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Published: 10 December 2022
Last updated: 29 January 2023

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1

Ricard, Cervera, Khamashta Munther A. A, and Hughes Graham R. V, eds. Antibodies to endothelial cells and vascular damage. Boca Raton, Fla: CRC Press, 1994.

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2

Kelleher, Siobhan. Signal transduction by endothelial cells: Investigation of early effects. Dublin: University College Dublin, 1998.

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3

Herrera, Esperanza Meléndez, Bryan V. Phillips-Farfán, and Gabriel Gutiérrez Ospina. Endothelial cell plasticity in the normal and injured central nervous system. Boca Raton: CRC Press/Taylor & Francis, 2015.

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4

1959-, Lewis Thomas J., and Robinson James 1958-, eds. Angiogenesis research progress. New York: Nova Science Publishers, 2008.

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5

L, Gordon J., ed. Vascular endothelium: Interactions with circulating cells. Amsterdam: Elsevier, 1991.

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6

W, Siemann Dietmar, ed. Vascular-targeted therapies in oncology. Chichester, West Sussex: J. Wiley, 2006.

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7

E, Sumpio Bauer, ed. Hemodynamic forces and vascular cell biology. Austin, Tex: R.G. Landes, 1993.

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8

Modeling tumor vasculature: Molecular, cellular, and tissue level aspects and implications. New York: Springer, 2012.

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9

Triton Biosciences-UCLA Symposium (1985 Park City, Utah). Perspectives in inflammation, neoplasia, and vascular cell biology: Proceedings of a Triton Biosciences-UCLA Symposium, held in Park City, Utah, February 2-8, 1985. Edited by Edgington Thomas S, Ross Russell, and Silverstein Samuel C. New York, N.Y: A.R. Liss, 1987.

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10

S, Edgington Thomas, Ross Russell, and Silverstein Samuel C, eds. Perspectives in inflammation, neoplasia, and vascular cell biology: Proceedings of the Triton Biosciences-UCLA Symposium, held in Park City, Utah, February 2-8, 1985. New York: Liss, 1987.

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11

Fleming, Ingrid, Brenda R. Kwak, and Merlijn J. Meens. The endothelial cell. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0006.

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The endothelium, a monolayer of cells that lines blood vessels, acts as a physical barrier between circulating blood and vascular smooth muscle cells. The purpose of this chapter is to provide a general overview on the structural heterogeneity of the endothelium. Moreover, the most important physiological functions of the vascular endothelium in blood vessels are discussed. More detailed insights into the pathogenesis of specific diseases, including atherosclerosis and hypertension, are provided in other chapters of this book.
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12

Coomber, Brenda Lynn. Quantitative ultrastructure of endothelial cells from blood-brain barrier and permeable microvessels. 1986.

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13

Greece) NATO Advanced Study Institute on Vascular Endothelium: Source and Target of Inflammatory Mediators (2000 : Crete. Vascular Endothelium: Source and Target of Inflammatory Mediators (Nato Science Series. Series I, Life and Behavioural Sciences, 330). Ios Pr Inc, 2000.

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14

Engin, Ayse Basak, and Atilla Engin. Endothelium: Molecular Aspects of Metabolic Disorders. Taylor & Francis Group, 2013.

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15

Engin, Ayse Basak, and Atilla Engin. Endothelium: Molecular Aspects of Metabolic Disorders. Taylor & Francis Group, 2013.

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16

Engin, Ayse Basak, and Atilla Engin. Endothelium: Molecular Aspects of Metabolic Disorders. Taylor & Francis Group, 2013.

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17

Engin, Ayse Basak. Endothelium: Molecular Aspects of Metabolic Disorders. Taylor & Francis Group, 2013.

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18

Banjara, Manoj, and Damir Janigro. Effects of the Ketogenic Diet on the Blood-Brain Barrier. Edited by Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0030.

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Ketone bodies (KBs) are always present in the blood, and their levels increase after high-fat diet intake, prolonged exercise, or extended fasting. Thus, one can predict effects on the brain capillary endothelium from high levels of ketones in the blood. Prolonged exposure of blood-brain barrier (BBB) endothelial cells to KBs induces expression of monocarboxylate transporters and enhances brain uptake of KBs. In addition, cell migration and expression of gap junction proteins are up-regulated by KBs. Thus, beneficial effects of the ketogenic diet may depend on increased brain uptake of KBs to match metabolic demand and repair of a disrupted BBB. As the effects of KBs on the BBB and their transport mechanisms across the BBB are better understood, it will be possible to develop alternative strategies to optimize the therapeutic benefits of KBs for brain disorders where the BBB is compromised.
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19

Herrera, Esperanza Meléndez, Gabriel Gutiérrez Ospina, and Bryan V. Phillips-Farfan. Endothelial Cell Plasticity in the Normal and Injured Central Nervous System. Taylor & Francis Group, 2015.

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20

Herrera, Esperanza Meléndez, Gabriel Gutiérrez Ospina, and Bryan V. Phillips-Farfan. Endothelial Cell Plasticity in the Normal and Injured Central Nervous System. Taylor & Francis Group, 2015.

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21

Bochaton-Piallat, Marie-Luce, Carlie J. M. de Vries, and Guillaume J. van Eys. Vascular smooth muscle cells. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0007.

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To understand the function of arteries in the regulation of blood supply throughout the body it is essential to realize that the vessel wall is composed predominantly of smooth muscle cells (SMCs) with only one single layer of luminal endothelial cells. SMCs determine the structure of arteries and are decisive in the regulation of blood flow. This review describes the reason for the large variation of SMCs throughout the vascular tree. This depends on embryonic origin and local conditions. SMCs have the unique capacity to react to these conditions by modulating their phenotype. So, in one situation SMCs may be contractile in response to blood pressure, in another situation they may be synthetic, providing compounds to increase the strength of the vascular wall by reinforcing the extracellular matrix. This phenotypic plasticity is necessary to keep arteries functional in fulfilling the metabolic demands in the various tissues of the body.
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22

The Textbook Of Angiogenesis And Lymphangiogenesis Methods And Applications. Springer, 2012.

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23

(Editor), Elga de Vries, and Alexandre Prat (Editor), eds. The Blood-Brain Barrier and Its Microenvironment: Basic Physiology to Neurological Disease. Informa Healthcare, 2005.

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24

de, Vries Elga, and Prat Alexandre 1968-, eds. The blood-brain barrier and its microenvironment: Basic physiology to neurological disease. New York: Taylor & Francis, 2005.

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25

Rubanyi, Gabor M., and Werner Risau. Morphogenesis of Endothelium (Endothelial Cell Research Series). CRC, 2000.

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26

Kovanen, Petri T., and Magnus Bäck. Valvular heart disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0015.

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The heart valves, which maintain a unidirectional cardiac blood flow, are covered by endothelial cells and structurally composed by valvular interstitial cells and extracellular matrix. Valvular heart disease can be either stenotic, causing obstruction of the valvular flow, or regurgitant, referring to a back-flow through the valve. The pathophysiological changes in valvular heart disease include, for example, lipid and inflammatory cell infiltration, calcification, neoangiogenesis, and extracellular matrix remodelling. The present chapter addresses the biology of the aortic and mitral valves, and the pathophysiology of aortic stenosis and mitral valve prolapse.
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27

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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28

Guzik, Tomasz J., and Rhian M. Touyz. Vascular pathophysiology of hypertension. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0019.

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Hypertension is a multifactorial disease, in which vascular dysfunction plays a prominent role. It occurs in over 30% of adults worldwide and an additional 30% are at high risk of developing the disease. Vascular pathology is both a cause of the disease and a key manifestation of hypertension-associated target-organ damage. It leads to clinical symptoms and is a key risk factor for cardiovascular disease. All layers of the vascular wall and the endothelium are involved in the pathogenesis of hypertension. Pathogenetic mechanisms, whereby vascular damage contributes to hypertension, are linked to increased peripheral vascular resistance. At the vascular level, processes leading to change sin peripheral resistance include hyper-contractility of vascular smooth muscle cells, endothelial dysfunction, and structural remodelling, due to aberrant vascular signalling, oxidative and inflammatory responses. Increased vascular stiffness due to vascular remodelling, adventitial fibrosis, and inflammation are key processes involved in sustained and established hypertension. These mechanisms are linked to vascular smooth muscle and fibroblast proliferation, migration, extracellular matrix remodelling, calcification, and inflammation. Apart from the key role in the pathogenesis of hypertension, hypertensive vasculopathy also predisposes to atherosclerosis, another risk factor for cardiovascular disease. This is linked to increased transmural pressure, blood flow, and shear stress alterations in hypertension, as well as endothelial dysfunction and vascular stiffness. Therefore, understanding the mechanisms and identifying potential novel treatments targeting hypertensive vasculopathy are of primary importance in vascular medicine.
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29

García-Martín, Elena, George E. Barreto, José A. G. Agúndez, Rubem C. A. Guedes, and Ramon Santos El-Bachá, eds. Cerebral endothelial and glial cells are more than bricks in the Great Wall of the brain: insights into the way the blood-brain barrier actually works (Celebrating the centenary of Goldman’s experiments). Frontiers Media SA, 2015. http://dx.doi.org/10.3389/978-2-88919-572-5.

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30

Albert, Tyler J., and Erik R. Swenson. The blood cells and blood count. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0265.

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Blood is a dynamic fluid consisting of cellular and plasma components undergoing constant regeneration and recycling. Like most physiological systems, the concentrations of these components are tightly regulated within narrow limits under normal conditions. In the critically-ill population, however, haematological abnormalities frequently occur and are largely due to non-haematological single- or multiple-organ pathology. Haematopoiesis originates from the pluripotent stem cell, which undergoes replication, proliferation, and differentiation, giving rise to cells of the erythroid, myeloid, and lymphoid series, as well as megakaryocytes, the precursors to platelets. The haemostatic system is responsible for maintaining blood fluidity and, at the same time, prevents blood loss by initiating rapid, localized, and appropriate blood clotting at sites of vascular damage. This system is complex, comprising both cellular and plasma elements, i.e. platelets, coagulation and fibrinolytic cascades, the natural intrinsic and extrinsic pathways of anticoagulation, and the vascular endothelium. A rapid, reliable, and inexpensive method of examining haematological disorders is the peripheral blood smear, which allows practitioners to assess the functional status of the bone marrow during cytopenic states. Red blood cells, which are primarily concerned with oxygen and carbon dioxide transport, have a normal lifespan of only 120 days and require constant erythropoiesis. White blood cells represent a summation of several circulating cell types, each deriving from the hematopoietic stem cell, together forming the critical components of both the innate and adaptive immune systems. Platelets are integral to haemostasis, and also aid our inflammatory and immune responses, help maintain vascular integrity, and contribute to wound healing.
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31

Goligorsky, Michael S., Julien Maizel, Radovan Vasko, May M. Rabadi, and Brian B. Ratliff. Pathophysiology of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0221.

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In the intricate maze of proposed mechanisms, modifiers, modulators, and sensitizers for acute kidney injury (AKI) and diverse causes inducing it, this chapter focuses on several common and undisputable strands which do exist.Structurally, the loss of the brush border, desquamation of tubular epithelial cells, and obstruction of the tubular lumen are commonly observed, albeit to various degrees. These morphologic hallmarks of AKI are accompanied by functional defects, most consistently reflected in the decreased glomerular filtration rate and variable degree of reduction in renal blood flow, accompanied by changes in the microcirculation. Although all renal resident cells participate in AKI, the brunt falls on the epithelial and endothelial cells, the fact that underlies the development of tubular epithelial and vascular compromise.This chapter further summarizes the involvement of several cell organelles in AKI: mitochondrial involvement in perturbed energy metabolism, lysosomal involvement in degradation of misfolded proteins and damaged organelles, and peroxisomal involvement in the regulation of oxidative stress and metabolism, all of which become defective. Common molecular pathways are engaged in cellular stress response and their roles in cell death or survival. The diverse families of nephrotoxic medications and the respective mechanisms they induce AKI are discussed. The mechanisms of action of some nephrotoxins are analysed, and also of the preventive therapies of ischaemic or pharmacologic pre-conditioning.An emerging concept of the systemic inflammatory response triggered by AKI, which can potentially aggravate the local injury or tend to facilitate the repair of the kidney, is presented. Rational therapeutic strategies should be based on these well-established pathophysiological hallmarks of AKI.
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32

Magalhaes, Eric, Angelo Polito, Andréa Polito, and Tarek Sharshar. Sepsis-Associated Encephalopathy. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0032.

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Brain dysfunction is a major complication of sepsis and is characterized by alteration of consciousness, ranging from delirium to coma and marked electroencephalographic changes. It reflects a constellation of dynamic biological mechanisms, including neurotransmitter imbalance, macro- and microcirculatory dysfunction resulting in ischaemia, endothelial activation, alteration of the blood-brain barrier impairment with passage of neurotoxic mediators, activation of microglial cells within the central nervous system, cumulatively resulting in a neuroinflammatory state. Sepsis-associated brain dysfunction is associated with increased mortality and long-term cognitive decline, whose mechanisms might include microglial activation, axonopathy, or cerebral microinfarction. There is no specific treatment, other than the management of the underlying septic source, correction of physiological and metabolic abnormalities, and limiting the use of medications with neurotoxic effects.
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33

Vascular endothelium: Mechanisms of cell signaling. Amsterdam: IOS Press, 1999.

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34

Siemann, Dietmar W. Vascular-Targeted Therapies in Oncology. Wiley & Sons, Limited, John, 2006.

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35

Wentzel, Jolanda J., Ethan M. Rowland, Peter D. Weinberg, and Robert Krams. Biomechanical theories of atherosclerosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0012.

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Atherosclerosis, the disease underlying most heart attacks and strokes, occurs predominantly at certain well-defined sites within the arterial system. Its development may therefore depend not only on systemic risk factors but also on locally varying biomechanical forces. There are three inter-related theories explaining the effect of biomechanics on atherosclerosis. In the first theory, a central role is played by lipid transport into the vessel wall, which varies as a result of mechanical forces. In the second theory, haemodynamic wall shear stress-the frictional force per unit area of endothelium arising from the movement of blood-activates signalling pathways that affect endothelial cell properties. In the third, strain-the stretch of the wall arising from changes in blood pressure-is the key biomechanical trigger. All three theories are discussed from historical, molecular, and clinical perspectives.
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36

Rubanyi, Gabor M., Victor J. Dzau, and John P. Cooke. Vascular Protection: Molecular Mechanisms, Novel Therapeutic Principles and Clinical Applications (Endothelial Cell Research). CRC, 2002.

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37

(Editor), John D. Catravas, Una S. Ryan (Editor), and Allan D. Callow (Editor), eds. Vascular Endothelium: Mechanisms of Cell Signaling (Nato a S I Series Series a, Life Sciences). IOS Press, 1999.

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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

van Hinsbergh, Victor W. M. Physiology of blood vessels. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0002.

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This chapter covers two major fields of the blood circulation: ‘distribution’ and ‘exchange’. After a short survey of the types of vessels, which form the circulation system together with the heart, the chapter describes how hydrostatic pressure derived from the heartbeat and vascular resistance determine the volume of blood that is locally delivered per time unit. The vascular resistance depends on the length of the vessel, blood viscosity, and, in particular, on the diameter of the vessel, as formulated in the Poiseuille-Hagen equation. Blood flow can be determined in vivo by different imaging modalities. A summary is provided of how smooth muscle cell contraction is regulated at the cellular level, and how neuronal, humoral, and paracrine factors affect smooth muscle contraction and thereby blood pressure and blood volume distribution among tissues. Subsequently the exchange of solutes and macromolecules over the capillary endothelium and the contribution of its surface layer, the glycocalyx, are discussed. After a description of the Starling equation for capillary exchange, new insights are summarized(in the so-called glycocalyx cleft model) that led to a new view on exchange along the capillary and on the contribution of oncotic pressure. Finally mechanisms are indicated in brief that play a role in keeping the blood volume constant, as a constant volume is a prerequisite for adequate functioning of the circulatory system.
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40

Curry, Nicola, and Raza Alikhan. Normal platelet function. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0281.

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The platelet is a small (2–4 µm in diameter), discoid, anucleate cell that circulates in the blood. In health, it plays a vital role in haemostasis, and in disease it contributes to disorders of bleeding and thrombosis. Platelets are produced from the surface of megakaryocytes in the bone marrow, under tight homeostatic control regulated by the cytokine thrombopoietin. Platelets have a lifespan of approximately 7–10 days, and usually circulate in the blood stream in a quiescent state. Intact, undamaged vessel walls help to maintain platelets in this inactive state by releasing nitric oxide, which acts both to dilate the vessel wall and to inhibit platelet adhesion, activation, and aggregation. After trauma to the blood vessel wall, platelets are activated and, acting in concert with the endothelium and coagulation factors, form a stable clot. This chapter addresses platelet structure and function, and the response of platelets to vessel injury.
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41

Jackson, Trachette L. Modeling Tumor Vasculature: Molecular, Cellular, and Tissue Level Aspects and Implications. Springer, 2014.

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42

Perspectives in inflammation, neoplasia, and vascular cell biology: Proceedings of a Triton Biosciences-UCLA Symposium, held in Park City, Utah, February ... symposia on molecular and cellular biology). A.R. Liss, 1987.

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43

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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44

Tissue Engineering of Vascular Prosthetic Grafts (Tissue Engineering Intelligence Unit). Landes Bioscience, 1999.

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45

P, Zilla P., and Greisler Howard P, eds. Tissue engineering of prosthetic vascular grafts. Austin: R.G. Landes Co., 1999.

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46

Bhopal, Raj S. Epidemic of Cardiovascular Disease and Diabetes. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198833246.001.0001.

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Coronary heart disease (CHD) and stroke, collectively cardiovascular disease (CVD), are caused by narrowing and blockage of the arteries supplying the heart and brain, respectively. In type 2 diabetes (DM2) insulin is insufficient to maintain normal blood glucose. South Asians have high susceptibility to these diseases. Drawing upon the scientific literature and discussions with 22 internationally recognized scholars, this book focuses on causal explanations and their implications for prevention and research. Genetically based hypotheses are considered together with the developmental origins of health and disease (DOHAD) family of hypotheses. The book then considers how CHD, stroke, and DM2 are closely linked to rising affluence and the accompanying changes in life-expectancy and lifestyles. The established causal factors are shown to be insufficient, though necessary, parts of a convincing explanation for the excess of DM2 and CVD in South Asians. In identifying new explanations, this book emphasizes glycation of tissues, possibly leading to arterial stiffness and microcirculatory damage. In addition to endothelial pathways to atherosclerosis an external (adventitial) one is proposed, i.e. microcirculatory damage to the network of arterioles that nourish the coronary arteries. In addition to the ectopic fat in their liver and pancreas as the cause of beta cell dysfunction leading to DM2, additional ideas are proposed, i.e. microcirculatory damage. The high risk of CVD and DM2 in urbanizing South Asians is not inevitable, innate or genetic, or acquired in early life and programmed in a fixed way. Rather, exposure to risk factors in childhood, adolescence, and most particularly in adulthood is the key. The challenge to produce focused, low cost, effective actions, underpinned by clear, simple, and accurate explanations of the causes of the phenomenon is addressed.
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