and AT1 receptor in an animal model of spontaneous MH. Other vasoactive mediators such as the endothelin and the inflammatory response may be important contributing to and increasing endothelial damage. There have been no randomized controlled trials to define the best treatment approach, but progressive lowering of pressures over days is considered safest unless made more urgent by critical clinical state. It seems logical to introduce ACE inhibition cautiously and early, but in view of the risk of rapid pressure lowering some recommend delay.
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32

Monaco, Claudia, and Giuseppina Caligiuri. Molecular mechanisms. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0014.

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The development of the atherosclerotic plaque relies on specific cognate interactions between ligands and receptors with the ability to regulate cell recruitment, inflammatory signalling, and the production of powerful inflammatory and bioactive lipid mediators. This chapter describes how signalling is engaged by cell-cell surface interactions when the endothelium interacts with platelets and leukocytes enhancing leukocyte recruitment during atherogenesis. It also exemplifies intracellular signalling pathways induced by the activation of innate immune receptors, the most potent activators of inflammation in physiology and disease. Differences are highlighted in innate signalling pathways in metabolic diseases such as atherosclerosis compared to canonical immunological responses. Finally, the key lipid mediators whose production can affect endothelial function, inflammation, and atherosclerosis development are summarized. This Chapter will take you through these fundamental steps in the development of the atherosclerotic plaque by summarizing very recent knowledge in the field and highlighting recent or ongoing clinical trials that may enrich our ability to target cardiovascular disease in the future.
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33

Vascular Endothelium:Receptors and Transduction Mechanisms. Springer, 1989.

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34

Alharbi, Yousef, Manish S. Patankar, and Rebecca J. Whelan. Antibody-Based Therapy for Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0006.

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With their role in connecting disease-associated antigens to the cellular immune response, antibodies hold considerable promise as therapeutic agents. This chapter discusses three classes of therapeutic antibodies that have been developed for use in ovarian cancer therapy. The first includes antibodies selected against tumor-associated antigens such as MUC16/CA125, mesothelin, epithelial cell adhesion molecule, and folate receptor α‎. Antibodies in the second class target proteins such as CTLA-4 and PD1 that act as immune response checkpoint receptors. The third class of antibodies target secreted factors that promote tumor growth: targets in this class include vascular endothelial growth factor, cytokines, and chemokines. The development of each of these is described. The chapter also discusses the complications presented by soluble antigens, which serve to limit the applicability of antigens (such as MUC16/CA125) that are both cell-surface associated and circulating and the prospects for the combination of antibody-based immunotherapy and chemotherapy.
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35

Jones, Nina. Identification and characterization of downstream signaling partners of the endothelial cell-specific receptor tyrosine kinase, Tek/Tie-2. 2000.

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36

Vasoconstrictor effect of endothelin-1 (ET-1) in human skin: The role of et[subscript]a and et[subscript]b receptors. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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37

Cimpean, Anca Maria, Andreea Adriana Jitariu, and Marius Raica. Growth Factors and Their Corresponding Receptors as Targets for Ovarian Cancer Therapy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0011.

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Ovarian cancer remains one of the most aggressive and difficult to manage malignancies regarding evaluation and therapeutic options. The high mortality persists despite extensive research in the field. Current conventional chemotherapy does not improve disease-free survival and does not decrease recurrences amongst patients. This calls for a stringent reconsideration of the drugs selection, focused on the most targeted strategies and personalization of the therapy. Targeted agents against growth factors and their corresponding receptors are already approved as first- or second-line neoadjuvant therapy with controversial results. This chapter critically discusses the role of growth factors as vascular endothelial growth factor, fibroblast growth factors, or platelet-derived growth factors and their corresponding receptors in the pathogenesis, progression, and selection of therapeutic strategies. Other growth factors, such as nerve growth factor or endocrine gland derived growth factor, seem to have a strong involvement in ovarian carcinogenesis but their actual impact is not fully understood.
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38

Phipps, Lisa M., Titi Chen, and David C. H. Harris. Radiation nephropathy. Edited by Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0091_update_001.

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Radiation nephropathy usually arises after inadvertent exposure of kidneys to radiotherapy. It may manifest as acute nephropathy as early as 6 months after exposure, or later as chronic nephropathy, hypertension, or asymptomatic proteinuria. Glomerular and peritubular endothelium and renal tubular cells are especially radiosensitive. There are no pathognomonic histological features, but renal pathology may be similar to that of haemolytic uraemic syndrome. Radiation nephropathy may be prevented by renal shielding and mitigated by radiation dose fractionation. Control of hypertension is important and angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists appear to have protective effects beyond those of blood pressure control.
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39

Karaman, Sinem, Aleksanteri Aspelund, Michael Detmar, and Kari Alitalo. The lymphatic system. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0009.

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The lymphatic vascular system is an integral component of the circulatory system; it forms a one-way conduit that transports tissue interstitial components back to the venous circulation through lymph nodes. Lymphatic vessels extend to most tissues and contribute to the regulation of interstitial fluid homeostasis, trafficking of immune cells, and absorption of dietary fats from the gut. Developmentally, lymphatic vessels originate from embryonic veins and specialized angioblasts. A number of molecules have been identified in the commitment of endothelial cells to the lymphatic lineage, and the sprouting, expansion and maturation of the lymphatic vascular tree. Importantly, the vascular endothelial growth factor (VEGF) family members VEGFC and VEGFD, together with their receptors VEGFR2 and VEGFR3 have been implicated as critical regulators of lymphangiogenesis. Lymphatic vessels are involved in several human diseases, including cancer, where they contribute to tumour metastasis, the leading cause of cancer-related deaths. Lymphatic vessels regulate immune responses against foreign pathogens by transporting leucocytes to lymph nodes, but are also in involved in the regulation of self-tolerance. Defects in the lymphatic vascular system are causal for the development of lymphoedema.
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40

Imai, Shoichi, Masatsugu Hori, and Michitoshi Inoue. Regulation of Coronary Blood Flow. Springer, 2014.

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41

1937-, Inoue Michitoshi, and International Symposium on Adenosine and Adenine Nucleotides (4th : 1990 : Yamanaka Lake, Japan), eds. Regulation of coronary blood flow. Tokyo: Springer-Verlag, 1991.

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42

Imai, Shoichi, Masatsugu Hori, Michitoshi Inoue, and Robert M. Berne. Regulation of Coronary Blood Flow. Springer, 2013.

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43

Imai, Shoichi, Masatsugu Hori, Michitoshi Inoue, and Robert M. Berne. Regulation of Coronary Blood Flow. Springer London, Limited, 2013.

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44

1937-, Kanno Morio, and Hattori Yuichi, eds. Current aspects of cellular and subcellular mechanism of drug actions. Sapporo, Japan: Hokkaido University School of Medicine, 2000.

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45

Gutiérrez, Orlando M. Fibroblast growth factor 23, Klotho, and phosphorus metabolism in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0119.

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Fibroblast growth factor 23 (FGF23) and Klotho have emerged as major hormonal regulators of phosphorus (P) and vitamin D metabolism. FGF23 is secreted by bone cells and acts in the kidneys to increase urinary P excretion and inhibit the synthesis of 1,25 dihydroxyvitamin D (1,25(OH)2D) and in the parathyroid glands to inhibit the synthesis and secretion of parathyroid hormone. Phosphorus excess stimulates FGF23 secretion, likely as an appropriate physiological adaptation to maintain normal P homeostasis by enhancing urinary P excretion and diminishing intestinal P absorption via lower 1,25(OH)2D. The FGF23 concentrations are elevated early in the course of chronic kidney disease (CKD) and may be a primary initiating factor for the development of secondary hyperparathyroidism in this setting. Klotho exists in two forms: a transmembrane form and a secreted form, each with distinct functions. The transmembrane form acts as the key co-factor needed for FGF23 to bind to and activate its cognate receptor in the kidneys and the parathyroid glands. The secreted form of Klotho has FGF23-independent effects on renal P and calcium handling, insulin sensitivity, and endothelial function. Disturbances in the expression of Klotho may play a role in the development of altered bone and mineral metabolism in early CKD. In addition, abnormal circulating concentrations of both FGF23 and Klotho have been linked to excess cardiovascular disease, suggesting that both play an important role in maintaining cardiovascular health.
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46

Karmali, Mohamed A., and Jan M. Sargeant. Verocytotoxin-producing Escherichia coli (VTEC) infections. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0008.

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Verocytotoxin (VT)-producing Escherichia coli (VTEC), also known as Shiga toxin producing E. coli (STEC), are zoonotic agents, which cause a potentially fatal illness whose clinical spectrum includes diarrhoea, haemorrhagic colitis, and the haemolytic uraemic syndrome (HUS). VTEC are of serious public health concern because of their association with large outbreaks and with HUS, which is the leading cause of acute renal failure in children. Although over 200 different OH serotypes of VTEC have been associated with human illness, the vast majority of reported outbreaks and sporadic cases of VTEC-infection in humans have been associated with serotype O157:H7.VTs constitute a family of related protein subunit exotoxins, the major ones implicated in human disease being VT1, VT2, and VT2c. Following their translocation into the circulation, VTs bind to endothelial cells of the renal glomeruli, and of other organs and tissues via a specific receptor globotriosylceramide (Gb 3), are internalized by a process of receptor-mediated endocytosis, and cause subcellular damage that results in the characteristic microangiopathic disease observed in HUS.The incubation period of VTEC-associated illness is about 3–5 days. After ingestion VTEC (especially of serotype O157:H7) multiply in the bowel and colonize the mucosa of probably the large bowel with a characteristic attaching and effacing (AE) cytopathology. Colonization is followed by the translocation of VTs into the circulation and the subsequent manifestation of disease.The majority of patients with uncomplicated VTEC infection recover fully with general supportive measures. Historically, the case-fatality rate was high for HUS. However, improvement in the treatment of renal failure and the attendant biochemical disturbances has substantially improved the outlook, although long-term sequelae may develop.Ruminants, especially cattle, are the main reservoirs of VTEC. Infection is acquired through the ingestion of contaminated food, especially under-cooked hamburger, through direct contact with animals, via contaminated water or environments, or via personto-person transmission.The occurrence of large outbreaks of food-borne VTEC-associated illness has promoted close scrutiny of this zoonoses at all levels in the chain of transmission, including the farm, abattoir, food processing, packaging and distribution plants, the wholesaler, the retailer and the consumer. While eradication of VTEC O157 at the farm may not be an option, interventions to increase animal resistance or to decrease animal exposure are being developed and validated. Hazard Analysis and Critical Control Programmes are being implemented in the processing sector and appear to be associated with temporal decreases in VTEC serotype O157 illness in humans. Education programmes targeting food handling procedures and hygiene practices are being advocated at the retail and consumer level. Continued efforts at all stages from the farm to the consumer will be necessary to reduce the risk of VTEC-associated illness in humans.
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